The Scientific Debate Blog

Excellent report on the cause of "heart disease."

2009-02-11T16:35:00.000-08:00

I quoted this great report on my old site, but now the page is gone, so I thought I should post it here. The process that is described doesn't just "clog the arteries," but also can cause all kinds of other "chronic diseases."

QUOTE:

Chemist unlocks mysteries of cholesterol, heart disease
Contact Susan Griffith, 216-368-1004 or s...@po.cwru.edu

Graffiti on a building's wall can be a nuisance, but the kind sticking
to proteins in the blood can be used as a new indicator for
cardiovascular disease.

"It is like chemical fingerprints," said CWRU chemist Robert Salomon.

Research on the oxidation of low density lipoproteins (LDL), the so
called "bad cholesterol," led to the discovery by Salomon, professor
of chemistry, of isolevuglandins and other toxic oxidized lipids that
form this graffiti on proteins.

Pure samples of isolevuglandins and other oxidized lipids prepared
synthetically in Salomon's research provide doctors at the Cleveland
Clinic (John Crabb, Stanley Hazen, Henry Hoff, Joe Hollyfield and
Eugene Podrez), with valuable tools and information for studies of
heart disease, macular degenerative disorders and other diseases
brought on by oxidative damage of lipids.

He credits the research link between CWRU and the Clinic as making the
connection between the chemistry lab and biological processes.

The clinical groups suspected the involvement of oxidized lipids in
pathological processes they were studying, he said, but the amounts of
these lipids in biological specimens were so minute that progress was
stymied until methods were developed for making virtually unlimited
amounts of pure oxidized lipids in the chemical laboratory.

The National Institutes of Health recognized Salomon's ground-breaking
research with a new four-year, $1.4 million research grant for the
study, "Preprostaglandin Endoperoxides." The grant continues 23 years
of NIH support and expands upon research that has resulted in patents
on detecting a variety of these "fingerprints" of lipid oxidation that
can be used to read the "graffiti" on oxidatively damaged proteins in
the blood.

Through the development of antibodies that recognize the modified
proteins, the researchers can measure the accumulation of them in
human blood that may occur over days, weeks or even months.

The quantity of the modified proteins correlates with cardiovascular
disease, Salomon said.

While many people have high levels of LDL, only a small fraction of
them will develop heart disease. Salomon found that the "graffiti"
resulting from oxidized lipids sticking to proteins is a better
indicator of cardiovascular disease than the classical risk factors,
high LDL or total cholesterol levels in the blood.

Salomon also found that some people have an allergic reaction to the
"graffiti" because their immune system responds to the altered
proteins as if they were alien invaders.

Preprostaglandin endoperoxides are unstable intermediates, produced
throughout the body, from which hormone-like oxidized lipids are
formed to promote blood clotting or thinning, depending upon the needs
of the organism. Other endoperoxide-derived oxidized lipids produce
pain and inflammation. The medicinal actions of aspirin and other
nonsteroidal antiinflammatory drugs such as Celebrex, result from
their ability to block the enzyme responsible for generating the
endoperoxides.

"We stumbled onto a non enzymatic process that transforms
endoperoxides into toxic oxidized lipids, levuglandins, that stick to
proteins and DNA," Salomon said.

Similar endoperoxides are produced by nonenzymatic oxidation of lipids
caused by free radicals. Salomon realized that when these
endoperoxides are transformed into isolevuglandins they become "very
reactive materials that act like a magnet that sticks to everything,
including the protein in LDL particles."

Macrophage cells, described as the garbage trucks of the blood, try to
carry away oxidatively damaged LDL. When macrophages get gummed up
with oxidized lipids, they "become bloated with partially digested
lipoprotein and globules of cholesterol" and form "foam cells,"
Salomon said.

Eventually foam cells develop into the atherosclerotic plaque found in
cardiovascular disease.

"Macrophages are supposed to clean up oxidatively damaged LDL but are
covered with these toxic oxidized lipids that bring the whole process
to a grinding halt," Salomon said.

Isolevuglandins "spoil" the protein, according to Salomon, who added
that antioxidants, like vitamin E, help protect the body against this
bad chemistry. When the antioxidants fail, the damage from free
radical oxidation occurs.

Over the past decade, Salomon's research has expanded to other
diseases such as macular degenerative diseases that result in
blindness and involve "brain lipids" that contain an omega-3 fatty
acid that is abundant in fish oil. Brain lipids are very rare in the
body, but are found in nerve cells and in the photoreceptor rod cells
of the eye. Salomon and Clinic researchers suspected that the energy
from light on the receptors might promote oxidation and damage.
Through mass spectroscopy studies, they have begun to see protein
modifications that are similar to those in heart disease.

Salomon's discoveries started with pure chemistry.

"It became apparent that this chemistry was significant to human
health," he said. "For years, I was in the mind frame that anything
biological was magical, and that the chemistry that occurs in test
tubes had little relevance to the chemistry that occurs in biological
processes. "Slowly over the past decade, I have begun to realize that
chemistry is part of the problem and part of the solution. Biology
must adapt to the chemistry inherent in the molecules we're made of,"
he added. UNQUOTE.

Note the point made: "When macrophages get gummed up
with oxidized lipids..."
This cannot happen if you ate a diet rich in saturated fatty acids and
very low in unsaturated fatty acids (assuming you don't consume
cholesterol that is already oxidized). Cholesterol can be oxidized by
in vivo lipid peroxidation, and that cannot occur with saturated fatty
acids. In a sense, this is as simple as "2+2=4," yet our great
"experts" are advising the opposite !

Let's take a look at a new study that can be misleading.

2008-11-12T21:28:00.000-08:00

Here's the abstract:

Controversy exists over how much linoleic acid (LA) should be consumed in a healthy diet. Some claim that high LA intake promotes inflammation through accumulation of tissue arachidonic acid (AA) and subsequent production of pro-inflammatory lipid mediators. Here the author reviews the current available evidence from human studies that address this issue. The data indicate that high LA in the diet or circulation is not associated with higher in vivo or ex vivo pro-inflammatory responses. Surprisingly, several studies showed that those individuals consuming the highest level of LA had the lowest inflammatory status. Recent findings suggest that LA and AA are involved in both pro- and anti-inflammatory signaling pathways. Thus, within the ranges of intake that are achievable for most human populations, the evidence do not support reducing LA intake below current consumption levels.

Title: Too much linoleic acid promotes inflammation-doesn't it?

Source: Prostaglandins Leukot Essent Fatty Acids. 2008 Nov 4. [Epub ahead of print].

Author: Fritsche KL.

Perhaps the biggest "problem" here is that the author appears unaware of a couple of pieces of crucial evidence from the professional scientific literature. One Asian study found that vegetarians had less oxidized LDL than meat eaters, despite consumed more LA. Another study found that the incidence of certain cancers (now considered due to "chronic inflammation") increased significantly once one reached a certain level of LA consumption, but consuming more than that amount did not result in even more cancers. In other words, there is a threshold amount for LA consumption and certain cancers. Why might this be the case?

First of all, if you eat a certain amount of LA, your body will replace the natural Mead acid (if you were born with it in your cells - it depends upon your mother's diet) with AA, and then "chronic inflammation" is possible, even if only minor stressors are present. Again, above that amount and you are not going to incorporate more AA. The author doesn't tell us how many calories were being consumed. It could be that those with higher LA intake also consumed less calories. They could also have consumed more antioxidant-rich foods, and less cooked meat, etc. There is also no mention of people who consume hardly any LA, such as myself, and the author doesn't even explain why this is the case. Basically, what we see in this study is someone who has not considered that multiple factors might be at work. Instead, it's the same old "nutritional science" game, which is to create abstract categories, then do "epidemiological" studies (originally designed for infectious diseases, not dietary studies) that only control for one or more of these categories. Instead, I've suggested for years now that studies be done on actual diets that people are consuming now. By doing so, investigators can then "work backwards" and determine what is healthy and what is not. Of course, they should have studied the scientific literature (including biochemical) that appears to be relevant, such as:

J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.

"...Intake of total and saturated fat from meat was associated with statistically significant increases in pancreatic cancer risk but that from dairy products was not. CONCLUSION: Red and processed meat intakes were associated with an increased risk of pancreatic cancer. Fat and saturated fat are not likely to contribute to the underlying carcinogenic mechanism because the findings for fat from meat and dairy products differed. Carcinogenic substances related to meat preparation methods might be responsible for the positive association."

Because they have not used my type of approach, what the public sees, especially now with almost all adults having internet access, are all kinds of contradictory "studies." Even in the study directly above, the phrase "saturated fat" is used, which is sometimes used in a misleading way. The authors should have said "saturated fatty acids" (the actual molecules) because "saturated fat" is yet another potentially misleading abstract concept. For example, lard is classified as a "saturated fat" (and is unhealthy, generally-speaking), but is only about 40% saturated fatty acids. It also contains quite a bit of LA, as well as cholesterol, which can get oxidized during cooking. Coconut oil is about 92% saturated fatty acids and is a healthy food item (so long as it's not going rancid), as the best "natural" nutritional study of al time demonstrates (that is, the documented good health of many millions of Asian people consuming diets rich in coconut products).

As I said, if "nutritional scientists" would not ignore this kind of evidence, which is undeniable and direct, unlike their "epidemiological" studies of abstract categories, they would realize that classifying both lard and coconut oil as "saturated fats" makes no sense at all, and that dietary saturated fatty acids are not likely to be unhealthy (since there is no unhealthy biochemical mechanism that they are involved in, unlike LA and AA). This unfortunate situation illustrates how "science" can go terribly wrong, leading to dangerous advice being given to the general public. And now that you have this information, you can confront various "experts" yourself, and you will likely find that they are not willing to talk to you at all or else their responses don't make sense or don't address the issue. One "expert" told me he didn't have time to learn the basic biochemistry involved and could not speak to the point I was raising, which concerned oxidized cholesterol. Many people ask me how such a situation could have occurred, but as a historian I realize that it's too complex to reduce to a simplistic explanation, one that would require a major investigation in its own right.

Is eating "meat" unhealthy or dangerous?

2008-11-12T13:03:00.000-08:00

This is a good question because the apparent answer must include the problems with "nutritional science" (and science in general) that are misleading many people today. Below is a post of mine from another site which address this question:

The "meat" issue is very interesting, because it demonstrates a huge problem with "nutritional science" today. Even if we use the phrase "red meat," as many "experts" now do, that is still very misleading, because the question everyone wants answered is, "is this food item healthy or is it not?" Abstract categories which have no scientific integrity (such as "meat" or "red meat") dominate a great deal of "expert advice," yet there is more than enough evidence now to avoid such language, and instead connect diet with biochemical evidence in a direct way.

I'll provide an example. I eat small amounts of gelatin each day, but I never eat "meat," or do I? Who is to say, and if they do say, what does it mean, scientifically? Instead, the biochemical evidence is clear and the semantics can be avoided; HCAs are generated in dangerous amounts when "meat" is cooked with the usual oils (rich in polyunsaturated fatty acids). Mary Enig has suggested freezing "meat" for two weeks or more, then eating it raw. The question I have is, why do I need "meat?" I know I need a certain amount of high-quality protein, but do I need meat? I consume small amounts of nutritional yeast and gelatin each day, along with a lot of cheese, and that seems to replace anything that "meat" supplies.

If this combination was not a sufficient replacement, I surely would not have recovered from my wasting disorder (from less than 100 pounds to the mid 130s now), as well as the severe osteoporosis and other problems I had several years ago. Thus, I avoid HCAs, lipid peroxidation, oxidized cholesterol, and excess iron, among other potentially unhealthy things, without "giving anything up." I have to admit that my thinking is largely "risk reward ratio," which isn't that far from the "first do no harm" part of the Hippocratic Oath (as far as I can tell). Now I'll be the first to admit that small amounts of high-quality raw "red meat" (frozen 2 weeks or more) now and is not likely to cause problems, but it's expensive, I don't know if it's really high-quality (I have to take the word of the "health food store" people), and I don't know how to prepare it. Moreover, I don't want to develop a taste for something I don't like now and isn't doing anything to maintain my health.

Here's a study that few Americans hear about, even with all the time devoted to "health and science" issues in the news these days:

Mutat Res. 2002 Sep 30;506-507:9-20. "Comments on the history and importance of aromatic and heterocyclic amines in public health." Weisburger JH.

"The carcinogenic risk of aromatic amines in humans was first discovered when a physician related the occurrence of urinary bladder cancer to the occupation of his patients. They were employed in the dyestuff industry, chronically exposed to large amounts of intermediate arylamines… Epidemiological data suggest that meat eaters may have a higher risk of breast and colon cancer. HCAs induced cancer in rats in these organs and also in the prostate and the pancreas. In addition, there is some evidence that they affect the vascular system... The amounts of HCAs in cooked foods are small, but other components in diet such as omega-6-polyunsaturated oils have powerful promoting effects in target organs of HCAs..."

Pictures from the old MSN site.

2008-11-11T15:54:00.001-08:00

There were only two. This is a description of the first:

This was pictured in CNN's special TV show entitled, "America's Killer Diet." It shows how in the early 1960s soybean oil consumption in the USA began to increase significantly, and continued to do so up to the present. This makes clear my point about people having arachidonic acid in their cells now, whereas prior to about 1960, this would not have been the case for the overwhelming majority of Americans. One the bottom left, the year is 1909. Middle bottom is 1954, Bottom right appears to be 1999. Note that there was no canola oil being consumed until the 1980s, and that has also risen in a similar way since its introduction, which means the situations is even worse that the chart indicates. Note that this chart is just for the four fat sources listed. Butter consumption, for example, has decreased (at least relative to calories consumed).

[IMG]http://i237.photobucket.com/albums/ff196/Backgammon1/Oil_Consumption_Chart.jpg[/IMG]

And this is the description of the second:

I created this chart from the one at the Canola Council of Canada's website, and it seems to be a good indication of how canola oil consumption has risen since the 1980s in many nations (Canada is or was the biggest producer of canola). Of course, you can go to your local food store and read ingredients lists to see how much canola oil (and rapeseed, which is a "cousin" of canola) is in the food you eat these days. The numbers on the left are to be multiplied by 10,000 tons. The internet source of the Council's chart is: http://www.canola-council.org/manual/GMO/gmo4.htm This chart shows the general trend, and it's not clear (to me) exactly what year is represented by the end of the line. Again, this appears to be a good graphic representation of the general trend, and is not intended (by me) to be considered beyond this gross conception.

[IMG]http://i237.photobucket.com/albums/ff196/Backgammon1/Canola_Oil_Production.jpg[/IMG]

44 th (last) page of the old MSN site.

2008-11-11T15:50:00.001-08:00

The EFA Claim Was Refuted Long Ago

I read the following statement in the Wikipedia.org entry on "essential fatty acids:"

QUOTE: ...Biologist Ray Peat has pointed out flaws in the studies purportedly showing the need for n-3 and n-6 fats. He notes that so-called EFA deficiencies have sometimes been reversed by adding B vitamins or a fat-free liver extract to the diet. In his view, 'the optional dietary level of the "essential fatty acids" might be close to zero, if other dietary factors were also optimized...' UNQUOTE.

This is not a complicated matter. Either these molecules are necessary to the life of a full-grown, non=pregnant adult human or they are not. I saw my great grandparents live to ages 100 and 96 without any source of omega 3s (except for whatever tiny amounts they might get in the small portion of meat they ate, for example - they didn't eat oily fish at all), so I know this is a nonsensical claim, but "experts" cite studies involving rats (from what one can tell by the wikipedia article), such as:

Burr, G.O., Burr, M.M. and Miller, E. (1930). "On the nature and role of the fatty acids essential in nutrition" (PDF). J. Biol. Chem. 86 (587). Retrieved on 2007-01-17.

The problem is that rats are not people, the needs of periods of growth should not be compared to fully-grown adults, who don't want to grow any more, and the complete knowledge of vitamins did not exist in1930. Fortunately, a group of scientists did what they were supposed to do (at M.I.T.), and tried to directly verify or refute the Burr hypothesis/claim of 1930. This is what they found in the mid 1940s:

QUOTE: ...fed a pyridoxine-deficient diet, rats develop a scaliness of the paws and tails which is hardly distinguishable from the syndrome which develops from a deficiency in "essential" fatty acids. Others have demonstrated that pyridoxine is necessary for the formation of fat from protein. From this we have reasoned that there may be an interrelationship between pyridoxine and "essential" fatty acids.

We have demonstrated that this deficiency condition can be cured by feeding pyridoxine but that it is not affected by feeding linoleic acid. The effects of pyridoxine have been confirmed in a repeat experiment. The evidence indicates that pyridoxine deficiency not only decreases the appetite of rats but also the efficiency of food utilization... UNQUOTE.

Source: http://www.gwu.edu/~nsarchiv/radiation/dir/mstreet/commeet/meet4/brief4.gfr/tab_e/br4e1c.txt

So why are our "experts" not telling us about the M.I.T. results? If they are ignorant of these results, how can they call themselves "experts?" If they know about these results and are remaining silent purposefully, they are guilty of academic dishonesty, at the very least. If I try to edit the wikipedia entry and provide this information, what will happen? It's one thing to argue "interpretation" of experimental results, but this was a direct, undeniable, total refutation of the 1930 Burr experiment, so if this information is not included, what reason could the wikipedia entry have to exist in the first place? Is it there to make people feel comfortable about destroying our oceans to eat more "essential omega 3s?" I'm not suggesting there is any sort of "grand conspiracy." In general, people (including the "experts") are so concerned with obtaining "truth" quickly, have such a "herd mentality," and are so resistant to ideas that contradict what they think they "know," that it only takes a "little push" (supplied here by Burr) to get things moving in the wrong direction. Once that happens, self-interested parties (such as those who want to sell refined, highly-unsaturated oils to the masses) show up to "cash in."

Those of you who haven't read about arachidonic acid on this site yet may be saying to yourselves, "yes, I've come across these kinds of things before on the internet, and even if you are correct, why should I care?"

As I tell people, understanding the implications of this may save you a whole lot of suffering and provide you with a few more decades of life. The causes of death today are quite different from those before the middle of the twentieth century (in the USA, at least). Before circa 1950, most Americans ate a diet that led to a polyunsaturated fatty acid (PUFA) called the Mead acid being incorporated into their cells. You need PUFAs in your cells, because they are used for clotting and the inflammatory process, among other things. However, if you eat a diet rich in the typical dietary "essential fatty acids," your body will displace the Mead acid with another one, called arachidonic acid (AA).

AA is released from cells just as Mead acid is, when there is a major stressor. However, AA is much more biochemically acid than the Mead acid, so inflammation can be more intense if you have AA in your cells. What is even worse (for most people) is that AA, because of its extreme biochemical reactivity, is also released when there are minor stressors, unlike the Mead acid. Inflammation can become chronic much more easily (with AA in your cells), and and chronic inflammation is the cause of most "chronic disease" in nations like the USA. On this site, you will find plenty of evidence which demonstrates that if you follow the disease process back to its source, chronic inflammation, and by definition, having AA in your cells, is the underlying or "root" cause. If this isn't a lot more important than other claims you've read about it, I suggest you use the forums here and post about what you've found that seems more crucial to know.

Lastly, I'll mention my own experiments (on myself) with "essential fatty acid deficiency." For more than a few years, starting in 2001, I refrained from eating any food with more than trace amounts of omega 3 or omega 6 PUFAs. I witnessed some interesting changed in my body. I seemed to breathe with greater ease, I haven't had a cold since then (when I used to get at least 2 colds per year), and when I got cut the inflammation only lasted hours, not days (as used to be the case). I also had a terrible case of rosacea, which didn't go away until I also started to eat more high-quality protein and some gelatin, so it's hard to say exactly what was causing that condition. I was raised on a diet rich in corn oil, and I had several inflammatory conditions which are based upon having AA in one's cells (chalazions and keloids).

However, I also noticed that I seemed to need to drink a bit more, and I occasionally had small dry spots on my face. On the other hand, my hair didn't get "greasy," and I was able to go nearly two weeks without washing my hair, whereas I used to wash my hair every day before going "EFAD." As I began to examine "junk food" more closely, about two years ago, I noticed that it probably wasn't too unhealthy, so long as it was low in unsaturated fatty acids and cholesterol (because the cholesterol can get oxidized during processing). I began to eat some baked good that had a fat content that was a bit more than 50% saturated (paying no mind to trans fatty acids one way or the other and had little or no cholesterol.

Adding small amounts of this kind of food item led to an end to the dry spots, but my hair usually began to get greasy in 5 to 7 days. This is consistent with the M.I.T. findings and suggests that foods with more than trace amounts of unsaturated fatty acids that are not PUFAs (meaning monounsaturated fatty acids) may prevent the mild skin conditions that many of today's "experts" argue are signs of horrible ill health to come. Here is the M.I.T. finding mentioned above: QUOTE: ...The animals on the fat-free diet developed a very mild scaliness of the feet and tails. Since, in a later experiment, this condition was prevented by feeding additional amounts of the various vitamins in the supplement, it is considered possible that olive oil or elaidin in the diet exerts a vitamin-sparing action... UNQUOTE. Note that you can also find this statement in the Encyclopedia Britannica Book of the Year, 1948 in the biochemistry section (page 121): "Pyridoxine [a B vitamin] was found to relieve the deficiency state resulting from the absence of dietary fat, and to cause the deposition of linoleic [the most common omega 6 PUFA in diets] as well as di- and tetraenoic acids in the tissues of rats on fat-free diets… This contradicts the idea that linoleic acid cannot be synthesized by by rat tissues..."

43 rd page of the old MSN site.

2008-11-11T15:49:00.001-08:00

Okay, so when is this diet going to kill me?

You’ve probably heard various “experts” tell you to “avoid saturated fat,” “cut down on your salt intake,” “replace sugar-rich foods with fiber-rich complex carbohydrates,” “be sure to consume the recommended amounts of essential fatty acids,” etc. But what if you do the exact opposite of all these suggestions? Shouldn’t something very bad happen to you fairly quickly? We all know that when a non-expert is correct if he or she tells you not to jump into an active volcano if you value your life. Certain undeniable things will happen to your body if you do. One could use lab rats and create a volcano like contraption to study the sequence of events, but most people are not interested in the molecular-level detail – they just want to be alive and in reasonably good physical condition. Thus, turning back to eating a supposedly terribly unhealthy diet, if one can eat a diet this is theoretically horrible (according to present nutritional dogma), what would the “experts” say to someone who decided to consume such foods? Obviously, nobody would be able to predict exactly how long one could live on this diet, but there would have to be general guidelines, or else their claims to be presenting “science” would not be valid. For example, with the “essential fatty acid” claim, one is supposed to experience “deficiency symptoms” within a month’s time, according to most nutrition books that talk about this subject in detail.

In my case, I decided to adopt this supposedly terribly unhealthy diet in 2001, and then continued to “waste away,” down to under 100 pounds (at 5’9” tall and usually around 130 pounds), before I discovered just how deficient I was in stomach acid. Then I began to “recover,” though it took me nearly another year to realize that my protein consumption was too low. After eat more good quality protein (along with some other “adjustments,” such as taking the citrate forms of calcium and magnesium instead of the oxide forms), my various “diseases” (such as severe osteoporosis) began to improve greatly. And here I am, six years later, still eating a diet “deficient” in “essential fatty acids,” yet rich in saturated fatty acids, cholesterol, salt, and whole milk dairy products. Moreover, I avoid “heart-healthy” oils, such as olive and canola, but eat coconut products (the fat in coconut is about 92% saturated), and my “fiber” intake is very limited. I don’t eat any food that has more than perhaps the tiniest trace amounts of omega 3 PUFAs. My fruit and vegetable consumption would be considered low, compared to what “experts” advise.

Thus, the obvious question is, how can these “experts” be correct if someone who is at death’s door adopts what appears to be the unhealthiest diet possible, and then recovers from all these terrible “diseases” and appears to be quite well 6 years later? It’s one thing to say something like, “well, our advice is based upon statistical correlations and we can only tell you if you are raising you risk for a certain disease,” but it’s another thing to expect people to believe that your claims are accurate when someone in terrible health adapts the “worst” diet possible, even for a healthy person, then recovers and appears fine, six years later. Either the diet is really “bad,” and the results speak for themselves, or else the “risk” must be so low (even if there is one, which I dispute, of course) as to be laughable. They may know how to ignore the scientific method and still keep their jobs, spewing out their dangerous advice as they go, but when this advice violates basic common sense, just about anyone can see that these Emperors are strutting nude fools.

On the other hand, I would like to see what happens to a person who consumes a typical amount of fat, but just about all in the form of canola oil (with some fish oil supplementation that is considered "optimal"). One researcher decided to go on a diet very rich in omega 3s from animal products and discovered that when markers for oxidative stress were measured, they were incredibly high (source: Sinclair, H., Prog. Lipid Res. 25: 667-72, "History of EFA & their prostanoids: some personal reminiscences."). This brings up an interesting point about many researchers today; they don't seem to care about previous research, even if on-point experim nts were conducted with conclusive results. Instead, they rely upon "markers" that are based upon assumptions, some of which have been refuted by older, on-point experiments! Perhaps they simply don't know about the older studies, though there seems to be an attitude that only recent research is worth considering, as if the universe that existed a few decades or so ago is different than the one we live in now. Obviously, this is a very unscientific view. The "essential fatty acid" experiements may be the best example of this problem. In 1948, rats fed a totally fat-free diet were fine, yet decades later, experiments were conducted that sought "markers" of "essential fatty acid deficiency," such as having Mead acid in one's cells. It didn't matter if these animals lived longer and healthier lives; the mere fact that they had Mead acid in their cells was enough for the researchers to pronounce that a serious "deficiency" in "essential fatty acids" existed, and that the animals were "diseased," making it seem as if the animals had serious medical problems, which could occur in something like vitamin C deficiency ("scurvy"). Again, this makes no sense on any level, and is clearly an unscientific attitude.

Here is another example of an unscientific attitude held by scientists (I like to call it a scientific "shell game"):

QUOTE: ...the researchers say women should not make too much of these results, which are based on reports of what women said they ate over many years -- not a rigorous, scientific experiment where specific dietary factors could be studied in isolation... UNQUOTE.

What they don't tell you is that most studies that they cite when giving the general public dietary advice are just like this one. The other kind of study that is very common involves getting some healthy college students and giving them two different diets for several weeks, measuring various "markers" at points considered most revealing. However, the diets are usually both unhealthy. For instance, one diet might be rich in safflower or corn oil, while the other has less of this oil, with a fish oil supplement added so that the overall fat intake is the same. I agree that over the course of a few weeks or so, the markers will appear "better" most of the time on the fish oil supplemented diet, due to the affect on AA metabolization. This does not mean that either diet is good for long-term health, however. Thus, these experiments start subjectively, that is, they choose which diets to give the volunteers, and in the example I mentioned, there is no reason to refrain from providing other diets, such as my current diet. There are other misleading points made by the researchers in this report, so I suggest you read it in its entirety. It can be found at: http://www.newsday.com/news/nationworld/wire/sns-ap-diet-ice-cream-pregnancy,0,367279.story

Biologist Ray Peat recently wrote an essay about how some scientists are basically deciding beforehand what they want their experiments to suggest:

QUOTE: ...The study's lead author, Eva Lee, quoted by a university publicist, said "We found that progesterone plays a role in the development of breast cancer by encouraging the proliferation of mammary cells that carry a breast cancer gene." But they didn't measure the amount of progesterone present in the animals. They didn't "find" anything at all about progesterone. The "anti-progesterone" drug they used has been used for many years to treat uterine, ovarian, and breast cancers, in some cases with progesterone, to intensify its effects, and its protective effects are very likely the result of its antiestrogenic and anti-cortisol effects, both of which are well established, and relevant. In some cases, it acts like progesterone, only more strongly.

"Other more specific progesterone blockers are under development," Lee notes. And the article in Science magazine looks like nothing more than the first advertisement for one that her husband, Wen-Hwa Lee, has designed.

According to publicists at the University of California, Irvine, "Lee plans to focus his research on developing new compounds that will disrupt end-stage cancer cells. The goal is a small molecule that, when injected into the blood stream, will act as something of a biological cruise missile to target, shock and awe the cancerous cells." "In this research, he will make valuable use of a breast cancer model developed by his wife." "She developed the model, and I will develop the molecule," Lee says. "We can use this model to test a new drug and how it works in combination with old drugs."

"Previously we blamed everything," Lee says of his eye cancer discovery. "We blamed electricity, we blamed too much sausage - but in this case it's clear: It's the gene's fault."

The things that these people know, demonstrated by previous publications, but that they don't say in the Science article, are very revealing. The retinoblastoma gene (and its protein product), a specialty of Wen-Hwa Lee, is widely known to be a factor in breast cancer, and to be responsive to progesterone, RU486, and p21. Its links to ubiquitin, the hormone receptors, proteasomes, and the BRCA gene are well known, but previously they were seen as linking estrogen to cell proliferation, and progesterone to the inhibition of cellular proliferation.

By organizing their claims around the idea that RU486 is acting as an antiprogesterone, rather than as a progesterone synergist in opposing estrogen, Eva Lee's team has misused words to argue that it is progesterone, rather than estrogen, that causes breast cancer. Of the many relevant issues that their publication ignores, the absence of measurements of the actual estrogen and progesterone in the animals' serum most strongly suggests that the project was not designed for proper scientific purposes... UNQUOTE.

Source: http://raypeat.com/articles/articles/ru486.shtml

Lastly, I'll mention that a close relative who is also male and a few years younger than I am. He eats a diet that is different than mine in the following ways: 1. High polyunsaturated to saturated fatty acid ratio, whereas my diet is high in SFAs relative to PUFAs. 2. He eats a lot of cooked meat, and most likely a lot more oxidized cholesterol. I do consume small amounts of gelatin (which is almost all protein, with a little calcium), and if I heat up dairy, it's on low temperature (though I usually don't heat it at all). When I eat eggs, I only boil them. Otherwise, I am "vegetarian." 3. He does not eat any nutritional yeast, whereas I eat very small amounts with each meal. 4. He most likely eats quite a bit more calories than I do. 5. He has no interest in supplementing his diet with minerals, whereas I take small amounts of certain ones each day.

How is his health different than mine?

1. He had his gallbladder removed several years ago, after a couple of years of terrible pain, whereas I never had this problem. 2. He has high blood pressure, whereas mine is on the low end of "normal." 3. On his blood tests, his triglycerides have been very high at times, whereas mine have always been in the normal range. 4. He is about 5'10" tall and 215 pounds (and looks "inflamed"), whereas I am 5'9" tall and about 135 pounds. 5. He had "walking pneumonia" for a couple of months, is often ill, and often takes antibiotics, whereas I haven't been ill for at least a couple of years now, and have only taken antibiotics a few times in my adult life (I'm in my early 40s now).

42 nd page of the old MSN site.

2008-11-11T15:48:00.000-08:00

A unified "AIDS" hypothsis without "HIV." Part II.

Whatever “HIV/AIDS” is now (apologists have refused repeatedly to provide a hypothesis for it), one point is crucial; the way it is presented to the general public makes it an impossibility to “cure.” That is, there will never be a way to demonstrate scientifically (down to the molecular level) how a few “retroviral” particles cause an “HIV infected” woman to die of cervical cancer, for example. Instead, there will likely be more “models” presented (such as David Ho’s impossible scenario about how the “virus” destroys the T cells in question) that are little more than a child’s fanciful wishes. Thus, funding for “HIV experts” will continue, as will profits for pharmaceutical companies that produce “medicine” designed to “fight HIV.” What’s interesting, sociologically, is that this is how many “conspiracy theories” likely start out, that is, in retrospect, it appears to nicely fit together to help a few people at the expense of millions, and so some conclude that the few who benefit greatly planned it all out from the beginning. My sense is that the appeal of the “germ theory” for those in charge of the “biomedical establishment” came to dovetail with what major pharmaceutical companies had to offer, and politicians wanted to be able to reassure an anxious public. The irony, of course, is that a sense of certainty was bought at a very high price, because almost all resources have been devoted to various aspects of the ludicrous “HIV/AIDS” notion, which is now impossible to cure due to the way it is perceived.

A recent report makes the same point about "IBS" that I'm making for "HIV/AIDS:" QUOTE: Irritable bowel syndrome (IBS) is a common gastrointestinal disorder in the developed world. It is characterized by altered bowel function, abdominal discomfort, and pain. However, there are few effective treatments for IBS, in part because the molecular mechanisms underlying the disease symptoms have not been well defined. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2007/02/070215181503.htmp

In any case, what I am interested in doing involves trying to understand what the molecules in question are doing and what can be done to restore normal physiology and biochemistry. Most “HIV experts,” of course, think that they need to devise a way to “kill the germs,” not realizing that germs are almost always a problem due to conditions, and not because of some inherently malevolent quality. And they are basically repeating the many of the same mistakes made in the “war on cancer,” particularly in terms of using highly toxic “medicines” or “therapies,” which will often result in killing the patient anyway (though he or she may live a few more months). After teaching the scientific method to college students for many years, and after researching “HIV/AIDS” and related issues for several years, it is obvious to me that controlled experiments should be conducted in which those said to be “HIV infected” change their lifestyles so that they are subject to very little stress (especially oxidative), rather than taking very toxic “medicines” aimed at destroying particles that are just effects of the stress that led to the “positive” “HIV” test in the first place. Instead, such people are sometimes told to avoid “doing drugs” that may lead them to becoming “uninhibited,” leading to “unprotected sex” and exposure to a “deadly retrovirus.” When they “test positive for HIV” or “develop AIDS,” the sex is blamed rather than the drugs (as there is almost always one episode of “unprotected sex” that has occurred), even though the drugs many young people use generate a lot of oxidative stress, particularly in the context of being “overloaded” with arachidonic acid. Since we can all probably agree that such an experiment will not be undertaken any time soon, one must rely upon the evidence that now exists, and fortunately, as the studies I cited in Part I demonstrate, there are many studies that are highly suggestive of one underlying mechanism, though with several “co-factors” that can enhance this mechanism. Moroever, as I have seen in the nutrition field, even if the right experiments were conducted, those in charge could simply dismiss them for some reason, and most of the "mainstream media" seem all too willing to just assume that whatever this small number of people claims is correct, for whatever reason.

One interesting point about the “HIV/AIDS” story is that it “makes sense” to most people (in terms of their “germ theory” preconceptions), and most can’t imagine that the claim (s) is based upon indirect and non-specific “markers” that correlate to some degree with what is conceived as the clinical syndrome, “AIDS,” though this syndrome (basically, a list of symptoms, some of which are considered “diseases”) has changed over time, for reasons that make little sense to me. I encountered a very similar situation when I began my research in the nutrition field, and was disappointed to see the same kinds of mistakes made in a field that I thought would be more scientifically rigorous. As with “HIV/AIDS,” the nutritional “story” is easier for almost everyone to think that they understand compared to trying to think about what is actually occurring biochemistry. The incoherent nature of the nutritional story is not problematic, as nutritionists themselves don’t seem to realize how silly some of their claims and organizing principles are, and so the “average” person just “goes along with the program,” no matter how unsatisfactory the results. What’s even more disappointing is how some biochemists actually “step aside” and accept nutritional claims that violate a basic understanding of biochemistry. An example of this can be found in a book like "The Cookbook Decoder" (1981), written by chemistry professor Arthur E. Grosser. In this book, the chemist tells people not to be "haunted by morbid thoughts of sagging stomachs or fatty deposits clogging our arteries..." in the context of making a sauce, because corn starch can be used, presumably instead of something like cream (page 141). Though it may not have been clear that only oxidized cholesterol was dangerous when this book was published in 1981, it is obvious that this chemistry professor simply assumed that whatever the nutritionists say about the health benefits (or hazards) of certain foods is accurate. Instead, biochemists should take every opportunity to point out that when nutritionists advise people to do things like “be sure to use heart-healthy unsaturated fats” they are actually telling people to expose themselves to incredibly toxic molecules (in terms of the way most Westerners prepare their food).

Getting back to "AIDS;" while, as the Perth Group argue, potent oxidative stress (probably much more problematic in cells containing arachidonic acid) can cause the T cell dysfunction/Th1 to Th2 shift that leads to the "opportunistic infections," and probably some of the other "AIDS"-related disorders, there is the "heart disease" model as well. Applying this to "AIDS," the following sequence of events likely occurs in many who have "progressed top AIDS:" a great deal of oxidized molecules are present, which can be due to a number of things, and then lymphadenopathy often occurs. The "inflammation" that accompanies having too many oxidized molecules in the body can then cause the T cell dysfunction and Th1/Th2 shift. Below are some studies that are supportive of this possibility:

1. Eur J Immunol. 2003 Aug;33(8):2178-85.

Title: Oxidative-stress-induced T lymphocyte hyporesponsiveness is caused by structural modification rather than proteasomal degradation of crucial TCR signaling molecules.

Cemerski S, van Meerwijk JP, Romagnoli P.

Tolerance and Autoimmunity section, INSERM U563, Toulouse, France.

QUOTE: In several human pathologies (e.g. cancer, rheumatoid arthritis, AIDS and leprosy) oxidative stress induces T cell hyporesponsiveness... UNQUOTE.

QUOTE: ...deficient allergen-specific Treg cell responses have been associated with a number of allergic and autoimmune disorders. Tolerization to allergens and autoantigens is associated with augmentation of Treg cell numbers and suppressive function... UNQUOTE.

Source: Journal of allergy and clinical immunology, 2005, vol. 116, n^o5, pp. 949-959 [11 page(s) (article)] (121 ref.).

On the web: http://cat.inist.fr/?aModele=afficheN&cpsidt=17266844

QUOTE: Microparticles are membrane-derived vesicles that are released from cells during activation or cell death. These particles can serve as mediators of intercellular cross-talk and induce a variety of cellular responses. Previous studies have shown that macrophages undergo apoptosis after phagocytosing microparticles. Here, we have addressed the hypothesis that microparticles trigger this process via lipid pathways. In these experiments, microparticles induced apoptosis in primary macrophage cells or cell lines (RAW 264.7 or U937) with up to a 5-fold increase... To evaluate further signaling pathways induced by microparticles, the extracellular signal regulated kinase (ERK-) 1 was investigated. This kinase plays a role in activating phospholipases A2 which cleaves membrane phospholipids into arachidonic acid; microparticles have been suggested to be a preferred substrate for phospholipases A2. As shown in our experiments, microparticles strongly increased the amount of phosphorylated ERK1/2 in RAW 264.7 macrophages in a time-dependent manner, peaking 15 min after co-incubation. Addition of PD98059, a specific inhibitor of ERK1, prevented the increase in apoptosis of RAW 264.7 macrophages. Together, these data suggest that microparticles perturb lipid homeostasis of macrophages and thereby induce apoptosis. These results emphasize the importance of biolipids in the cellular cross-talk of immune cells. Based on the fact that in clinical situations with excessive cell death such as malignancies, autoimmune diseases and following chemotherapies high levels of circulating microparticles might modulate phagocytosing cells, a suppression of the immune response might occur due to loss of macrophages. UNQUOTE.

TITLE: The role of membrane lipids in the induction of macrophage apoptosis by microparticles.

SOURCE: Apoptosis. 2006 Dec 26.

On the internet: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17191114&query_hl=2&itool=pubmed_docsum

4. QUOTE FROM THE ABSTRACT: C57B16 mice were fed for 6 weeks on a low-fat diet or on high-fat diets containing coconut oil (rich in saturated fatty acids), safflower oil [rich in n-6 polyunsaturated fatty acids (PUFAs)], or fish oil (rich in n-3 PUFAs) as the main fat sources. The fatty acid composition of the spleen lymphocytes was influenced by that of the diet fed... The ratio of production of Th1- to Th2-type cytokines (determined as the IFN-gamma/IL-4 ratio) was lower for lymphocytes from mice fed the safflower oil or fish oil diets... It is concluded that saturated fatty acids have minimal effects on cytokine production. In contrast, PUFAs act to inhibit production of Th1-type cytokines with little effect on Th2-type cytokines; n-3 PUFAs are particularly potent. The effects of fatty acids on cytokine production appear to be exerted at the level of gene expression. UNQUOTE.

Source: J Leukoc Biol. 2001 Mar;69(3):449-57. "Dietary fatty acids influence the production of Th1- but not Th2-type cytokines," by Wallace, FA, et al.

On the internet: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11261793

5. TITLE: Programmed Cell Death Protects Against Infections.

QUOTE: ...For more than hundred years it was known that neutrophil granulocytes kill bacteria very efficiently by devouring them. After eating the germs neutrophils kill tehm with antimicrobial proteins...

...scientists...discovered a second killing mechanism: neutrophil granulocytes can form web-like structures outside the cells composed of nucleic acid and enzymes which catch bacteria and kill them...

...Only after lengthy live cell imaging and biochemical studies it became clear how neutrophils make NETs. The cells get activated by bacteria and modify the structure of their nuclei and granules, small enzyme deposits in the cytoplasm.

"The nuclear membrane disintegrates, the granules dissolve, and thus the NET components can mingle inside the cells", explains Volker Brinkmann, head of the microscopy group. At the end of this process, the cell contracts until the cell membrane bursts open and quickly releases the highly active melange. Once outside the cell, it unfolds and forms the NETs which then can trap bacteria.

Surprisingly, this process is as effective as devouring bacteria... UNQUOTE.

Source of the quoted material: http://www.sciencedaily.com/releases/2007/01/070110124142.htm

41 st page of the old MSN site.

2008-11-11T15:47:00.000-08:00

A unified "AIDS" hypothsis without "HIV."

"The will to believe or disbelieve is neither data nor argument. At this point in the debate, there is a price of admission: one must either give an account of the composition of Q that is more cogent than those proffered hitherto, or explain clearly why such an account does not matter."

I'll add that claiming that an issue is "settled" because a "majority of experts" agree (even though only a small number of them has actually studied the issue in detail) is roughly equivalent to slapping a proverbial fig leaf on the reality that only the "will to believe" is present, and as stated by J.S. Kloppenborg Verbin, this "is neither data nor argument.

Source: the book, "The Sayings Source Q and the Historical Jesus" by Andreas Lindemann (ed.), 2001, page 164.

I found it somewhat amusing that a scholar of the New Testament would make a point that is certainly at least as applicable to those who assert that nobody should even consider questioning "HIV/AIDS." The problem with "HIV/AIDS" is that advocates will not accept its possible refutation, no matter what facts one presents to them (assuming they could even agree about what the "HIV/AIDS" claim actually is). For example, if the "viral load" test is as accurate as is claimed, then one could test "HIV negative" people who are afflicted with an acute bout of the flu. Obviously, such people should test "negative," but what if many test "positive?" Would the "HIV/AIDS" advocates then admit that something is terribly wrong?

February 17, 2007.

When I say "AIDS," I don't mean women who "test positive for HIV" and die of cervical cancer, which is classified as an "AIDS death" in the USA. Instead, I am interesting in those who die young of what are called "opportunistic infections." Of course, there is no way to know all of the things a person who is said to have "died of AIDS" in the USA did to his/her body, or endured for some other reason (such as work-related toxic exposures), but it is possible to examine the evidence and determine whether there is an underlying mechanism that is consistent with the experimental data, such that it is. My sense is that one reason this has yet to be done involves the way almost all scientists seem to view the phenomena they study. They seem to feel the need to argue that there is one cause for "syndromes" that should have only been created in the first place as a first step, but instead ossified into an entity that is viewed as more important than the underlying "disease" mechanism itself. With "HIV/AIDS," a press conference, not a scientific paper containing experimental data, announced to the world that the "probable cause" of "AIDS" had been found. After that, the mainstream media and the "AIDS experts" gradually made stronger and stronger claims about "HIV" causing "AIDS." One can go back and read coverage of this in the major newspapers of the time, such as the New York Times, to see exactly how this transition occurred. Also, a book entitled "Impure Science," by Steven Epstein, documents this phenomenon. Within a couple of years, few scientists were interested in considering whether the "probable cause," according to a small number of scientists, actually was the cause. Rather, most saw that there was a great deal of funding and career advancement opportunities in simply "going with the flow," and were content to force the square pegs of their experimental data into the round holes of "HIV/AIDS" ideology in the studies they were able to get published. My understanding the "immune system" problems often encountered in those said to have "AIDS" is based upon reading a great deal of health, nutritional, and medical literature over the course of several years. Moreover, I decided not to take any ideological notions for granted, but to allow the evidence to lead wherever it did. And this approach has "paid off," as it's now clear that there is indeed a clear underlying mechanism, though there are several factors that can greatly enhance it (or inhibit it), and as I said above, most scientists seem to have great difficulty thinking in a "flexible" way that allows for this. I, on the contrary, was trained as a historian, and I came to understand that it would be ridiculous, for example, to argue that Julius Caesar "caused" the downfall of the Roman Republic.

I will start with the best explanation put forth by scientists to date. The "Perth Group" has an "oxidative stress hypothesis," but they don't talk about what the body does when there are a great deal of oxidized molecules in the body (from what I've read of their work). Instead, most if not all who propose this kind of explanation talk about how it would affect the CD4 T "helper" cells. However, there is another model that is worthy of consideration, because it has a similar effect, and that is the heart disease/oxidized cholesterol one. Basically, the body attacks oxidized cholesterol as if it were "foreign" and potentially dangerous. If there is too much oxidized cholesterol, it causes macrophages to become dysfunctional, and they can accumulate in arteries, causing narrowing in an ongoing chronic inflammtory process. Clearly, if one does things like takes certain drugs, there will be plenty of oxidized molecules, and they could cause the lymphadenopathy characteristic of early stages of "AIDS," as most US doctors encounter it. At some point, the "immune system" loses the ability to tell the difference between "self" and "foreign" because there are so many kinds of similar molecules - when molecules get oxidized, they do so in diffferent ways. There are at least several different kinds of "oxidized cholesterol" molecules, for example. At some point this element of the "immune system" ("Th1") must be "shut down" in order to avoid an "all out attack" on all molecules that resemble the oxidized ones, and that includes molecules crucial for basic life functions. The CD4 T helper cells do this, and the "experts" have mistaken this phenomenon as a sign of "retroviral infection," apparently due largely to a lack of scientific imagination and a ideological belief in the "germ theory."

There is a "disease" that is similar to the "early stages of AIDS," and that is MAS. I will now quote an abstract of a study about this disease: QUOTE:"OBJECTIVE: To review and analyze the clinical features, treatment, and outcome of macrophage activation syndrome (MAS) in children with systemic onset juvennil rheumatoid arthritis (SOJRA). METHOD: Retrospective review and analysis were performed on cases with MAS from a prospectively collected database of children with SOJRA from the year of 2003 to 2006 in the Hospital. RESULTS: Twenty four patients (21 boys, 3 girls) were diagnosed as having MAS with SOJRA. Mean age of the patients with MAS at diagnosis was 7 years, and the duration prior to diagnosis of MAS was 12 months. No trigger factors were found except in one case whose MAS was triggered by use of methotrexate and in another by parvovirus B19 infection. High grade fever, new onset hepatosplenomegaly and lymphadenopathy, pancytopenia, liver dysfunction were common clinical features in all the 24 cases (100%). Bleeding from skin, mucous membrane and gastrointestinal tract were noted in 9 cases (38%). Twelve (50%) cases had CNS dysfunction (high intracranial pressure, seizure and coma). Six cases (25%) developed ARDS. One patient suffered from renal damage. The laboratory test revealed elevated live enzymes and ferritin, decreased value of ESR, albumin, complete blood count and fibrinogen in all the 24 cases. Bone marrow examination supported the diagnosis of definite hemophagocytosis in the 24 cases. Lymph node biopsy was done for one case and histopathological examination showed that the node was full of activated macrophage. As to treatment, five cases only received high dose steroids (three of them died), 14 cases were treated with high dose steroids plus cyclosporine (one died), two were treated with steroids plus cyclosporine and etoposide (none died). The causes of deaths were ARDS and CNS involvement. In three of the cases who died, treatment was given up by their parents. CONCLUSIONS: MAS is a rare and potentially fatal complication of SOJRA. Most of our patients were male. Bone marrow studies support the diagnosis. CNS involvement and ARDS were poor prognostic signs. Early diagnosis and aggressive therapy are essential." UNQUOTE.

Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17274865&query_hl=1&itool=pubmed_docsum

The "opportunistic infections" of "AIDS" occur when the body puts a halt to a "MAS"-like condition, thereby preventing serious damage from taking place. When one examines literature of cholesterol oxidiation, there is an obvious connection to this MAS-like phenomenon: QUOTE: Atherosclerosis. 1994 Nov;111(1):65-78.

Iron induces lipid peroxidation in cultured macrophages, increases their ability to oxidatively modify LDL, and affects their secretory properties."

Fuhrman B, Oiknine J, Aviram M.

The present study demonstrates for the first time that iron ions can induce lipid peroxidation in intact macrophages without causing cell death. Macrophage lipid peroxidation increases cell-mediated oxidation of LDL, enhances the release of interleukin 1... UNQUOTE.

Interleukin 1 (IL-1) is considered a "pro-inflammatory" cytokine and the following is characteristic of how "HIV/AIDS experts" view it: QUOTE: While some cytokines may promote or restore immunity, some can accelerate HIV replication and are associated with disease progression. Cytokines associated with inflammation, such as IL-1, IL-6 and TNF-alpha, have been associated with increased viral replication, wasting syndrome and progression of Kaposi’s Sarcoma... UNQUOTE.

Source: http://www.projinf.org/pip/14/pip14i.html

This is also true for IL-8, but it's not just for "HIV/AIDS," but for "heart disease" as well. For example: QUOTE: Oxidized low-density lipoproteins play important roles in the development of atherosclerosis and contain several lipid-derived, bioactive molecules which are believed to contribute to atherogenesis. Of these, some cholesterol oxidation products, referred to as oxysterols, are suspected to favor the formation of atherosclerotic plaques involving cytotoxic, pro-oxidant and pro-inflammatory processes. Ten commonly occurring oxysterols (7alpha-, 7beta-hydroxycholesterol, 7-ketocholesterol, 19-hydroxycholesterol, cholesterol-5alpha,6alpha-epoxide, cholesterol-5beta,6beta-epoxide, 22R-, 22S-, 25-, and 27-hydroxycholesterol) were studied for both their cytotoxicity and their ability to induce superoxide anion production (O2*-) and IL-8 secretion in U937 human promonocytic leukemia cells. Cytotoxic effects (phosphatidylserine externalization, loss of mitochondrial potential, increased permeability to propidium iodide, and occurrence of cells with swollen, fragmented and/or condensed nuclei) were only identified with 7beta-hydroxycholesterol, 7-ketocholesterol and cholesterol-5beta,6beta-epoxide, which also induce lysosomal destabilization associated or not associated with the formation of monodansylcadaverine-positive cytoplasmic structures. No relationship between oxysterol-induced cytotoxicity and HMG-CoA reductase activity was found. In addition, the highest O2*- overproduction quantified with hydroethidine was identified with 7beta-hydroxycholesterol, 7-ketocholesterol and cholesterol-5beta,6beta-epoxide, with cholesterol-5alpha, 6alpha-epoxide and 25-hydroxycholesterol. The highest capacity to simultaneously stimulate IL-8 secretion (quantified by ELISA and by using a multiplexed, particle-based flow cytometric assay) and enhance IL-8 mRNA levels (determined by RT-PCR) was observed with 7beta-hydroxycholesterol and 25-hydroxycholesterol. None of the effects observed for the oxysterols were detected for cholesterol. Therefore, oxysterols may have cytotoxic, oxidative, and/or inflammatory effects, or none whatsoever.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16142584

Now, if you read the following study abstract about findings concerning "HIV/AIDS," you should be able to see that it is very likely that the same mechanism is at work, though the tissue involved is different (and accounts for the different symptoms): QUOTE: An important role for selenium in human immunodeficiency virus (HIV) disease has been proposed. Decreased selenium levels, as found in persons with HIV infection or AIDS, are sensitive markers of disease progression. Selenium deficiency, an independent predictor of mortality in both HIV-1 infected adults and children, is an essential micronutrient that is associated with an improvement of T cell function and reduced apoptosis in animal models. In addition, adequate selenium may enhance resistance to infections through modulation of interleukin (IL) production and subsequently the Th1/Th2 response. Selenium supplementation up-regulates IL-2 and increases activation, proliferation, differentiation, and programmed cell death of T helper cells. Moreover, selenium supplementation may down-regulate the abnormally high levels of IL-8 and tumor necrosis factor-alpha observed in HIV disease, which has been associated with neurologic damage, Kaposi's sarcoma, wasting syndrome, and increased viral replication. Together, these findings suggest a new mechanism through which selenium may affect HIV-1 disease progression.

http://www.journals.uchicago.edu/cgi-bin/resolve?id=doi:10.1086/315911&erFrom=-5611785506958785470Guest

I can't emphasize strongly enough that as far as I'm concerned, there is no one "AIDS," except as a socio-political entity perhaps. Instead, it makes much more sense to investigate "from the inside out," that is, to carefully observe how the patient is living (and has lived) in order to understand how that lifestyle is causing certain molecular-level phenonema to occur. There is no technological barrier to this endeavor, but the "medical establishment" demands a sense of certainty (as does the general public), and the textbook categorizations supply this (and the drug companies need to craft their "medicines" to specific "diseases"). Even on the fictional TV show "Dr. House," though a thorough investigation is often performed (sometimes including actually going to the patient's residence for "evidence"), the resolution invariably involves matching up the patient's problems to a textbook entity (often a "rare" one). I was taught to look beyond what is considered the "standard," and while I understand why doctors are reluctant to do this, in light of all the promises of "cures" that have never occurred as well as the dire predictions of all kinds of health "epidemics" (along with ones that are supposed to be in full force already), it is an affront to basic common sense to brush aside alternative approaches. Some of you may be saying to yourselves, "this sounds like evidence-based medicine, so what is new about your idea?" Evidence with an improper interpretation of it can be worse than no evidence at all. Moreover, there can be a huge difference in the kind of "evidence" used (and much evidence is ignored). For example, the mainstream media often reports on epidemiological studies, but epidemiologists can only be as good as the underlying assumptions, which, if flawed, can produce results that lead to horrendous advice. Instead, molecular-level evidence should be taken much more seriously than it presently is.

40 th page of the old MSN site.

2008-11-11T15:46:00.000-08:00

A Rough Guide to a Gentle Diet.

I have been asked if I could write up a “basic” and practical shopping guide by people who want a tasty, ready-to-eat, satisfying diet, but who fear gaining weight and eating food that will lead to “chronic disease.” I took a close look at some of products at a local supermarket called “Stop & Shop.” Before I talk about the products, I should mention that I currently eat three meals a day, spaced at least three hours apart, and I don’t consume any calories between meals. I might drink some cold tea, but it has no sugar or anything else in it, except perhaps for a tiny amount of salt. I’ve found that I can eat as much as I want, so long as I eat slowly and only eat three meals a day. I don’t get hungry at night and my weight is stable (and I’m slim).

I’ve been buying dairy products and organic eggs (only boil eggs) from supermarkets, but little else. Once in a while I might buy sauerkraut from such stores, but I usually buy organic sauerkraut at the local “health food store.” Here, I should mention that I do not buy dairy that contains substances such as carrageenan, guar gum, locust bean gum, etc., but if you don’t have a choice, avoid carrageenan. Products like ricotta cheese and sour cream can vary a great deal, with some containing more than one of these substances, while others are made without any.

Now, as I looked throught the breads, cookies, wafers, cookies, candies, etc. at Stop & Shop, I noticed that some of their brand of cookies were rich in saturated fatty acids but low in unsaturated fatty acids, and also did not appear to be made with bleached flour. These items were iced oatmeal cookies, caramel dipped shortbread cookies, chocolate covered graham cookies, and chocolate covered mint cookies. I purchased them and have found that they are useful for making a meal more tasty – I eat one per meal, at most. Of the fat content, at least 70% is saturated, whereas some of the other cookies contained considerably more unsaturated fatty acids than saturated ones, and so I would not even consider eating them. Also, I noticed that they sell candy called “gum drops” which are mostly sugar and corn starch, and have tried them as well. The most I have eaten with a meal is two. Marshmallows are also an item that should not be a problem – it contains no fat or cholesterol. Some whip toppings contain 2 grams of fat per serving, both of which are saturated, and so this is something that I would much rather eat (on top of all kinds of things) than cake or pie that has a high PUFA content (which is very common these days).

A meal consisting of one of these cookies, a “gum drop,” two or three ounces of cheese, a mixture of ricotta and sour cream, several raisins, part of a banana, shredded coconut, some pineapple chunks, a small amount of sauerkraut, dark chocolate, and a couple of large mashmallows is easy to “throw together,” and I’ve found it to be incredibly satisfying but very gentle on the stomach. Of course, organic dried fruit is probably better, especially if you still have arachidonic acid in your cells, but not everyone likes fruit in this form, and it can be quite expensive, several times more expensive than cheap cookies and “gum drops.” It also may be difficult to get children to eat such fruit. Obviously, most fresh organic fruit is good, but again, expensive (and not alwayus available in certain places). My point here is to call your attention to what kinds of “junk food” appears to be reasonable “safe,” if you eat it the right way and in small amounts.

I took a look at some of these kinds of products in the homes of friend and relatives, and almost every one of them contained a lot more unsaturated fatty acids than saturated ones, and some also contained cholesterol, at least some of which will get oxidized by the time it reaches your mouth. Ironically, because the "experts" have been telling people that unsaturated fatty acids are good (in general) for the last several decades, those who eat things like cookies (the ones rich in unsaturated fatty acids, which represent the clear majority of what you can find in the supermarket) are often found to have higher rates of this or that "disesase" in epidemiological studies. The conclusion of the "experts" is that sugar is unhealthy, because they assume that the unsaturated fatty acids are healthy, or at least not unhealthy.

However, as I have argued elsewhere on this site, the scientific method requires that all possible factors be isolated and tested. If this were done, for instance by feeding one group of rats a lot of cookies rich in unsaturated fatty acids, while another group of rats were fed cookies that contained at least 90 percent saturated fatty acids (of the fat content), and then observed them until they all died (recording the ages of death, of course), we would then have strong evidence. However, today when these kinds of studies are conducted, the "diseases" that afflict the animal and the ages to which they live are hardly ever recorded, because the researchers instead rely upon "markers," such as a rise in total cholesterol levels. By doing this, they can conduct experiments in a much shorter period of time and less expensively (they can also have their studies published their "results" more quickly). Most such researchers would argue that "high cholesterol levels have been proven to correlate with a greater risk of heart disease." Of course, this was claimed before an understanding of the role of oxidized cholesterol was well known, as it is now (at least by those working on this area of research). In any case, it is common to verify scientific claims whenver there is a possibility that it may be incorrect, for whatever reason. Einstien's "relativity" has been tested over and over again, for example, but those in the bio-medical and nutritional seem to be much more reluctant to question and test old claims, perhaps because of the repercusions.

In doing some research, I came across a web page that featured people asking a dietitian questions about triglyceride levels and some related issues. I thought this was an interesting page because it demonstrates how people are confused about what they should eat and what they should avoid. We have all heard all kinds of conflicting dietarty advice. The reason I decided to write this page is because so many people tell me that they are unable to follow "rigid" diets, for whatever reason. On the dietitian's page, advice offerred includes avoiding "saturated fat." On the contrary, I advise eating foods that contain either no fat, or else at least 70% saturated fatty acids (and also to avoid cholesterol if it is likely to be oxidized). This allows one to find tasty, satisfying food in typical supermarkets. However, as I said above, it's important to eat only three meals a day, with no calorie consumption in between. You will likely need to eat quite a bit of fat in order to feel satisfied (along with enough high quality protein, of course), and eating slowly helps a great deal. In late 2000, my cholesterol was 131 (on a vegan diet rich in nuts, seeds, beans, and whole grains, with some fruit and vegetable), and in mid 2004 it was 209. However, my HDL rose from 40 to 63, and my LDL was still in the range considered healthy.

The dietitian, however, claims that: "Your cholesterol is also high. Saturated fats (any animal product, coconut and palm kernel oils) and high cholesterol foods increase blood cholesterol (the LDL portion). Read the cholesterol & saturated fat topic also. Recent research suggests that high cholesterol foods, especially egg yolks may play a lesser role in increasing blood cholesterol. A 25% fat, low saturated fat diet should lower your LDL cholesterol."

Those who follow this advice may find themselves facing an awful lot of ill health. Consuming cholesterol (probably much of it oxidized, due to cooking and processing) and all that unsaturated fat is the proverbial recipe for disaster. As I ask people, "how many more years will I feel great on a diet that is supposed to kill me so quickly?" Then I usually add, "this is a very similar diet to my great grandfather's, and he lived to be over 100, with no omega 3 supplements, and no fear of saturated fatty acids, sugar, cholesterol, salt, etc."

This dietitican is aware of the problem with telling people to eat unappealing diets: "Now, with regards to your food choices. Why don't you eat fruit and vegetables? No time, habit or taste? Does the cook in your house like to prepare vegetables and fruits with meals?"

However, what is the point of telling people something they are simply not going to do? Unfortunately, this dietitian appears to be unaware of the dangers of oxidized cholesterol only, and tells people to limit cholesterol consumption: "The current recommendations are to limit egg yolks to 4 per week. So substitute 142 grams (5 ounces) of shrimp for one of the egg yolks per week." In contrast, my sense is that two or three boiled eggs a day is fine, so long as you don't eat any of the food items that can oxidize that cholesterol in your body after you eat it.

Here are some of the questions asked of the dietitian:

Q: I went in for a physical recently and was informed that my triglycerides were the highest the doctor had ever seen (875) and my cholesterol was at 308. All other aspects of the physical went well. I went again today for another blood lab after fasting from the evening the night before.

I am 32 years, 5'11'', weighing 186# and am fairly active. I haven't been drinking at all due to illness (bronchitis) and also as a result of my efforts to quit smoking (1 week and 1 day today). I don't drink much soda at all and when I do it is "diet". I do tend to eat a lot of hard candies (a function of my efforts to quit smoking). I eat a lot of red meat and chicken, fried foods and eat little to no vegetables or fruit. I don't like most vegetables.

I have a wonderful family and want to see my children grow up. What can I do to get myself back in healthy condition? Thanks for your help.

Q: My triglycerides are over 700. My cholesterol was normal. I have done everything to bring it under 700. I cut out sugar, sweets and my cokes to only 2 a day. Is that still too many? I am 60 lb. overweight. I have cut fat to 15 grams a day and calories to 1700. I exercise 4 times a week for 30 min. I have been doing this for a year. Why cant I loose the weight and bring my triglycerides down?

Q: I'm a 28-year-old male that recently had a full-blown blood panel done. To my surprise, my cholesterol level was 220 (HDL = 39, LDL = 120) and my triglyceride level was 304!!! I'm not overweight, I seldom drink and I have what I consider an average diet for a male my age (O.K. maybe more fries than I should now and then). I don't eat sweets, except for a daily Mocha or two (with extra chocolate). Could these sweet little chocolate drinks be sending my triglyceride levels through the roof? I think I can work on reducing my cholesterol level through better diet and more exercise, but what about these triglycerides?

The dietitian's responses included the following:

"...Often a very high triglyceride level like yours can be caused by undiagnosed diabetes... Triglycerides are effected by sugar and alcohol, not the fat content in your diet... Any excess calories, irrelative of the source, from protein, fat or carbohydrate, are converted to fat, usually to triglycerides. If you consume sugar, then you do risk increasing your blood triglyceride levels. The problem is the body prefers to run on glucose, not triglycerides..."

I'm glad to see that the dietitian realizes that the body "runs" well on glucose, and that excess calories can contribute to "high triglycerides." But why should one fear "high triglycerides?" Basically, this is just another "maker," and not anything directly related to an actual "disease," though I would point out that having high levels of triglycerides that contain a lot of unsaturated fatty acids is probably quite unhealthy. In fact, one study found that the solution to the "problem" of high tryglycerides was more glucose:

J Clin Invest. 1973 March; 52(3): 732–740.

Diurnal Patterns of Triglycerides, Free Fatty Acids, Blood Sugar, and Insulin during Carbohydrate-Induction in Man and Their Modification by Nocturnal Suppression of Lipolysis

G. Schlierf and E. Dorow

Abstract: Previous studies have shown that carbohydrate induction of hypertriglyceridemia in normal subjects occurs at night and appears to be related to a rise of free fatty acids after diurnal feeding of high-carbohydrate formula diet. The present investigation was undertaken to observe the effect on 24-h triglyceride, free fatty acid, blood sugar, and plasma insulin profiles of inhibition of nocturnal lipolysis by glucose or nicotinic acid in normal subjects and in patients with type IV hyperlipoproteinemia.

In 10 normal subjects and 10 patients with primary type IV hyperlipoproteinemia, plasma triglyceride, free fatty acid, blood sugar, and insulin levels were followed in short intervals for 24 h while a 2,400 cal, 80% carbohydrate, fat-free formula diet was given in six equal portions during the day (control experiments). This procedure was repeated in the same subjects, 10 of whom (5 normal subjects and 5 patients) received additional feedings of glucose between 2000 and 0600 h while the other 10 persons (5 normal subjects and 5 patients) were given nicotinic acid by intravenous infusion during the same time interval. Both procedures resulted in maintained lowering of free fatty acid levels over 24 h. Mitigation of carbohydrate-induced hypertriglyceridemia appeared to result from the additional glucose in normals and in patients. Nicotinic acid abolished the nocturnal rise of plasma triglyceride levels which in the control studies of normal subjects had resulted in approximate doubling of triglyceride levels in 24 h...

Source of the quoted passages from the dietitian's web page: http://www.dietitian.com/triglyce.html

39 th page of the old MSN site.

2008-11-11T15:45:00.000-08:00

An example of an anti-"saturated fat" study that is flawed.

On July 19, 2003, a report of a study appeared in New York's "Newsday" newspaper, page A8. The study in question is typical of the kind of evidence nutritionists and other "experts" cite when they make their claims. The title of this report was "Cancer, Fatty Foods Linked." I agree with this title, but in the report, an author of the study is quoted as saying, "The [pro-breast cancer] effect seems to be related particularly to saturated fat found mostly in high-fat milk, meat and some cereals such as biscuits and cakes."

The study was based upon "detalied food diaries of 13,000 older women in Norforlk in eastern England..."

The result of an analysis of these diaries was that: "The women who were eating 90 grams of fat [a day] had a twofold risk of those who were eating who were eating 40 grams..."

Again, this makes perfect sense to me - I wouldn't be suprised if the risk was higher, actually. But my question is, why is "saturated fat" being blamed? First of all, we will assume that by "saturated fat" they mean "saturated fatty acids," and are not discriminating among the many different kinds of saturated fatty acids - this is likely the case and there is nothing else that could be said if these assumptions were not made. Secondly, most people eating a typical Western diet and 90 grams of fat per day are going to be eating more PUFAs than a person eating a similar diet but containing only 40 grams of fat per day. Are they assuming that because PUFAs are considered "essential" that they do not have to consider the possibility that the PUFAs may be a major factor? The author of the report does not say. Since it is now known that oxidized cholesterol is very dangerous, and since foods typical in Western diets that are rich in saturated fatty acids are also rich in cholesterol (and also that much of this kind of food is cooked at high temperatures), this is a factor that would need to be controlled, but again there is no way to know from this report if it was. Of course, it is highly unlikely that these elderly British women consumed large amounts of coconut or palm kernel oil - these are products that are rich in saturated fatty acids, low in unsaturated fatty acids, and contain no cholesterol. A control group consuming one or both of these oils is absolutely essential for this kind of study to be reasonable, scientifically.

Moreover, The National Research Council of the USA published an exhaustive review of the literature up to the late 1980s, and titled this book, "Diet and Health: Implications for Reducing Chronic Disease Risk" (1990). A key point the authors make is: "Dietary fats increase the yield of mammary tumors only when they contain adequate amounts of omega-6 PUFAs, which are normally present as linoleate in fats derived from plants and land animals. This probably explains why fats such as butter, coconut oil, and beef tallow have little effect on mammary carcinogenesis (carroll et al., 1981). The requirements for omega-6 PUFAs in mammary tumor promotion have been explored systematically by Ip et al. (1985), who reported 4 to 5% of total calories as the threshold at which the yield of mammary tumors increased." Page 213. Moreover, I would add that both older and recent studies suggest that cooked "meat" is particularly dangerous, and this is now understood down to the molecular level. Even in "Diet and Health" this point is made: "...some dietary fats, e.g., lard and beef tallow... enhance mammary tumorigenesis when fed only at or before exposure to a carcinogen..." Page 214.

Here are some studies of note in this context:

Free Radic Biol Med. 1988;5(2):95-111.

"The ways in which dietary polyunsaturated fats and antioxidants affect the balance between activation and detoxification of environmental precarcinogens is discussed, with particular reference to the polycyclic aromatic hydrocarbon benzo(a)pyrene. The structure and composition of membranes and their susceptibility to peroxidation is dependent on the polyunsaturated fatty acid (PUFA) content of the cell and its antioxidant status, both of which are determined to a large degree by dietary intake of these compounds. An increase in the PUFA content of membranes stimulates the oxidation of precarcinogens to reactive intermediates by affecting the configuration and induction of membrane-bound enzymes (e.g., the mixed-function oxidase system and epoxide hydratase); providing increased availability of substrates (hydroperoxides) for peroxidases that cooxidise carcinogens (e.g., prostaglandin synthetase and P-450 peroxidase); and increasing the likelihood of direct activation reactions between peroxyl radicals and precarcinogens. Antioxidants, on the other hand, protect against lipid peroxidation... It has been concluded that dietary factors exert the greatest environmental influence on carcinogenesis and Doll and Pet have estimated that diet is responsible for approximately 35% of the total cancer deaths in the USA… The polycyclic aromatic hydrocarbon benzo(a)pyrene (BP) is a widely occurring environmental pollutant formed by the combustion of organic materials including cigarettes. It is present in smoked foods and as a contaminant in a wide range of crops, particularly vegetables… In 1975, Marnett and coworkers demonstrated the conversion of BP from BP-7,8-diol to BPDEs during the formation of prostaglandins from arachidonic acid… An increase in both the number of tumour-bearing animals and the multiplicity of respiratory tract tumors induced by BP has been demonstrated when hamsters were fed high fat diets and this effect was most pronounced in the group fed unsaturated fat (sunflower oil)…Taken together, these studies demonstrate that the oxidation of carcinogens catalysed by the MFO system in most tissues studied is dependent upon the presence of dietary EFA [omega 6 and/or omega 3 PUFAs]… The double bonds of PUFAs are suspectible [sic – presumably this should be susceptible] to attack by free radicals and this results in the formation of lipid radicals which combine with oxygen to yield peroxy radicals. These species may then react with another molecule of an unsaturated fatty acid resulting in a chain reaction and the formation of lipid hydroperoxides whicfh break down in the presence of transition metals to a complex mixture of short-chain molecules including aldehydes and hyrdrocarbon gases… In one study, the increase in the number of DMBA-induced mammary tumours as a result of selenium deficiency was particularly pronounced when the diet was rich in polyunsaturated fats and chemoprevention by increasing the intake of selenium was potentiated by additional vitamin E intake… Precarcinogens such as BP may oxidised to mutagenic and toxic species in foodstuffs which contain polyunsaturated fatty acids and are subjected to conditions which induce peroxidation… Unprotected PUFAs undergo peroxidation which can be initiated by intracellular free radicals produced in small quantities under normal circumstances or by a wide variety of environmental toxins…”

Cancer Res. 2005 Sep 1;65(17):8034-41.

"Cooking meat at high temperatures produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Processed meats contain N-nitroso compounds... Greater intake of bacon and sausage was associated with increased colorectal adenoma risk... Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma."

Thus, the fact that today's meat (from pigs, chickens, and cows especially) is richer in omega-6 PUFAs these days is highly likely to be a very important factor in carcinogenic processes. Yet all most of us hear about in the "mainstream media" are the same kinds of studies, which make the same kinds of claims, while other (much stronger evidence) is never, or hardly ever even mentioned. Fortunately, with the resources now available on the internet, one does not need to rely upon newspapers, popular magazines or books, and TV news programs for his or her nutritional information.

Recently, I came across a web site with the following information:

QUOTE: Cholesterol enters the body from saturated fats in animal sources, such as meat, poultry, egg yolks, liver, butter, cheese, and other dairy products. The cholesterol goes to the liver where it joins the cholesterol that is made there. The cholesterol is transported from the liver to the cells by low density lipoproteins (LDL), which acts like a nutritional ferry boat, loading up the cholesterol and navigating through the bloodstream, stopping at cells and depositing cholesterol to the cells that need it. If a cell already has enough cholesterol, it "refuses delivery" of the cholesterol cargo. The excess LDL stays in the blood where the cholesterol is deposited in the walls of arteries, causing atherosclerotic plaque. The more plaque that builds up, the narrower the arteries become, until eventually the blood supply to vital organs is reduced. This is why LDLs are known as the "bad cholesterol."*

But take heart, a nutritional rescuer is also present in the bloodstream, the high density lipoproteins, or HDLs. These are known as "good cholesterol," since they travel like a vacuum cleaner through the bloodstream, picking up excess cholesterol in the bloodstream, and also possibly sucking the cholesterol from the fat-laden plaques. The HDLs carry this excess cholesterol back to the liver, which converts it to bile, which is eliminated into the intestines. How your liver handles cholesterol is determined primarily by genetics, and secondarily by your diet.

While this is an oversimplification of a complicated biochemical process, it helps us understand two conclusions:

Any diet that raises cholesterol and LDLs and/or lowers HDL is bad.
Any diet that lowers cholesterol and/or raises HDL is good. UNQUOTE.

SOURCE: http://www.askdrsears.com/html/4/T040800.asp

Note how the author assumes that "excess LDL" will be "deposited in the walls of arteries." Rather, the molecular-level evidence demonstrates that oxidized LDL are "attacked" by macrophages, which can then become dysfunction and lodge in arteries, eventually causing plaque buildup if the process continues. Also; if, as the author says, HDL takes excess cholesterol bck to the liver and it's converted to to bile, abstructed ducts and gallbladder problems can occur, if too much of the cholesterol is oxidized. The issue is oxidation of cholesterol. The idea that "LDL is bad" is based upon an emphasis on "heart disease" in the context of unhealthy Western diets (rich in foods that act as oxidizing agents, like refined and highly polyunsaturated oils). Low LDL means a higher risk of certain cancers, amongst other unpleasant things. The author does make a point that many people are not aware of: QUOTE: For most people, about eighty percent of the cholesterol in their blood is made by their own body, with the rest coming from their diet. In fact, your body needs cholesterol so much that it makes around 3,000 milligrams per day that's ten times the maximum recommendation for daily dietary cholesterol. UNQUOTE.

38 th page of the old MSN site.

2008-11-11T15:44:00.000-08:00

What "viral infections" really do to the body.

A recent report explained this issue well:

QUOTE: ...The key to curbing any excess activity by the immune system apparently rests with Carabin, a newly discovered protein made by the specialized white blood cells that march in when a virus attacks...

When people are infected with a cold virus, for example, the virus enters cells and hijacks its works so that the cells become viral factories. The immune system's white blood cells go after these infected cells not only by fielding chemicals that kill them directly, but also by turning on genes that help out. When Liu and his group added Carabin to cells and then studied such genes, they discovered that Carabin disabled the "on" switches, keeping the genes off...

Tracking Carabin to its origins, the researchers said they were surprised to learn that viral infection not only turns on the immune system machinery, but also triggers the making of Carabin, which in turn shuts off the immune response.

"It's like having a built-in timer to keep the immune system in check," says Liu.

If Carabin turns out, after further study, to be a keystone natural inhibitor of immune responses, Liu added, it may prove useful in stopping such unwanted immune reactions as the rejection of transplanted organs... UNQUOTE.

Source of the quoted material: http://www.sciencedaily.com/releases/2007/01/070117134429.htm

Here are some factors that would need to be taken into account when assessing why people supposedly live longer today:

1. The percentage of women who died during childbirth then (whenever that is) as opposed to now.

2. Deaths due to diseases that are rare today, but that are usually easy to prevent or cure, such as TB.

3. The living conditions, for example, people not having refrigerators, yet living in cities like New York, where it can get very hot in the summer.

4. The fact that jobs were more hazardous 100 years ago. Compare the percentage of the population of the US that were coal miners then as compared to now, for example.

5. The fact that many substances were not known to be dangerous, and thus were no avoided, as is usually the case today.

6. The much higher death rates among infants and children.

7. In some time periods, the number of deaths of young men due to war.

8. Various epidemic deaths, which again is rare today, even if death due to "HIV/AIDS" is taken into account in nations like the USA.

9. Vitamin or mineral deficiencies, which are not nearly as common today.

10. Lack of medical knowledge, which would mean that many died of things that could be easily prevented today.

11. Lack of medical technology or equipment.

12. Lack of today's drugs, some of which are useful, of course, while others keep people alive longer than would otherwise be the case.

Thus, any claim that today's diet is better because people appear to live longer is quite presumptious, and would require a degree of evidence analysis that is not possible (due to the inability to quantify these factors as well as a lack of evidence for the "Industrial Revolution" period or previous epochs).

37 th page of the old MSN site.

2008-11-11T15:43:00.000-08:00

The use of hypotheticals in science.

In the history of science, there are many examples of the use of hypotheticals or analogies. In the case of Einstein’s relativity, for example, one can ask another to imagine a train passing by a person and it’s horn or whistle being activated. A person standing near the tracks would hear a sound that changes its pitch, whereas a person on the train would hear a uniform sound. One such thought experiment should be simple enough for just about everyone to understand. Let us imagine a time when some suggested that air is necessary for people to live. An animal that appears to need air in the same way is put in a large, sealed glass container, and an apparatus withdraws all the air from the container. The animal, however, does not die, but looks perfectly well – for several days! If this was so, just about everyone would agree that there is nothing in the air that is essential to life – that notion was directly and completely refuted. This is exactly what was done with a claim made in 1930 that rats required certain kinds of fatty acids. In 1948, rats were deprived of all fatty acids and lived without any difficulties. The researchers noted that they had provided a B vitamin to the rats that the 1930 researchers had not, and that that was the cause of the apparent ill health, not a deficiency of any kind of fatty acid. This experiment was discussed in the Encyclopedia Britannica Book of the Year in 1948, and yet for some reason most “nutritional experts” act as if it never occurred. Moreover, if anyone wanted to verify this experiment, it would not be difficult or expensive to conduct. In fact, even someone with no scientific credentials could conduct it, as long as he or she knew the basics of rat nutrition (minus the fatty acids, of course) and maintenance – information that could be readily obtained over the internet.

Here is another useful hypothetical: let us imagine that we only have a small number of choices if we want to ingest anything with more than trace amounts of fatty acids. We can choose chicken fat, which is about 30% saturated fatty acids (SFAs), lard, which is just under 40% SFAs, coconut oil at 92% SFAs, or palm kernel oil, around 87% SFAs. Now, we decide to ask our local nutritional expert about these choices. This person insists that “saturated fat is unhealthy,” and argues that lard is a “saturated fat.” We point out that it makes no sense to classify lard as a “saturated fat” because it is much closer to chicken fat than to the other fat sources at our disposal, which are highly unsaturated. We also suggest that if lard is to be called a “saturated fat” (even though we think it is nonsensical), then palm kernel and coconut oil should be called “highly unsaturated fats,” and that if experiments are done, lard and the “highly saturated fats” should not be used interchangeably.

It is easy to see how ridiculous this situation is. I point I have made in the past is that there are times in history when the best policy is what one might call “consolidation,” meaning that the “experts” should be asked to put all their preconceptions aside and reconsider everything they assume to be correct. It makes sense for this to occur when many scientific predictions have been made, yet few if any have actually come to pass. The “war on cancer” was supposed to be “won” by 1980, an “AIDS vaccine” was supposed to be available by the mid to late 1980s, there was supposed to be “epidemics” or even “pandemics” of “Mad Cow Disease,” “Bird Flu,” etc., and there were supposed to be terrible “infectious disease outbreaks” in the aftermath of the great tsunami and Hurricane Katrina. And just the other day, a report with the following statement appeared: “Experts believe the world is overdue for influenza pandemic” (source: http://www.sciencedaily.com/releases/2006/11/061112094603.htm). We have made great strides in technology over the past few decades, yet this has not been much of a help, in general. Under the circumstances, it is only reasonable to ask if there is any chance that at least some of the underlying assumptions are flawed, if not totally false. The use of some simple hypotheticals demonstrates that this appears to be the case.

One thing that is clearly not hypothetical is the claim that a virus is causing a deadly disease. One virus particle cannot kill a person, or even make a person ill, on its own. At some point, there must be an amount of virus present that present technology can detect and the reasonable mind would consider to be enough to cause the “disease” in question. This has never happened with “HIV/AIDS,” and most of the people I have explained this to are surprised, if not shocked. Moreover, particles that match the textbook descriptions of the “HI” virus have never been found in anyone. And, as Nobel Prize winner (in biochemistry) Kary Mullis pointed out, when he asked for the foundation study of the “HIV/AIDS” claim, such a paper has yet to be written. Instead, it is often the case that “HIV experts” argue that there is an “abundance of evidence,” apparently mistaking research for foundation or supporting evidence. Another common mistake (or technique, if it is being used intentionally) is to cite a large number of papers from the relevant literature, along with a short statement that “there is abundant evidence,” but with no analysis of the actual experimental findings. The person who does this appears to be unaware of the undeniable fact that the findings of an experiment are not always in accord with the interpretation of those findings by the people who conducted the study or experiment. For example:

QUOTE: Rebecca [Culshaw] clearly has never looked at studies of the origins of HIV-1 and HIV-2. See the attached papers, if you have any interest.

Mokili J, Korber B. ,The spread of HIV in Africa., J Neurovirol. 2005;11 Suppl 1:66-75. Review.
Zhu T, Korber BT, Nahmias AJ, Hooper E, Sharp PM, Ho DD. An African HIV-1 sequence from 1959 and implications for the origin of the epidemic., Nature. 1998 Feb 5;391(6667):594-7.
Korber B, Muldoon M, Theiler J, Gao F, Gupta R, Lapedes A, Hahn BH, Wolinsky S, Bhattacharya T. Timing the ancestor of the HIV-1 pandemic strains. Science. 2000 Ju" UNQUOTE.

Culshaw replied: QUOTE: Dear Dr. Foley, If you would compose an actual presentation of the data in these "papers", which of course I have read and studied, and that you think support the counter-propositions to what I wrote, by all means do so and it will be published here, along with my reply. UNQUOTE.

Source: http://barnesworld.blogs.com/barnes_world/

In other words, there is a disagreement about the interpretation of the findings, and so the only reasonable thing to do when this occurs is to examine the issue in depth, point by point. A formal, academic debate can be useful under such circumstances. However, what taxpayers are funding (to a large degree) is a group of people who keep making predictions and promises, rarely if ever deliver on them, and refuse to even explain how they can believe that the experimental findings are in accord with assumptions that have never been demonstrated to be accurate. I’ve also pointed out, particularly in the “saturated fat” and “essential fatty acid” claims, that the experimental designs clearly violate the scientific method. Unlike politicians, however, it seems that the scientists who hold most of the power in the biomedical establishment will never be held accountable. Rather, new promises will be made, the mainstream media will trumpet the notion that all “diseases” will be cured within ten or fifteen years, the biomedical agencies will continue to get funding, and then the cycle will repeat itself every so often. As I used to tell my students, one should use history as a guide. One should not predict that a “golden age” of peace and reason will prevail in the near future if such an age has never existed.

36 th of the old MSN site.

2008-11-11T15:42:00.001-08:00

Why many nutritional claims make no sense

One thing I have been pointing out to people for years now is that claims like "saturated fat is bad" or "cholesterol causes heart attacks" do not make sense on many levels. Obviously, some people find it difficult to understand the molecular-level evidence. One thing that is clear to everyone I've talked to is that when you look at common recipes, you find that cholesterol and saturated fatty acid contents are similar. In fact, "vegetarian" and "Mediterranean diet" dishes are clearly higher in saturated fatty acid (SFAs) content than beef and pork dishes, if the sample of recipes I clipped out of my local newspaper over a period of several months is any indication. The vegetarian dishes averaged 4.875 grams of SFAs per serving, while the beef and pork ones averaged 3.222. Below are some examples taken from this local, but major newspaper, New York's "Newsday:"

Roast Pork With Grapes: 10 grams of fat, 3 of it saturated (SFAs); 75 mg of cholesterol (1/2/2004, page B27).

Pasta With Chicken And Broccoli: 9 g fat, 3 SFAs; 76 mg cholesterol (11/5/2003, page B31).

Beef Picadillo With Toasted Corn Tortillas: 9 g fat, 2 SFAs; 60 mg cholesterol (8/6/2003).

Chicken Pizza With Vegetables: 9 g fat, 4 SFAs; 50 mg cholesterol (12/5/2003, page B39).

Pasta With Tomatoes, Chickpeas, and Feta (vegetarian): 23 g fat, 7 SFAs; 33 mg cholesterol (12/17/2003, page B23).

Greek Tomato And Green Bean Soup (vegetarian): 9 g fat, 3 SFAs; 17 mg cholesterol (10/14/2003, page B17).

Curried Beef Kabobs: 7 g fat, 2 SFAs; 71 mg cholesterol.

Bean and Corn Burritos With Salsa Fresca (vegetarian): 12 g fat, 3 SFAs; 9 mg cholesterol (8/4/2003).

Individual Greek Pitzas (vegetarian): 16 g fat, 6 SFAs; 33 mg cholesterol (8/13/2003).

Meatless Pad Thai (vegetarian): 23 g fat, 4 SFAs; 106 mg cholesterol (2/12/2004).

Chinese Style Beef In Barbeque Sauce: 10 g fat, 3 SFAs; 78 mg cholesterol (1/26/2004, B16).

Mediterranean Tortellini (vegetarian): 15 g fat, 5 SFAs; 28 mg cholesterol (1/30/2004, page B31).

Pork Medallions With Pears In Port Wine Sauce: 8 g fat, 2 SFAs; 74 mg cholesterol (2/3/2004, page B19).

Pork Tenderloin With Orange Balsamic Glaze: 4 g fat, 1 SFAs; 74 mg cholesterol (10/6/2003).

Tex-Mex Sausage And Rice: 13 g fat, 5 SFAs; 95 mg cholesterol (1/8/2004, page B19).

Pink Pasta Primavera (vegetarian): 15 g fat, 5 SFAs; 15 mg cholesterol (9/19/2003, page B39).

Chicken Po' Boys: 6 g fat, 1 SFAs; 60 mg cholesterol (7/29/2003, page B17).

Inside Out Cheeseburger: 17 g fat, 7 SFAs; 86 mg cholesterol (7/22/2003, page B19).

Shrimp And Sausage Jambalaya: 6 g fat, 1 SFAs; 106 mg cholesterol (9/26/2003, page B35).

Buffalo Turkey "Wing" Sandwiches: 16 g fat, 3 SFAs; 74 mg cholesterol (10/3/2003, page B37).

Lemon Garbanzo Beans Over Polenta (vegetarian): 16 g fat, 6 SFAs; 33 mg cholesterol (10/31/2003 page B35).

Chilean Beef And Peppers: 13 g fat, 4 SFAs; 59 mg cholesterol (10/28/2003, page B19).

Most of these dishes are in the 300-500 calorie range, per serving. Of course, what matters is how satisfying the dish is, because if it is not, one will likely eat more than one serving, or eat a big dessert. The only recipes that are significantly different from the ones above are the ones that use a lot of coconut oil, chocolate, or butter. For example. a chocolate mousse recipe I found on the internet was as follows:

Per serving: 122 calories, 3 g, 17 g carbohydrate, 3.5 g fat (3 g saturated fat), 3 mg cholesterol, <1>

Source: http://onhealth.webmd.com/script/main/art.asp?articlekey=59751

This recipe, if tripled to the amount of calories found in many "main dishes," would be about 10.5 g fat, 9 SFAs, and 9 mg cholesterol. If we quadruple it, to 488 calories, which is also similar to many main dishes, the numbers are: 14 g fat, 12 SFAa, 12 mg cholesterol. I use this example because it is similar to a typical meal of mine, and also because it shows what kinds of food you would have to consume large amounts of in order to be within a range many US "nutritional experts" claim is unhealthy. It is common for me to eat a lot of whole milk cheese and yogurt, dark chocolate, and some butter or coconut (either in the oil or shredded form) with each meal. This is not a diet that has been found to be unhealthy, actually. The evidence suggests it is healthy. The only stuides that appear not to involve those that do not discriminate among the sources of saturated fatty acids and cholesterol, do not take cooking techniques and "freshness" into account, do not take iron content into account, do not take all possibly relevant "cultural" or socio-economic factors into account, etc., but instead estimate the amount of SFAs consumed and then try to see if there is a "statistically significant" rise in the incidence of one or more "diseases" among those who eat more SFAs overall. This makes little sense, since one can now easily devise several different diets that are tasty (so that many people will continue to eat this way if they know it is healthy) and consistent with the molecular-level evidence. These diets can then be fed to species like dogs, which live significantly shorter lives than humans, but are fairly good animal models for overall health, and then we would have very strong evidence indicating which diet is healthiest. Such experiments were done many decades ago, but are now out of favor, since it is much easier to do a short term study to determine if a particular "marker" (such as LDL) rises or falls due to a dietary change, even though it is known that LDL must be oxidized in order to cause "disease," and so is only a potentially useful marker if people are eating diets rich in oxidized cholesterol (or diets that oxidize cholesterol inside the body).

Below is the most typical kind of study that is conducted these days in nations like the USA concerning possible dietary connections to “disease.” I ask the reader to think of the information above while reading though this abstract (summary), and then I will comment on it below it.

Arch Neurol 2003 Feb;60(2):194-200.

Dietary fats and the risk of incident Alzheimer disease.

Morris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, Schneider J, Wilson RS.

Rush Institute for Healthy Aging, 1645 W Jackson, Suite 675, Chicago, IL 60612, USA. martha_c_morris@rsh.net

BACKGROUND: Few studies have investigated the effects of dietary fats on the development of Alzheimer disease. We examined the associations between intake of specific types of fat and incident Alzheimer disease in a biracial community study. METHODS: We performed clinical evaluations on a stratified random sample of 815 community residents aged 65 years and older who were unaffected by Alzheimer disease at baseline and who completed a food-frequency questionnaire a mean of 2.3 years before clinical evaluation. RESULTS: After a mean follow-up of 3.9 years, 131 persons developed Alzheimer disease. Intakes of saturated fat and trans-unsaturated fat were positively associated with risk of Alzheimer disease, whereas intakes of omega-6 polyunsaturated fat and monounsaturated fat were inversely associated. Persons in the upper fifth of saturated-fat intake had 2.2 times the risk of incident Alzheimer disease compared with persons in the lowest fifth in a multivariable model adjusted for age, sex, race, education, and apolipoprotein E epsilon4 allele status (95% confidence interval, 1.1-4.7). Risk also increased with consumption of trans-unsaturated fats, beginning with the second fifth of intake (relative risk, 2.4 compared with the lowest fifth; 95% confidence interval, 1.1-5.3). We observed linear inverse associations between Alzheimer disease and vegetable fat (P =.002), and, after further adjustment for other types of fat, marginally significant associations with intake of omega-6 polyunsaturated fat (P =.10 for trend) and monounsaturated fat (P =.10 for trend). Intakes of total fat, animal fat, and dietary cholesterol were not associated with Alzheimer disease. CONCLUSION: High intake of unsaturated, unhydrogenated fats may be protective against Alzheimer disease, whereas intake of saturated or trans-unsaturated (hydrogenated) fats may increase risk.

The first thing I will say is that they are incorrect about what they are studying! They say "dietary fats," but then talk about the actual molecules, which are fatty acids in this case. A "dietary fat" would be something like butter, coconut oil, or corn oil. Thus, if they had "investigated the effects of dietary fats," they would have examined the difference between people who used butter versus those who used margarine as their primary sources of fatty acids, for example. This would be much better, though cooking techniques would certainly be a relevant factor that would need to be controlled for, unless hardly anyone cooked their primary dietary fat. Another point that is worth noting is that they assumed that the questionnaires were accurate, even though 131 of the 815 people studied here developed Alzheimer’s Disease (AD) within four years. Since this is a disease that involves mental impairment, especially memory loss, one would think that the authors would want to address this point. They also do not mention that AD is an inflammatory disorder, and that SFAs cannot be made into inflammatory molecules. In fact, if anything, SFAs act as a buffer against inflammation, due to their biochemical inertness. Among 131 cases of AD, to say that those who consumed the most SFAs and TFAs were 2.2 times more likely to develop AD really only means that a small number of people developed it above the other fifths.

In any case, I don’t necessarily think that their findings are incorrect, but the notion that there is likely causation here is a clear case of “jumping the gun.” We do not know if those who consumed the most SFAs and TFAs also consumed the most overall calories per day, or the most iron per day, or any number of other items that could act to “fuel” inflammation, unlike SFAs, which do not. The most glaring mistake made here, from what I can tell, is that they did not control for SFAs and TFAs separately. That is, there was no group of people who consumed a large amount of SFAs, but not TFAs, and vice versa, as far as we know. The scientific method demands that this be done. If it is not done, the result can be a highly misleading study such as this one seems to be. After all, if a high relative consumption of SFAs meant a much greater risk of AD (and if the risk was a tiny one, who would care at all?), then Asians on diet rich in coconut products should have very high rates of AD, when in fact the opposite is the case. It certainly may be the case that foods rich in TFAs also tend to be rich in SFAs, and so they both look like they may be “guilty.” In light of what is known now, the researchers also should have mentioned that the double bonds of the TFAs may be to blame, in terms of dangerous lipid peroxidation reactions, and so this should have been controlled for as well. Those using high quality oils such as sunflower would at least be provided with some natural antioxidant protection, whereas TFAs may be provided with synthetic antioxidants that are only used to prevent rancidity before the expiration date is reached. Moreover, someone using lard would also not get any of the antioxidant protection found in something like a good quality olive oil or sesame oil.

However, considering the fat content of the dishes listed above, how would one go about trying to follow the researchers’ tentative conclusions about the meaning of their findings? Many of the vegetarian dishes, including “Mediterranean” ones, have more SFAs than beef and pork dishes, for example (per serving). Thus, assuming that people avoid TFAs completely, these researchers would have us believe that at least some beef and pork dishes are among the healthiest things one could eat! Notice that they also don’t take cooking techniques into account in their study, which is one of the main reasons a diet rich in high quality beef, for example, may not be healthy. And why do they not address the evidence that suggests that only meat is unhealthy in “diseases” like AD? It is as if they are totally unaware of the relevant literature. My examination of the evidence leads me to agree with researchers who claim that meat in general is dangerous, at least the way it is usually cooked in nations like the USA. On the other hand, uncooked dairy and coconut products are among the healthiest things one can eat these days. The SFA content is irrelevant. Only in a highly saturated food, such as coconut, will the SFA content act to prevent rancidity, which is the main problem. And other than coconut, there is really nothing else that is close (except for the very similar palm kernel oil, which is rarely used in the kitchens of Western peoples), in terms of the SFA content. This means that except for coconut, one should be very careful about eating anything that contains more than trace amounts of fatty acids (or cholesterol). Foods that are fairly rich in SFAs, such as whole milk yogurt, are generally good, unless one cooks it at high temperature and while exposed to air, or if you can taste that it is “going bad.’

35 th page of the old MSN site.

2008-11-11T15:41:00.000-08:00

The latest on "inflammation."

The following report appeared on www.sciencedaily.com on 8/18/2006:

Research Reveals Inner Workings Of Immune System 'Thermostat'

When bacteria, viruses or parasites attack, immune system cells unleash the soldiers. These “hot” protein compounds kill invaders – but also trigger inflammation, which, if unchecked, can destroy tissue, induce shock and kill the host. So immune system cells let loose another protein compound to cool down the immune response. Precisely how this immune system “thermostat” operates is unclear. The leading hypothesis is that these compounds – which act as furnace and air conditioner – battle it out over control of the system’s inflammatory response. But new research, led by George Yap of Brown University, shows that these cytokines don’t operate independently and in opposition. They operate in harmony and are controlled by the same master. In work published in the Journal of Immunology, Yap and his team show that the “cool” anti-inflammatory protein compound known as Interleukin 10 is activated by Interferon-γ, a class of proteins secreted by a class of white blood cells known as T helper 1 cells. The team then traced secretion of Interferon-γ indirectly to tyrosine kinase 2, or tyk2, the same protein that signals “hot” inflammatory cytokines Interleukin 12 and Interferon-α and Interferon-β. “Under the prevailing paradigm, scientists believe that the pro- and anti-inflammatory arms of the immune system just antagonize each other,” Yap said. “Here we show that they actually induce each other. ‘Hot’ cytokines don’t inhibit ‘cool’ ones – they trigger their production. Wounding, in effect, triggers a healing process.” In previous research, Yap discovered that mutant mice with a naturally defective tyk2 gene were immune to arthritis, a condition caused by inflammation. But these mutants were much more susceptible to opportunistic infections. Why? Without tyk2, Yap found, mice didn’t make enough of the pro-inflammatory warriors that destroy harmful bugs and cause inflammation. This finding established the notion that tyk2 signaling controlled Interleukin 12, the furnace side of the system. But what controlled Interleukin 10, the air conditioner? To find out, Yap and his team conducted a series of experiments in mutant mice infected with the parasite Toxoplasma gondii. They found that Interleukin 10 production by T helper 1 cells is triggered by Interferon-γ - but not directly. Another cell, an antigen presenting cell or APC, sends a stimulatory signal back to the T helper 1 cell, ordering it to make Interleukin 10. “What we see is that the ‘hot’ and ‘cool’ arms of the immune system aren’t independently regulated,” Yap said. “They talk to each other and respond in a dynamic and coordinated fashion.” Yap said the findings should send a message to drug companies designing and testing tyk2-inhibiting medicines for arthritis and other autoimmune diseases. Block tyk2 function, Yap said, and patients will be more prone to infection – and their arthritis may not be relieved. “There could be a downside to these drugs,” he said.

Source: http://www.sciencedaily.com/releases/2006/08/060818012429.htm

My claim is that the evidence suggests that with arachidonic acid in your cells the inflammatory response is "hyperactive" on both the "hot" and "cold" sides of the process, whereas if you allow your body to make its own polyunsaturated fatty acid, the Mead acid, your inflammatory response will be optimal. Interestingly, the same day the above report appeared the one below did:

QUOTE: Harvard Medical School researchers report in the August 17 Science Express that adult mice lacking the immune system protein paired-immunoglobulin like receptor-B (PirB) had brains that retained the plasticity of much younger brains, suggesting that PirB inhibits such plasticity. Intriguingly, brains of immature PirB-deprived mice also exhibited greater plasticity than brains endowed with the protein. Taken together, the results have important implications for the future study and repair of the brain. "Our study of mutant mice lacking PirB function reveals that at all ages, even during critical periods when circuits are prone to change, there are active molecular mechanisms that function to limit synaptic plasticity," said Josh Syken, HMS instructor in neurobiology and lead author of the study. One way to promote new connections in brains damaged by disease or injury might be to target PirB. "The implications here should attract broad interest outside the field of developmental neuroscience because molecules and mechanisms that oppose neuronal plasticity represent new targets for therapy to re-establish damaged connections following spinal cord injury, head injury or stroke," said Syken, who carried out the study with Carla Shatz, Nathan Marsh Pusey professor of neurobiology at HMS, and colleagues. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/08/060818012553.htm

This is evidence that what is considered "normal" is actually a dangerous condition, in that with AA in your cells, the threshold for an inflammatory response is much lower than with Mead acid, leading to the real damage done by "pathogens," various kinds of irritants, and physical insults. It would not be difficult to determine if I am correct, but because it is considered normal for cells to have AA in them, such an experiment is probably not going to be conducted any time soon.

There is a lot of "chatter" these days in certain biomedical circles of the connection between "inflammation" and "heart disease," even though it is known that LDL oxidation is the root of the problem. Here, the evidence about which fatty acids to fear is clear, for example:

Biochim Biophys Acta. 1995 Feb 9;1254(3):250-6.

Oxidation of low-density lipoproteins: effect of antioxidant content, fatty acid composition and intrinsic phospholipase activity on susceptibility to metal ion-induced oxidation.

Croft KD, Williams P, Dimmitt S, Abu-Amsha R, Beilin LJ.

The oxidative modification of low-density lipoprotein (LDL) may play an important role in atherogenesis. Our understanding of the mechanism of LDL oxidation and the factors that determine its susceptibility to oxidation is still incomplete. We have isolated LDL from 45 healthy individuals and studied the relationship between LDL fatty acid, vitamin E and beta-carotene composition, intrinsic phospholipase A2-like activity and parameters of LDL oxidation. LDL was exposed to a copper ion-dependent oxidising system and the kinetics of oxidation studied by monitoring formation of fatty acid conjugated dienes. The length of the lag phase of inhibited lipid peroxidation was measured as well as the rate of lipid peroxidation during the propagation phase. There was no significant correlation between LDL antioxidant vitamin or fatty acid composition and lag time to LDL oxidation. Oleic acid was negatively correlated with the rate of LDL oxidation (r = -0.41, P < r =" 0.34," r =" 0.28," r =" 0.43," r =" 0.43," r =" 0.44,">

Note what they say about the possible dangers of vitamin E supplementation, which is why I prefer to avoid this by avoiding any major source of dietary polyunsaturated fatty acids. In another study, the point about PUFAs and LDL oxidation is as explicit as possible:

"Oxidizability of antioxidant-depleted LDL was largely determined by LDL PUFA content."

Source: Free Radic Res. 1996 Feb;24(2):135-47.

How different constituents of low density lipoprotein determine its oxidizability by copper: a correlational approach.

Kontush A, Hubner C, Finckh B, Kohlschutter A, Beisiegel U.

And here is another example of the true cause of most "infectious" diseaes:

QUOTE: LIAI scientist Mitchell Kronenberg, Ph.D., and an international team of scientists, have identified that Borrelia burgdorferi, the bacteria that causes Lyme disease, contains a glycolipid which triggers an immune response from the body's natural killer (NK) T cells, a type of white blood cell. The finding is particularly exciting because it is one of the few glycolipids found to naturally induce an immune response from the body's NK T cells, which are prized for their ability to initiate a fast and vigorous attack against infection. UNQUOTE.

And a key point is made about this mechamism:

QUOTE: Most white blood cells respond to foreign proteins to protect the body, but NK T cells are unique in that they respond to glycolipids, which are natural biochemicals made of linked fat and sugar. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/08/060822150046.htm

With excessive free radical activity, there will be more glycolipids that are deemed "foreign" and attacked by NT K cells, and with AA in your cells, the attack will be much more pronounced (than if you had Mead acid in your cells). Thus, these "diseases" may never be seen in healthy individuals who are eating an optimal diet, with the possible exception of a massive, and very unlikely exposure to a "pathogen." And here are some more researchers "jumping on the bandwagon:"

QUOTE: "This research validates our hypothesis that immune cells are harmful in gum disease," said Dr. Kawai. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/08/060828074634.htm

The following makes the point that it's the inflammatory response that is causing the damage, not the "germs:"

QUOTE: Many patients with CF develop chronic lung infections from a strain of bacteria known as Pseudomonas aeruginosa. During chronic infection, the inflammatory response is never "shut off", and the continuous inflammation, mediated by IL-23 and other cytokines, may eventually lead to lung damage... Children with CF have an abnormality in the function of a cell protein called the cystic fibrosis transmembrane regulator. This affects the flow of water and certain salts in and out of the body's cells, leading to the production of abnormally thick mucus. The thickened mucus can affect many organs and body systems, including the sinuses and lungs, pancreas, liver, gallbladder, intestines, and reproductive and sweat glands. In the sinuses and lungs, this thickened mucus allows bacteria that would normally be cleared from the airways to multiply and cause chronic infection. UNQUOTE.

Whether or not the CF protein abnormalities can be prevented or lessened by feeding children the right diet is an issue that I won't address here (my guess is that the rates of CF on those consuming certain diets is very low), but note that an "abnormal" (that is, stressful) condition allows the bacteria to prompt the dangerous chronic inflammation.

Source of the quoted passage: http://www.sciencedaily.com/releases/2006/11/061106164725.htm

A new report trumpets the great new discovery of how the 1918 flu pandemic actually killed people: QUOTE: ...the new work shows that infection with the virus prompted an immune response that seems to derail the body's typical reaction to viral infection and instead unleashes an attack by the immune system on the lungs. As immune cells attack the respiratory system, the lungs fill with fluid and victims, in essence, drown. UNQUOTE.

I have been pointing out for well over a year now that this is the way almost all "infectious diseases" cause damage, and the evidence just keeps mounting in favor of this mechanism, which some of the "virus hunters" themselves have acknowledged. The problem is that there is little attention paid to the simple things people can do to prevent the inflammatory response from becoming dangerous.

Source of the quoted passage: http://www.sciencedaily.com/releases/2007/01/070117134419.htm

34 th page of the old MSN site.

2008-11-11T15:40:00.000-08:00

It's stress, not germs, part II.

In the case of "mad cow" types of neurodegeneration, a damaged protein has been said to act as an infectious "germ" or sorts. If you have read the other essays, you can probably guess what my response is: it is certainly possible, but the inflammatory response to the proteins would be the cause of the damage, and inflammation can be attentuated, so that experiments should be done that control for possibly relevant factors that might render the "disease" negligible or non-existant. However, here are some facts that few people are aware of, which suggest that the supposedly dangerous prion proteins are an effect, not a cause. With this knowledge, it is obvious that those who have claimed that prions act as a sort of infectious agent have not followed the scientific method:

"High-manganese, low-copper environments can create prion diseases without the organophosphate catalyst, as seen in deer and elk herds in Colorado who eat manganese-rich pine needles."

Source: http://madcow.pamrotella.com/

QUOTE: Cambridge University prion biochemist, David R. Brown is dismissive of the science behind the infectious model of BSE. He terms it "a very limited amount of science by a few assumed -- reputable scientists." He insists there is "no evidence an infectious agent is present in either meat or milk." "Simple tests on udder walls of cows -- which could easily detect an infectious prion -- have not been done, why I don't understand."

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same Dr. David Ray was appointed to the UK Veterinary Products Committee (VPC) -- a government body that licences animal medicines. Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey chemical poisoning model matches with the epidemiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither. The question is rhetorical, and Purdey has an eye-opening answer. He argues that the prion molecule acts as a shock-adsorber of damaging energy from ultraviolet rays and other oxidizing agents. Once this prion defence system is rendered ineffective by organophosphates, these oxidizing effects have an unmediated impact on tissues.

UNQUOTE.

Source: http://www.cqs.com/opmadcow.htm

"Several US trials failed to invoke BSE in cattle after feeding or injecting them with massive doses of scrapie-contaminated brain tissue. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass-and-silage system without any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding."

Source: http://www.ourcivilisation.com/madcow/madcow.htm

And this comment by virologist Stefan Lanka suggests that the "deadliness" of a "germ," as demonstrated in a lab, may have little to do with the "germ:" QUOTE: These experiments have been used already since over 100 years back, in order to "prove" the existence of several "viruses" quite different from each other, for instance also that of the purported smallpox virus. In these experiments, extracts are being injected through the eggshell into the embryo. Depending on how much is injected and where in the embryo the supposedly "virus-infected" extract is injected, the embryo dies faster or more slowly. It would die from such injections in precisely the same manner too if the extracts were sterilized in ad- vance. This killing then is presented by those virologists, firstly, as direct proof of the existence of the respective virus, secondly as proof of the possibility of multiplying the virus, and thirdly and simultaneously as proof of the isolation of the virus. From hen embryos killed in this way, millions of which are dying silently each year at the vaccine manufacturers', various vaccine substances are being produced. Besides hen embryos, also cells are being killed in test-tubes in order to present the dying of these cells as proof of the existence, the multiplying and the isolation of a disease- causing virus. Nowhere however is a virus being isolated in this manner, photographed in an electron microscope and its component parts described in processes of the type called electrophoresis. UNQUOTE.

Source: http://www.gatago.com/misc/health/aids/2472802.html and: http://www.gnn.tv/A02138

The other thing you have likely heard about is that “defective genes” cause various “diseases,” but what you rarely hear is that oxidative stress (probably involving lipid peroxidation) and other stressors caused the genes to become defective in the first place, and thus the “disease” is entirely preventable – if one follows a correct diet and lifestyle. It is no mystery that so many “diseases” have reached what we are told are “epidemic” levels in recent years. The following is one of the few reports that includes a discussion of “inflammation” and stressors along with the results that defective genes were detected:

Title: Genetic variation linked to age-related macular degeneration.

QUOTE: "...These data suggest that CFH Y402H [the gene in question] may be a causal factor in more than 50 percent of all AMD cases in the general population."

"Genetic predisposition to a malfunctioning CFH can only be of importance when the complement system is switched on," the authors write. "This is demonstrated by the significant interaction between chronic as well as acute inflammation and CFH Y402H."

"The effect of CFH is significantly influenced by environmental and genetic factors that determine the inflammatory response and activate the complement pathway." (JAMA. 2006;296:301-309. Available pre-embargo to the media at www.jamamedia.org). UNQUOTE.

Source: http://www.eurekalert.org/pub_releases/2006-07/jaaj-gvl071306.php

Note that this was a study of correlations, and not of direct molecular-level mechanisms. Here is a much better kind of study, discussing molecular-level mechanims, yet also presenting a comprehensive view of disease:

Eur Respir J. 2006 Jul;28(1):219-42.

Oxidative stress and redox regulation of lung inflammation in COPD.

Rahman I, Adcock IM.

Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (c-Jun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kappaB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kappaB-mediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kappaB-alpha kinase or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-kappaB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression. Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity. The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/quercetin and reserveratol), specific spin traps, such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kappaB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells. Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.

Another group of researchers has reached similar conclusions: QUOTE: ...the research team studied what precedes inflammation - the injury of hepatocytes caused by toxic chemicals, which sets in motion the inflammation process.... We now understand development of liver cancer in mice. Since inflammation drives both damage and regeneration in liver tissue, it is the repeating cycle of damage, inflammation and regeneration that leads to liver cancer..." UNQUOTE. Source: http://health.ucsd.edu/news/2006/06_21_Karin.htm.

And here's the latest point about free radical damage/oxidative stress being the root cause of "infectious disease:"

QUOTE: Dr. Howard Taylor Ricketts, who eventually died of typhus, identified rickettsia in the late 1800s. Sahni's research group first began investigating the rickettsia bacteria as a model to study the biological changes that occur in the lining of the blood vessels (endothelium) as the bacteria travels through the blood stream. Initially they were looking at what types of cellular changes occur in response to the infection. They discovered that cells undergo oxidative stress and produce harmful free radicals, causing inflammation and other complications.

Researchers hypothesized that antioxidants might serve as useful therapies after examining the damage to infected cells, as seen by electron microscopy, and through biochemical evidence proving oxidative stress (OS), a term used to describe a level of damage in cells, tissue and organs. Antioxidants can generally neutralize free radicals and reduce oxidative damage. Earlier experiments in which scientists infected cells with rickettsia bacteria and then treated the cells with alpha-lipoic acid, a powerful antioxidant, showed that the infected cells did, indeed, marshal a defense against the bacteria. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/08/060809232944.htm

And here's a study that supports the connection between "infectious diseases" and damage from free radicals:

J Am Coll Cardiol. 2006 Jun 20;47(12):2436-43. Oxidized low-density lipoprotein autoantibodies, chronic infections, and carotid atherosclerosis in a population-based study. Mayr, M., et al. OBJECTIVES: We investigated whether associations exist between immune reactions to oxidized low-density lipoproteins (OxLDLs), chronic infections, and carotid atherosclerosis as quantified by ultrasound. BACKGROUND: Atherosclerosis is a chronic immuno-inflammatory disease wherein both oxidized lipids and infectious agents are incriminated as possible contributors. METHODS: We measured immunoglobulin (Ig)G and IgM autoantibody titers to copper-oxidized-LDL and malondialdehyde-LDL (OxLDL-AB), IgG and IgM apolipoprotein B-100-immune complexes (ApoB-IC), and titers of antibodies to Escherichia coli and chlamydial lipopolysaccharide (LPS), mycobacterial heat shock protein 65 (mHSP65), Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus and evaluated their relationship to cardiovascular risk factors, chronic infections, and incident/progressive carotid atherosclerosis in the Bruneck study. RESULTS: The OxLDL-AB and ApoB-IC levels remained stable over time as indicated by strong correlations between 1995 and 2000 measurements (p <>

Though I've debunked several claims often seen in nutritional and biomedical textbooks (as have others before me), I think my most important "discovery" is that the "immune system" can only work optimally with Mead acid in your cells (rather than arachidonic acid or an omega 3 PUFA). The reason is that with the Mead acid in your cells, if there is an insult that triggers the immune system, you will get a short burst of "inflammation," then it will recede and allow the humoral immune system (antibodies) to do its job. With arachidonic acid in your cells, the inflammatory response will last too long, and may do tremendous damage. If the inflammatory response with AA does become chronic, you run a great risk of having vital biomolecules getting damaged and becoming dysfunction or being attacked by the immune system become they now appear to be "foreign," due to modifcation by free radicals. And if this continues, at a certain point the body will produce so many antibodies that everything appears foreing; it is then that the Th1 to Th2 shift occurs, leading to "AIDS" (the "opportunistic infections"), because the body needs to prevent self-destruction. In some cases, this fails and "autoimmune diseases" occur instead. With the fatty acids from fish oil in your cells, the situation appears to be even worse, which may be what led some "experts" to suggest that one needs to "balance" omega 3s and 6s. It's not clear that this is possible, because when cells are stressed, one fatty acid must predominate, in terms of being metabolized into inflammatory molecules. In any case, the Mead acid appears to be clearly the best choice in the microscopic "Goldie Locks" story.

33 rd page of the old MSN site.

2008-11-11T15:39:00.000-08:00

Epidemiology: Facts versus "factoids."

I was thinking about the difference between "studies" one often hears about in the mainstream media - studies that contradict each other (and therefore cannot be considered "factual") - and pieces of information that are more substantive. Rather than listen to one "expert" talk about how great red wine is while another drones on about the perils of alcohol consumption, which might be best described as "factoidal" (in a new, more apt, language designed to reconsider findings deemed "scientific"), my tentative opinion is that something like feeding an animal species (such as dogs) different diets and seeing if any was substantially better or worse than the rest (in terms of health, but mostly longevity) would be best thought of as "factual." Feeding dogs a diet no human would or has ever eaten, then looking for markers of this or that "disease" (even though dogs rarely die of it - unlike humans), and not determining whether the dogs live shorter and less healthy lives, is at best "factoidal" information. And yet this is what most "science" these days (on biomedical and nutritional issues, at least) amounts to for the most part.

This brings me to the subject of "epidemiololgy," which is a statistical study of "disease" that starts with all kinds of assumptions, one of which, in the "infectious disease" context, is that "germs" are the direct and sole cause of these kinds of "diseases." I have written about the problems and misleading advice that has been derived from epidemiology in some of the other essays, but here I want to turn my attention to a study that is very interesting, though most likely flawed. The question worth asking, after examining it, is: is it factual or factoidal? And in this case, I think the answer has to do with how wise the investigator is, rather than what is contained within the study itself.

The study in question is J.C. Annand's "Further evidence in the case against heated milk protein," published in Atherosclerosis journal; 1972 Jan-Feb;15(1):129-33. Annand points out that pasteurization, cooking, or improper storage can make make lactose much more allergenic. He then states that: "It seems possible therefore that this same response against denatured MP [milk protein] may be a factor in the development of atherosclerosis or of arterial thrombosis." After that, he talks about the correlations found or not found in the epdiemiological evidence: "...the dietary factor which seemed to correlate consistently throughout these surveys appeared to be MP which had received relatively prolonged heat treatment. Thus the consumption of flash-pasteurized milk, saturated fatty acids, milk fat and sugar all failed to correlate on this historical basis in the UK."

Now he may indeed be on to something here, but note that at this point he can only suggest a scientific hypothesis. In order to present a hypothesis like Annand's, at this point in history, one would need to do an experiment that controlled for oxidized cholesterol, since there is now a great deal of evidence, down to the molecular level, that this is the root cause of "heart disease." In 1972, this was not known, and so Annand's idea was reasonable. In fact, his point about milk protein is still worth considering, an should certainly be controlled for in relevant experiments. However, my point is that while Annand's investigations were thoughtful, one still needs to follow the scientific method to determine what the reality is. Unfortunately, in the case of various "diseases," it is now routine to take all kinds of "short cuts" that directly violate the scientific method, and the results of this are all too obvious. Also worthy of note, though in this the "mainstream media" is at least complicit, is the scant attention paid to results that contradict the simplistic and misleading notions that abound these days. For example, in the July 17, 2006 edition of Newsday (page 26), in an article entitled, "Midlife clues to dementia," we learn that after studying "cholesterol in a group of 1,027 men over three decades. Among many who developed dementia, records showed that their cholesterol levels had dropped about 15 years earlier, and had remained low." No explanation was offerred; the author merely characterized it as a "contradiction."

Now I'll discuss some problems with non-epidemiological "scientific" claims. Below are some citations that I will use in the remainder of this essay, when I have the time to finish it.

Genetic variation linked to age-related macular degeneration "The effect of CFH [a gene "turned on" by stressors] is significantly influenced by environmental and genetic factors that determine the inflammatory response and activate the complement pathway." (JAMA. 2006;296:301-309. Available pre-embargo to the media at www.jamamedia.org). http://www.eurekalert.org/pub_releases/2006-07/jaaj-gvl071306.phpHigh-manganese, low-copper environments can create prion diseases without the organophosphate catalyst, as seen in deer and elk herds in Colorado who eat manganese-rich pine needles. http://madcow.pamrotella.com/Cambridge University prion biochemist, David R. Brown is dismissive of the science behind the infectious model of BSE. He terms it "a very limited amount of science by a few assumed -- reputable scientists." He insists there is "no evidence an infectious agent is present in either meat or milk." "Simple tests on udder walls of cows -- which could easily detect an infectious prion -- have not been done, why I don't understand." A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same Dr. David Ray was appointed to the UK Veterinary Products Committee (VPC) -- a government body that licences animal medicines. Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey chemical poisoning model matches with the epidemiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither. The question is rhetorical, and Purdey has an eye-opening answer. He argues that the prion molecule acts as a shock-adsorber of damaging energy from ultraviolet rays and other oxidizing agents. Once this prion defence system is rendered ineffective by organophosphates, these oxidizing effects have an unmediated impact on tissues. http://www.cqs.com/opmadcow.htm IT HAS BEEN DEMONSTRATED HOWEVER THAT H5N1 kills hen embryos and can be cultivated in eggs. Where is the rat to be smelled in this? These experiments have been used already since over 100 years back, in order to "prove" the existence of several "viruses" quite different from each other, for instance also that of the purported smallpox virus. In these experiments, extracts are being injected through the eggshell into the embryo. Depending on how much is injected and where in the embryo the supposedly "virus-infected" extract is injected, the embryo dies faster or more slowly. It would die from such injections in precisely the same manner too if the extracts were sterilized in ad- vance. This killing then is presented by those virologists, firstly, as direct proof of the existence of the respective virus, secondly as proof of the possibility of multiplying the virus, and thirdly and simultaneously as proof of the isolation of the virus. From hen embryos killed in this way, millions of which are dying silently each year at the vaccine manufacturers', various vaccine substances are being produced. Besides hen embryos, also cells are being killed in test-tubes in order to present the dying of these cells as proof of the existence, the multiplying and the isolation of a disease- causing virus. Nowhere however is a virus being isolated in this manner, photographed in an electron microscope and its component parts described in processes of the type called electrophoresis. http://www.gatago.com/misc/health/aids/2472802.html and: http://www.gnn.tv/A02138 Several US trials failed to invoke BSE in cattle after feeding or injecting them with massive doses of scrapie-contaminated brain tissue. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass-and-silage system without any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding. http://www.ourcivilisation.com/madcow/madcow.htm

32 nd page of the old MSN site.

2008-11-11T15:38:00.000-08:00

It's stress, not "germs" that causes disease.

This is a page that I will be working on for a while. Basically, there are some quotations from reports or studies that show how most "experts" are "barking up the wrong tree," finding "germs" where the underlying cause is one or more known stressors. In the case of Hep C., for example, whether or not a "germ" is actually present appears to be beside the point; what determines whether illness manifests itself is the amount and kinds of stress (and also things that keep stress under control, such as antioxidants). The report about a possible connection between "prion disease" and "heart disease" is evidence that some scientists don't realize that they are mistaking effect for cause; damaged proteins will likely be found in all kinds of "diseases," but again, the stressors caused that damage, and the proteins are just an effect, not a cause.

While working at her clinic at the military hospital, Sjogren noted that at least half of her patients tested positive for the hepatitis C virus. She then started wondering about how servicemembers were faring with treatments and how the disease affected the quality of their lives. From the start, Sjogren wanted to answer specific questions for servicemembers who have Hepatitis C: What happens to these people over time? How does it affect their quality of life? What happens when you treat them? "We just don't know what the impact of hepatitis C is. The rate of hepatitis C has been studied in the military but not the outcomes," she said. "Nobody has talked to them as a research population ... and captured the story the way we do." Sjogren's research endeavors were funded by a grant from the DoD's Peer Reviewed Medical Research Program. Congress created the program in 1999 to promote research in health issues the military faces. Since its inception through 2005, the program has spent almost $300 million to fund nearly 200 projects in a range of medical topics, including combat casualty care and technology and infectious disease research like Sjogren's. Once members from any of the military services were diagnosed as positive for the hepatitis C virus, their doctors told them about Sjogren's study so they could learn more about joining it. If they decided to participate, Sjogren's team performed a liver biopsy, if one hadn't already been done, to see how advanced the disease was. At the end of four years, a second biopsy was taken. "It's the only way to establish the progression of the disease," Sjogren said. Her patients, ranging in age from 18 to the upper 50s, mostly come from the Northeast because of its proximity to Walter Reed. Thirty percent of the study volunteers had minimal liver disease, Sjogren said. Of the 70 percent with more advanced liver disease, 15 to 20 percent had cirrhosis, a condition in which scar tissue replaces healthy tissue, blocking the flow of blood through the organ and preventing it from working as it should. Cirrhosis is the twelfth leading cause of death by disease, killing about 26,000 people each year, according to The National Digestive Diseases Information Clearinghouse Web site. Sjogren's clinic provided treatment to "just about everybody unless they have very minimal disease or liver damage," she said. "We may not offer them treatment because chances are that person's disease may not progress." The standard treatment--24 to 48 weeks of a once-a-week injection with interferon and several pills of ribavirin each day--are what Sjogren speculated would cause a decrease in quality of the volunteers' lives. "The medications are tough to take," she said. On initial questionnaires, study volunteers reported that they were depressed; anxious about their health, families, and careers; and having trouble sleeping. Once treatment began, however, they reported that their quality of life had improved. "We've been very surprised. When we asked the patients why (they felt better), they said, 'I'm doing something for my infection,'" Sjogren said. Another factor that may have calmed study volunteers is the patient education Sjogren's staff offers. "Sometimes they don't fully understand hepatitis C, and the patients are very anxious. They think they have HIV or something that's going to kill them overnight," she said. "We like to talk to the patient and put them at ease, and say 'Look this is the story, let's work together.'"

http://www.sciencedaily.com/releases/2006/07/060707152257.htm

These findings raise the possibility that heart infection could be a new aspect of prion diseases, including those that affect humans and livestock, and that these diseases could travel through the blood… "Until now, prion disease has been thought of as a chronic neurological condition," says Scripps Research Professor Michael B. Oldstone, M.D., who led the research. "Our study has shown, however, that it can have other manifestations, therefore expanding the types of conditions it could cause."

http://www.sciencedaily.com/releases/2006/07/060707151953.htm

A new study shows that statins, which are typically used as anti-cholesterol medications, can inhibit the replication of the hepatitis C virus (HCV). They could replace ribavirin in combination therapy with interferon. These findings are published in the July 2006 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD), published by John Wiley & Sons, Inc. Currently, 170 million people worldwide are infected with HCV. The standard treatment is a combination therapy of interferon and ribavirin, which is only effective in about 55 percent of patients. The remaining 45 percent face a threat of the disease progressing to cirrhosis and liver cancer. Based on recent reports that one statin, lovastatin, inhibits HCV replication, researchers led by Masanori Ikeda of Okayama University in Japan, tested other statins in search of a more effective anti-HCV therapy. Using the OR6 cell culture assay system, they evaluated the anti-HCV activities of five statins: atorvastatin, fluvastatin, lovastatin, pravastatin and simvastatin. When the statins were tested alone, all except pravastatin inhibited HCV replication. Fluvastatin had the strongest effect. Atorvastatin and simvastatin had moderate effects while lovastatin had a weak effect. While pravastatin exhibited no anti-HCV activity, it did work as an inhibitor for HMG-CoA reductase, suggesting that the anti-HCV activities of the other stains are not due to the direct inhibition of HMG-CoA. The researchers determined that the anti-HCV activities of statins were not related to cytotoxicity, meaning they did not kill the host cell. Additional experiments also suggested that, "the statins possess the ability to inhibit the replication of HCV RNA via a specific antiviral mechanism," the authors report. The researchers tested the theory that certain proteins are required for HCV RNA replication and that statins block the replication by inhibiting those proteins. In support of this theory, they found that the addition of both mevalonate and geranylgeraniol restored HCV RNA replication in the statin-treated cells. To evaluate statins as potential replacements for ribavirin in combination therapy, the researchers tested the anti-HCV activities of each one when combined with interferon. Each combination, except the one including pravastatin, had even stronger inhibitory effects on HCV RNA replication than when the statin was used alone. Again, fluvastatin plus interferon exhibited the strongest effect. "We clearly demonstrated that co-treatment of interferon and fluvastatin was an overwhelmingly effective treatment," the authors report. This combined therapy was more effective against HCV RNA replication than interferon alone and more effective than the standard combination therapy of interferon and ribavirin.

http://www.sciencedaily.com/releases/2006/07/060709125024.htm

Circulation Journal. 2005 Apr;69(4):475-80. Title: Fluvastatin ameliorates the hyperhomocysteinemia-induced endothelial dysfunction: the antioxidative properties of fluvastatin.

…CONCLUSIONS: Hyperhomocysteinemia, even mild to moderate, induces endothelial dysfunction through its oxidative effect. The antioxidant fluvastatin was able to cancel out the oxidative stress induced by hyperhomocysteinemia and ameliorate endothelial dysfunction.

Here is a recent report that shows how a virus actually does cause "disease."

Viral disease outbreak in Mauritius PORT LOUIS, Mauritius, July 15 [2006] (UPI) -- A rare mosquito-borne virus has killed at least 77 people on Mauritius and other Indian Ocean Islands this year.

The chikungunya virus causes fever, joint pain and other symptoms, the Times of London reported. Some tourists have been infected along with local inhabitants.

Most of the dead were elderly.

The outbreak was reported in The Lancet after researchers at the University of Lausanne reported finding the virus in a woman who had recently returned from Mauritius.

The disease usually makes itself felt within four to seven days after a person is bitten by an infected mosquito. About 12 percent of people with the infection continue to experience joint pain for at least three years.

The outbreak peaked in the first three months of the year, although health officials advise tourists in the area to take precautions against mosquito bites.

Note that the most of the deaths were among the elderly, and that the symptoms occurred within days, and are characteristic of a pronounced inflammatory response. In fact, many victims continued to have these symptoms for years, due to this "autoimmune" problem. Whether or not the diet of the people was a major factor was apparently not explored, as one would guess (after reading many such reports and studies). There was no direct cytopathic effect here, and this "deadly" virus killed a tiny percentage of the population that was exposed to it - the very weak in particular - just as evolutionary theory would predict. I would like to see one piece of evidence that demonstrates a direct cytopathic effect by any "germ" in a healthy, non-"geriatric," adult human. I have yet to find any. Please post the evidence of this in the general message board forum if you can find any. What is interesting is how "HIV/AIDS" is also said to be viral, and yet in this "condition," one can be asymptomatic for years, then all of a sudden one or more of several very different disorders might afflict you, and it does not matter how healthy you are. In a sense, "HIV/AIDS" is a charicature of a realistic understanding of how "germs" cause "infectious disease." In fact, what can do direct cytopathic damage to a tissue or organ are the kinds of drugs being given to the "HIV infected," which explains why so many of them now die of liver failure. At this point, the only interesting question to me is, will future historians regard the "virus hunters" of today in more or less the same light as the witch hunters of several hundred years ago?

Ane here's a report today about how molecules in cranberry juice prevent "infectious bacteria" from becoming a problem, by preventing the bacteria from becoming "clingly" (as one scientist phrased it):

QUOTE: Compounds in cranberry juice have the ability to change E. coli bacteria, a class of microorganisms responsible for a host of human illnesses (everything from kidney infections to gastroenteritis to tooth decay), in ways that render them unable to initiate an infection... The new results build on previously published work, in which Camesano and her team showed that cranberry juice causes tiny tendrils (known as fimbriae) on the surface of the type of E. coli bacteria responsible for the most serious types of UTIs to become compressed. Since the fimbriae make it possible for the bacteria to bind tightly to the lining of the urinary tract, the change in shape greatly reduces the ability of the bacteria to stay put long enough to initiate an infection. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/09/060910142246.htm

And here's another good passage from a recent report:

"Bacteria use chemical signals to initiate the majority of human infections. When these signals reach a certain threshold (in a process known as quorum sensing), pathogenic bacteria will change their mode of growth and produce virulence factors that lead to infection. These chemical signals also trigger the bacteria to produce slimy biofilms that cloak the bacteria and make the colony physically resistant to antibiotics."

Source: http://www.sciencedaily.com/releases/2006/09/060911103419.htm

31 st page of the old MSN site.

2008-11-11T15:37:00.000-08:00

Saturated fatty acids are the solution, not the problem.

The following study makes the point that when doing an epidemiological study on the effects of "saturated fat," one must take the other food constituents into account. As I've said in the other essays, failure to do so is a violation of the scientific method and should not be considered science.

J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.

"Intake of total and saturated fat from meat was associated with statistically significant increases in pancreatic cancer risk but that from dairy products was not. CONCLUSION: Red and processed meat intakes were associated with an increased risk of pancreatic cancer. Fat and saturated fat are not likely to contribute to the underlying carcinogenic mechanism because the findings for fat from meat and dairy products differed. Carcinogenic substances related to meat preparation methods might be responsible for the positive association.

In a study entitled "The fish nobody knows," it was found that those who rarely ate fish had a much lower heart attack risk that those who did, apparently because the people in the study usually ate fried fish. Source: Barnett and Barone, 1989.

But it's important not to miss all the important factors involved here. While it's true that studies have demonstrated how dangerous cooked meat can be, one should ask if there is any way of minimizing the danger. First, let's take a look at one study that is clear about the dangers of cooked meat:

Cancer Res. 2005 Sep 1;65(17):8034-41.

Cooking meat at high temperatures produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Processed meats contain N-nitroso compounds... Greater intake of bacon and sausage was associated with increased colorectal adenoma risk... Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma.

Now let's take a look at a study that examines the role that the kinds of fat in one's diet can play:

Free Radic Biol Med. 1988;5(2):95-111.

The ways in which dietary polyunsaturated fats and antioxidants affect the balance between activation and detoxification of environmental precarcinogens is discussed, with particular reference to the polycyclic aromatic hydrocarbon benzo(a)pyrene. The structure and composition of membranes and their susceptibility to peroxidation is dependent on the polyunsaturated fatty acid (PUFA) content of the cell and its antioxidant status, both of which are determined to a large degree by dietary intake of these compounds. An increase in the PUFA content of membranes stimulates the oxidation of precarcinogens to reactive intermediates by affecting the configuration and induction of membrane-bound enzymes (e.g., the mixed-function oxidase system and epoxide hydratase); providing increased availability of substrates (hydroperoxides) for peroxidases that cooxidise carcinogens (e.g., prostaglandin synthetase and P-450 peroxidase); and increasing the likelihood of direct activation reactions between peroxyl radicals and precarcinogens. Antioxidants, on the other hand, protect against lipid peroxidation...

Fat consumption patterns are well documented, and correlate very well to what is known about molecular-level mechanisms, for example:

"Fat available in the food supply increased from an average of 124 g/day per capital in 1909 to 172 g/day in 1985. Although the chief sources of fat during that time have been fats and oils; meat, poultry, and fish; and dairy products, great changes within each of these groups have occurred. The proportion of animal fat declined from 83 to 58% as butter and lard use declined, whereas the proporion of vegetable fat (in margarinesand in salad and cooking oils) rose from 17 to 42%."

Source: The book, "Diet and Health," by the National Research Council, page 160.

I would further add that the lard of 1909 was considerably higher in saturated fatty acid content than most lard sold in a nation like the USA is today.

Here are some more frightening statistics from this book: "The percentage of calories contributed by linoleic acid [the most common form of dietary omega 6 polyunsaturated fatty acid - also called PUFAs] to total fat fat itake increased from 7% during 1909-1913 to about 16% in 1985... In 1985, linoleic acid was available at 7% of total calories..." Also from page 160. This is important, because the statistics also tell us that: "The requirements for omega-6 PUFAs in mamary tumor promotion have been explored systematically by Ip, et al. (1985), who reported 4 to 5% of total calories as the threshold at which the yield of mammary tumors increased..." Page 213. In the early 1900s, these kinds of cancers, common today, were rare. Thus, both the molecular-level evidence and all the statistics point to the same "culprit." I can't tell you why this receives so little attention in the "mainstream media," but you are certainly free to contact some "science reporters" and ask. Please post your experiences in this endeavor in the newsgroup section of this site if you do.

As I've pointed out in other essays, having AA in your cells makes you more susceptible to "diseases" thought to be caused by something like excess alcohol consumption. For example:

Toxicol Appl Pharmacol. 2006 Jul 1. "Nitric oxide donors prevent while the nitric oxide synthase inhibitor l-NAME increases arachidonic acid plus CYP2E1-dependent toxicity." Wu D, Cederbaum A.

QUOTE: Polyunsaturated fatty acids such as arachidonic acid (AA) play an important role in alcohol-induced liver injury. AA promotes toxicity in rat hepatocytes with high levels of cytochrome P4502E1 and in HepG2 E47 cells which express CYP2E1. Nitric oxide (NO) participates in the regulation of various cell activities as well as in cytotoxic events. NO may act as a protectant against cytotoxic stress or may enhance cytotoxicity when produced at elevated concentrations… These results indicate that NO can be hepatoprotective against CYP2E1-dependent toxicity, preventing AA-induced oxidative stress. UNQUOTE.

Notice how one event follows another, creating a "pathway," which might not have to be therre in the first place. In the above example, NO may be a "protectant," but it can also cause harm if too much is produced, or if it is produced too often. Again, without AA in your cells, this will either not happen, or else it will take more of an insult for it to be triggered, and even then less damage will likely result. Below is a report that is best summed up by a quotation from it:

QUOTE: "What happens four hours after that high-fat meal is that your artery looks just like the arteries of a person who has heart disease," said co-author Janet P. Wallace... UNQUOTE.

The title of this report, however, is as misleading as one could imagine: "A Serving Of Exercise After That Saturated Fat." Why is it so misleading? Because we are not told what the fatty acid content of the meals was, and worse, as the researchers themselves point out: "Wallace said the oxidation of high-fat meals causes oxidative stress markers that harm the arteries and contribute to such conditions as heart disease, diabetes, Alzheimer's and cancer..." Now it is biochemical fact that saturated fatty acids in the form of food do not have this effect - something like fresh coconut oil could be used as the only form of fat in a high-fat meal in order to demonstrate this experimentally, something that obviously should have been done by these researchers. However, as is usual, they simply accept linguistic conventions about "saturated fat" and probably don't even know about the low rates of the diseases Wallace mentioned among those who eat very large amounts of SFAs but very low amounts of unsaturated fatty acids.

Thus, I agree with them on their findings. They appear to have fed the subjects meals featuring a lot of lard (which is 39% saturated) as well as highly unsaturated oils (used for the cooking). And I would expect such findings, and I agree with their interpretation up to this point. I disagree that lard should be called a "saturated fat," however, because they also call coconut oil a "saturated fat," and fresh coconut oil will not have this effect. It is therefore appropriate for them to repeat the experiment using fresh coconut oil instead of whatever fat source they used, and then report on the results (I am assuming the coconut oil would be consumed fresh, so that other factors will not be in play). However, they probably cannot even conceive of this possibility, which is ne reason owhy I am writing these essays. Another major problem is that the "high-fat" meals served to the subjects were high in cholesterol cooked while exposed to air. The scientific method requires that factors be isolated, so we don't know if the animal fat used plus the oxidized cholesterol was mostly to blame, or if it was one or the other. Here is the meal in question: "The high-fat breakfast included eggs, sausage and hash browns. It included 48 grams of fat (16.5 grams saturated fat and 4.5 grams trans fat), 33 grams protein, 91 grams carbohydrates, 280 milligrams of cholesterol and 2,220 milligrams of sodium." As to the "exercise," it was desribed as follows: "...all 25-year-olds who were determined to be physically active and apparently healthy, walked on a treadmill for 45 minutes two hours after eating..." It's difficult to know what this accomplished, as it's known that at least some forms of "exercise" cause a great deal of oxidative stress, so at the very least, the claim is as tentative as can be.

Source of this report: http://www.sciencedaily.com/releases/2006/09/060901192519.htm

And here's a passage from a recent study supporting the point made above about how PUFAs cause damage: "Arachidonic acid epoxides, previously suggested to be involved in apoptosis, oncogenesis and cell proliferation, are generated by cytochrome P450 epoxygenases..."

Source: J Mol Histol. 2006 Sep 7.

Finally, here is Lancet study that has received almost no attention: Lancet. 1994 Oct 29;344(8931):1195-6.

"Dietary polyunsaturated fatty acids and composition of human aortic plaques." Felton CV, Crook D, Davies MJ, Oliver MF.

QUOTE: How long-term dietary intake of essential fatty acids affects the fatty-acid content of aortic plaques is not clear. We compared the fatty-acid composition of aortic plaques with that of post-mortem serum and adipose tissue, in which essential fatty-acid content reflects dietary intake. Positive associations were found between serum and plaque omega 6 (r = 0.75) and omega 3 (r = 0.93) polyunsaturated fatty acids, and monounsaturates (r = 0.70), and also between adipose tissue and plaque omega 6 polyunsaturated fatty acids (r = 0.89). No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered. UNQUOTE.

QUOTE: High-fat dairy foods contain many potentially anticarcinogenic factors, including conjugated linoleic acid (CLA). However, few epidemiologic studies have specifically evaluated high-fat dairy food consumption, and none have evaluated CLA intake, in relation to colorectal cancer risk... These prospective data suggest that high intakes of high-fat dairy foods and CLA may reduce the risk of colorectal cancer. UNQUOTE.

And this is excellent: Mutat Res. 2002 Sep 30;506-507:9-20. "Comments on the history and importance of aromatic and heterocyclic amines in public health." Weisburger JH.

QUOTE: The carcinogenic risk of aromatic amines in humans was first discovered when a physician related the occurrence of urinary bladder cancer to the occupation of his patients. They were employed in the dyestuff industry, chronically exposed to large amounts of intermediate arylamines… Epidemiological data suggest that meat eaters may have a higher risk of breast and colon cancer. HCAs induced cancer in rats in these organs and also in the prostate and the pancreas. In addition, there is some evidence that they affect the vascular system. The formation of HCAs during cooking can be decreased by natural and synthetic antioxidants, by tryptophan or proline, or by removing the essential creatine through brief microwave cooking prior to frying or broiling. The amounts of HCAs in cooked foods are small, but other components in diet such as omega-6-polyunsaturated oils have powerful promoting effects in target organs of HCAs. On the other hand, the action of HCAs may be decreased by foods containing antioxidants, such as vegetables, soy, and tea… Possibly, the carcinogenic effect of HCAs is accompanied by the presence of reactive oxygen species (ROS), which are also inhibited by antioxidants.. UNQUOTE.

Finally, from a recent report: QUOTE: ...The researchers couldn't explain why eating more animal fat was associated with breast cancer risk. It may be that factors other than fat are involved. For instance, grilling red meat can create cancer-causing chemicals… Earlier studies had suggested one reason for the increased cancer risk, relating this to the heterocyclic amines (HCAs) that form when red meat is cooked at high temperatures (like frying and grilling), especially well-done. In laboratory studies, HCAs bond to estrogen receptors and create estrogen-like effects. In earlier research with
women past menopause, those who consistently ate hamburger, beef steak and bacon very well done thus getting high levels of HCAs -had more
than four times the breast cancer risk in comparism with women who consumed these meats raw or medium done… Like many carcinogens, HCAs have to be activated to be able to damage our DNA and pose cancer risk... UNQUOTE.

Source: http://www.tribune.com.ng/22032007/hlt2.html

30th page of the old MSN site.

2008-11-11T15:36:00.000-08:00

Some thoughts on a book by Robert Gallo.

I’d like to talk briefly about Robert Gallo’s book, “Virus Hunting” (1991). Gallo is considered the “co-founder of HIV,” and in this book he provides a window into his thought process and into what a “top expert” understands about viral phenomena specifically, and “pathogenic” organisms more generally. It is worthy of note how often he mentions that something is “poorly understood” – many times.

He mentions how some microbes are beneficial, while others are innocuous, and: “Others have been harmful under certain circumstances, and a few fatal even under the best circumstances.” Page 44. There are no citations. Moreover, unless all factors are controlled for, how would he know that a few “microbes” are always fatal, since he acknowledges that “circumstances” can play a decisive role here? The role of quantity has been discussed by other “virus hunters,” but Gallo does not mention that the amount of exposure can play a decisive role as well in the initial “infection.”

Next, he describes a virus as: “A chemical entity simply following the rules of physical chemistry.” True enough, but since the rules of physical chemistry are known, why are there so many statements about things that are “poorly understood” in this context? And why has he not “stepped in” and clarified the issue when “AIDS experts” claim that “HIV” is “wiley,” “mysterious,” “paradoxical,” etc., which they have done many times and continue to do so to the present? Is “HIV” the only virus that does not follow the rules of physical chemistry? If it does, then there should be no “mystery,” “paradox,” etc.

Next, still on page 44, Gallo states: “Once inside a cell, specific viruses will, in time, exploit the machinery of certain cells to their own reproductive advantage…” Again, this can be demonstrated in an artificial lab environment, to be sure, and also can occur in some people, but why doesn’t it occur in everyone who is “infected?” Obviously, it cannot be the sole cause – other factors must play a role or else basic logic is violated here. Gallo, along with all the other “virus hunters’” work I’ve read display an alarming lack of interest in what these other factors might be. However, in this book, Gallo does supply some important clues, for example:

"Some viruses burst from the host cell, destroying it in the process. Others 'pinch off' or 'bud' from the cell membrane, giving them an added outer envelope, which includes fatty components from the cell membrane.” Page 49. On page 50, Gallo talks about how viruses attach to the “cell membranes” of cells, and then states: “After this interaction takes place, a poorly understood process occurs that allows some viral components to penetrate the cell, and in this process the fatty component of the viral envelope will fuse with a fatty layer of the cell membrane.” It is also worth mentioning that he says that when an “infected cell” bursts, whatever that means (apoptosis? necrosis? something else?), “The bursting is believed to be brought on by the harmful effects on the cell of the proteins of these kinds of viruses [that is, RNA viruses], but our understanding of the phenomenon is incomplete.” What I would like to know is exactly what that “understanding” at this point actually is. It does not seem to amount to much, does it?

In any case, he does mention fatty acids, and what is known for sure is that highly unsaturated fatty acids can be much, much more biochemically active than saturated ones or monounsaturated ones. Since the way the virus damages cells is “poorly understood,” but since we do know that viruses need to use the cellular machinery, it may be that cells with a lot of polyunsaturated fatty acids in their “cell membranes” may be “sitting ducks,” of sorts, for at least some viruses. Simple experiments could be done to determine this, feeding a group of animals a diet rich in safflower and fish oil, while the other group only gets fresh coconut oil, and then both could be exposed to a virus that usually kills 10% of that species, but I have yet to find one that does exactly this.

On page 52, Gallo remarks: “When large amounts of virus are formed and released at a certain time, the viruses can be found ‘free’ (that is, not in a cell) in the blood plasma. We call this a viremia. Usually, this is very transient and associated with acute clinical symptoms, such as fever and headache.” Later, on page 241, when discussing “HIV,” he talks about “Numerous HIV particles, having replicated in the follicular dendritic cells…” I agree with the point made on page 52, which makes the statement on page 241 so puzzling. That is, if there is “HIV” viremia, why has it yet to be detected in any person, ever? Despite several attempts, all we have to show are “markers” that can occur due to other factors (some not related to any virus at all). Thus, any claim about “HIV” causing “AIDS” violates the scientific method just on this one point alone (and there are more than a few others). Gallo does say that, “During this [early] period, then, the virus has its field day and replicates extensively, so much so that scientists can readily find free virus in the blood, the viremia mentioned in the previous chapter.” Page 243. Yet no matter where one looks for the evidence of this (he provides no references), all one finds are “markers” that are assumed to be evidence of “HIV,” but can be evidence of all kinds of unrelated phenomena.

Gallo actually provides what, in light of the evidence, appears to be the cause of almost all “disease,” for example: “…the macrophage can also be activated to release virus in conjunction with certain cytokines, small proteins with biological activities, that are likely to be released during inflammatory processes…” and that this “…may cause some of the disease symptoms.” Page 247. Now the obvious thing to do, for anyone even somewhat familiar with the scientific method, would be to develop an animal model (which has been done) and then subject animals to their version of “HIV,” such as “SIV” in some primate species. Some animals would be healthy controls, while others would be subjected to the kinds of stressors that were experienced by the first “AIDS patients” in the early 1980s (since “inflammation” can occur even when no “pathogenic organisms” are present). However, as I have pointed out in one of the other essays, the way “AIDS” has been defined, one cannot have “AIDS” without the markers thought to be indicative of “HIV infection,” even if one has all the symptoms of this clinical syndrome. What one is to make of this ludicrous situation is a personal decision, I suppose, but the illogical element is basic and obvious. Moreover, since a virus needs the “help” of the cell: “it [the virus] enters a cell and, with the help of the cell itself, synthesizes what it needs and reassembles these elements into new virus particles” (page 49), but not everyone who is exposed to the virus will in fact become ill, the scientific method demands that one attempt to control for all factors that may be relevant. Until this is done, what is being presented to the public is not science. What one wishes to call it has yet to be determined.

29 th page of the old MSN site.

2008-11-11T15:35:00.000-08:00

Odds and ends.

Here are some important items that I want readers to have access to, even if I have yet to use them in an essay.

ITEM: http://www.mercola.com/2002/aug/17/cooking_cancer.htm

...Boiling at 100 degrees Celsius appears to be the only safe cooking method. In potato-based foods, even cooking at a moderate temperature of 120 degrees Celsius began the process of acrylamide formation. a control group -- an increase similar in magnitude to the high levels observed in non-smoking humans.

ITEM: http://www.mercola.com/2006/jun/29/wendys_is_changing_to_healthy_cooking_oil_or_is_it.htm

Wendy's is Changing to 'Healthy' Cooking Oil, or is It?

Wendy's, the third largest burger chain in the United States, has been revamping its menu to include healthier choices and will soon begin using a non-hydrogenated cooking oil. The oil, slated to begin use in August 2006 in the United States and Canada, is a blend of corn and soy oils with zero grams of trans fat. The move will reduce trans fat in Wendy's French fries and breaded chicken items by 95 percent. Trans fat is a known artery-clogger that raises bad cholesterol while lowering the good kind. Studies have found that just 5 grams of trans fat a day can raise heart disease risk by 25 percent. Using the new oil, the restaurant's chicken sandwiches, nuggets and strips will contain zero grams of trans fat, while a large order of fries will go from 7 grams to 0.5 grams. Wendy's also removed all trans fat from their salad dressings earlier in 2006. Four years ago, McDonald's said they planned to switch to a cooking oil that would reduce the trans fat in their French fries by 50 percent, but they are still in testing mode.

Yahoo News June 8, 2006

Dr. Mercola's Comment:

Most people don't realize that the average American has four orders of fries a week, so this issue is important for many. McDonald's fries now come from huge manufacturing plants that can peel, slice, cook, and freeze 2 million pounds of potatoes a day. The major issue with French fries may not be trans fat, although some fast food chains' fries contain over 30 percent trans fat. What most people fail to understand is that once you heat oil to a high temperature in the presence of oxygen and light you can produce all kinds of different damaged toxic oil molecules that are cyclized, cross-linked, fragmented, bond-shifted, and polymerized. If food turns brown during the cooking process, it has dried out, been overheated, and become toxic. The toxic molecules change the expression of many genes in the direction of inflammation and cancer. When you exceed a safe temperature and turn food brown you not only change the chemistry of the food, you also damage the oil. The nature of chemical reactions is that for every 10-degree Celsius rise in temperature, the rate of chemical reactions (with oxygen, light, metals) at least doubles, and may even triple or quadruple. In addition to the damaged fats, other toxic substances, like acrylamide, are created when you fry potatoes. Acrylamide appears to be a potent carcinogen and was only recently discovered a few years ago.

ITEM (an old post of mine on another newsgroup): ...here is the citation from Keys' Seven Countries (the 1979 book, page 135): "At levels below 200 mg/dl, decreasing cholesterol concentrations tend to be associated with increasing rates of non-coronary death."

...On page B17 of New York's Newsday newspaper (March 1, 2005), AHA spokesperson Dr. Richard Stein states: "What we've learned in the last 15 years is that LDL has to be oxidized in the vessel wall... [in order for plaque to accumulate and become dangerous]."

SOME IMPORTANT STUDIES ABOUT DIET AND HEALTH:

Cancer Res. 2005 Sep 1;65(17):8034-41.

Meat, meat cooking methods and preservation, and risk for colorectal adenoma.

Sinha R, Peters U, Cross AJ, Kulldorff M, Weissfeld JL, Pinsky PF, Rothman N, Hayes RB.

Environ Mol Mutagen. 2004;44(1):44-55.

Meat-related mutagens/carcinogens in the etiology of colorectal cancer.

Cross AJ, Sinha R

Diets containing substantial amounts of red or preserved meats may increase the risk of various cancers, including colorectal cancer. This association may be due to a combination of factors such as the content of fat, protein, iron, and/or meat preparation (e.g., cooking or preserving methods). Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Humans can be exposed to NOCs by exogenous routes (from processed meats in particular) and by endogenous routes. Endogenous exposure to NOCs is dose-dependently related to the amount of red meat in the diet. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs).

J Nutr. 2004 Apr;134(4):776-84.

Meat consumption patterns and preparation, genetic variants of metabolic enzymes, and their association with rectal cancer in men and women.

Murtaugh MA, Ma KN, Sweeney C, Caan BJ, Slattery ML.

Meat consumption, particularly of red and processed meat, is one of the most thoroughly studied dietary factors in relation to colon cancer. However, it is not clear whether meat, red meat, heterocyclic amines (HCA), or polycyclic aromatic hydrocarbons (PAH) are associated with the risk for rectal cancer... These data suggest that mutagens such as HCA that form when meat is cooked may be culpable substances in rectal cancer risk, not red meat itself.

J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.

Meat and fat intake as risk factors for pancreatic cancer: the multiethnic cohort study.

Nothlings U, Wilkens LR, Murphy SP, Hankin JH, Henderson BE, Kolonel LN. CONCLUSION: Red and processed meat intakes were associated with an increased risk of pancreatic cancer. Fat and saturated fat are not likely to contribute to the underlying carcinogenic mechanism... Carcinogenic substances related to meat preparation methods might be responsible for the positive association.

In the "good ole days," many of the cancers were very slow-growing, and the following report may hold a key to the explanation for this:

QUOTE: Edinburgh scientists have identified the way a specific cell protein can trigger the spread of cancer... The protein, MDM2, normally functions to control the activity of a key cancer preventing protein called p53. In some of the body's cells, the biochemical ratio between MDM2 and p53 can become unbalanced causing MDM2 to act as a cancer-promoting agent... In the current study, funded by Cancer Research UK, we have identified protein fragments which can bind to MDM2, inhibiting its activity... UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/07/060724105039.htm

As one ages, such protein fragments accumulate (perhaps due mostly to glycation), and can cause all kinds of problems in this way. Cancers that occur due to this mechanism are not being "fueled" by AA metabolites, and thus usually take much longer to become potentially deadly. Though this report actually shows the mechanism working in the opposite direction (senescence rather than "immortality"), it can work either way. Again, though, there are simple ways to prevent this protein fragment problem, and the first thing to consider is limiting the amount of cellular stressors, as one can do by eating a diet that contains few unsaturated fatty acids and no animals products cooked while exposed to air.

Update (7/26/2008): In a recent report, the following statement is made:

QUOTE: Age may not be rust after all. Specific genetic instructions drive aging in worms, report researchers at the Stanford University School of Medicine. Their discovery contradicts the prevailing theory that aging is a buildup of tissue damage akin to rust, and implies science might eventually halt or even reverse the ravages of age... UNQUOTE.

Source: http://www.sciencedaily.com/releases/2008/07/080724123234.htm

What I find amusing about this is that they are basically claiming that "science" may be able to raise the maximum human life expectancy, which seems to be about 120 years, yet so many people are dying before the age of seventy! It would make sense to first get the overwhelming majority of people to live to be around 110, then concern oneself with going beyond that point. If people continue to eat the kinds of diets that are typical in most "advanced, modern" nations, then getting beyond the 120 year limit is only going to benefit a very small percentage of the population, because the rest will diet of cancer, heart disease, etc., way before the age of 120, or 110, or 100, or 90, or 80.

28 th page of the old MSN site.

2008-11-11T15:34:00.000-08:00

The science "show" must go on?

I don't know how many people in the world do as much research as I've done (on nutritional/health/medical topics) in the last few years, but what amazes me is how I keep reading the same things in reports of scientfic studies. One thing is how some group of researchers think they've uncovered something new, when in fact it is "old news." I've come to realize that unlike historians, most scientists don't know where "they are at" - they have little knowledge of the literature to which they are supposed to be contributing.

Another thing is how those who have detected a protein doing something in a "disease" think that the protein is the underlying cause or show no interest in the cause. Of course, telling people just to avoid a stressor that renders the protein dysfunctional would not pay any bills, now would it? Think of a broken hinge on a door, which makes the door difficult to open and close. One can try to design a much more elaborate hinge or one can replace the hinge, but why not observe the people who use the door to see if they are doing something that is beyond the threshold of what the hinge can bear?

And finally, for now, I often read about how research scientists are so suprised about something that should not be at all surprising to them. The latest example dovetails with a point I've made in my essays here about how the body mostly damages itself. Really, what would be a tremendous aid to most of us would be an "owner's manual" of sorts, rather than a bunch of narrow-minded scientists attempting to "reinvent the wheel," and almost always failing.

QUOTE: The gene makes a protein called STAT1, and its production is triggered whenever the immune system senses a foreign bacterium, virus or other pathogen. STAT1 activation is a critical step in the immune system response, as this protein activates other key immune substances.

So it didn't make sense to the researchers that mice that couldn't produce STAT1 would remain healthy.

“It took us completely by surprise,” Satoskar said. “We knew from previous work that mice that lack the substances produced in response to STAT1 develop serious infections. We thought we'd see that in this study, too...”

The researchers infected groups of mice with L. donovani. Mice in one group lacked the gene that makes STAT1. Mice in another group lacked the gene that makes an immune system protein called T-bet. In a normal immune response to infection, STAT1 triggers the production of T-bet. Together, these proteins are responsible for the production of interferon gamma, an important protein that helps launch a full-blown immune system attack against foreign pathogens.

A group of mice with both STAT1 and T-bet genes intact served as a control.

About two weeks after infection, the researchers began measuring the number of L. donovani parasites in the animals' livers.

The pathogen went wild in the mice that lacked T-bet – the researchers found thousands upon thousands of the parasites in the livers of these animals.

Yet there were next to no parasites in the mice without STAT1.

“Two weeks after infection, the mice without STAT1 had 25-fold fewer parasites in their liver tissue than the normal mice, and about 100-fold fewer parasites than the mice without T-bet,” Satoskar said. “Visceral leishmaniasis never developed in the animals without STAT1 – the parasites weren't able to establish an infection in the animals' livers and spleens.”

The researchers also measured parasite levels in the livers two months after infection. Again, levels were quite high in the mice without T-bet, while normal mice and mice without STAT1 showed no sign of the disease.

While the normal mice weren't sick – they showed no physical signs of having leishmaniasis, such as inflammation of the liver and spleen – Satoskar said the parasite was still in their systems.

“Once infected, the parasite never goes away completely,” Satoskar said. “It's always hiding somewhere.”

Ironically, L. donovani thrives in the liver and spleen by infecting the very cells that the immune system uses to rid the parasite from the body. These cells are called macrophages – a kind of garbage collector for the immune system, as they clean out everything from red blood cells that have died to infectious pathogens. But enough L. donovani parasites can overtake a macrophage's ability to clean up.

“L. donovani infection failed to launch in mice without STAT1 because there weren't enough macrophages in the liver for the parasite to infect, and these are the very immune cells that are essential for successful survival and replication of Leishmania parasites in the host,” Satoskar said.

The researchers aren't suggesting that STAT1 activation should be stopped in order to prevent visceral leishmaniasis. However, they want to figure out how this protein's absence keeps macrophages from flooding into the liver during the early stages of infection. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/06/060625124244.htm

Note that they say that the animals "showed no physical signs of having leishmaniasis, such as inflammation of the liver and spleen." The "disease" is the inflammatory response run amuck, and not a "bug gone wild" for some inexplicable reason. So what are we to make of this? We know (citations in essays above) that the inflammatory response can be ehanced or inhibited by the fatty acid content of one's diet, but they don't appear to know this. We know that stress is what causes "bugs" to become problematic/"pathogenic," but they don't seem to be aware of this either. Where, exactly, are they? Why are taxpayers asked to pay for studies that are so unrelated to medical reality? If this was one study, it wouldn't make much difference, but most medical studies are like this, that is, little interest is shown in trying to understand a "big picture," Instead, we get all kinds of minutiae that never seems to add up to anything (unless someone like myself comes along and tries to make sense of it all). And yet the promises keep coming - soon all "disease" will be curable, they tell us. But when you read the reports, you see what appear to be the "lost souls" of the academic world.

In order to adhere to the scientific method, one must know what factors might be relevant, and then of course controls must be used for them. But if one is unfamiliar with the professional literature on the topic, it is likely that proper controls will not be utilized in the experiments. Here, they could have subjected a group of rats to a diet rich in oxidizing agents and low in antioxidants, while feeding another group a diet rich in antioxidants and low in oxidizing agents. This would tell us whether these genes can be "turned on" or "off" by dietary/environmental factors. The literature suggests this is likely to be the case.

However, they don't seem to know the literature, nor do they seem to think in a comprehensive way. And they appear to be uninterested in underlying causes. It's almost like they are just trying to "put on a show" to justify the money they are being paid - obviously, it is not about results. If it were, those who pledged to win the "war on cancer," develop a vaccine against "HIV," etc., would have been ousted long ago, and replaced by those with new ideas and approaches. Because there is a political/bureaucratic structure in place and because the public doesn't understand enough about the issues, however, the "show" will continue to play on, at the doctor's office or hosptial near you. But at least now you know about it, and may decide not to attend when you are sent an invitation.

A couple of days after writing the above, two articles appeared in a local paper, Newsday (New York metro area). One was titled "Circadian key to cancer?" and the other was "Study IDs gene triggers to liver cancer" (both on page A50 on 6/28/06). In the former, there is no mention of vitamin D and breast cancer (which is what the article addressed), even though there is an extensive literature on this connection to breast cancer and sunlight issues, demonstrating my point about how ignorant so many research scientists seem to be these days on the subject about which they are supposed to have expertise.

The latter article is another thing you see all the time in mainstream biomedical science reports, that is, a discovery of a gene said to be the "key" to one or another "disease." Yet, of course, there never seems to be a cure after such a momentous "breakthrough," does there? Here, however, the author admits that: "...toxins can increase the risk for liver cancer." At the end of the article, there is the usual: "'You can use these mouse-model systems to test compounds that stop of slow these genetic alterations,'" stated by one of the researchers. Thus, as usual, the experiment appears to be about designing very profitable drugs that slow down "disease" progression enough to make people afflicted with the disease demand that they get their medicine, even though there are usually nasty side-effects and life will only be extended a few weeks or months. Most people, don't realize that this is the kind of game being played, and that they are the field upon which these athletes trod.

And the show continues, in yesterday's Newsday newspaper for example, on page A40 (6/29/06). First, we learn that in "Lyme Disease," "The initial symptom is... a red, circular inflammation of the skin." Again, it's about the body's response, not necessarily a "bug" doing direct damage. Below this article is one titled, "Research advance in colon cancer," but the author (it's an AP report) notes that "...doing $3000 genetic tests on every colon cancer patient to find the 4 percent who have such mutations is expensive..." They then talk about a less expensive test that is about 67% accurate. They do not talk about prevention at all, and considering how much is known about the causes of colon cancer, one is compelled to ask why studies such as the following are not mentioned:

Cancer Res. 2005 Sep 1;65(17):8034-41.

Meat, meat cooking methods and preservation, and risk for colorectal adenoma.

Sinha R, Peters U, Cross AJ, Kulldorff M, Weissfeld JL, Pinsky PF, Rothman N, Hayes RB.

An obvious point I have never heard anyone make is, how much can we afford to spend on attempting to make drugs or design "therapies" that either help very few people (and almost always in a very limited way) or only extend lives for a few weeks or months (often with nasty side-effects)? When a society reaches a certain technological boundary, attempting to go beyond it will mean devoting huge resources to it while achieving little in the way of results. Why not just spend a reasonable amount of money on educating the public about what to avoid in the first place? Then, fortuitous accidents, like the discovery of antibiotics (which are now being abused terribly) will occur at times when knowledge and technology are working in tandem.

27 th page of the old MSN site.

2008-11-11T15:33:00.000-08:00

A new report that "says it all."

University of Wisconsin-Madison

June 19, 2006

E. Coli Research Identifies Two New Keys To Regulation Of Bacterial Gene Expression

The cellular process of transcription, in which the enzyme RNA polymerase constructs chains of RNA from information contained in DNA, depends upon previously underappreciated sections of both the DNA promoter region and RNA polymerase, according to work done with the bacterium E. coli and published today (June 16) in the journal Cell by a team of bacteriologists from the University of Wisconsin-Madison.

This fundamental research about a key step in RNA synthesis has important implications for the study of gene expression in other organisms, and adds to the wealth of knowledge about E. coli contributed by scientists from the UW-Madison.

"The kinds of processes that we study in E. coli happen in a wide variety of bacteria of medical, environmental and agricultural importance," notes Rick Gourse, a professor of bacteriology who published the Cell paper along with a team from his lab. "This knowledge can ultimately be put to use in systems that aren't so amenable to investigation, such as bacteria that cause cholera, produce anthrax toxin or lead to ulcers and stomach cancer."

Scientists use model organisms because they are relatively easy to work with and because there is a vast amount of previous knowledge about them. They can then test whether their findings in model organisms hold true in other species, says Gourse, who studies a strain of E. coli that while harmless, is closely related to disease-causing varieties like E. coli 0157:H7.

"Basic research in E. coli is very important," says Gourse. "Much of what we know about gene expression both in bacteria and in higher life forms comes from work performed originally on this model organism." The strain that Gourse works with is one of the most well-studied species in biology and has important ties to the UW-Madison. In his most recent study, Gourse investigated the interaction between RNA polymerase and promoters from the E. coli chromosome. RNA polymerase reads the information in DNA and transcribes it into chains of RNA, which are later translated into proteins. Promoter regions are specific sequences within the DNA chain that tell RNA polymerase when and where to begin transcription, and how much product to make from specific genes.

Gourse's group found that there is a specific region within DNA promoters that makes contact with a highly conserved but previously underappreciated segment of the sigma subunit of RNA polymerase. While the contact with sigma is very strong at promoters for most genes, it is particularly weak at promoters that make ribosomal RNA, which means that other factors like nutritional and environmental signals ultimately regulate the expression of those genes.

"In this case, regulation is achieved not because the promoter makes a special contact, but because it can't establish contact at all," says Gourse. "This is an example of how sometimes less is more, and a probably very ancient example of one of the methods that arose through evolution to regulate gene expression."

Ribosomal RNA makes up the bulk of ribosomes, the molecular machines that make proteins and are present in huge numbers in all cells. Since so much of the cell's energy is used to make ribosomes, control of ribosomal RNA transcription is particularly crucial to a cell's well-being.

"This work is basic to the growth of all bacteria," says Gourse. "By understanding transcription and control of ribosome synthesis in E. coli, we can understand more about these processes in bacterial species that we need to control, like those that cause disease or make toxins. E. coli is also the workhorse of the biotechnology industry. Understanding E. coli gene expression in detail allows us to harness these cells for producing products of biotechnological importance, like pharmaceuticals."

Source: http://www.sciencedaily.com/releases/2006/06/060618223905.htm

As is quite common, the report concludes with a vague promise of great "breakthrough medicines" to come in the near future (if the researchers continue to get their funding, of course). And yet the researchers make the explicit point that nutritional and environmental factors appear to be paramount, and certainly not the "genetic code" by itself. Another point is how a "model" is created from what is observed in one species of bacteria, and from that all kinds of assumptions are made, which of course all too often find their way into textbooks, appearing as "absolute fact" to many students (and teachers as well). It's worth mentioning that with "HIV/AIDS," a model was generated from clinical observations, and not from cellular-level or molecular-level ones. Then, shared "markers" that were thought to be consistent with this model were sought, and some were found, though only in some patients. Attempts at determining underlying mechanisms were undertaken, and all have failed, though the technology is available to do so - thus it is basically one big pile of assumptions and models. And yet even models that were demonstrated to be incorrect are still being touted as "what happens" when a person is "HIV infected." Before the clinical observations, there was speculation about various phenomena that came to be deemed an "infection" by a "retrovirus," but nothing beyond this hazy, presumptuous sheen of technical "knowledge." At a loss for a truly scientific explanation, the "bug hunters," who were in charge of things, decided to force the square pegs into round holes.

If you'd like to get a sense of how little evidence there is of "HIV," go to this link, which discusses what a recent attempt at "isolation" actually revealed:

http://theperthgroup.com/REJECTED/StructureLetterPG.pdf

They (the Perth Group) are responding to a particular study. One media report of it contains the following:

QUOTE: [Professor Stephen Fuller said] "You say can you show me the structure of the HIV virus and the question is which one.

"HIV is very variable. It varied in diameter by a factor of three."

The way the research team, from the Wellcome Trust Centre for Human Genetics at Oxford University, dealt with this was by taking multiple images at different tilts.

Working with colleagues in Heidelberg and Munich, they took about 100 images of 70 individual HIV viruses and then looked at similarities.

Despite the variability, the team found some consistent features... This included the finding that the core of virus - which is cone-shaped - spans the width of the viral membrane. But there are spikes on the outside which bind to human immune cells, called T cells, and allow the virus to invade them. UNQUOTE.

Exactly how this can pass as "isolation" is beyond comprehension, though one has to give some credit to Fuller, who is reporting his findings accurately (though he assumes that "HIV" must be there, somewhere). Another thing that makes no sense is that there is no explanation about how the "virus" "invades" cells. A virus needs to be activated before it does anything, remaining inert until the proper signals are received, and thus this statement about binding and invading is at the very least incomplete. Of course, even if we decided to accept this assumption (with no evidence to support it), there should still be ample evidence of "HIV" killing off these cells, and no such evidence exists to date. The cells sometimes, but not always, tend to decrease in those said to be afflicted with "AIDS" over time, and so it is assumed that "HIV" is the cause of this (though again, not all "AIDS deaths" are due to this loss of cells anway).

Source of this report: http://newsvote.bbc.co.uk/mpapps/pagetools/print/news.bbc.co.uk/2/hi/health/4642940.stm

26 th page of the old MSN site.

2008-11-11T15:32:00.000-08:00

How a latent virus actually causes "disease."

An interesting report on sciencedaily.com made the following reports about a virus that can cause symptoms but is often latent for long periods of time.

"Infected for life: How the Herpes Simplex Virus Uses MicroRNA to Hide Out in Cells

Researchers at the University of Pennsylvania School of Medicine have discovered part of the reason why cold sores, caused by a herpes virus, come back again and again. The new study, published online last month in Nature, points to a small RNA molecule, called a microRNA (miRNA) as the culprit that keeps the latent virus-infected cell alive. These findings could one day lead to a new way to fight the virus and offers the first target for intervention in the latent infection.

A research team led by Nigel W. Fraser, PhD, Professor of Microbiology, has found that herpes simplex virus-1 (HSV-1), the virus that causes cold sores and ocular keratitis, produces an miRNA molecule. This miRNA is encoded by the Latency-Associated Transcript gene (LAT) in the viral genome and works through a process called RNA interference to prevent normal cell death or apoptosis. Thus, the latent viral infection is maintained for the lifetime of the individual because the latently infected cell does not die."

“Although miRNAs encoded by cellular genes are known to be an important mechanism for controlling gene expression, this is one of the first miRNA found to be encoded by a viral genome,” says Fraser. “Our study helps show how HSV-1 can maintain a latent infection for the lifetime of an infected individual.”

The LAT gene was discovered by Fraser and colleagues in 1984, but a protein product from this gene has never been found. This caused Fraser and his research team to hypothesize that LAT may work through an miRNA molecule, which is a small piece of the LAT gene. It interferes with the translation of two cell proteins that are required for cell death: TGF-b and SMAD-3. The LAT miRNA binds to specific sequences of messenger RNA from these two genes and causes them to be degraded. Thus, the amount of TGF-b and SMAD-3 protein is reduced in the cell and apoptosis is prevented. Because the latent virus is not producing any viral proteins the immune system of the infected individual cannot detect the infected cell.

Latent HSV-1 infections form in neuronal cells of the peripheral nervous system. When a latent infection is reactivated (by stress of many kinds), HSV-1 proteins are synthesized and new infectious virus particles are formed. These virus particles migrate along the neuronal axons to the epithelial cells of the skin. Viral growth in the skin, or other mucous membranes where nerves are found, causes cell damage and an immune reaction that results in a painful sore. Although the latency-to-reactivation process is not fully understood, it is known to involve stress, such as physical damage, ultraviolet light, hormones, or even fever.
Fraser is currently testing whether HSV-2, a relative of HSV-1 that causes genital herpes, also encodes an miRNA molecule in its LAT gene. “MiRNA may be a more general mechanism that latent viruses use to remain alive in the host cell,” suggests Fraser.

Present treatments of HSV-1 rely on acyclovir-based drugs that target the viral polymerase and inhibit viral DNA replication during the acute infection. However, they do not target the latent infection, and thus cold sores return throughout the lifetime of the infected individual..."

Note that they explicitly point out that stress is the key to reactivation, and also that they have a good understanding of what is occurring at the molecular level. They may be unaware of how much stress certain diets can produce, relative to others, but there are simple tests that can be done to demonstrate this (such as ORAC and the Rancimat). Notice that the "medicine" is used to control the symptoms temporarily, and does nothing to prevent them. In fact, if used too often, such medication will cause so much stress that it will become a contributor to the underlying problem. This report is useful because it demonstrates how "far off the mark" the "HIV/AIDS" claims are. If "HIV" exists in latent form and causes "disease" many years later, this would be the way it would happen. On the hand, the body can compensate wioth minor disruptions easily, such as a small loss of certain T cells. On the other hand, if the following claim was true, "HIV infected" people would experience pronounced symptoms, at the very least:

"People infected are quickly swarmed by a virus that replicates at warp speed by hijacking its host genes... HIV is a retrovirus, an insidious pathogen... Because of HIV's tendency to swarm, a mind-boggling number of viruses are continuously produced. Nabel estimates there can be more AIDS viruses in an infected individual than there are influenze viruses in global circulation at the height of the flu season."

Source: Page A41 of Newsday newspaper (6/4/06).

Even a science fiction writer would realize that if you are going to make such a claim of there being more "HI" viruses in a sinlge individual than there are flu viruses in the entire world's human population at the height of flu season, there would have to be symptoms present in that individual. In actuality, such a quantity of active virus would prevent life from being possible. I challenge any scientist to load up an animal with this amount of active virus (any virus, that is) and keep that animal alive for more than a few days (though I doubt it could live for more than a few minutes).

So, what the "HIV/AIDS" claimants are telling us is that, despite their inability to demonstrate exactly how "HIV" kills years later, after many years of no symptoms, even though the technology is available to determine this "pathogenicity" issue, we should simply believe their notions, even though these assertions are based only on older models and assumptions about how "germs" kill which have been demonstrated to be incorrect. They talk about "swarming" at "warp speed" and about a "wiley retrovirus" that "mutates rapidly," and yet such phenomena would produce pronounced symptoms and probably a quick death, but instead it takes years for problems to occur? And of course anyone who questions this is deemed a "quack!"

Clearly, for any latent virus to cause symptoms, stress needs to occur that will reactivate it. At the very least, if the "HIV/AIDS" claimants are correct about "HIV infection," deadly symptoms will only occur if certain cellular stressors are in play, and one can certainly avoid these stressors, and therefore, disease. Apparently, the "HIV/AIDS" claimants do not realize how inconsistent their notions are with what is now known about how viruses and other "pathogens" actually cause "disease" - once again, excessive specialization appears to be a major factor in this sad chapter of medical history.

Interestingly, these "experts" sometimes make the same point I am making, for example:

"Soon after the introduction of antiretroviral therapy for HIV infection, some patients may develop an inflammatory immune reconstitution syndrome..."

Source: Rev Mal Respir. 2006 Feb;23(1):69-72.

In some cases, the "experts" appear to be in some sort of intellectual fog, for example:

"Clinical deterioration after initiation of antiretroviral therapy may result from restored immunity."

Source: Clin Infect Dis. 2006 Jun 1;42(11):1639-46.

If the "disease" causes a failure of the "immune system," then how can restoring it lead to deterioration? They freely admit:

"There is no standard clinical definition for immune reconstitution syndrome."

This is quite an admission, and one could certainly say the same thing about "AIDS" itself. But how can you investigate something that has no standard definition without at least putting forth a definition that you intend to use in your study? What, exactly, are they studying? Basically, their conclusion is something like; people who are the most ill are more likely to be afflicted with this unknown entity, which seems to be like saying that sick people are more likely than healthy people to be sick a year from now than heathy people. But if you read the entire study, you can judge for yourself.

One important point I would make is that you can't "restore" an "immune system," though you can do particular things, such as enhance the production of certain molecules (or even provide those molecules from exogenous sources). "AIDS patients" do not become ill with all kinds of "diseases," but with particular ones. This seems to happen after an excessive amount of antigenic exposure, and may also be related to fatty acids in the body, high levels of oxidative or other stressors, and perhaps a few other "co-factors," such as high iron levels.

The "anti-retroviral therapy" may indeed "kill bugs" or prevent the reproduction of some of them, but if "germs" are not the issue, which the evidence suggests (especially in "diseases" that are supposed to take several years to develop), then such an approach will not work, though it may be that more conscientious people take the "medicines" and live a little longer, providing the tiniest of fig leaves with which such "experts" use to clothe the ugly, naked reality. However, the fact that the difference is so small, and the side effects often terrible, is a clear demonstration that the "HIV/AIDS" claim is incorrect - when something is right in science, it works, and when it is wrong, it does not. With "HIV/AIDS," those with alternative ideas - ones that actually fit the data - are not permitted (or do not have the funding) to demonstrate that a healthy, but "HIV infected" person has nothing to fear from a particular "germ" that appears to be a figment of certain "experts'" imaginations, but does have to worry about changing his or her "immune system" in a way that can lead to major health problems within a period of several years, especially if he/she continues to engage in behavior that results in a great deal of antigenic exposure.

Now here's something really puzzling, from an "HIV expert:"

QUOTE "A strong immune response can be good in the short term, but if sustained for a long time as in those with HIV, it can exhaust the immune system," he said. "If you could somehow dampen the response, it might effectively convert the condition to the more chronic, asymptomatic infection seen in monkeys." UNQUOTE

Source: http://www.sciencedaily.com/releases/2006/06/060616091615.htm

I agree, if it were in fact the case, but a strong inflammatory resonse is something a person feels, especially if it is supposed to be ongoing for many years, as in "HIV/AIDS." But this is not (or rarely) the case. Moreover, this notion is not related to the "mainstream" claims about "HIV" depleting particular T cells over time, which the body could certainly compensate for, assuming the person was eating well, etc. With "HIV/AIDS," it is like a religion in which if you agree with a main theological point, you can then go off and make up all kinds of stories that you can say are central to that religion - even if the stories actually contradict the main theological point itself!

25 th page from the old MSN site.

2008-11-11T13:02:00.000-08:00

Because “germ theory” assumptions are so central to the many recent failures (both to cure and predict) of the biomedical establishment over the last few decades, I will post new information about why the “germ theory” is not correct, though in the certain situations uncommon during most of human evolutionary history, it undeniably can appear to be correct. That is, if everyone, or the vast majority of a society’s population is engaging in activities that cause certain bacteria to become “pathogenic” then the use of toxic “medicines” may seem to be a godsend (though they may cause some of the symptoms of the “disease,” not to mention long-term adverse effects). Of course, most “experts” blame the bacteria, as if they were the direct and sole cause, instead of blaming themselves for not emphasizing exactly how “bugs” cause “disease.”

As I have pointed out in some of the other essays here, the "bugs" basically act according to conditions, that is, some become "pathogenic" when there is too much stress present (often oxidative). Under such circumstances, they become "clingy" and prompt an inflammatory response. If the stress is continual, the clinging continues, and the inflammatory response does serious damage (and fatty acids in your body seem to play a major role at this point, in terms of keeping the dangerous inflammation going longer than it should). In the case of viruses, the case is even weaker, and claims made by various "experts" are contradictory (or absent), as I've demonstrated in some of the other essays.

First, below, I will quote from the book, “The Secret Life of Germs,” by Philip M. Tierno.

Page 15: “An apparently spotless glass at the bar in an exclusive Upper East Side hotel was actually spotted, invisibly, with group D strep, another of the many germs passed in feces; no doubt, a bartender or busboy handled the glass improperly. Pseudomonas aeruginosa, a common environmental organism which can produce a whopping eye infection, thrived on a nail dryer at an exclusive beauty salon and in the shower at a fashionable sports club. The sports-club shower also contained Klebiesella penumoniae; as its name indicates, this germ, which is found naturally in the human intestine, can cause pneumonia if it manages to get into the lungs. Finally, among other germ-ridden locales, consider a public phone at Madison Avenue and Seventy-first Street. Lingering on the handset were S. aureus and beta-hemolytic strep group A, a flesh-eating bacterium. These are the sorts of germs we run into every day… if enough of them get into the wrong part of the body, serious illness, even death, can result. For example, if S. aureus infects an open sore or cut and goes untreated, it could lead to a minor infection or possibly to something as potentially lethal as toxic shock syndrome… Fortunately, people with healthy immune systems usually beat off most germs pretty easily, including some of the nastier ones.”

The only thing to add here is that it is often the “inflammatory” response that does damage; the minor cellular-level damage that some “bugs” do can be repaired promptly. A quick and potent inflammatory response is what is needed, but due to the cellular-level stress people subject themselves to on a regular basis (such as from foods that act as oxidizing agents), the "bugs" get "clingy," and then, duet to the fatty acids in the cells in many people these days, the inflammatory response is too potent. I will post more interesting quotations from this book, including ones that do discuss the role of the inflammatory response, in the near future.

Page 40: “At least two billion people around the world harbor the toxoplasmosis parasite; most don’t know they have it and will never be troubled by it. Almost one hundred percent of the French population, for example, has contracted taxoplasmosis…”

In general, the reason Americans in particular have seen so much “disease” is because they are engaged in activities that prompt powerful inflammatory responses to various “pathogen” that have caused few problems in other populations, and at other times in history.

Page 41: “…there is often a fine line between mutualism and parasitism. For example, the bacterium Streptococus pneumoniae can give people pneumonia if it gets a foothold in their lungs. Yet the same germ resides benignly, elsewhere in the respiratory tract, in fifteen percent of the population… Another good example is Staphylococcus aureus, a mutualistic component of most people’s normal skin flora. But if S. aureus gets into an open wound site, as can happen to patients after surgery, an infectious illness could occur and the germ would then become parastic…”

If you’ve read the other essays, you know that what happens is that the “germ” prompts and inflammatory response, which then does the real damage, so calling it a “parasite” needs to be clarified. It may indeed become “clingly,” but it is just trying to survive. Under less stressful conditions, it lives inside a person without becoming clingly and prompting an inflammatory response, but when your body is subjected to certain kinds and amounts of stress, the “germ” can become clingly, resulting in what we perceive as “disease.”

Page 140: “…scientists have discovered that animals may develop a subclinical form of prion disease [such as “Mad Cow disease”]. Although they carry lethal levels of prions in their brains, they have no symptoms. Yet prions from their bodies can produce a lethal form of the disease in other animals.”

Again, the only reasonable explanation is an inflammatory response to something perceived as a threat. I would also point out that calling something a “disease” when no symptoms are present makes little sense, and obfuscates more than it illuminates an attempt to understand the basic mechanisms involved.

Page 204: “The immune system detects the presence of [H. pylori] and repeatedly sends T cells to wipe them out, but the T cells are stymied by the mucous coating and they accumulate futilely on one side of it, along with other immune-system cells. Eventually, they die, spilling their cell killing contents onto the stomach lining instead of H. pylori and initiating an inflammatory process… The inflammatory immune response and the growth of H. pylori reinforce each other… which can lead to the formation of ulcers.”

Page 214: “Quantitative changes in the gut flora can often trigger an inflammatory process… a person may pick up a toxin-producing strain of a germ that is usually beneficial, like Shingella-bearing E. coli 0157:H7. In this connection, immunological responses may also have an impact."

Page 218: “…in people infected with Coxsackie virus, the immune system can send antibodies that will attack both the virus and the pancreatic cells it resembles.”

And as I’ve pointed out in some of the other essays, the fatty acids most Americans now have in their cells can make the situation much worse.

Below are passages from a recent sciencedaily.com report:

“Probiotics can help prevent and treat disease through a number of mechanisms. One way is by interacting directly with the disease-causing microbes, making it harder for them to cause disease... ‘Exposure to commensal organisms is necessary for the appropriate development of both the innate and acquired immune systems. Once established, probiotic organisms interact with these immune defenses, possibly changing the nature of the immune response to other antigens, including commensal and pathogenic organisms…’”

Source: http://www.sciencedaily.com/releases/2006/06/060610225845.htm

Note the vague language of the reporter – this is why it is difficult to understand exactly what is occurring. I found that when I began to ask this question, and also tried to visualize the molecular-level situation, it helped a great deal. In any case, when it is said that “probiotic” bacteria make things more difficult for “pathogenic” bacteria, this likely means that the “bad bugs” can’t become “clingy” because the probiotic bacteria basically beat them to it. The probiotic bacteria, however, does not prompt an inflammatory response, and this is what is implied when the author states that the probiotic bacteria may change the nature of the immune response. The point is that “germs” do no cause “disease;” it is always contextual and contingent upon several factors, as would be the virulence, duration, etc., of the “disease,” should what we perceive as disease result.

Note that many "experts" have suggested that a bacteria or virus is the cause of the "heart disease epidemic," and some still do, even though the molecular-level cause is now known. While "pathogens" may "take advantage" of damage in the body, they rarely, if ever, do much damage directly, and one also has to take into account how humans are trying to do things that have never been done before by other species, such as to have millions living in close quarters and subjected to powerful stressors, such as pesticides and estrogenic substances, on a continual basis.

Studies such as the following demonstrate what the scientific reality is regarding common "diseases," because they focus on molecular-level events:

Free Radic Biol Med. 2002 Jan 1;32(1):38-45.

Lipid peroxidation contributes to immune reactions associated with alcoholic liver disease.

Mottaran E, Stewart SF, Rolla R, Vay D, Cipriani V, Moretti M, Vidali M, Sartori M, Rigamonti C, Day CP, Albano E.

Increasing evidence indicates the involvement of immune reactions in the pathogenesis of alcoholic liver disease. We have investigated whether ethanol-induced oxidative stress might contribute to immune response in alcoholics. Antibodies against human serum albumin modified by reaction with malondialdehyde (MDA), 4-hydroxynonenal (HNE), 2-hexenal, acrolein, methylglyoxal, and oxidized arachidonic and linoleic acids were measured by ELISA in 78 patients with alcoholic cirrhosis and/or hepatitis, 50 patients with nonalcoholic cirrhosis, 23 heavy drinkers with fatty liver, and 80 controls. Titers of IgG-recognizing epitopes derived from MDA, HNE, and oxidized fatty acids were significantly higher in alcoholic as compared to nonalcoholic cirrhotics or healthy controls. No differences were instead observed in the titers of IgG-recognizing acrolein-, 2-hexenal-, and methylglyoxal-modified albumin. Alcoholics showing high IgG titers to one adduct tended to have high titers to all the others. However, competition experiments showed that the antigens recognized were structurally unrelated. Anti-MDA and anti-HNE antibodies were significantly higher in cirrhotics with more severe disease as well as in heavy drinkers with cirrhosis or extensive fibrosis than in those with fatty liver only. We conclude that antigens derived from lipid peroxidation contribute to the development of immune responses associated with alcoholic liver disease.

The above study is excellent, in that it shows how stress and too much polyunsaturated fatty acid content in your diet can lead to the body essentially destroying itself. This mechanism also seems to be the cause of at least many "AIDS" cases. In stark contrast:

"The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known..."

Source: Hepatology. 2005 Sep;42(3):568-77.

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice.

You M, Considine RV, Leone TC, Kelly DP, Crabb DW.

And:

"Rats fed a saturated fat diet are protected from experimentally induced alcoholic liver disease... Increases in dietary saturated fat increased liver membrane resistance to oxidative stress..."

Source: J Nutr. 2004 Apr;134(4):904-12.

Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition.

Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.

And here is something that ties everything together nicely:

"Bacteria and parasites often use special toxins to perforate the membranes of target cells. These pore-forming toxins are a key weapon in the attack arsenal of some common and virulent bacteria, such as Staphylococcus aureus, well-known for its role in hospital-acquired infections, Streptococcus pneumonie, responsible for middle ear infections and pneumonia, and Helicobacter pylori, implicated in ulcers. Pore-forming toxins compose about a quarter of all known protein toxins that increase the infectivity and severity of bacterial diseases.

Once the toxin perforates the host membrane, ions begin to leak out of the cell. Sensing a drop in its potassium concentration, the cell reacts by forming a multi-protein complex known as an inflammasome. Scientists know that inflammasomes act like a sort of roving security force inside the cell, detecting a variety of danger signals such as bacterial RNA or bits of bacterial flagellin. The inflammasomes join together and activate a protein, caspase-1, that in turn triggers an inflammatory response."

Most likely, the cell would be much more resistant to various "germs" if there were significantly less unsaturated fatty acids at the cell surface. Simple experiments could determine this.

Source: http://www.sciencedaily.com/releases/2006/09/060922093757.htm

24 th page from the old MSN site.

2008-11-11T13:01:00.000-08:00

How language impedes science, part II.

A simplified way of thinking about this is: we are being told that even if the symptoms are exactly like "AIDS," people cannot have it if they are "HIV negative," and yet there is nothing exact about "AIDS." It is based on observations, and it has changed over the years, now including things like cervical cancer, even though few attempts are being made to understand how this can be the case at the molecular and cellular levels. There is also nothing exact about "HIV," as only markers are involved in the tests, and these markers are not unique to "retroviruses," let alone a specific one. At this point, after more than a quarter of a century of research, one can only regard "HIV/AIDS" claims as a kind of "fool's gold" that does not even have the appearance of real gold.

How could this "AIDS" situation be resolved in the most sensible way? By "going back to basics," that is, first, attempt to delineate clinical syndromes based upon observations and markers that are shared, doing so without any preconceptions. Once this is accomplished, researchers could investigate what the patients who are afflicted by these syndromes have in common, such as a great deal of antibiotic usage. It would also be important to follow such people around without their knowledge, because they may be doing illegal things, such as taking certain drugs, that they don't want to mention to their doctors. If this is kind of investigation is not legal, there is a loss of controls and it will be impossible to advance beyond the CS, though if enough people are afflicted, it's likely that at least some will be honest and the problem will be more comprehensible.

If the stressor that is the root cause can be determined, then it is not just a scientific issue any longer, that is, the government may decide that it will not devote resources to those who knowingly harm themselves. If this is not done, various "therapies" and "treatments" can be tried, but I'm not especially interested in this sort of endeavor because there is so much conflict of interest involved and because things become so complicated so quickly that attempting to use the scientific method is impossible.

23 rd page from the old MSN site.

2008-11-11T13:00:00.000-08:00

How language can impede science.

The alternative “HIV/AIDS” hypothesis and why the “experts” will not address it.

I shall begin with the second point first, because it is central to the problem. Before one can attempt to construct a scientific hypothesis, one must have access to precise language (or create it himself/herself), lest science degenerate into ideological blather. For example, if someone accuses you of being a “liberal” or a “conservative” because of something you have said or done, you will not necessarily be able to convince him/her otherwise – ever. In such a situation, because there is no one definition of “liberal” or “conservative” that all agree upon and is flexible enough to be useful in all situations, attempting to resolve such claims is often a futile endeavor – even between two people only.

Something similar has occurred in the “HIV/AIDS” field. These claimants argue that if one’s symptoms fit perfectly into the clinical syndrome (CS) called “AIDS,” but if one is “HIV negative,” the person cannot possibly have “AIDS.” CSs exist because an understanding of the molecular-level sequence of events is absent or clearly incomplete. CSs are based upon observed symptoms, and as all agree, a “positive HIV test” does not mean that any symptoms are present. Even in the case of something like “liver failure,” it may not be known (and never be known) exactly what happened at the molecular level, but in this case it was known that the damage originated in a particular organ. Anything could have caused it, or it could have been a combination of factors that was toxic. With “AIDS,” there is a multiplicity of very diverse pathological phenomena, and thus to claim that “HIV” is the only cause of “AIDS” invalidates the professional terminology, rendering an objective investigation impossible (because those in power can simply redefine whatever they want to, whenever they want wish). One must either explicitly reinvent or modify significantly the medical language or agree that if symptoms fit a clinical syndrome, then that person’s condition is to be classified as that syndrome.

The other possibility is to determine exactly what is occurring at the molecular level, and then different classifications might indeed be possible. In “HIV/AIDS” and many other “diseases,” for example, there is damage that is done directly by TNF-alpha, but this molecule is generated by the body as part of the normal “inflammatory” process. Any cellular-level stressor can cause this problem. Thus, if damage to the body was done by TNF-alpha (and there is certainly plenty of evidence for this notion), resulting in various “diseases,” there may never be anything more than a TNF-alpha Syndrome, because there are too many ways it can occur. The intelligent thing to do, once this was determined, would be to look for the kinds of stressors that would generate such a result, remove it, and see if the syndrome resolves. Our “health experts,” however, have been smitten with the “germ theory,” and seek to destroy the “bugs” that are causing the “disease,” when in fact the “bugs” are just opportunistic, in a way, responding to conditions in a manner that works for them, in an evolutionary sense.

“HIV/AIDS” claimants have placed themselves in an impossible position, because if “AIDS” is due to “HIV,” then there is no reason for the “syndrome” designation. They use it because they do not know exactly what is occurring at the molecular level. They have placed models and assumptions in a privileged position, above the scientific method, and anyone who questions such a bizarre practice is labeled a “quack,” while it is they who are engaged in the actual quackery. In this way, they hope to deflect attention from those who insist that before telling millions of people to take highly toxic “medications,” the claims being made in support of this prescription must meet the criteria of the scientific method. It is interesting to note how much more media coverage those who claim to have been abducted by “UFO aliens” receive than those who point out how flawed the “HIV/AIDS” claim is, and how it is not even consistent with accepted medical terminology.

Now on to point one; there is a very well-known reason why certain practices often lead to an “immune-deficiency” problem, though even this makes little sense, since “AIDS” patients do not die of just any “disease.” Rather, they possess “immune systems” that have been altered. But we are back to the first problem again, because the “AIDS” CS was created, as all CSs are, to help doctors determine the best course of action in the absence of complete knowledge (and often in a situation where very little is known or understood). “AIDS” has, in fact, been modified over the years, but in a ludicrous expansive way, to include those who “test positive for HIV” rather than to attempt to make the CS “leaner,” and to place it into a more coherent overall framework. Thus, any attempt to suggest that “AIDS” should be changed in way that would exclude certain patients is met by the illogical response that if “HIV” is present, then it has to be “AIDS.” Of course, if “HIV” was in fact present and doing damage, then this would be demonstrable, and one could simply abandon the syndrome designation. A scientist could examine blood or tissue samples and determine whether the “HIV” was doing certain kinds of damage or not, and then if it was not, the person would no longer be considered an “AIDS patient.” Those in charge have thus created something of a fairy tale existence for this disease/syndrome. It is a “disease” when it is convenient for it to be for them, but it is a syndrome when it is convenient for it to be for them. However, if one could demonstrate “AIDS” in the absence of “HIV,” the scientific method requires that one conclude that “HIV” does not cause “AIDS.” The reason those in charge refuse to accept the scientific method in this instance, presumably, is that they believe that certain markers indicate that a “retrovirus” must be present. But if this is accurate (and the whole notion of a “retrovirus” is rather obscure, especially in the sense of whether it is the cause or effect of stressors), it makes their actions even more egregious, because if a CS is present, but the “pathogen” is not, then the pathogen cannot be the cause of the CS. It does not get much simpler than this, in terms of adhering to the scientific method. Thus, they have insulated themselves from science while at the same time calling others who point out the necessity of adhering to the scientific method “quacks” by a use of terminology that is patently illogical.

Finally, as to point one, I will mention that it is rather simple to induce “AIDS,” at least in humans, by excessive antigenic exposure. When a certain threshold is reached (which will vary somewhat from one person to another, obviously), “immune system” cells that are “regulatory” stimulate certain T cells to undergo apoptosis. Why? It’s really quite simple. If they body is exposed to too many different antigens, there is nothing certain T cells can do, because just about everything that they might “attack” either looks “foreign” or like “self.” The body must not let these cells “do their thing,” because that would mean massive autoimmune damage, and perhaps a quick death. It is also true that a certain amount of oxidative stress, perhaps exacerbated by other factors (even the fatty acids one eats), will cause a loss of certain T cells. The “HIV tests” measure the amount of antigenic exposure or the amount of apoptopic bodies circulating, and such tests may indeed be a good indicator of future “illness,” but not because of a specific virus that attacks and destroys these cells in an asymptomatic way. Viruses causing damage elicit a very noticeable inflammatory reaction. Too much antigenic exposure, leading to a loss of these cells, would not do this, and of course this is consistent with the evidence, while the “HIV” notion is not.

But again, once they claim that in the absence of a “positive HIV test” there can be no CS of “AIDS,” even if all the observable and measurable criteria are met, they have closed the door on those who wish to present alternative explanations, preventing the scientific method from being utilized here. It would not matter, for example, if a scientist could create “AIDS patients” simply by excessive antigenic stimulation alone, thereby demonstrating that this is at least one cause of “AIDS,” because the powers that be have decided that “HIV” was not present, but obviously, that is the whole point of doing such an experiment! One of the most basic principles of the scientific method is that if something is deemed to be the sole cause of a particular phenomenon, and yet an experiment is done and it is demonstrated that something else can also cause the same phenomenon, then the claim that there is a sole cause is not accurate. And so what appears to be the case, in light of the evidence, that is, that what they perceive as “retroviral infection” is just the effect of excessive antigenic exposure, is disallowed, and pursuing this possibility will get one labeled a quack, even if that person in fact follows the scientific method “to the letter.” Until this situation is corrected, “HIV/AIDS” claimants are like a child who closes his eyes, put his hands over his ears, and says, “la la la la la – I can’t hear you,” over and over again. Hopefully, such a child will never be given the kind of power the “HIV/AIDS” claimants now possess.

I used to think of “HIV/AIDS” as a cult, but it’s more than that; there is a self-fulfilling prophecy element to it as well. Imagine the following; a leader of a small group who consider themselves “fundamentalist” Christians decide that because Jesus favored the lowest strata of society, and because criminals are now viewed in this light, that they should commit crimes. The leader also tells them that they will know that they are truly following the correct Christian path because they, like Jesus, will be persecuted, while other Christians in the USA are not. Of course, they will be “persecuted” because they commit crimes, not because of their beliefs, but you will never be able to convince them of this, just like the “HIV/AIDS” claimants will not allow the scientific method to be used to determine what the causes of the various “AIDS” phenomena are. In both instances, a self-fulfilling prophecy is at play. Moreover, those who have and continue to expose themselves to large amounts of antigens, and who “test positive for HIV” will likely continue to live their lives in a way that will mean the same or more antigenic exposure (because they are already “infected with HIV” and don’t think that “AIDS” can be caused by anything else), while at the same time taking “medicines” that are highly toxic but totally unnecessary. Years later, when “AIDS” presents, these drugs may “keep the bugs down” due to their toxicity, and so the drugs may indeed keep these people alive for several months longer, on average. However, the opportunity to completely prevent “AIDS” from occurring in the first place will be missed, and instead those who “test positive” are involuntary converts to the cult, and become the self-fulfilling prophecy the “HIV/AIDS” claimants point to when they argue that the “case is closed” with regard to “HIV” causing “AIDS.”

This alternative hypothesis does not originate with me, but with those who specialize in the "immune system," for example: “…the basic function of all cells of the organism is appropriately timed death "from natural causes". This type of cell death, or apoptosis, generates no stress signals. If, on the other hand, a cell is "murdered" by an infectious agent or dies an untimely death due to necrosis or ischemia, the cell undergoes a stress response with the liberation of stress protein-peptide complexes into the extracellular environment upon cell lysis. Not only do they serve as a "danger signal" to alert the immune system to the death of a cell under stress, but their role as protein carriers allows the immune effector cells to survey the peptides released by this stressed cell and to activate against new or unrecognized peptides carried by the stress protein. Matzinger bases the Danger Theory of Immunity on three "Laws of Lymphotics". These laws state that: (1) resting T lymphocytes require both antigen stimulation by an antigen-presenting cell (APC) and co-stimulation with a danger signal to become activated; (2) the co-stimulatory signal must be received through the APC; and (3) T cells receiving only antigen stimulation without the co-stimulatory signal undergo apoptosis.”

Source: Immunopharmacology. 2000 Jul 25;48(3):299-302.

A more technical explanation is:

"It is likely that suppression of cytotoxic T-lymphocyte function has evolved as a mechanism to control the immunopathological damage that can occur as a consequence of cytolytic killing by CD8+ T cells. For example, in the mouse model for hepatitis B infection CD8+ T cells exhibit virus control via gamma interferon and tumor necrosis factor alpha production without causing the liver tissue destruction that would result from active cytolysis (18). In human immunodeficiency virus infections, the down-regulation of perforin in virus-specific CD8+ T cells from gut-associated lymphoid tissue may be a mechanism to protect the integrity of the rectal mucosa from cytotoxic T-lymphocyte activity..."

Source: Journal of Virology, August 2005, p. 10619-10626, Vol. 79, No. 16

Excessive antigenic exposure without the proper "danger" signals can lead to what one might call “opportunistic infections AIDS,” whereas in some other instances of “AIDS,” inflammatory molecules like TNF-alpha do the damage that leads to what gets called an “AIDS case” (in other cases, malnutrition is the underlying cause - of the "positive HIV test," that is). If you examine the mainstream “HIV/AIDS” studies, you soon realize that at least several different molecular-level mechanisms are at play, for instance, compare “AIDS” wasting” with “AIDS dementia.” If “AIDS” were a useful CS, there would not be diverse molecular-level phenomena, as there undeniably is. If one wishes to use the CS designation correctly, it should be reorganized into several different syndromes, and, as I pointed out above, there is no reason to insist on “HIV infection,” because that implies that the molecular-level mechanisms are known to such a degree that one can explain how “HIV” causes “dementia” with certain molecules involved (such as gamma-interferon or TNF-alpha), but also causes wasting with different molecules doing the damage. It is undeniable that such knowledge does not exist at present. In the case of Africans, there indeed may be a pathological amount of apoptosis occurring, due to a poor diet and other factors, but again, this should be a separate CS. In my case, back in 2000, there was oral thrush, anti-nuclear antibodies, wasting, raised EBV levels, severe osteoporosis, pronounced skin rashes, soft fingernails, frequent GI track infections (food poisoning like episodes), tendonosis, “floaters” appearing in my vision, and other symptoms that would lead to a typical diagnosis of “AIDS” in Africa today. I now realize that my supposedly healthy vegan diet was at least partly to blame. I ate little salt, for example, and at some point was unable to produce stomach acid. My tendonosis lasted for over two years – I eventually ate more and better quality protein, along with supplementing with stomach acid, and the tendonosis pain was gone in about two to three months, at most.

Note that one would expect Africans said to have “AIDS” to have high levels of apoptopic bodies, indicating that they are not receiving adequate nutrition, but this is also a sign of excessive antigenic exposure, and so the claim that the “disease” is the same only makes sense on this level, that is, on the level of markers that the “experts” decided (due to their belief in models and “germ theory” assumptions) was “proof” that a viral infection is the cause in both cases, despite how ridiculous this claim is when examines the evidence as a whole.

22 nd page from the old MSN site.

2008-11-11T12:59:00.000-08:00

HSWC "in action."

Here is the page I am responding to in this post of mine (on another newsgroup):

http://www.anaesthetist.com/icu/infect/virus/dues2.htm

Response:

Now this is the kind of essay a student might have written in one of my courses. I would have advised the student to rewrite it, realizing that the student is "trying" but does not understand certain essentials about the scientific method.

Quote: We cannot simply make bland statements like "HIV causes AIDS". We must provide practical, relevant, and testable (falsifiable) assertions that should allow "dissident scientists" to attack our standpoint using the scientific approach of falsification. Needless to say, we should welcome well-formulated attacks, for science can only proceed by the identification of problems, the creation and refinement of explanatory hypotheses, and the testing of these hypotheses for their ability to withstand the sharpest arrows we can shoot at them. In this sense, and this sense alone, we should welcome criticism from Professor Duesberg and his colleagues. We should perhaps be grateful to Prof. Duesberg for providing us with an opportunity to explore the nature of science, and see how badly one can go off the rails if one concentrates on "proof of causation" rather than "falsification". Unquote.

This is good, and I would mention that Copernicus was correct about the heliocentric notion but not about the perfectly circular orbit. In a similar way, Duesberg was correct about certain obvious problems with the "HIV/AIDS" claims but appears to be wrong about the notion that "HIV" is a virus the way the flu is, for example, and that there are "antibodies to HIV." He has only been able to think so far "outside the box," like Copernicus.

The onus is on the person or people making the claim to demonstrate that it meets the criteria of the scientific method. All factors have to be controlled for in on point experiments. Talking about "AIDS in Africa" is supposed to demonstrate what, exactly? Most of these "AIDS patients" are not even given the tests considered basic in other nations. This is a terrible argument, if one can even call it an argument.

Some, like Ho, have diligently tried to demonstrate causation, but they have all failed. The Perth Group points out that "testing positive" is an indicator (not necessarily a great one) of cellular level damage or distress, and so "correlations" with 30 or so "diseases" several years later would make perfect sense (while Duesberg's notions do not).

Some "dissidents" do spend a lot of time of questins of "isolation" but this is irrelevant for the claimant, as his/her burden is clear; there needs to be a formal scientific hypothesis stated, then tests must be done that control for all possible factors. This has not been done with the "HIV/AIDS" claims, and hence it cannot be regarded as "science" at this point, regardless of what any "dissident" remarks.

The person who wrote the essay, however, has decided to state a hyothyesis:

Quote: AIDS can be defined as a syndrome of acquired immunodeficiency characterised by lowered CD4 counts and 'disseminated tuberculosis or unusual opportunistic infections or certain aggressive neoplasms'. (1) Most cases of African AIDS are associated with repeatable serological evidence of 'HIV infection'. (2) Prevention of transmission of 'HIV' (as indicated by repeated negative serology) prevents AIDS. (3) Continued suppression of 'HIV' replication (as indicated by lowered 'viral load' in the blood) constitutes an effective therapy, and is associated with improvement in immune function, and a lower incidence of opportunistic infections. Unquote.

Now defining a clinical syndrome has nothing to do with meeting the criteria of the scientific method. It is used by doctors to try and help patients in the absence of such an attainment, hopefully without doing harm (Hippocratic Oath). Then he talks of "associations" in Africa and "repeated serological evidence." Associations are used to point a scientist in the right direction and do not meet the criteria of the scientific method. If this were so, it should be quite easy to demonstrate that because there is an association between people with the smelliest socks at the end of the day and a "disease" that the smelly socks caused the disease. Moreover, talking about "evidence" of "HIV infection" is assuming what needs to be demonstrated. The markers now used to claim that a person is infected are ubiquitous, and that comes from the relevant "non-dissident" literature. First, "HIV/AIDS" claimants need to demonstrate that the markers they are using are specific for a particular virus, and then the would need to show how this particular virus causes harm ten or so years later.

The statement "Prevention of transmission of 'HIV' (as indicated by repeated negative serology) prevents AIDS" demonstrates the problem with this way of thinking. "AIDS" can only be deemed present if there are "positive HIV tests," so there is nothing here but circular reasoning. The alternative that makes the most sense is that these markers demonstrate cellular level damage and/or cellular debris in amounts larger than normal, demonstrating that there is pathological process, and so one would expect such people to be more likely to develop certain "diseases" 10 or so years later. Taking "medication" that is highly toxic makes it impossible to determine why one of the "AIDS defining diseases" develop. Just telling a person that he/she is going to die in 10 years (a terrible death) introduces a stressor that is not present in a control population (not that controls are used by "HIV/AIDS experts" anyway). If one argues that "HIV positives" who don't take the "medication" die a bit sooner (not exactly a great argument to make when prescribing such "medicine"), then one has to have convincing evidence that this is indeed the case, along with controlling for all factors. It may be, for example, that most who refuse the "medicine" are people who continue to do what caused the cellular level damage in the first place, and therefore one would expect them to "develop and AIDS defining disease" a bit sooner. Again, circular reasoning is present but the scientfic method is not.

Also not mentioned is the fact that two or more hypotheses can exist at the same time, but only one can become a scientifc theory (though none may). It is only with time and properly controlled experiments (that are repeated for verification) that one can claim that a hypothesis should be considered a theory. If one reads the literature on dangerous viruses, as I have, one is struck by how these "experts" (who don't question the "HIV/AIDS" claim) point out that deadly viruses appear to kill indirectly, buy provoking a powerful inflammatory response. This explains the 1918 pandemic, for example, because there the young, healthy, and physically active died in greater proportions. Their "good health" meant that their bodies responded with a more potent inflammatory response, and from there direct damage and/or a bacterial pathogen could have done the deadly damage. We now have the technology to determine exactly what is going on at the molecular level, so there is no reason for speculation. However, it is true that those who determine who gets the money to do the kinds of experiments to make such determinations don't often see the value in doing so. And thus those who understand the scientific method realize that one must refrain from making definitive statements until such experiments are done. Too many these days do what the author has done, that is, assume that textbook statements or models are correct, and then engage in circular reasoning as "proof."

First and foremost, I would ask the author to restate the "working hypothesis" (in a sense, all hypotheses must be "working" in order for them to be of much use). I have tried to think of one, but in light of the evidence, it is difficult. The best I could do would be something like: "there is evidence of what is considered by most virolgists to be a retroviral infection. This seems to correlate with a clinical syndrome some number of years later at this point in time. I propose to isolate people who test 'HIV negative' and expose them to all the stressors present among the early 'AIDS patients,' including chronic use of 'poppers,' antibiotics, corticosteriods, receptive anal sex, a 'junk food diet,' etc., for three years, then have them take AZT for at least two years. At that point, it will be observed whether they suffer from conditions that appear to be consistent with the clinical syndrome that is now called 'AIDS.' The subjects (volunteers, of course) will be male homosexuals who agree to be monitored in a way that will prevent any possibility of becoming what is now considered to be 'infected with HIV.' In this way, we eliminate the possibility that any other factor present in this population but not others could be the cause of 'AIDS' rather than what is considered to be a retroviral infection."

I hope everyone sees the problem here: "HIV/AIDS" claimants would argue that what these volunteers might develop is "non-HIV AIDS" (or some other phrase meaning the same thing). Thus, they preclude the possibility of using the scientific method because they hold their definition of the phenomena to be more important than the scientific method. This is unacceptable and such people should not be allowed to call themselves scientists, among other things. At this point, It has become something much more like a cult than science, actually, and attacking critics, who may indeed be incorrect about something specific (or more likely, overstate their case) does nothing to remedy the situation. Only an understanding and willingness to meet the simple standards of the scientific method will acheive this.

I think I should make an important point explicitly: one can refute a hypothesis by showing that it's essential points are wrong. For example, in 1930 and experiment was done on rats (Burr & Burr), and from that experiment (done with improper controls) came the claim that certain animals require dietary sources of specific fatty acids. In 1948, a properly controlled experiment was done in which one group of rats was given no fat source and there was did not develop any symptoms of disease or deficiency. It was determined that a B vitamin (unknown in 1930) was what the rats needed. This is a direct refutation, and there is nothing that can be done to resurrect the 1930 claim, assuming the 1948 experiment was not outright fraudulent (it found its way into the Enclycopedia Britannica). There is no reason to pursue the 1930 claim beyond this point (at least in rats), and yet it is a darling of "health and nutrition gurus" these days, so the "HIV/AIDS" situation is hardly unique or new. The point is that the "HIV/AIDS" claimants, if they truly want to do science, can define "AIDS" precisely, then my experiment could be conducted, and if the volunteers developed "AIDS" the "HIV/AIDS" claim would be directly refuted and would need to be abandond completely. There would be no need to attack "dissidents" or argue that this or that correlation "proved" that "HIV/AIDS" is "true." However, because of the circular reasoning present (which is not in the "essential fatty acid" claim) they are basically asserting something akin to Papal Infallibility.

End of response.

Note that a "typo" error or two occur in my response.

And here's a response to a person who wanted to know about how to "prove" the existence of a deadly virus:

"Proof" is for math and logic. Here, there is a need for a clear demonstration, done in a way that is consistent with the scientific method. If that has been done, I'd like to see it. I asked about the "SIV" monkey studies on another post, but it didn't seem like anyone knew about what was asking. Now, in order for any virus to be deadly it has to provoke a strong inflammatory/immune response or it has to have a direct cytotoxic effect on at least one kind of cell. However, if you demonstrate that animals in poor health are killed off by a direct cytotoxic effect, you have demonstrated evolutionary theory, not virus theory. That is, if you want to demonstrate that a virus is deadly, you need to kill off healthy animals in a way that is just like conditions in the wild. Otherwise, you do not have proper controls, and there is no way to know exactly what you have demonstrated. However, even viruses that are considered "the worst" usually kill no more than about 25% of the population, and all of this may be due to the inflammatory response, not a direct cytotoxic effect (except perhaps in the very weak). Since one can modulate the inflammatory response by doing rather mundane things (dietatry, for example), my sense is that this is where the resesarch should be directed now.

As I've said elsewhere, there is more than enough evidence and the technology is now available: if a virus is killing a person, there is no reason to be unable to demnonstrate exactly how, down to the molecular level. Instead, we get models derived from old assumptions that found their way into textbooks. Then, the evidence is "massaged," in an attempt to force the square pegs into the round holes. This is true for other claims as well (such as the lipid bilayer membrane and "essential" fatty acids), and represents a failure to understand the scientific method. I've had students who were majors in a scientific discipline tell me that they never really understood the fundamental principles upon which science was based until they took my history class. They would say that after taking my class, their science classes made a lot more sense to them. Moreover, my interactions with scientists has led me to conclude that most of them either don't understand or don't pay much attention to the scientific method. Career advancement, developing things that can be patented, etc., seem to be more important than "worrying" about the scientific method, and so here we are, in the midst of the great failure of the modern biomedical establishment.

21 st page from the old MSN site.

2008-11-11T12:58:00.001-08:00

Some studies worthy of note.

Here I will post studies that I have posted on other newsgroups in the past that are instructive in one way or another, along with brief commentary.

Animal Science Journal

Volume 73 Issue 5 Page 389 - October 2002 doi:10.1046/j.1344-3941.2002.00054.x

Comparison of the antioxidant activities of 22 commonly used culinary herbs and spices on the lipid oxidation of pork meat Hisako TANABE1, Masami YOSHIDA1 and Nanae TOMITA2 The antioxidant activities of 22 selected culinary herbs and spices (i.e. ginger, cinnamon, clove, bay, sage, rosemary, thyme, savory, oregano, sweet basil, parsley, coriander, tarragon, sansho, allspice, cumin, black and white peppercorns, nutmeg, caraway, dill and fennel) when they were added to pork homogenate were measured and expressed as a thiobarbituric acid (TBA) value. The addition of liquid extracts of all the herbs and spices significantly suppressed lipid oxidation of the pork, especially the extracts of sansho, sage and ginger, which showed the strongest inhibition of lipid oxidation.

This study is important because it shows that lard, a "saturated fat" according to many "nutritional experts" is very susceptible to lipid peroxidation, which is very dangerous to cells. If this study were done with fresh coconut oil, it would be worthless, because the coconut oil generates so little lipid peroxidation that there would be little contrast among the herbs and spices. Thus, in a sense, many Westerners are "held hostage" by the nonsensical classification scheme of "nutritional experts," many of whom don't seem to have much, if any understanding of the biochemistry involved. If they did, they would be advising people to avoid food that acts as an oxidizing agent, regardless of how it ranked in the older nutritional framework. Instead, many stubbornly try to figure out how to make it look like the old framework is correct, despite the incredible contradictions and also the fact that another explanation is much better and is not contradicted by any of the evidence.

Here are some studies that try to determine why "meat" seems to be so dangerous:

"Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma."

Source: Cancer Res. 2005 Sep 1;65(17):8034-41. Meat, meat cooking methods and preservation, and risk for colorectal adenoma. Sinha R, Peters U, Cross AJ, Kulldorff M, Weissfeld JL, Pinsky PF, Rothman N, Hayes RB.

"These data suggest that mutagens such as HCA that form when meat is cooked may be culpable substances in rectal cancer risk, not red meat itself."

Source: J Nutr. 2004 Apr;134(4):776-84. Meat consumption patterns and preparation, genetic variants of metabolic enzymes, and their association with rectal cancer in men and women. Murtaugh MA, Ma KN, Sweeney C, Caan BJ, Slattery ML.

"Red and processed meat intakes were associated with an increased risk of pancreatic cancer. Fat and saturated fat are not likely to contribute to the underlying carcinogenic mechanism because the findings for fat from meat and dairy products differed. Carcinogenic substances related to meat preparation methods might be responsible for the positive association."

Source: J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65. Meat and fat intake as risk factors for pancreatic cancer: the multiethnic cohort study. Nothlings U, Wilkens LR, Murphy SP, Hankin JH, Henderson BE, Kolonel LN.

What these studies don't mention is the role played by dietary PUFAs in this situation, for example:

"Dietary heterocyclic aromatic amines (HCA) and polyunsaturated fatty acids (PUFA) are both believed to play a role in colon carcinogenesis... These results show that COX, and COX-2 in particular, can play a substantial role in HCA activation, especially in extrahepatic tissues like the colon. Furthermore, the obvious interactions between PUFA and HCA in COX-2 expressing cancer cells may be important in modulating colorectal cancer risk."

Source: Mol Carcinog. 2004 Jul;40(3):180-8.

Title: "Effects of polyunsaturated fatty acids on prostaglandin synthesis and cyclooxygenase-mediated DNA adduct formation by heterocyclic aromatic amines in human adenocarcinoma colon cells."

Moonen HJ, Dommels YE, van Zwam M, van Herwijnen MH, Kleinjans JC, Alink GM, de Kok TM.

Here's something interesting from the "HIV/AIDS" experts:

"The highest levels of total intake (from food and supplements) of vitamins C and B1 and niacin were associated with a significantly decreased progression rate to AIDS... The relation between total vitamin A intake and progression to AIDS appeared to be U-shaped; the lowest and highest quartiles of intake did most poorly, while the middle two quartiles were associated with significantly slower progression to AIDS... Increased intake of zinc was monotonically and significantly associated with an increased risk of progression to AIDS..."

Source: Am J Epidemiol. 1993 Dec 1;138(11):937-51.

As one group of zinc researchers, who have pointed out how dangerous low levels of zinc can be, stated:

"To our surprise, zinc salts at 80–200 µmol/L added exogenously to standard RPMI 1640 cultures for 8 h could induce 30–40% apoptosis in thymocytes..."

You can read this excellent study (Journal of Nutrition. 2000;130:1399S-1406S) at:

http://jn.nutrition.org:80/cgi/content/full/130/5/1399S

My point is that the evidence is overwhelming that "diseases" ("AIDS," in this instance) are at best tangentially related to "bugs" (especially considering that they were here before we were), and that much of this evidence is of the best quality, that is, molecular-level. Most "experts" have placed the emphasis on the the wrong agents, and due to excessive specialization (and perhaps a few other factors), simply go along with "the program." And here the "program" is that "HIV causes AIDS," even though if that were true this evidence of vitamins and minerals and "AIDS progression" (and plenty of other studies) should not exist. It contracts the model the "bug hunters" have put forth.

It is worthy of note that I've been struck by how uninquistive so many "people of science" actually are. I, on the other hand, was trained to examine evidence in an exhaustive and highly critical way (in history graduate school).

Twentieth page from the old MSN site.

2008-11-11T12:56:00.000-08:00

The Latest Evidence.

Rather than write up more essays, which, in a sense, are variations on the same theme, I think it might be best for you to read the other essays, then come to this page, where I will post evidence as it is published. If there was new evidence that appeared to contradict the points I've made in the other essays, and did not seem to be flawed (and also if the data was made public so that all could examine it, which is not always the case) then I would write up a new essay for it.

The points I've made about TNF-alpha (being released when cells are stressed), free radical damage, and "inflammation" are supported by new calorie-restriction experiments. Here is a passage from one report:

"The researchers also found that calorie restriction (CR) decreases the circulating concentration of a powerful inflammatory molecule called tumor necrosis factor alpha (TNF). They say the combination of lower T3 levels and reduced inflammation may slow the aging process by reducing the body's metabolic rate as well as oxidative damage to cells and tissues."

Source: http://www.sciencedaily.com/releases/2006/05/060531164818.htm

I would add that the issue is stress, not calories consumed, unless one eats so much that it in itself becomes stressful. Most likely, people on calorie-restricted diets ate a lot less unsaturated fatty acids. As I suggested in the essay about doing experiments, all one needs to do is the substitute fresh coconut oil for the usual fat sources in lab animal diets and see what the results are. If this was done, the results would be similar to calorie restriction, if not better, assuming the animals were not being fed much more food than is necessary.

This is suggested by their statement: "The thyroid gland produces critical hormones that play an indispensable role in cell growth and development as well as in lipid and carbohydrate metabolism. T4 is the main product secreted by the cells of the thyroid gland, but most actions of thyroid hormone are initiated by T3."

In other words, if the T3 levels are higher, there is more lipid metabolism, and that means more AA metabolites around to do damage.

In a study just published, the point I've made about my argument about "inflammation" is stated explicityly:

"Blockade of cytokines, particularly of tumour necrosis factor alpha (TNF-alpha), in immuno-inflammatory diseases, has led to the greatest advances in medicine of recent years... TNF-alpha is of crucial importance in the development of antigen-dependent and antigen-independent models of inflammation, and that these results correlate well with clinical success..."

The only thing not mentioned is the role fatty acids play, again, probably due to the excessive specialization in today's biomedical establishment.

Source: Springer Semin Immunopathol. 2006 Jun;27(4):391-408.

Title: "Inhibition of IL-1, IL-6, and TNF-alpha in immune-mediated inflammatory diseases."

Moller B, Villiger PM.

Today, there was a report about a study showing the long-term effects of surgery, something that few if any patients are told:

"'The first insight we take away from this is that when bad things happen down the road, months, maybe even years later, that we cannot, as we have in the past, just attribute it to the natural course of illness.'"

But what is this mostly due to? Again, we are back to "inflammation," macrophages, etc:

"Inflammation is a player in most major diseases, from cardiovascular disease to cancer. A heart patient, for example, already has chronic inflammation and the coronary bypass surgery he needs, ironically, may accelerate it. ...research is showing the impact of even a small infection [common after even minor surgery] in the face of chronic inflammation. Using an animal model of sickle cell disease, a disease marked by systemic inflammation, he’s studying the host’s defense to microbial products such as lipopolysaccharide. He’s found a resulting transformation of macrophages, which typically work like garbage collectors for the immune system, into large, pro-inflammatory cytokine-spewing cells."

This is similar to the oxidized cholesterol role in "heart disease." The only thing missing, as usual, is an understanding of the role fatty acids play, which explains why certain common "diseases" of today were not at all common a hundred years ago, when people's cells were not overloaded with arachidonic acid.

Source: http://www.sciencedaily.com/releases/2006/06/060605155505.htm

You may have heard that recently a scientist "infected" himself with H. pylori, giving himself an ulcer and "proving" that this was the "cause" of ulcers - a bacterial infection. However, it is undeniably true that not everyone who has been exposed to H. pylori develops an ulcer. Thus, this claim of "causation" appears to violate the scientific method. A recent experimental study shows what is really going on in this "disease," and guess what? Arachidonic acid metabolites appear to be what causes the "disease:"

"Our findings are the first to demonstrate that the detrimental consequences of H. pylori LPS on gastric mucin synthesis involve ERK-dependent cPLA2 activation that leads to up-regulation in PAF generation and ET-1 production..."

Source: IUBMB Life. 2006 Apr;58(4):217-23.

As in other "diseases," a stressor compels cells to release AA, which is made into particular molecules (such as LTB4), which cause some bacteria to become "clingly," prompting the body to attack it with molecules (such as TNF-alpha) that do terrible damage if cells are chronically exposed to it, and leading to what people perceive as "disease."

For more on this, see the essay, "The AA connection to today's common 'diseases.'" Now here is something recent that makes some important points:

"Just as immune cells recognize and attack foreign invaders in the human body to protect against harmful infections, single-cell organisms have a protein called H-NS that recognizes foreign DNA and prevents it from becoming active, the researchers discovered. But bacteria can also benefit from foreign DNA. When Salmonella is infecting an animal or person, for instance, many proteins the bacteria need to cause disease are encoded by DNA acquired from other bacteria. The researchers found that when the bacteria is infecting a host, other molecules can compete with the H-NS protein, allowing the disease-causing genes to be expressed. When the bacteria are in the environment, H-NS turns these genes off to avoid detrimental consequences if all the disease-causing genes were to be expressed at once. These findings give scientists new insight into how bacteria can protect themselves from an invasion by foreign DNA, yet still take in genetic information from diverse sources that makes them more virulent. 'By harnessing foreign DNA, bacteria that cause typhoid, dysentery, cholera and plague have evolved from harmless organisms into feared pathogens...'"

Source: http://www.sciencedaily.com/releases/2006/06/060608225847.htm

Note how it is mentioned that certain proteins and also biochemical activity are needed for "disease" to occur (meaning that a damaging inflammatory response will be provoked). My argument is that the evidence, when viewed as a whole, suggests that there is a "ramping up" of "the war" between the "immune system" and the "pathogens" that is not necessary and that does the person more harm than good. The proper diet and lifestyle can largely prevent this from occurring (in almost all practical situations).

And here is something very interesting about multiple sclerosis:

QUOTE: It may sound like a case of blame the victim, but researchers at Washington University School of Medicine in St. Louis have shown that cells in the central nervous system can sometimes send out signals that invite hostile immune system attacks. In mice the researchers studied, this invitation resulted in damage to the protective covering of nerves, causing a disease resembling multiple sclerosis.

Eliminating a molecular beacon can help protect a neuron (shown here) from destructive immune system cells. (Image courtesy of Washington University School of Medicine)Ads by Google Advertise on this site

"It's been clear for quite a while that our own lymphocytes (white blood cells) have the ability to enter the central nervous system and react with the cells there," says John Russell, Ph.D., professor of molecular biology and pharmacology. "Under normal circumstances, the brain and the immune system cooperate to keep out those cells that might harm the brain. But in people with multiple sclerosis, they get in."

The researchers found that they could prevent destructive immune cells from entering nervous system tissue by eliminating a molecular switch that sends "come here" messages to immune cells. Ordinarily, flipping that switch would cause immune cells to rush to the vicinity of the cells that sent the signals and destroy whatever they consider a danger — including nerve cell coatings.

But in the mice in which the switch was removed, the researchers saw that immune cells previously primed by the scientists to attack the central nervous system (CNS) did not enter the CNS, and the mice stayed healthy. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/06/060616125632.htm

So once again we see that a terrible "disease" is caused by the body attacking itself because of some cellular-level stressor. If you read the other essays, you know that just through diet alone this "attack" might be prevented, with no inhibition to the "immune system." The evidence is now clear - none of these ideas originate with me. Every day, it seems, the evidence, which is consistent down to the molecular level, mounts, for example:

"Hepatocellular carcinoma (HCC), the most common form of liver cancer, is the third leading cause of cancer deaths worldwide. Its major risk factors are persistent infection with hepatitis B and C viruses, and exposure to toxic chemicals, including alcohol, all of which cause chronic liver injury and inflammation... 'Since inflammation drives both damage and regeneration in liver tissue, it is the repeating cycle of damage, inflammation and regeneration that leads to liver cancer,' said [Michael] Karin."

Source: http://www.sciencedaily.com/releases/2006/06/060623001538.htm

I would just add that excess polyunsaturated fatty acids in the diet have the potential to be toxic in the same way, as is clear from the literature. Here's a less technical explanation:

"...when highly unsaturated vegetable oils are heated at frying temperature (365 F) for extended periods--or even for half an hour--a highly toxic compound, HNE (4-hydroxy-trans-2-nonenal) forms in the oil... Csallany's work underscores the risk of repeated heating, or reusing, highly unsaturated oils for frying because HNE accumulates with each heating cycle. In future studies, Csallany and her colleagues plan to determine how long polyunsaturated oil must be heated at lower temperatures in order to form HNE and its related compounds."

Source: http://www.medicalnewstoday.com/medicalnews.php?newsid=23733

Nineteenth page from the old MSN site.

2008-11-11T12:55:00.000-08:00

Why cancers today are more aggressive than those of the past.

One thing you don't hear about is how aggressive many cancers are today, which was uncommon in the past, and the only scientific explanation that makes any sense inovolves AA and other unsaturated fatty acids. I will be working on this page for a while, and so I will just post a few abstracts of studies here (at the end) as write, because these items are representative of the literature in general.

I remember reading something biologist Ray Peat wrote about how in experiments from the early to mid twentieth century it was found that animals on a fat-free diet did not develop cancer. It surprised me, to say the least; not so much the experimental results but how these results have received little, if any, mainstream media coverage (at least in recent years). Now, it's possible that this is due to a lack of familiarity with the old evidence on the part of journalists too young to know and to busy to do the research, and yet there are plenty of the kinds of studies presented below (in their abstract forms) published in recent years. In one, there is the following passage:

"In conclusion, here we demonstrate that: a) breast cancer cells retain dependence on endogenous fatty acid synthesis and sensitivity to FAS inhibition in the presence of supraphysiological levels of dietary fatty acids..."

And in another one there is:

"It is well documented that arachidonic acid (AA) and its metabolites are intimately linked to cancer biology."

In that study, the point is made that AA metabolites have the direct, cancer-causing effects, while "free" AA is so toxic that it kills cells, even cancer cells, quite easily. These researchers seem to be interested only in cancer cells, so they appear to have negelected to ask themselves the simple question, "what would happen if people ate food that depleted their bodies of AA (and also omega 3 PUFAs)?" A fat-free diet is not practical, but one that rids the body's cells of AA is (and is also very tasty). Not doing this can create a "frying pan into the fire" situation, that is, if one tries to inhibit AA metabolization, worse problems and eventually "diseases" can result.

And here are some other examples of the kind of evidence now available:

Carcinogenesis. 2006 May 15; [Epub ahead of print]

Arachidonic acid induced gene expression in colon cancer cells.

Monjazeb AM, High KP, Connoy A, Hart LS, Koumenis C, Chilton FH.

Department of Cancer Biology, Wake Forest University Baptist Medical Center, Medical Center Boulevard, Winston-Salem, NC 27157.

It is well documented that arachidonic acid (AA) and its metabolites are intimately linked to cancer biology. However, the downstream mechanism(s) that link AA levels to cancer cell proliferation remain to be elucidated. Initial experiments in the current study showed that exogenous AA and inhibitors of AA metabolism that lead to the accumulation of unesterified AA are cytotoxic to the colon cancer cell line, HCT-116. Additionally, exogenous AA and triacsin C, an inhibitor of AA acylation, induced apoptosis and related caspase-3 activity in a transcriptionally dependent manner. Gene array analysis revealed that both exogenous AA and triacsin C alter the expression of similar genes in HCT-116 cells. For example, both down-regulate several genes with well documented roles in cell survival and apoptotic resistance. Conversely, both up regulate genes encoding AP-1 transcription factors, which have known roles in inducing apoptosis, and genes which counteract ras (Erk/MAPK) growth signaling pathways. Realtime PCR and immunoblotting demonstrated that mRNA and protein levels of one of the major AP-1 transcription factors, c-Jun is markedly elevated by exogenous AA and triacsin C. Additionally the cyclooxygenase-2 inhibitor, sulindac sulfide, increase c-Jun mRNA levels. Together, these studies reveal that the generation of intracellular AA and its subsequent impact on gene expression likely represents a critical step that regulates colon cancer cell proliferation.

Free Radic Biol Med. 2006 Feb 1;40(3):364-75. Epub 2005 Nov 4.

Role of cytochrome P450 in phospholipase A2- and arachidonic acid-mediated cytotoxicity.

Caro AA, Cederbaum AI.

Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, Box 1603, One Gustave L. Levy Place, New York, NY 10029, USA. Andres.Caro@mssm.edu

Phospholipases A2 (PLA2) comprise a set of extracellular and intracellular enzymes that catalyze the hydrolysis of the sn-2 fatty acyl bond of phospholipids to yield fatty acids and lysophospholipids. The PLA2 reaction is the primary pathway through which arachidonic acid (AA) is released from phospholipids. PLA2s have an important role in cellular death that occurs via necrosis or apoptosis. Several reports support the hypothesis that unesterified arachidonic acid in cells is a signal for the induction of apoptosis. However, most of the biological effects of arachidonic acid are attributable to its metabolism by mainly three different groups of enzymes: cytochromes P450, cyclooxygenases, and lipoxygenases. In this review we will focus on the role of cytochrome P450 in AA metabolism and toxicity. The major pathways of arachidonic acid metabolism catalyzed by cytochrome P450 generate metabolites that are subdivided into two groups: the epoxyeicosatrienoic acids, formed by CYP epoxygenases, and the arachidonic acid derivatives that are hydroxylated at or near the omega-terminus by CYP omega-oxidases. In addition, autoxidation of AA by cytochrome P450-derived reactive oxygen species produces lipid hydroperoxides as primary oxidation products. In some cellular models of toxicity, cytochrome P450 activity exacerbates PLA2- and AA-dependent injury, mainly through the production of oxygen radicals that promote lipid peroxidation or production of metabolites that alter Ca2+ homeostasis. In contrast, in other situations, cytochrome P450 metabolism of AA is protective, mainly by lowering levels of unesterified AA and by production of metabolites that activate antiapoptotic pathways. Several lines of evidence point to the combined action of phospholipase A2 and cytochrome P450 as central in the mechanism of cellular injury in several human diseases, such as alcoholic liver disease and myocardial reperfusion injury. Inhibition of specific PLA2 and cytochrome P450 isoforms may represent novel therapeutic strategies against these diseases.

Int J Oncol. 2004 Mar;24(3):591-608.

Novel signaling molecules implicated in tumor-associated fatty acid synthase-dependent breast cancer cell proliferation and survival: Role of exogenous dietary fatty acids, p53-p21WAF1/CIP1, ERK1/2 MAPK, p27KIP1, BRCA1, and NF-kappaB.

Menendez JA, Mehmi I, Atlas E, Colomer R, Lupu R.

Department of Medicine, Evanston Northwestern Research Institute, Evanston, IL 60201, USA.

A biologically aggressive subset of human breast cancers has been demonstrated to overexpress fatty acid synthase (FAS), the key enzyme of endogenous FA biosynthesis. This breast cancer-specific activation of FAS-dependent lipogenesis, an anabolic-energy-storage pathway of minor importance in normal cells, would render breast cancer cells more vulnerable to anti-metabolite interventions with FAS as therapeutic target. Not surprisingly, pharmacological inhibitors of FAS have been reported to produce both cytostatic and cytotoxic effects in human breast cancer cells, as well as to suppress DNA replication. However, the signal transduction pathway(s) that link FAS hyperactivity and breast cancer cell growth has been unresolved. Here, we have attempted to provide a systematic approach to assess the role of FAS signaling on the survival and proliferation of human breast cancer cells. First, we assessed the level of FAS protein in a panel of human breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-453, MDA-MB-435, ZR-75B, T47-D, BT-474, and SK-Br3). FAS expression was graded from ++++ (overexpression) in SK-Br3 cells to + (very low expression) in MDA-MB-231 cells. No correlation was noted between FAS overexpression and estrogen receptor (ER) or progesterone receptor (PR) status, whereas a positive correlation was found between high levels of FAS expression and the amplification and/or overexpression of HER-2/neu oncogene. Because metabolic adaptation of breast cancer cells to the ambient fatty acid concentration may be relevant to the goal of utilizing FAS inhibition as a chemotherapeutic target, we evaluated the effect of exogenous dietary fatty acids on the cytotoxicity resulting from the inhibition of FAS activity. Pharmacological inhibition of FAS activity by the natural antibiotic cerulenin [(2S,3R)-2,3-epoxy-4-oxo-7E,10E-dodecadienamide] resulted in a dose-dependent cytotoxicity which positively paralleled the endogenous level of FAS. Supraphysiological levels of exogenous oleic acid (OA), a omega-9 monounsaturated fatty acid synthesized from a primary-end product of FAS palmitate, significantly diminished cell toxicity caused by cerulenin. Indeed, OA exposure significantly reduced FAS activity and expression by 55% in FAS-overexpressing SK-Br3 cells. omega-3 (alpha-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid) and omega-6 (linoleic acid and arachidonic acid) polyunsaturated fatty acids (PUFAs), however, were unable to rescue breast cancer cells from cerulenin-induced cytotoxicity. Pharmacological blockade of FAS activity in FAS-overexpressing SK-Br3 cells resulted in apoptosis as determined by an enzyme-linked immunosorbent assay for histone-associated DNA fragments, and confirmed by TUNEL DNA-end labeling experiments. We further characterized signaling molecules that participate in the cellular events that follow inhibition of FAS activity and precede apoptosis in breast cancer cells. In SK-Br3 cells, cerulenin-induced inhibition of FAS activity resulted in down-regulation of p53, and up-regulation of cyclin-dependent kinase inhibitor (CDKi) p21WAF1/CIP1. Treatment with cerulenin or a novel small-molecule inhibitor of FAS C75 resulted in a dramatic accumulation of CDKi p27KIP1, which was accompanied by a noteworthy translocation of p27KIP1 from cytosol to cell nuclei. Strikingly, FAS inhibition also caused a significant activation of the Raf-mitogen-activated protein kinase (MEK) extracellular signal-regulated kinase (ERK1/2) cell survival pathway. Interestingly, we demonstrated that inhibition of FAS activity increased the nuclear-to-cytoplasmic ratio of BRCA1, a breast cancer tumor suppressor protein, as well as it induced a nuclear translocalization of the anti-apoptotic nuclear transcription factor-kappaB (NF-kappaB). In conclusion, here we demonstrate that: a) breast cancer cells retain dependence on endogenous fatty acid synthesis and sensitivity to FAS inhibition in the presence of supraphysiological levels of dietary fatty acids, supporting the notion that FAS inhibition may be useful in treFAS inhibition may be useful in treating breast cancer in vivo; b) endogenous fatty acid synthesis is functional in breast cancer cells and is vital since its pharmacological inhibition is cytotoxic by promoting apoptosis, and c) specific blockade of FAS activity induces the accumulation, activation, and/or cellular relocalization of multiple and diverse pro- and anti-apoptotic signaling pathways, suggesting that p53-p21WAF1/CIP1, ERK1/2 MAPK, p27KIP1, BRCA1, and NF-kappaB play a novel role in the breast cancer cell response to a metabolic stress after perturbation of FAS-dependent de novo fatty acid biosynthesis.

Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11280-5.

Intracellular unesterified arachidonic acid signals apoptosis.

Cao Y, Pearman AT, Zimmerman GA, McIntyre TM, Prescott SM.

The Huntsman Cancer Institute, and Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.

Cyclooxygenase-2 (COX-2) is up-regulated in many cancers and is a rate-limiting step in colon carcinogenesis. Nonsteroidal antiinflammatory drugs, which inhibit COX-2, prevent colon cancer and cause apoptosis. The mechanism for this response is not clear, but it might result from an accumulation of the substrate, arachidonic acid, an absence of a prostaglandin product, or diversion of the substrate into another pathway. We found that colon adenocarcinomas overexpress another arachidonic acid-utilizing enzyme, fatty acid-CoA ligase (FACL) 4, in addition to COX-2. Exogenous arachidonic acid caused apoptosis in colon cancer and other cell lines, as did triacsin C, a FACL inhibitor. In addition, indomethacin and sulindac significantly enhanced the apoptosis-inducing effect of triacsin C. These findings suggested that unesterified arachidonic acid in cells is a signal for induction of apoptosis. To test this hypothesis, we engineered cells with inducible overexpression of COX-2 and FACL4 as "sinks" for unesterified arachidonic acid. Activation of the enzymatic sinks blocked apoptosis, and the reduction of cell death was inversely correlated with the cellular level of arachidonic acid. Inhibition of the COX-2 component by nonsteroidal antiinflammatory drugs restored the apoptotic response. Cell death caused by exposure to tumor necrosis factor alpha or to calcium ionophore also was prevented by removal of unesterified arachidonic acid. We conclude that the cellular level of unesterified arachidonic acid is a general mechanism by which apoptosis is regulated and that COX-2 and FACL4 promote carcinogenesis by lowering this level.

Int J Urol. 2006 Aug;13(8):1086-91.

Inhibition of 5-lipoxygenase pathway suppresses the growth of bladder cancer cells.

Hayashi T, Nishiyama K, Shirahama T.

Many stimuli, including growth factors and cytokines, activate arachidonic acid (AA) metabolic pathways, which are involved in cancer development and progression. We examined the effects of a series of pharmacological inhibitors of AA metabolic enzymes on bladder cancer cells to determine the role of AA pathway in this malignancy. Human bladder cancer cell lines were treated with various AA metabolic enzymes inhibitors for lipoxygense (LOX) and cyclooxygenase (COX) pathways, and the growth suppression effects were examined. The enzyme expression in cancer cells was examined by immunoblot analyses. A 5-LOX-specific inhibitor, AA861, dose-dependently inhibited the growth of bladder cancer cells. The growth inhibitory effects were greatly abolished by 5-LOX product, 5-HETE, but not by other LOX products examined. They were observed in four cancer cells that expressed 5-LOX, but not in one that did not. Of a series of LOX and COX pathway inhibitors, AA861 was the strongest one to suppress the growth of cancer cells. Bladder cancer cells frequently expressed 5-LOX. A 5-LOX-specific inhibitor, AA861, revealed the strongest growth suppression of those cells compared to other LOX and COX pathway inhibitors, and the growth suppression effects were considered to be due to inhibition of the enzymatic activity. Therefore, 5-LOX may play a regulatory role in proliferation and/or survival of bladder cancer, and may be a therapeutic target for the disease.

Eighteenth page from the old MSN site.

2008-11-11T12:53:00.000-08:00

Why you have to be careful with antioxidants.

A report today (May 18, 2006) really put a smile on my face, I must admit, because it is so consistent with my interpretation of the scientific evidence, but it also demonstrates why you should be careful about taking large amounts of antioxidant supplements. So let's get to the report, which opens with:

"Doctors have long been encouraging Americans to add more fruits and vegetables to their daily diets. Now, UC Davis researchers have discovered one way in which flavonoid-rich apples inhibit the kinds of cellular activity that leads to the development of chronic diseases, including heart disease and age-related cancers."

Source: http://www.sciencedaily.com/releases/2006/05/060517185449.htm

As I point out, much of this "cellular activity" involves AA metabolites, which one can easily avoid with the right diet. But then comes the really interesting part:

"In the current study, Gershwin and his colleagues exposed human endothelial cells to an extract of an apple mash made from different apple varieties. The researchers then challenged these cells by exposing them to tumor necrosis factor (TNF), a compound that usually triggers cell death and promotes inflammation via a mechanism called the 'nuclear factor (NF) kappa B pathway.' This pathway involves chemical signaling between cells. The apple extract was able to protect the cells from the normal lethal effects of TNF."

If you've read the other essays, you know that the more unsaturated the fatty acids in your cells, the more TNF gets generated during stress to cells. But the nuclear factor kappa B pathway is important here as well. I'll let some scientists who seem to really understand the material explain it:

"N-6 polyunsaturated fatty acids (N-6 PUFAs), major constituents of corn oil and natural ligands for peroxisome proliferator-activated receptors, increase the rate of growth of established tumors. It has been proposed that chemical peroxisome proliferators increase hepatocyte proliferation by mechanisms involving activation of nuclear factor-B (NF-B) and production of low levels of tumor necrosis factor (TNF) by Kupffer cells; however, how N-6 PUFAs are involved in increased cell proliferation in liver is not well understood. Here, the hypothesis that N-6 PUFAs increase production of mitogens by activation of Kupffer cell NF-B was tested. A single dose of corn oil (2 ml/kg, i.g.), but not olive oil or medium-chain triglycerides (saturated fat), caused an ~3-fold increase in hepatocyte proliferation. Similarly, when activity of NF-B in whole rat liver or isolated hepatocytes and Kupffer cells was measured at various time intervals for up to 36 h, only corn oil activated NF-B. Corn oil increased NF-B activity ~3-fold 1–2 h after treatment exclusively in the Kupffer cell fraction. In contrast, increases were small and only occurred after ~8 h in hepatocytes. The activation of NF-B at 2 h and increases in cell proliferation at 24 h due to corn oil were prevented almost completely when rats were pretreated for 4 days with either dietary glycine (5% w/w), an agent that inactivates Kupffer cells, or the NADPH oxidase inhibitor, diphenyleneiodonium (s.c., 1 mg/kg/day). Furthermore, arachidonic acid (100 µM) activated superoxide production ~4-fold when added to isolated Kupffer cells in vitro. This phenomenon was not observed with oleic or linoleic acids. Interestingly, a single dose of corn oil increased TNF mRNA nearly 2-fold 8 h after treatment. It is concluded that corn oil rapidly activates NF-B in Kupffer cells via oxidant-dependent mechanisms. This triggers production of low levels of TNF which is mitogenic in liver and promotes growth of hepatocytes...

In conclusion, the data presented here support the hypothesis that corn oil activates NF-B in Kupffer cells via oxidant-dependent mechanisms. This is probably a key early event resulting in subsequent increases in TNF leading to increased cell proliferation in the liver"

Source: Carcinogenesis, Vol. 20, No. 11, 2095-2100, November 1999

So here again the connection between diet and the "disease" common in the West today is clear. As I've said in other essays, my main point is that there is enough scientific evidence to make clear suggestions about diet, and that most of what you hear in the media is the opposite of what you should be doing, especially concerning which fatty acids are best and which are the worst.

Now for the point about antioxidants: if you follow my diet, for example, you may do harm if you use antioxidant supplements in large amounts (and that might happen with any diet). Why? Because molecules like TNF are useful under certain circumstances, and if you inhibit them in a strong way you might cause "disease." The reason why antioxdant "studies" look "good" has to do with the fact that almost everyone is eating a diet that produces a lot of free radical damage. In theory, one might be able to "balance" these two sides of the coin (called the redox balance), but much more experimentation would have to be done to see what the long term effects are of various combinations. Until then, I will stay with my diet and no antioxidant supplements (though as I get older I might take small amounts of CoQ10).

Seventeenth page from the old MSN site.

2008-11-11T12:52:00.000-08:00

How many 'scientific studies' violate the scientific method?

In some cases, what you hear about in the media is just "hype." In other words, the resesarchers say that a finding is "promising" and "may lead to an eventual cure for disease X." But it may get reported as "a cure for disease X appears to be just around the corner." An example of this is:

"'Research Uncovers Signaling Pathways Related To Brain-immune System Links'

New research on signaling pathways in immune cells bolsters evidence of connections between the central nervous system and the immune system. The findings may also advance the scientific foundation for a potential HIV treatment that may block the virus that causes AIDS... Because macrophages are a reservoir for HIV, a strategy that denies the virus entry into those immune cells may be important in combating HIV infection."

Source: http://www.sciencedaily.com/releases/2006/05/060515230947.htm

If you read the whole report you see that they observed some molecular phenomenon, then tried to fit the square peg into the round hole. If a virus was damaging, destroying, or rendering dysfunctional macrophages, then it would be detectable, just as what happens to macrophages when there is too much oxidized cholesterol in the body is detectable (and the entire "disease process" is clear). Instead, these researchers are assuming that the textbook models and claims are accurate, and so they come to tentative conclusions (notice how many times "may" is used in these kinds of reports/studies) that don't consider the process as a whole, and in this case their conclusions are inconsistent with basic observation. There is not a great deal of macrophage dysfunction or destruction in a person "infected with HIV," though after taking toxic drugs for many years there can be all kinds of damage done to the body. So what are they talking about?

If I asked them to cite one piece of scientific evidence (where controls are used and a few hundred people or more are involved) that demonstrates that within even a year of "HIV infection" there is massive macrophage death and/or dysfunction, what would they cite? I have yet to find such evidence for such claims as theirs. Moreover, the "proof is in the pudding" when it comes to "diseases." If they can't "cure" it (and they've had 25 years now), then they have failed. I'd like to see others with fresh ideas that are focused on the process as a whole get proper funding, but instead those who mouth the dogma seem to get the lion's share of it.

Another problem in these kinds of studies, that is, ones that appear to be so specific and focused on molecular-level phenomena is that many researchers, who are often highly specialized in their research, may be so fixated on one gene or protein, for example, that they don't realize that even if it were easy to change, inhibit, or enhance genetic or protein expression, it is likely that the long-term consequences will be worse than doing nothing at all. For example:

"A gene commonly involved in cancer onset, c-myc, has been found to have a role in the immune system's normal function according to a study published today in Blood."

Source: http://www.sciencedaily.com/releases/2006/05/060515100316.htm

A good example of how many research scientists "miss the forest because the trees get in the way" is the following:

"The cellular activity of PI-103 was traced to its ability to cooperatively inhibit both the p110Ã¡ subunit of PI3 kinase and a downstream molecule called mTOR that also plays a critical role in cell growth. Although both of these molecules are members of the same signaling cascade, the researchers found that they must be concurrently inhibited because of a regulatory feedback loop that renders a monospecific inhibitor ineffective. Importantly, dual inhibition of p110Ã¡ and mTOR with a low dose of PI-103 elicited no drug-related toxicity and was highly effective against human gliomas transplanted into mice."

Source: http://www.sciencedaily.com/releases/2006/05/060516075929.htm

Now this sound like they are incredible geniuses, to be sure, but what have they to show for it? You can go back many years and find reports like this, and nothing ever seems to come of the "momentous discoveries." The simple reality is that such aberrant cellular signaling is due to the fatty acids people are now consuming in much of the world (and low intake of antioxidant-rich foods, etc.). Yes, you can then inhibit what should never have been enhanced in the first place, but you risk "side-effects" that are worse than the "disease" that you were originally trying to "cure."

Also note that they are trying to inhibit cell growth, and yet in other studies, researchers with similar or the same credentials argue that arachidonic acid is "essential" because it stimulates cell growth (as does the Mead acid, but not as potently). One does not need to have any credentials, however, to realize that growth needs to take place at certain times and to a certain degree (or else cancer can result, among other deleterious possibilities). Yet in many studies the researchers never talk about what the thresholds are, and thus to say that something is "good" or "beneficial" because it "stimulates growth," without any context, is worse than meaningless - it can lead people to do things that are very dangerous.

A very common problem with many studies is that they focus on "markers," which again is indirect and possibly totally wrong. The most obvious example of this involves measuring serum cholesterol (or LDL) levels and then claiming that X "lowers the risk of heart disease." Especially now, because it's known that oxidation of cholesterol/LDL is the main problem, such a claim is very misleading, and could cause cancer rates to rise, because low LDL has this effect in most people. This approach is based upon a statistical evaluation of this marker and rates of one "disease." They hardly ever consider the possibility that "high" cholesterol (between 200 and 220) may be best for overall mortality (as Ancel Keys himself noted in his 1979 "Seven Countries" book). Today, many "beneficial" claims are made for fish oil, yet if one only looks for markers of AA damage, one can miss the damage done by omega 3 fatty acids in fish oil. For example:

J Biol Chem. 2005 May 13; [Epub ahead of print]

Regiochemisry of neuroprostanes generated from the peroxidation of docosahexaenoic acid in vitro and in vivo.

Yin H, Musiek ES, Gao L, Porter NA, Morrow JD.

Departments of Pharmacology and Medicine, Vanderbilt University Medical Center, Nashville, TN 37235.

Isoprostanes (IsoPs) are isomers of prostaglandins (PGs) that are generated from the free radical-initiated peroxidation of arachidonic acid (C20-4 omega-6). IsoPs exert potent bioactivity and are regarded as the "gold standard" to assess oxidative stress in various human diseases. Analogously, autoxidation of docosahexaenoic acid (DHA, C22:6 omega-3) generates an array of IsoP-like compounds that are termed neuroprostanes (NPs). A major class of NPs identified in vitro and in vivo contain F-type prostane rings and are know as F(4)-neuroprostanes (NPs). A number of different F(4)-NP regioisomers are formed from the peroxidation of DHA. Among the eight possible regioisomeric groups, we hypothesize that 4- and 20-series NPs are generated in greater amounts than other classes because the precursors that lead to regioisomers other than those of the 4- and 20-series can be further oxidized to form novel dioxolane-IsoP-like compounds, analogous to those generated from arachidonate. Various mass spectrometric approaches, including electron capture atmospheric pressure chemical ionization mass spectrometry, were utilized to analyze NPs formed in vitro and in vivo based on their characteristic fragmentation in the gas phase. Experimental results are consistent with our hypothesis that 4- and 20-series NP regioisomers are preferentially generated. The discovery of regioselectivity in the formation of NPs will allow studies of the biological activities of NPs to focus on the more abundantly generated compounds in order to determine their role in modulating the pathophysiological consequences of DHA oxidation and oxidant stress.

The most common problem, however, is the finding of a "link," "association," or "correlation." This compounds the problem of looking for markers, adding another level of "noise" instead of just employing the scientific method. The "link," or whatever they call it, is often due to socio-economic or other "non-scientific" factors. For example, from sciencedaily.com (on 1/20/2006) was the following:

"Wine Drinkers Have Healthier Diets Than Beer Drinkers:

People who buy wine also buy healthier food and therefore have healthier diets than people who buy beer, finds a study published online by the British Medical Journal.

Studies have shown that drinking wine is associated with lower mortality than drinking beer or spirits. Some studies have also suggested that wine drinkers have healthier diets than beer or spirits drinkers, and this may explain wine's beneficial effect on health.

To study this theory, researchers in Denmark investigated the link between the purchase of beer and wine and various food items from supermarkets.

They analysed 3.5 million transactions chosen at random from 98 outlets of two large Danish supermarket chains over a six month period (September 2002 to February 2003).

Customers were categorised as "wine only," "beer only," "mixed," or "non-alcohol" buyers. Details of items bought, the number and price of the items, and the total charge for each customer's transaction were recorded.

They found that wine buyers bought more olives, fruit and vegetables, poultry, cooking oil, and low fat cheese, milk, and meat than beer buyers. Beer buyers bought more ready cooked dishes, sugar, cold cuts, chips, pork, butter or margarine, sausages, lamb, and soft drinks than wine buyers.

These results indicate that people who buy (and presumably drink) wine purchase a greater number of healthy food items than those who buy beer, say the authors. They also support findings from the United States, Denmark, and France showing that wine drinkers tend to eat fruit, vegetables, and fish and use cooking oil more often and saturated fat less often than those who prefer other alcoholic drinks.

The health benefits of drinking wine may be due to specific substances in wine or to different characteristics of people who drink other types of alcohol, they add. Thus, it is crucial that studies on the relation between alcohol intake and mortality adjust for other lifestyle factors such as drinking patterns, smoking, physical activity, education, or income."

Source: http://www.sciencedaily.com/releases/2006/01/060119232848.htm

Most of these kinds of studies are called "epidemiological," which is derived from their first use to understand "infectious diseases," which were said to cause "epidemics." I am using quotation marks here because of the fact that all factors are not controlled for, which is required by the scientific method. If you've read though some of my essays here, you realize that the fatty acids you eat can play a huge role in your health, whether you develop particular "diseases," etc., but of course there are many other factors that are rarely or never taken into account (such as the socio-economic ones). Indeed, one could argue that it is impossible to do so, yet that does not explain how a "scientist" can decide to not control for factors that have been demonstrated to be important (such as the fatty acids). I call the worst abuses of this approach "smelly socks epidemiology," because it would be easy to find an "association" between how much a person's socks smell at the end of the day to just about any "disease," and yet hardly anyone would think that the socks caused the disease, though if you substitute "sugar," "salt," "cholesterol," or any number of things most people view as "unhealthy," few question the results, and the existing dogma is reinforced.

One way to refute a supposedly scientific claim is to demonstrate that there is another explanation that accounts for all the data without any problems. It is not difficult to validate experimentally the points I've made on this site; all a researcher needs to do is to feed one group of animals the diet and supplements I suggest while feeding another group a diet that is consistent with the "typical American" diet, and then expose the animals to various "infectious diseases." If the latter group becomes ill but the former does not (or if the incidence of "disease" is much lower and/or the manifestation of it greatly attentuated) it would be clear that at least most "infectious diseases" are epiphenomenal - resulting from a combination of factors that one could avoid or manipulate to best effect.

Of course, this would then mean a loss of jobs for many very powerful people n the biomedical establishment, a huge loss of profits for companies that make certain "medicines," etc., so even if such exeperiments are performed, do not expect the mainstream media to explain to you what the implications are. As I said in another essay here, experiments like this are being done, but the researchers are not controlling for the variables that appear to play a major (if not the major) role, due to excessive "professional" specialization (since I have cited other studies which point to the roles these variables play in "disease" in several essays here).

Sixteenth page from the old MSN site.

2008-11-11T12:49:00.000-08:00

Where the "immune system" fits into this view of "disease."

Have you ever wondered why so few “experts” and “journalists” ask how it could be that something that is supposed to be “scientific” fails over and over again? How many predictions have you heard about “outbreaks of infectious disease” that never come to pass? How many “flu pandemics” have been predicted in the last few decades? And let's not forget the "Mad Cow Disease" scare a few years back, which frightened many people I know. What about the massive death from “infectious diseases” in the wake of the tsunami disaster and Hurricane Katrina that were predicted and never occurred? On the other hand, it is estimated that each year 90,000 hospital patients die of infections they acquired while in this supposedly “antiseptic” environment in the USA alone. Something is very wrong here, and when something is this wrong, it is usually because the underlying assumptions are not accurate. Fortunately, some have investigated why the predominant notions about the “immune system” and “inflammation” do not seem to work in the “real world” the way it is said that they operate in models presented in the major textbooks.

Nobody really knows what the “immune system” is. New molecules and processes are being “discovered” all the time, and basically what is known is based upon observations (often made under specific, “un-natural” conditions) and assumptions derived from untested or partially tested models. What we do know is that it developed via evolutionary processes, but not that it was designed to be a “system,” so it is important not to take anything for granted, or to assume that a “promising marker” that was found upon preliminary investigations should be reified into textbook dogma (unfortunately, this situation is all too common in recent years). Because of the many problems with existing notions about the “immune system,” some scientists have reevaluated the textbook notions, and today there is Matzinger’s “Danger Model” and Cuniliffe’s “Morphotstatic” one. Cunliffe’s is more “radical,” but also more consistent with the notion that an inflammatory response that is too strong is very dangerous. Below, I will present a few passages from Cunliffe’s web site, along with my comments in brackets (the specific page is http://www.morphostasis.org.uk/Papers/Phlog199803.htm). After this, I will discuss a recent report which provides a common example of how this works in practice.

Here is Cunliffe’s view:

A morphostatic system works in a different way. "Ooopppss! Something's making a tissue mess. Better go tidy up the mess and fix any losses. While we're about it we'll take a snapshot of this mess. We'll remember the most unusual signature of it. Then, if we meet a similar mess in the future, we'll ramp up the accumulation of mess eaters and make these act more aggressively when they get there."…

It is almost a scorched earth (scorched extracellular space) policy that sequesters away nutrients and metabolites from potential invaders. Invaders must dedicate genetic resources to ensuring the generation of supplies and other metabolites - or, alternatively, get themselves invited into the host's cells where there are more accessible resources. These conditions are, naturally, proinflammatory for phagocytes and APCs so the invading organisms are obliged to be proinflammatory (pathogenic) themselves.

[This does not need to be the case, but it is usually the case for those with AAOS (arachidonic acid overload syndrome). With Mead acid in the place of AA, “pathogens” come in, find the environment to be rather placid (since cells are packed with saturated fatty acids and non-oxidized cholesterol) and do little reproducing and little harm. Some “pathogens,” in fact, only become dangerous to people when they are placed under enormous stress, such as when bacteria often found in peoples’ GI tracts is exposed to the stresses of surgery. This is a major reason for the hospital deaths from normally benign bacteria. With “flu outbreaks” of the common variety, people who are either not healthy or who are enduring a great deal of biochemical activity, for example, if they are doing manual labor for many hours a day, act as incubators because the “pathogen” has the resources under these circumstances to adapt to the “immune system.” They are still only deadly for a small number of people, however, and a personal story is illuminating in this context. Up until the time I decided to rid my body of AA, I used to experience at least two “colds” a year, on average, and the symptoms were usually very uncomfortable and lasted for at least two weeks. Once I began avoiding dietary PUFAs, it took a few years before I “caught” something at a family gathering. One relative was very ill for several days with pain in the throat and other nasty symptoms, and had to try two different antibiotics, then she developed another infection, while another relative was told by his doctor that he had “strep throat” and was also prescribed antibiotics. I had a mildly uncomfortable sensation in my throat for several hours one day, then felt a bit tired the next, but there was little else – a few sneezes and a bit of nose blowing over the course of a couple of days. What was the difference? They experienced a stronger inflammatory response than I did, which everyone agrees will occur with Mead acid instead of AA in one’s cells, but they also had problems containing the infection, while my body appears to have had no problem coming to some sort of “settlement” with the “pathogen.” Thus, without AA in your body, you basically have a different “immune system.”]

So, microbes have two distinct influences when encountered by phagocytes (including antigen presenting cells like dendritic cells). First they have features characteristic of microbes (in general) and the phagocyte remembers these, from its evolutionary roots, as potential food: an encounter with them up-regulates the phagocyte's activity (probably, in part, by TLRs). Second, microbes have mechanisms to generate extracellular debris (and this equates to pathogenicity). Little wonder, then, that a macerated wound (from a physical pathogen like, for example, excessive heat) is a breading haven for microbes.

Cells that die suddenly in trauma (e.g. heart attacks, burns) have not been preparing for apoptosis. Cells that die of viral infections or other intracellular nasties have probably moved somewhere along the path towards apoptosis. This means that cells that die by trauma do not spill much Il-1 whereas infected cells do. Spilt Il-1 is a strong contender to be one of the danger signals (eicosanoids, which are released after membrane perturbations, are another). Nevertheless, Dressler's syndrome is the occasional autoimmune sequel to a heart attack - so trauma does increase the risk of autoimmunity. Similarly, in burns and major trauma, autoimmune activity is easy to demonstrate. Indeed, it is the probable precipitant of the phagocytic anergy that precedes multiple organ failure. Any system that allows auto-rejection of normal cells must sport a failsafe cut off device to inhibit the piecemeal destruction of self (6).

[Another key point is contained here: since AA metabolites/eicosanoids are very strong in comparison to Mead acid metabolites/eicosanoids, “danger signals” will have to be quite a bit of “danger” for such signals to occur in a person who has Mead acid in place of AA, whereas the AAOS person’s “immune system” will experience these danger signals in situations where there really is little, if any danger. And there is a price to be paid for these unnecessary danger signals; first, an inflammatory response that has self-destructive qualities, perhaps to the point of “autoimmune disease,” and in some people, T-cell anergy and “AIDS”-like conditions.]

· Th1 cells evolve as an elaboration of the Tc cell system. Now, the cellular and cytoplasmic debris of leaking cells can be digested by APCs and then processed so that representative peptides can be presented on the APC's surface. Apoptosis of these APCs will favour tolerance to ClassII+peptide epitopes. But, when these APCs fail to contain the problem and start to rupture, Th1 aggression will be favoured. On any future encounter with a similarly caricatured APC (not of the pathogen nor of its native antigen), the inflammatory response can be quickly ramped up - bringing in copious aggressive phagocytes and Tnk cells. This is designed to give inflammation a memory. The newly immigrant phagocytes still have to sort healthy-self-cells from the rest but they are now stirred up into a frenzy of eagerness to get on with this job.

· Since extensive tissue destruction is undesirable, phagocytes must be inhibited when the Th1 cell amplification process becomes too intense. Phagocyte activity is consequently inhibited (as, e.g. in a boil) and this increases the amount of debris left to be cleaned up; the IgM free antibody system arose to act as a debris mop. (Macrophage derived cells (B-cells) have an immunoglulin receptor that internalises only targeted debris and processes this into peptide+ClassII epitopes. (Then, when a suitable CD4 T-cell receptor encounters this epitope, it triggers the respective B-cell to produce a sea of free IgM.) B-cells (cells that evolve from the macrophage line) have an immunoglulin receptor that internalises only targeted debris and processes this into peptide+ClassII epitopes. Then, when a suitable CD4 T-cell receptor encounters this epitope, it triggers the respective B-cell to differentiate into a plasma cell that then secretes free IgM. This then tags the debris and enhances its clearance. So, progression to Th2 activity is most likely to occur when cell-mediated auto-rejection is inhibited in the interests of inhibiting piecemeal self-destruction. But this inhibits the clean disposal of mess. The release of IgM is an attempt to compensate for this. All the other immunoglobulins have evolved as shells that envelop IgM (e.g. IgG, IgA, IgE).

[This kind of tissue destruction is what the “HIV” protein band test detects. IgM tries to deal with the cellular “mess,” but at some point this fails too, and then comes the anergy and “full-blown AIDS.” Molecules like TNF-alpha and AA metabolites do great damage to cells, tissues, and organs, so cellular debris continues to accumulate (and tangential “syndromes” develop, such as “AIDS dementia).” At some point the body is so devastated that TNF-alpha and/or AA metabolites may begin to be generated in much smaller amounts, and this may be the “point of no return,” when death in the near future is a certainty. Note that other effects of this process can be insufficient stomach acid and digestive enzyme production, which would cause an “AIDS wasting syndrome,” along with multiple physiological failures. Without the ability to digest protein especially, thyroid hormone, for example, is going to be produced in insufficient quantities, leading to fatigue, etc.]

And now for the report I mentioned in the second paragraph:

"'Sepsis represents a patient's response to severe infection,' explains senior author William C. Aird, MD, Chief of the Division of Molecular Medicine and Associate Director of the Center for Vascular Biology at BIDMC. 'We know that antibiotics will take care of the primary infection, but 30 percent of patients with severe sepsis will die in spite of successful antibiotic therapy because the body's host response is out of control and turns on its bearer. Sepsis develops when the immune system becomes overactivated in response to an existing infection, setting in motion a cascade of dangerous inflammatory and coagulation responses throughout the body. A leading cause of organ failure and intensive care unit (ICU) hospitalizations, severe sepsis accounts for 200,000 deaths...'"

So the question is, why is there such an "out of control" response? "Experts" who recently examined records written by surgeons a couple of hundred years ago were surprised that these kinds of problems were very rare, with most people recovering from amputations of limbs with no such "out of control" response. Animals experiments have shown that if the animal is fed coconut oil, there is no such "out of control" response, but once again, we are dealing with the problem that comes with the extreme specialization that characterizes today's biomedical establishment.

Source for the passage above: http://www.sciencedaily.com/releases/2006/05/060519152635.htm

As the scientific literature on "viruses" makes clear, viruses can prompt a powerful inflammatory/"immune system" response, which in turn can do the actual damage, and which can also make the body susceptible to various "pathogens" that are not normally problematic. There is really no debate on this subject, though some "experts" seem to be blissfully unaware of it (and these people might be best be referred to as crude germ theory adherents). A "retrovirus" is not something that can do this (except perhaps when cells are subjected to un-natural laboratory conditions), but instead is activated by it (if one believes this phenomenon should be termed a "virus"). It may be that "retroviruses" evolved into "real viruses" (that is, agents capable of "infecting" cells), but the point is that in light of what is known, real damage cannot be done by a "retrovirus" to a person who is in good health - there is no known, nor plausible explanation for such a claim. The entire concept is illogical, because "retroviral" phenomenona is found in cells that are under great stresses, and while a person may appear healthy to others for a while, at some point the powerful stressors will cause what most people think of as "disease." Thus, the all-too-common mistake of concluding that effect was cause was made by many of the early "HIV/AIDS" investigators.

Not all of these investigators, however, have (consciously or otherwise) decided to accept the mainstream model of the "disease" and attempted to fit the evidence into the model, even when it is clearly contradictory. For example, one group's findings are consistent with Cunliffe's view:

Ironically, and sadly, the "medications" many "HIV/AIDS patients" are given result in just such damage - damage that the body possesses mechanisms to prevent in this situation.

Source: Journal of Virology, August 2005, p. 10619-10626, Vol. 79, No. 16

"CD8+ T-Cell Dysfunction due to Cytolytic Granule Deficiency in Persistent Friend Retrovirus Infection."

Gennadiy Zelinskyy,1 Shelly J. Robertson,2 Simone Schimmer,1 Ronald J. Messer,2 Kim J. Hasenkrug,2, and Ulf Dittmer1.

Fifteenth page from the old MSN site.

2008-11-11T12:47:00.000-08:00

Fish oil quotes you might want to read.

I thought I'd create a page with quotations from the professional nutritional literature (which "experts" are supposed to have read), along with a few other "gems." If a "health professional" advises you to consume flax, canola, or fish oil, I suggest you print this out and have him or her read it.

In "Modern Nutrition in Health and Disease" (by Shils and Young, 7th edition, page 102), for example, they say the "data certainly do not support the widely published assumption that n-3 fatty acids possess a specific retarding effect on atherogenesis... in rabbits at least, they seem to stimulate atherosclerosis." The animals had liver damage as well as "Periportal fibrosis, lipogranulomas filled with lipofuscin, and bile duct hyperplasia." The authors go on to say: "Other potentially harmful effects of 20:5 n-3 and 22:6 n-3 [that is, EPA and DHA] rich fish oils are neglected by the advocates of increased human consumption of fish oils. The pathologically increased bleeding times, as observed after aspirin ingestion, also occurs in Eskimos on a high fish oil diet."

The authors go on to talk about "a promoting role of [EPA/DHA] in the development of carrdiac necrosis and an increased sensitivity to catecholamine stress." They then talk about extreme tocopherol ("vitamin E") deficiency in animals and say that to repeat the experiments in humans might be dangerous.

Another telling quotation: "...the most severe degree of atherosclerosis was observed in rabbits fed fish oil, with a similar trend in the [flax] oil group., rather than after feeding palm oil with its high concentration of palmitic and stearic acid [saturated fatty acids]."

In the second addition of Maria C. Linder's "Nutritional Biochemistry and Metabolism," second edition, page 462, we learn of the "potential toxic effects of such fatty acids [the omega 3s in fish oil], causing inreased bleeding, 'yellow fat disease,' cardiac necrosis... as well as ulcers, platelet and immune malfunction..." Another interesting point about how toxic and potent fish oil is: "...fish oils may be...better than cyclosporine in suppressing the immune system..." Page 77.

In "Diet and Health," by the National Research Council, page 192, they say: "...it has not been established that inake of omega-3 fish oils per so will reduce the risk of CHD ["heart disease"]. Furthermore, it is not known whether long-term ingestion of these PUFAs will lead to undesirable side effects. The information available does not support a rcommendation to use fish oil supplements to reduce the risk of CHD." They also note that the use of the native Greenlander diet as an example of the supposed benefits of fish oil need to be considered more carefully, since these people "...usually die before middle age." And they point out a basic and disturbing biochemical fact that many medical doctors are not even aware of, that is "...the extreme susceptibility of the omega 3 fatty acids in fish oil to oxidation." Page 601.

The following abstract is all too familiar these days, but you hardly ever hear about anything resembling this in the mainstream media. Notice how they mention that both arachidonic acid and docosahexaenoic acid, which is found in high amounts in fish oil, are responsible for the dysfunction and "diease." Here again, I agree with them completely, but I go on to ask the obvious question, "why are we consuming these substances at all if there is no need for them?" If the only reason is that a flawed experiment was done in 1930 that was refuted directly in 1948 became entrenched in textbooks, then it's time to "get the word out," which is what I am trying to do. I welcome new experiments, and may even pay for all expenses if I am wrong about this (if we can agree on the experimental design so that it does not repeat the mistakes of 1930 and other similar experiments), but nobody who believes in the "essential fatty acid" claim has ever expressed interest in this offer.

Neuroscientist. 2006 Jun;12(3):245-60.

Phospholipase A2-generated lipid mediators in the brain: the good, the bad, and the ugly.

Farooqui AA, Horrocks LA.

Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus.

Phospholipase A2 (PLA2) generates arachidonic acid, docosahexaenoic acid, and lysophospholipids from neural membrane phospholipids. These metabolites have a variety of physiological effects by themselves and also are substrates for the synthesis of more potent lipid mediators such as eicosanoids, platelet activating factor, and 4-hydroxynonenal (4-HNE). At low concentrations, these mediators act as second messengers. They affect and modulate several cell functions, including signal transduction, gene expression, and cell proliferation, but at high concentrations, these lipid mediators cause neurotoxicity. Among the metabolites generated by PLA2, 4-HNE is the most cytotoxic metabolite and is associated with the apoptotic type of neural cell death. Levels of 4-HNE are markedly increased in neurological disorders such as Alzheimer disease, Parkinson disease, ischemia, spinal cord trauma, and head injury. The purpose of this review is to summarize and integrate the vast literature on metabolites generated by PLA2 for a wider audience. The authors hope that this discussion will jump-start more studies not only on the involvement of PLA2 in neurological disorders but also on the importance of PLA2-generated lipid mediators in physiological and pathological processes.

Fish oil also changes one's "immune system" in a way that is similar to what happens in many "AIDS" cases, for example:

"...the anti-inflammatory effects of FO may be explained in part by a shift in the Th1/Th2 balance, due to the direct suppression of Th1 development, and not by enhancement of the propensity of CD4+ T cells to be polarized toward a Th2 phenotype..."

Thus, the "anti-inflammatory" effect is "toxic," that is, it prevents the body from protecting itself, and so it counteracts the effects of arachidonic acid overload syndrome by creating a condition that may be much worse!

Source: J Nutr. 2005 Jul;135(7):1745-51.

In a book that appears to me to be designed for undergraduate college students, "Perspectives in Nutrition," by Gordon M. Wardlaw, et al (fourth edition), there is:

"An upper limit of 10% of energy intake as polyunsaturated fatty acids is often recommended, in part because the breakdown (oxidation) of those present in lipoproteins is linked to increased cholesterol deposition in arteries [note that it is more than a "link," as the molecular evidence is clear about exactly what is occurring]... This breakdown may alkso increase the risk of cancer. Depression of immune function is also suspected to be caused by an excessive intake of polyunsaturated fats." Page 135.

"An excess of omega-3 fatty acid intake can allow uncontrolled bleeding and may cause hemorrhagic stroke... Overall, excessive consumption of omega-3 fatty acids as such can be as problematic as inadequate consumption. Currently, health experts do not recommend that healthy people use fish oil supplements..." Page 120.

What is interesting here is that the National Research Council noted that one would have to consume a great deal of omega 3s to acheive the "desired effects," and thus one will be taking great risks in doing so. Is it necessary to take such a risk? Not until it is clear that "essential fatty acid deficiency" in a non-pregnant adult human is possible on a diet that substitutes something like fresh coconut oil for all other major sources of fat. I've done this experiment on myself for several years now and have seen only benefits, but if we look at the molecular-level evidence, we can see why.

For example, Watkins, et al. found that the AA metabolite, PGE2, is responsible for bone degeneration, and that omega-3 fatty acids, as anyone who understands the biochemistry would know, block the formation of PGE2. But these researchers also found that: "Saturated fat intake led to increased bone density..." and that "...butter fat... reduced ex vivo bibe PGE2... and increased bone formation rates... compared to those given diets higher in n-6 [omega 6] fatty acids," and they talk about how "saturated fatty acids... can benefit bone modeling."

Source: "Bioactive fatty acids: role in bone biology and bone cell function," in Porgress in Lipid Research 40 (2001) 125-148.

Now a key point here is that if they had used lard, which some "experts" call a "saturated fat," it is highly unlikely that they would have gotten the same result. Butter is a safe "saturated fat," whereas the lard sold in the West is not (and I trim off the yellowed sides of the butter stick before using it, because that is oxidized lipid and is dangerous). Turning back to omega 3s, what this shows is that you do not have to ingest something dangerous to counteract something dangerous, because there are much safer alternatives: butter, yogurt, coconut oil, dark choclate, etc. Now that the molecular evidence has made it clear that oxidation is the problem, a highly saturated fat source, like coconut oil, is undeniably very healthy, whereas a fat source with a great deal of unsaturated fatty acids and little or no antioxidant protection (like today's lard) is very dangerous.

In another study:

"...addition of cod liver oil to to the diet elevated the rate of peroxidation by 20-fold."

And that was on top of the 10-fold increase over rats on the fat free diet (when corn oil was added).

Source: from the text of the following (which is just the abstract):

Free Radic Biol Med. 1988;5(2):95-111.

A role for dietary lipids and antioxidants in the activation of carcinogens.

Gower JD.

Division of Comparative Medicine, Clinical Research Centre, Harrow, Middlesex, U.K.

Biologist Ray Peat has cited much older studies, such as how dogs fed fish oil all died of cancer:

"Fifty years ago, it was found that a large amount of cod liver oil in dogs' diet increased their death rate from cancer by 20 times, from the usual 5% to 100%. A diet rich in fish oil causes intense production of toxic lipid peroxides, and has been observed to reduce a man's sperm count to zero. [H. Sinclair, Prog. Lipid Res. 25, 667, 1989.]"

Source: http://www.healthythyroid.com/vegetableoils.htm

Peat notes of the Sinclair experiment:

"An oil researcher spent 100 days eating what he considered to be the Eskimo diet, seal blubber and mackerel paste. He observed that his blood lipid peroxides (measured as malondialdehyde, MDA) reached a level 50 times higher than normal, and although MDA is teratogenic, he said he wasn't worried about fathering deformed children, because his sperm count had gone to zero." Original source: Sinclair, H., Prog. Lipid Res. 25: 667-72, "History of EFA & their prostanoids: some personal reminiscences."

Finally, I recommend reading "The Cholesterol Conspiracy" by Russell L. Smith (1991). He cites a great deal of the pre-1990 literature and also gives a good account of the politics involved in medical and nutritional advice. About fish oil, he notes:

"...the Eskimo study was yet another example of poor scientific analysis and reporting. First, the authors of the study offered no convincing evidence that the Eskimos had low CHD ["heart disease"] rates. The few hundred Eskimos located over a very large area had little in the way of physician care and autopsy data confirming cause of death were rare. Primitive Eskimos rarely live beyond age 50, long before CHD symptoms emerge in the vast majority of people. The Eskimo study authors neither mentioned this fact, nor provided the reader with such basic data as average age of Eskimos in their study. Such an omission was incredible for a 'scientific' article because of the interpretation of CHD rates depends heavily on age. The average cholesterol level of the Eskimos was higher than the average value of Americans." Page 79.

And: "...diets high in polyunsaturates seriously suppress the body's natural immune system... a possible third contributor to cancer is the process of 'auto-oxidation' of polyunsaturated fatty acids..." Page 96.

And: "And since omega-3 fatty acids are more unsaturated than the common polyunsaturated vegetable fats (omega-6), they are even more prone to oxidation than the vegetable fats..." Page 103.

Omega 3s are said to be necessary for eye health, but the opposite may be the case:

QUOTE: "Over the past decade, Salomon's research has expanded to other diseases such as macular degenerative diseases that result in blindness and involve "brain lipids" that contain an omega-3 fatty acid that is abundant in fish oil. Brain lipids are very rare in the body, but are found in nerve cells and in the photoreceptor rod cells of the eye. Salomon and Clinic researchers suspected that the energy from light on the receptors might promote oxidation and damage. Through mass spectroscopy studies, they have begun to see protein modifications that are similar to those in heart disease." UNQUOTE.

Source: http://www.cwru.edu/pubaff/univcomm/2002/june/cholesterol.htm

So at this point, you might be asking, "then why are all these studies we hear about in the media saying that fish oil is so good?" Many of the studies are obviously flawed, and others simply reveal the socio-economic reality in nations like the USA, that is, oily fish that people like to eat costs more, and so the more affluent, who have better health care, live easier lives, eat higher quality food, are more aware of what is considered healthy, etc., are more likely to eat such items, and also to cook them in less dangerous ways. Mostly, the results (almost all short term) reflect how two unhealthy items in small amounts are usally less dangerous than one unhealthy item in large amounts. However, it is also true that in some ways fish oil is not quite as dangerous as arachidonic acid, for example:

"These data suggest that the cardioprotective properties of n-3 fatty acids may derive in part from their less reactive oxidized lipid metabolites."

Source: J Nutr Biochem. 2005 Apr;16(4):213-21.

And this one is important: J Lipid Res. 2006 Oct 30.

Immunosuppressive effects of polyunsaturated fatty acids on antigen presentation by HLA class I molecules.

Shaikh SR, Edidin M.

Dietary supplementation with polyunsaturated fatty acids (PUFAs) has immunosuppressive effects... [lowering] target cell susceptibility to lysis by effector T cells. Treatment of B lymphoblast targets with the -6 PUFA arachidonic acid (AA) or -3 docosahexaenoic acid (DHA) lowered their susceptibility to lysis by alloreactive CD8+ T cells by ~20-25%... PUFAs significantly lowered APC-T cell conjugate formation, by ~30-40%...

Fourteenth page from the old MSN site.

2008-11-11T12:45:00.000-08:00

The best practical diet and the explanation for it.

When a "disorder" that befuddled my doctors appeared to be well on its way to killing me, several years ago, I decided to take it upon myself to research the issues and use my academic skills in a "last ditch" effort to save my life. Let me make it clear that I did not engage in any "high risk" behavior and have never even smoked a cigarette. I did not drink alcohol, though I took a tablespoon or organic red wine at the end of a meal once in a while. I was eating plenty of whole grains, beans, nuts, seeds, legumes, and I was supplmenting with omega 3s. I ate very little salt and no cholesterol. Yet somehow, my body was deteriorating rapidly, and I was only 36 years old.

I decided that I would put all preconceptions aside, and just examine the evidence behind any claim. At the same time, I read books on biochemistry, physiology, nutrition, etc., in an attempt to develop an deep understanding of the processes involved. If I thought that I had "come up short" in this endeavor, I would not be writing these essays (and I probably would not be alive to do it anyway). The rationale for my present diet is simple: avoid foods that act as direct stressors (such as any food that contains more than a small amount of unsaturated fatty acids); avoid foods that inhibit normal physiology (such as legumes); avoid foods that contain natural toxins (such as potatoes with green colors); avoid foods that contain cholesterol that is likely to be oxidized (meat, eggs, or dairy cooked while exposed to air, powdered eggs or dairy as one might find in baked goods, and homogenized dairy); eat at least some antioxidant-rich foods with each meal (such as berries or dark chocolate); be sure to eat enough high quality protein each day to meet your needs (probably at least 50 grams for a "moderately active" adult).

Below is my current diet, though I do also use some supplements, and I will add a section on them at a future date. Note that one often hears about the "dangers of sugar" and other such nonsense all the time in the mainstream media. Moreover, all one seems to hear is how "beneficial" fish oil is, when in fact the National Research Council and the major works of the professional nutriitonal literature warn about its dangers. I have quoted passages from this literature in other essays, but I'll just mention here that when one says something like "sugar" or "saturated fat," take it with a grain of salt, because such terms and phrases have no scientific meaning. The molecules in a bag of refined white sugar are different than the molecules in a something like Rapadura unrefined sugar, and other "sugars," such as malitol have specific physiological effects. Most people have been convince that "sugar is bad," but in fact it is the safest form of energy for mitochondria, with the possible exception of short/medium chain saturated fatty acids (though these are not found in more than trace amounts in most Western diets).

What follows is a diet of mine that I no longer follow; after that is my current diet. I don't think the "old" diet is a "bad" one, but I like my current one better. Both are practical and not very expensive, so almost every Westerner should be able to obtain these foods. I would not claim that it is "best," but that it does no harm and supplies the body with what it needs. Note that you may need more protein in your diet, depending upon your lifestyle, and also that I am assuming that a person is in excellent health (and also that I am going to add a supplement section that I also feel is necessary, at least for me).

3 slices of homemade bread (coconut oil is the only major source of fat used, and it is only used to "greasse" the pan), made with all-purpose, organic, unbleached flour, organic sugar (Rapadura brand), bananas, spices, and a touch of salt

All of the dairy products listed below are not from grass-fed cows, and have little if any omega 3 content:

3-4 ounces of whole milk cheese (mozzarella, cheddar, swiss, or monterey jack)

4-5 ounces of whole milk yogurt

1 ounce or less of butter

½ ounce of bittersweet chocolate

1/8 ounce of dark chcocoate (70% cocoa mass)

3 ounces of whole milk ricotta cheese

1 boiled egg (organic, but not enhance with omega 3s)

1 large banana or 2 small ones

1 or 2 prunes

a few dozen raisins, rehydrated slightly

1 ounce of strawberry preserve

3 ounces of shredded coconut (which I then grind into a powder with a burr grinder)

1 apple, 1 pear, or several pineapple chunks

less than one level teaspoon of nutritional yeast

an occasional carrot

a small amount of sauerkraut (washed off first) is okay, and goes well with boiled eggs

boiled potatoes are good, but they should be organic, and the organic ones around here are often very green - do not eat green potatoes

if you can get organic berries (blueberries are the most available and least expensive, from what I've seen), go ahead and eat at least several with each meal.

My current diet:

Aside from fresh fruit, especially bananas (though I'm not sure if bananas are technicaly a "fruit"), I eat a lot of cheese along with ricotta, which can be the same as cheese, or be made with whey, which will change the amino acid profile a litte. I make a "milk shake" type of item by adding strong coffee (after it has cooled) to ricotta, and mixing it with sugar, a touch of salt, and small amounts of cocoa powder, cinnamon, and ginger. I also eat other dairy, such as butter, sour cream, and yogurt, but never with additives such as carrageenan. I eat dark choclate and bittersweet chocolate chips. I let raisins soak in water for several hours, then drain the water - you can also use this water if you want to make a bread. I also eat figs, prunes, and other dried fruits, which I soak in water too, but not as frequently. I eat boiled potatoes with butter. I often eat pickled/fermented cabbage with cheese. I eat pasta, with an herbal tomato based sauce on top (ricotta is mixed into it). I also eat oatmeal sometimes, made with cinnamon and ginger, along with sugar and some salt. I make a pudding with pineapple juice, crushed pineapple, a mashed banana, sugar, coconut oil, a touch of salt, ginger, and flour to thicken it up. You can make this with other fruit as well. Once in a while, I will eat a boiled egg. Lastly, I eat shredded coconut, though I put it through a burr coffee grinder first, because I like the texture better this way. I still take tiny amounts of nutritional yeast, and even tinier amounts of gelatin, each day.

A word about "cooking:"

High temperature heating of food while exposed to air is something I avoid entirely, in order to prevent dangerous chemical reactions from occurring. It may sound impossible to eat such a diet after you've been raised on fried food, but I found that the key is to let your sense of taste predominate over your sense of smell. This takes a few days, but once you "have it," you can appreciate subtle nuances in your recipes. I make sauces with tomato paste and pureed corn. I add herbs and/or spices, along with a pinch of salt and sugar, then add ricotta cheese and mix well. This all occurs at low/medium heat on the stove top. After it is warm throughout, I add organic pasta, and let it heat to the level I like. It is not very hot, and while I eat I keep a top on it so that it doesn't cool quickly, which will happen. I eat slowly, and like to "rotate" among several different dishes or combinations of items (such as a couple of raisins, a small amount fo dark chocolate, and some shredded coconut).

Those who feel the need to eat meat should read the thread in the nutrition forum on cooking meat. Basically, the best thing to do with meat, assuming it is fresh, seems to be to freeze it for at least two weeks, let it thaw, cut it into small pieces and then put it into a sauce, such as the ones I have described above, but not to use high heat. I don't know what this will result in, since I don't eat "meat," but you may need to squeeze the blood out of some cuts. If anyone tries this technique, please go to the cooking meat thread and post a message about your experiences there.

Supplements:

I take about 25-50% of the USRDA of potassium in the citrate form along with about .15 gram of calcium citrate before my first meal of the day, along with a tiny amount of a vitamin B complex powder (which I allow to dissolve under the tongue). Keep in mind that the more stress you place on your body, the more vitamin and mineral supplementation you will likely need.

In the middle of the meal I take about 25% of the RDA in vitamin D (I don't get a great deal of sunlight), then at the end of the meal I take about 25-30% of the RDA in zinc and magnesium citrate, and a very small amount of MSM. In the next two meals, I do the same thing except that I don't take the potassium or zinc, and instead take about 15% of the RDA of copper (gluconate form) in the middle of the meals.

Every week or so I take a gelatin supplement, and advise those with conditions where healing is not happening to do the same. For example, I had tendonosis in my right shoulder for over two years, but after using the gelatin and also eating more high quality protein, it felt normal again within a couple of months. I also take tiny amounts of selenium as selenomethionine a few times a week (avoid the selenite form of selenium).

Another thing you need to do is to determine whether you are producing enough stomach acid, because many conditions and also a poor diet can cause this deficiency. If you have "heart burn" once in a while you probably produce enough. If not, you can get a betaine HCl and pepsin supplement and cut the pill into thirds (I use Country Life brand, for example). You take a third and see what happens, then you take two thirds and see what happens. When you feel warmth, you know you took too much, so you drink a few ounces of water to neutralize it.

Even with enough stomach acid, you may have an inflammatory condition in your GI tract which is causing the cells that absorb nutrients to be dysfunctional (meaning that you are probably overloaded with AA, or eat a great deal of raw and/or rancid food). In such a situation you are in a lot of trouble, and this can happen in "celiac disease," where (as usual) an inflammatory response that is too potent causes damage and dysfucntion. If I were in such a situation now, I'd avoid food that could enhance the problem and eat more antioxidant-rich food, especially berries, but since I have taken the AA out of my cells, as I've seen, I just get a quick inflammatory burst and then the quick resolution, so I doubt that I would encounter a "chronic inflammatory" condition. Note that the evidence suggests that on a diet with only a trace amount of unsaturated fatty acids, it is unlikely that the body would invoke the inflammatory response against gliadin, and hence there would likely be hardly any "celiac disease," nor other kinds of problems like this.

A word about "salt:" I use mostly Celtic Sea salt, which you can get over the internet, just as I prefer Rapadura brand sugar over what is called unrefined organic cane sugar (but I use both, because they have different tastes). Sodium is not the problem in terms of developing high blood pressure, but eating a high salt diet will mean a lot of chloride, and if your diet is low in potassium, that combination seems to cause most cases of "hypertension" (which is why fruits and vegetables appear to counteract it in major studies done on this subject). Basically, if you make your own food, like I do, and eat foods that have good potassium content, then you can eat the salt "to taste." You may need time to adjust your sense of taste, but that only takes a few days to a week, in my experience. I've found that I don't like foods with strong odors, as most Americans do, but prefer little smell sensation (relatively speaking). Once you find that you have also adapted in this way, it is highly unlikely that you will eat too much of the salt (assuming you make your own food), but you can measure it out so that it is in the range of acceptable, then put it in a container and only eat that amount per day. If you eat salty cheese or something like that, you can take a little salt out of the container to compensate. Remember that if you already have hypertension, this advice is not for you, though you may want to eat more fruit and vegetables and make your own food (and in the process, change the way your experience food so that you don't eat as much salt).

Not enough salt may have been the root cause of the problem that almost killed me in 200-2001, for example:

American Society of Animal Science American Dairy Science Association

News from the Midwest Sectional Meetings, March 16-18, 1998, Des Moines, Iowa

Contact: Ted Wiseman, Ohio State University(614) 292-9052 Don Mahan, (614) 292-6987 By Kyle Sharp

Salt Doesn't Just Add Flavor to the Diets of Early-Weaned Pigs

COLUMBUS, Ohio – Hog producers who wean early and want healthier, faster-growing and more consistently sized pigs should be saying "pass the salt." Sodium chloride, commonly known as table salt, helps break down protein and prevent the growth of harmful bacteria in the stomachs of newly weaned pigs, said Ted Wiseman, Ohio State University animal science graduate research associate. The chloride component is particularly important. Early-weaned pigs with almost three times more sodium and chloride in their diets than the minimum recommendations of the National Research Council are more uniform with better growth rates, Wiseman said. Wiseman presented research regarding sodium chloride and early-weaned pigs at the American Society of Animal Science/American Dairy Science Association Midwestern Meeting, March 17 in Des Moines, Iowa. Several years ago, Ohio State researchers found that pigs weaned early have a greater need for chloride. While a young pig nurses the sow, lactose in the milk is broken down in the pig's stomach by bacteria called Lactobacilli, and as a result lactic acid is formed. This acidity in the stomach is what digests food proteins and prevents the growth of harmful bacteria that can cause diarrhea and other health problems. When pigs are weaned from milk, lactic acid production decreases and is replaced by the natural production of hydrochloric acid within the stomach. However, when a pig is weaned early, hydrochloric acid production has not yet begun, and the resulting low stomach acid levels can cause poor food digestion and bacterial concerns. Chloride helps digest food proteins and keep stomach acid levels high. "The chloride in sodium chloride helps sooth the transition period of early-weaned pigs from when lactic acid production decreases to when hydrochloric acid production begins," Wiseman said.

Source: http://www.asas.org/midwestern/press/ohsalt.html

Thirteenth page from the old MSN site.

2008-11-11T12:44:00.000-08:00

How easy the key experiments would be to do.

Biologist Ray Peat has written about experiments done on animals decades ago, and basically what one learns is that animals on a high omega 6 and/or 3 diet die of cancer at alarming rates while those on a fat free diet hardly ever develop cancers and live longer in general.

Such experiments are straightforward and can be repeated when new variables are considered or discovered. There is no need for "models," "markers," "surrogate endpoints," "correlations," "associations," or "further investigations." That is, if a species of animal such as a dog lives a long and healthy life on a diet that a humans have eaten and found to be tasty and satisifying, then one is in a position to give advice to those interested, especially in light of such experiments as the following:

Blood Coagul Fibrinolysis. 2006 Jun;17(4):259-64.

Inhibitory effects of cardiotonic pills on platelet function in dogs fed a high-fat diet.

Zhang L, Zheng J, Li HM, Meng YX.

Department of Cardiology, Tianjin 254th Hospital (Affiliated Hospital of the Medical College of Nankai University), China bInstitute of Research and Development, Tasly Pharmaceutical Company, Tianjin, China.

Insulin resistance and the consequent metabolic disorders are associated with a state of platelet hyperactivity. Oxidative stress is responsible for the persistent platelet activation. We sought to study the inhibitory effect of cardiotonic pills, an oral herbal component, on platelet function in a dog model with insulin resistance induced by high-fat feeding. We fed 18 dogs with a high-fat diet and six dogs with normal chow as control for 6 months. Then, six dogs were fed with a high-fat diet and received additional aspirin (250 mg/day), and another six dogs received additional cardiotonic pills (1000 mg/day) for 4 months. Time-course changes in metabolic parameters and platelet function were detected. After high-fat feeding for 6 months, In addition, a platelet hyperactivity state, characterized by increased agonist 18 dogs developed a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance.(arachidonic acid, ADP and collagen) induced platelet aggregation, platelet expression of adhesion molecules (P-selectin and GP IIb/IIIa), and platelet intracellular calcium concentration, was indicated. Cardiotonic pills showed a significant antioxidative activity by presenting an increase in plasma superoxide dismutase and decrease in erythrocyte glutathione, as well as a lipid-lowering effect (decrease in both plasma cholesterol and triglyceride). Either aspirin or cardiotonic pills could significantly reverse the platelet hypersensitivity and hyperfunction. Compared with aspirin, cardiotonic pills showed a more exaggerated inhibitory effect on platelet function (a significantly decreased collagen-stimulated platelet aggregation, and expression of adhesion molecules). In conclusion, cardiotonic pills inhibited platelet hyperfunction in dogs with insulin resistance. This inhibitory effect may mainly be explained by antioxidative activity and metabolic control.

Note that we do not know what kind of fat was used in the "high fat diet." The researchers are assuming, apparently, that any fat source, when fed in such amounts as they do here, will result in: "...a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance."

My modest proposal is to repeat this experiment, except to substitute fresh coconut oil for whatever fat source they used here, and see if such "disorders" result. In light of the rarity of these disorders among peoples who eat large amounts of coconut products, it seems highly unlikely, but the important point is that it would be conclusive, because the basic chemistry is known. That is, unsaturated fatty acids can cause damage in the oxidative stress context whereas saturated ones cannot, so if the dogs are fine on the high fat/coconut oil diet, then we know that unsaturated fatty acids are the "culprit," and people should be told to avoid such "food" products.

Experiments in alcohol related liver injury, interestingly, have demonstrated this point, though you don't hear about this in the media, for example:

Clin Biochem. 1989 Feb;22(1):41-9.

Biochemical basis for alcohol-induced liver injury.

French SW.

Department of Pathology, Faculty of Health Sciences, University of Ottawa, Ontario, Canada.

Chronic ethanol ingestion leads to hepatocellular injury and alcoholic liver disease (ALD) only if multiple factors combine to favor centrilobular hepatocellular hypoxia. It is hypothesized that these factors include a shift in the redox state, the induction of the microsomal ethanol oxidizing system (MEOS), a high blood alcohol level (BAL), a high polyunsaturated fat diet and episodic decreased O2 supply to the liver. The shift in the redox state favors a low cellular pH, decreased fatty acid oxidation and increased triglyceride formation. The increased MEOS activity increases O2 consumption and portal-central O2 gradient as well as favors acetaldehyde toxic effects including retention of hepatic lipids and export proteins causing cell swelling. The resultant increase in the concentration of acetaldehyde and lactate may stimulate fibrosis as they stimulate collagen synthesis in vitro. The resultant fatty liver narrows the sinusoids slowing sinusoid blood flow. The combination of events reduces available O2 leading to decreased levels of ATP and cellular pH making the liver vulnerable to episodes of systemic hypoxia. The role of membrane changes are reviewed, i.e., 1) membrane fluidity as related to changes in the species of phospholipids, 2) mitochondrial function as related to the changes in the lipid environment of the electron transport chain, and 3) linoleic acid-prostaglandin metabolism. Acute ethanol in vitro has been shown to affect liver cell metabolism regulation by triggering and increasing protein phosphorylation through the Ca2+-phospholipase C pathway. A high fat diet enhances the liver injury caused by chronic ethanol ingestion.

J Nutr. 2004 Apr;134(4):904-12.

And:

Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition.

Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.

Arkansas Children's Nutrition Center, Department of Pharmacology/Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. RonisMartin@uams.edu

Rats fed a saturated fat diet are protected from experimentally induced alcoholic liver disease, but the molecular mechanisms underlying this phenomenon remain in dispute. We fed male Sprague-Dawley rats intragastrically by total enteral nutrition using diets with or without ethanol. In 1 control and 1 ethanol group, the dietary fat was corn oil at a level of 45% of total energy. In other groups, saturated fat [18:82 ratio of beef tallow:medium-chain triglyceride (MCT) oil] was substituted for corn oil at levels of 10, 20, and 30% of total energy, while keeping the total energy from fat at 45%. After 70 d, liver pathology, serum alanine aminotransferase (ALT), biochemical markers of oxidative stress, liver fatty acid composition, cytochrome P450 2E1 (CYP2E1) expression and activity and cytochrome P450 4A (CYP4A) expression were assessed. In rats fed the corn oil plus ethanol diet, hepatotoxicity was accompanied by oxidative stress. As dietary saturated fat content increased, all measures of hepatic pathology and oxidative stress were progressively reduced, including steatosis (P <>

UPDATE: In recent study (Prostaglandins Other Lipid Mediat. 2006 Jul;80(1-2):1-14. Epub 2006 Jun 23.), the researchers state: "In this regard, we have shown that COX nitration occurs in human atherosclerotic tissue and in aortic lesions from ApoE(-/-) mice kept on a high fat diet." Again, we are not told what the fat source is, and it's likely that if the mice were raised on something like coconut oil as their primary fat source, this result would not occur. If only such experiments were properly controlled, in accordance with the scientific method - this is so obvious that it is quite frightening that the "brightest minds" (the ones most people trust their lives to) seem totally unaware of relevant factors that need to be taken into account.

And then there is more of the same: "Polyunsaturated free fatty acids (PUFAs) participate in normal functioning of the cell, particularly in control intracellular cell signalling. As nutritional components they compose a human diet with an indirect promoting influence on tumourogenesis... free AA levels are elevated in colon cancer, as AA is the precursor to biologically active eicosanoids." Those like myself who do the research with an open mind find these kinds of statements boring at this point, because there are so many of them in the literature, and yet mainstream media "journalists" appear to be completely ignorant of these matter-of-fact remarks about PUFAs.

Source: Mol Cell Biochem. 2006 Jul 21; [Epub ahead of print]

Title: "Altered membrane free unsaturated fatty acid composition in human colorectal cancer tissue."

Authors: Szachowicz-Petelska B, Sulkowski S, Figaszewski ZA.

Twelfth page from the old MSN site.

2008-11-11T12:43:00.000-08:00

The AA connection to today's common "diseases."

If you've read the other essays, you are familiar with the evidence for the cause of "disease" as we perceive it today being rooted in the inflammatory response (and TNF-alpha in particular), and not just the response of several hundred years ago, but one that is greatly enhanced by the "modern" diet (rich in omega 6 PUFAs). Here is evidence for the role of an AA metabolite in producing a common symptom of "disease:"

Am J Physiol Regul Integr Comp Physiol. 2006 May;290(5):R1262-70. Epub 2006 Jan 12.

Kupffer cell-generated PGE2 triggers the febrile response of guinea pigs to intravenously injected LPS.

Li Z, Perlik V, Feleder C, Tang Y, Blatteis CM.

Dept. of Physiology, Univ. of Tennessee Health Science Center, 894 Union Ave., Memphis, TN 38163. blatteis@physio1.utmem.edu). Because the onset of fever induced by intravenously (iv) injected bacterial endotoxic lipopolysaccharides (LPS) precedes the appearance in the bloodstream of pyrogenic cytokines, the presumptive peripheral triggers of the febrile response, we have postulated previously that, in their stead, PGE(2) could be the peripheral fever trigger because it appears in blood coincidentally with the initial body core temperature (T(c)) rise. To test this hypothesis, we injected Salmonella enteritidis LPS (2 mug/kg body wt iv) into conscious guinea pigs and measured their plasma levels of LPS, PGE(2), TNF-alpha, IL-1beta, and IL-6 before and 15, 30, 60, 90, and 120 min after LPS administration; T(c) was monitored continuously. The animals were untreated or Kupffer cell (KC) depleted; the essential involvement of KCs in LPS fever was shown previously. LPS very promptly (<10>

Arachidonic acid by itself is highly unstable and toxic, for example:

"We conclude that lethal injuries sustained by cells during short exposures to AA were caused by the fatty acid itself and were not mediated by the AA-induced influx of Ca2+/cations. Moreover, direct physical effects of AA on the plasma membrane (changes in membrane fluidity or detergent-like action) were also excluded."

Source: Biochem Pharmacol. 2004 Mar 1;67(5):903-9.

AA metabolites are even more potent, which suggests that what appear to be "diseases" are really just the epiphenomena of AA overload, which becomes manifest when a stressor is applied to cells. However, the amount and length of exposure to the stressor plays a major role in the kind of damage the "inflammation" will do (especially when one's cells contain omega 3 and 6 PUFAs), for example:

Infect Immun. 2003 May;71(5):2674-83.

Title: "The levels and patterns of cytokines produced by CD4 T lymphocytes of BALB/c mice infected with Leishmania major by inoculation into the ear dermis depend on the infectiousness and size of the inoculum."

"Diseases" are not necessarily caused by "germs," even when they are present and appear to be the "obvious" cause, for example:

"The bacteria [H. pylori] are found everywhere in the world, but are especially prevalent in developing countries, where up to 80% of children and 90% of adults can have laboratory evidence of an H. pylori infection--usually without having any symptoms."

What does cause "disease?"

"The vast majority of H. pylori in colonized hosts are free-living, but approximately 20% bind to gastric epithelial cells. This binding induces an immune response..." which can lead to "...peptic ulcer disease, gastric adenocarcinoma, and non-Hodgkins lymphoma of the stomach."

In the other essays, I showed how having the wrong fatty acids in your cells increases your chances of a chronic inflammatory condition significantly, and this is the case with H. pylori in the context of a typical "modern" diet:

"The means through which H. pylori causes gastric cancer are more complex but likely involve alterations in gastric epithelial cell responses that are perturbed within the context of a chronic gastric inflammatory infiltrate, which can persist for decades."

So far, so good, but then, as is so often the case, the interpreation of the findings is illogical:

"'Our results indicate that H. pylori can co-opt a host protein as a receptor and that it can increase expression of this receptor in gastric epithelial cells,' says Peek. 'Further, absence of this receptor abolishes the inflammatory response that H. pylori induces in infected mice, suggesting that this receptor mediates H. pylori-induced injury in the stomach.'"

Another group of researchers found that "disease" occurred only when cellular stress was present, though this has been known for some time (for instance, it was found that a common bacterium in the GI tract only became dangerous - possibly life-threatening - when subjected to stressors produced during surgery):

"The researchers discovered a new function for these glycolipids--they are cleaved in response to cell stress caused by changes in osmotic pressure and relative acidity or alkalinity... 'We found that putting these cells under stress similar to that initially encountered by the trypanosome inside the fly caused the parasites to cleave free GPIs...'"

Source: http://www.sciencedaily.com/releases/2006/05/060509174333.htm

Source for the above quotations about H. pylori "infection:"

http://www.sciencedaily.com/releases/2006/05/060506103846.htm

It is this "clinging" action when subjected to stressors that appears to make many "pathogens" dangerous to the "host." After "clinging," the body invokes the "inflammatory" process (the exact nature of which is determined by the fatty acids present), which then could do the actual damage that results in symptoms of a "diseases." Here's another example of this in "infections" common in the West:

"UTIs [urinary tract infections] begin when bacteria gain a foothold on cells lining the kidney or bladder and grow into colonies. They latch onto cells using tiny fibers known as pili. Similar fibers also are produced by bacteria responsible for a variety of gastric, respiratory and other infections."

Source:

http://www.sciencedaily.com/releases/2002/11/021115070154.htm

The key point in all of this is that arachidonic acid is very unstable and toxic, and is released from cells upon the most minor of stressors. Then it can stress the "germs," which cause "disease" by the "clinging" action, provoking the "inflammatory" process, which is too potent and sustained in people with arachidonic acid in their cells (and it appears to also be the case for people with long chain omega 3s as well), and then the damage that is called one "disease" or another eventually appears. Note that it would be very easy to confirm this idea by feeding one group of animals fresh coconut oil as their only fat source (at 30% of total caloric intake) while another group would be fed something like corn oil, canola oil, fish oil, or some combination of oils rich in omega 6s and/or omega 3s. The animals would then be exposed to knwon "pathogens" that cause "disease" in that species. The animals fed the high PUFA diet should not be given antioxidants, so that the fatty acids would cause the stress that would then allow the "pathgen" to become dangerous in the manner described above.

Another point I'll make here, though perhaps in the future I'll write up a new essay on it, has to do with "co-factors." If you read through studies concerning "chronic disease" you find iron, for example, to be "implicated" in many conditions. The evidence suggests that while iron may indeed by a co-factor that enhances various "disease," it can be neutralized by diet. For instance, it has been found that though Asians have high iron level (in general) they do not have the "disease" Western "experts" thought they should: "'The finding that Asians and Pacific Islanders have high levels of iron in the blood is surprising because they also have the lowest prevalence of the particular gene mutation that is found in Caucasians with the typical form of hemochromatosis,' he said. 'This may mean that the Asians and Pacific Islanders have a different genetic mutation that has not yet been discovered, or that they do not, for some reason, develop hemochromatosis/iron overload despite their high blood levels of iron.'"

Source: http://www.sciencedaily.com/releases/2005/04/050430222454.htm

Here again, the "experts" don't realize that having your cells packed with more stable fatty acids neutralizes this potential problem, and instead they go on to speculate about the role undiscovered genes may be playing, rather than examining the literature as a whole to see if there is an explanation already "in the books."

An excellent abstract that explains the role iron does play (in those overloaded with omega 6 PUFAs at least) is the following:

Med Hypotheses. 2003 Jan;60(1):69-83. Are lipid peroxidation processes induced by changes in the cell wall structure and how are these processes connected with diseases? Spiteller G. Lehrstuhl Organische Chemie, Universitatsstrasse 30, Bayreuth, Germany. gerhard.spiteller@uni-bayreuth.de

Apparently nature uses the unique sensitivity of polyunsaturated fatty acids (PUFAs) versus oxygen to generate chemical signals if the surface of a cell is influenced by an outside or inside event... It seems that mammalian and plant cells respond equally to such changes in their structures by transformation of polyunsaturated fatty acids localized in the phospholipid layer of the cell wall to lipidhydroperoxides (LOOHs). These lipid peroxidation (LPO) processes involve all PUFAs, not only arachidonic acid.Slight physiological changes of the cell wall for instance by proliferation seem to activate enzymes, e.g., phospholipases and lipoxygenases (LOX). When an outside impact (for instance by attack of microorganisms) exceeds a certain level LOX commit suicide and liberate iron ions. These start a nonenzymatic LPO. Enzymatic and nonenzymatic LPO distinguish fundamentally which has not been recognized in the past. In the enzymatic LPO processes peroxyl radicals generated as intermediates cannot leave the enzyme complex. In contrast in a nonenzymatic LPO process peroxyl radicals are not trapped. They attack nearly any kind of biological molecules, for instance proteins. Thus only the amount of an outside impact decides if proliferation, apoptosis, or necrosis is started... After consumption of food rich in linoleic acid its LPO products become increased in low density lipoprotein (LDL). This LDL is able to enter endothelial cells and damage cells from inside, long before an inflammatory response is detectable.

And this brings me to the topic of "HIV/AIDS." Various attempts at discovering the "pathogenesis" of the "virus" have been attempted, and all have failed, leading the "experts" to argue that there is enough circumstantial-type evidence to establish "causation" and thus the pathogenesis issue can be put on the proverbial back burner with no threat to public health. Therefore, at this point, there is little effort being put into trying to figure out exactly how "HIV" (assuming it exists, of course) can cause death by numerous means (including some cases of cervical cancer) several years after "infection."

But after reading through the essays on this forum, and of course what is written above, I hope that you now realize that in order for a virus to kill someone many years after infection and after several years of apparent good health, something has to be going on in the body that is doing damage. "HIV" could be doing something similar to what the researchers discovered about H. pylori, but if that were the case, this would have been uncovered long ago. Instead, the "experts" posit "models" of "pathogenesis" and are more or less content to do other things. What this demonstrates clearly is that they don't understand that if an "infectious disease" has the characteristics of "HIV/AIDS" it must have an "inflammatory" component, meaning that molecules like TNF-alpha, PGE2, and LTB4 are doing the damage, though it's also possible that the biochemical signals or free radicals generated by the "inflammatory" activity cause the changes seen not just in "HIV/AIDS," but also in "aging" and other "diseases."

The most common model of "HIV/AIDS" that one hears about in the mainstream media is that, over time, "HIV" destroys enough CD4 cells to cause "immune system collapse." However, the body can adapt to a small loss of cells, and if there was a large loss of cells, symptoms and death would occur much sooner, as was common in the early days of the "AIDS epidemic." Thus, what started out as a reasonable assumption that was consistent with the evidence (though, again, from what is known now the first thing that should be investigated in such a phenomenon is "inflammation") became reified into a cult-like belief system that is about as inconsistent with the evidence and what is known as an explanation could possibly be.

A similar thing has happened in the "nutritional science" field. For example, in the "early days" it was reasonable to classify fatty acids into broad categories: saturated, monounsaturated, and polyunsaturated. Yet now it is known that each kind of fatty acid has distinct biochemical and physiological effects. As science journalist Gary Taubes has noted, some saturated fatty acids tend to raise serum cholesterol levels while others tend to lower them. Despite calls from some experts in this field to reconsider this abstract system, which, over time, appears less and less consistent with the scientific reality, change comes at a pace that would make a snail appear to be an Olympic sprinter.

My proposal to deal with this situation is to approach the problem in two ways: at the molecular-level, where "hard science" prevails, and at the practical level, where researchers can focus on results, rather than on attempting to fit square evidence pegs into their round abstract, unverified model holes. For example, in "HIV/AIDS," why not follow around as many "AIDS patients" who will allow such an intrusion and record everything they do (and also try to get them to be honest about their pasts), while also measuring various markers, especially ones related to "inflammation" and free radical damage? After several years of gathering such information, researchers could then try to "connect the dots." Instead, the dots got connected before the black points were printed on the page, due to the preconceptions held or asserted by the authorities in charge. In nutrition, why not determine exactly what people are eating, here and in countries with very different diets and rates of "disease," as well as other lifestyle elements that may be relevant, and then compare this information database with what is known at the molecular-level.

Eleventh page from the old MSN site.

2008-11-11T12:42:00.000-08:00

What the "common cold" can teach us about illness.

If you've read some of the other pages I wrote here, you'll remember how I talked about stress generating molecules that possess potent qualities, especially the "pro-infalmmatory" TNF-alpha and the "anti-inflammatoyr" IL-10. You will also remember that the kinds of fatty acids in your cells have a significant effect on the response. The omega 6, arachidonic acid, promotes chronic inflammation and anti-inflammation; the long-chain omega 3s promote strong inflammation, but not much in the way of anti-inflammation, though because the symptoms of anti-inflammation have been associated with inflammation, the omega 3s are said to be anti-inflammatory (they also counteract AA metabolites); the omega 9, Mead acid, generates a powerful, but quick inflammatory response, and then a powerful and quick anti-inflammation.

As I've said in another essay, the last time there was an "infectious disease" that several family members fell ill to, I barely experienced symptoms, relative to what I've experienced with AA in my cells; first, my throat felt minor pain upon swallowing, and then minor sinus congestion, an occasional sneeze and cough, and mild fatigue, and it lasted about a week. In the past, the throat was more painful, and that lasted twice as long. The cough, sneezing, and congestion were also more pronounced and lasted longer. Overall, it usually took at least two weeks to "clear." My relatives who "caught" the same thing experienced major fatigue and very severe symptoms overall, and their bouts lasted longer. One had to try two different antibiotics. I took nothing, and did nothing unsusual.

According to what is known, the sore throat should be related to TNF-alpha, whereas the coughing/sneezing and congestion would be due to IL-10. Since fatigue does not occur at first, there is no way to know whether it is due mainly to the effect of TNF-alpha or the IL-10. Moreover, it is possible that both may be responsible.

Now certain claims have been made about perceived phenomena, such as "chronic fatigue syndrome" and "AIDS" with regard to TNF-alpha, IL-10, and similar molecules. Some claim that there is too much IL-10 in "CFS" and a shift from TNF-alpha to IL-10 in "AIDS," but unless the levels of these molecules are determined at different points during the "illness," and even during the course of a day, there is no way to know at this point.

But there is a different way of thinking about this. We hear about "good" and "bad" cholesterol in the media, with prominent "experts" making such remarks, and it's the same thing with molecules like TNF-alpha and IL-10. Both are necessary, and what matters is the context - there is no villian and hero. With AA in your cells, both are "hyped up" and can cause damage, whereas with the omega 3s, molecules like TNF-alpha are enhanced but IL-10 appears to be inhibited. With Mead acid, there is a short response for both, which means that it is not likely that your body will be damaged or become dysregulated by the exposure to the "pathogen," "irritant," "allergen," or "toxin." As I've said in other essays, it is about minimizing the damage the "immune system" can do to specific cells or tissues in its effort to protect the body as a whole, and not about taking a TNF-alpha pill or an IL-10 pill, or a pill that suppresses or enhances one or the other. If one is in an "emergency" situation, then "therapeutic" doses of such substances may be necessary to stave off immediate death, but the overwhelming majority of the time, it is not about suppressing one or enhancing the other, but rather what's best is to have a short burst of the inflammatory followed by a short burst of the anti-inflammatory, and this does not happen when your body is made hyper-reactive by the unstable omega 3 and omega 6 polyunsaturated fatty acids.

Another important point is that with AA in your cells, the threshold for the inflammatory response is much lower (compared to Mead acid, at least). This means that "allergies" that a person has might never have developed in the first place if he/she had Mead acid instead of AA in his/her cells. The explanation I have furnished here accounts for the Janus-like quality of the phenomenon, that is, we hear about attempts to "boost the immune system" and also about the benefits of substances that "reduce inflammation." How is it possible to want two things that contradict each other at the same time? It just shows how little the people making such claims understand. My point, that with Mead acid in your cells you get a strong but quick inflammation and then a quick resolution to it, solves this "riddle" that is befuddling the "experts," though many act as if there is no contradiction here, which may be the most frightening aspect of this, at least on an intellectual level. With the highly unstable arachidonic acid in your cells, minor stressors generate the inflammatory process, and a cycle of damage and "rebuilding" occurs, causing so much chaos to the "system" that eventually major failure will happen, whether it be an auto-immune problem, immunosuppression, cancer, tissue degeneration, or fibrotic changes that interfere with the functioning of a particular tissue or organ.

A recent report (5/3/06) on sciencedaily.com makes some very key points on this topic, yet also demonstrates where there is a major misunderstanding, which is responsible for the poor state of affairs with respect to the practical applications of the scientific findings:

"Human T cells respond much more robustly than chimpanzee [and other primate] cells do..." and this can "...account for the rarity of T-cell mediated liver damage, such as chronic active hepatitis, cirrhosis and cancer, following Hepatitis B or C infection in chimpanzees. In addition, several other common human T cell-mediated diseases, including bronchial asthma, rheumatoid arthritis and type 1 diabetes, have, so far, not been reported in chimpanzees or other great apes."

Moreover: "This study may also explain the severe human reactions observed in a recent clinical trial using a T cell activating anti-CD28 antibody produced by TeGenero, Inc. All six healthy volunteers who received doses at 500 times lower than what was tested in nonhuman primates became severely ill, requiring hospitalization."

The volunteers experience a hyperactive immune/inflammatory response that was nearly deadly. Thus, it's clear to those who possess some familiarity with the phenomenon that the problem is the hyperactivity, and this appears to be greatly enhanced by AA as well as long-chain omega 3 PUFAs (such as EPA). However, where they do terribly wrong is in their notions about the "germs" or "bugs" causing the "disease," leading them to make prescriptive suggestions that do much more harm than good, even though attentuating the immune/inflammatory response is very easy (and inexpensive) to do.

Let's take an example - here's what they say about "HIV/AIDS:"

"The study suggests that the expression of Siglecs [which are absent in human T cells] on chimpanzee T cells in essence puts the brakes on the cells during chronic HIV infection, preventing progression to AIDS in chimpanzees. In contrast, the onset of human AIDS occurs more rapidly due to the loss of T cells..."

This makes no sense whatsoever. Apparently, they think that "HIV" activates the T cells, which then get infected with the "HIV," and are killed off. However, this has never been demonstrated, though several attempts at doing so have failed, and thus they seem to hold notions that may be common, but are incorrect. If you want to read more about this, click on "links" and then click on the Perth Group. The key point here is that when the T cells are activated, they produce cytokines that do the damage, no matter what pathogens are present or absent.

At least one of the researchers appears to be aware of what I am suggesting: "...said Varki. 'It is reasonable to hope that drugs can be found to turn the Siglec brakes back on again in human T cells, to slow the T cells down when they become hyper-active and cause disease.'"

He also understands what happened to the volunteers in the other study that resulted in the hyperactive response that was nearly deadly:

"'In retrospect, the absence of natural restrictions on activation, such as that provided by Siglecs, could have predicted this striking disparity between humans and nonhuman primates,' said Varki. The human volunteers could have experienced rapid activation of T cells and a resulting 'cytokine storm.'"

Note that TNF-alpha is a cytokine.

The only thing Varki probably does not understand is how much of a difference diet can make, because just about everyone in nations like the USA are overloaded with AA these days.

Source for the above quotations: http://www.sciencedaily.com/releases/2006/05/060502224533.htm

Relevant study: Title: "Dietary fish oil increases tumor necrosis factor secretion but decreases interleukin-10 secretion by murine peritoneal macrophages."

J Nutr. 2002 Dec;132(12):3740-3.

This study is important because of the claims about fish oil being "anti-inflammatory." Actually, the fish oil appears to attenuate the anti-inflammatory component of the process, but because "experts" noticed that symptoms commonly thought of as being signs of "inflammation" are lessened by fish oil, they call fish oil "anti-infammatory." Instead, with fish oil, there is damage from the TNF-alpha, but it just keeps going until the stressor is removed, which can result in tremendous damage. This is pointed out in the professional nutritional literature, for example, the book "Modern Nutrition in Health and Disease," by Shils and Young, or "Diet and Health," by the National Research Council.

In the 7th edition of the Shils and Young book, page 102, we learn that the "the "data certainly do not support the widely published assumption that n-3 fatty acids possess a specific retarding effect on atherogenesis... in rabbits at least, they seem to stimulate atherosclerosis." The animals had liver damage as well as "Periportal fibrosis, lipogranulomas filled with lipofuscin, and bile duct hyperplasia."

The authors go on to say: "Other potentially harmful effects of 20:5 n-3 and 22:6 n-3 [that is, EPA and DHA] rich fish oils are neglected by the advocates of increased human consumption of fish oils. The pathologically increased bleeding times, as observed after aspirin ingestion, also occurs in Eskimos on a high fish oil diet." The authors then talk about "a promoting role of [EPA/DHA] in the development of carrdiac necrosis and an increased sensitivity to catecholamine stress." And then they state that extreme tocopherol ("vitamin E") deficiency occurs with fish oil supplementation. Another telling quotation: "...the most severe degree of atherosclerosis was observed in rabbits fed fish oil, with a similar trend in the [flax] oil group., rather than after feeding palm oil with its high concentration of palmitic and stearic acid [saturated fatty acids]."

Some "diseases," such as "heart disease," which were rare in the early 1900s (in the USA and most other nations), may be related to arachidonic acid overload, and may indeed be attenuated in the short term by fish oil supplements, but the molecular-level evidence suggests that damage will be done that will simply mean dying of a different "disease" or a different variation of "heart disease," perhaps at an earlier age than if one had just eaten the typical diet. The differences will be related to the powerful inflammatory and anti-inflammatory response with AA in your cells, or with the powerful inflammatory and weak anti-inflammatory response with EPA and DHA in your cells (using my definitions, which are based upon the molecules produced rather than the perceptions of doctors and common notions about what "inflammation" is). The powerful responses with omega 3s and/or omega 6s generate a great deal of free radical activity, and this is what has lead to the "epidemic" of "heart disease," for example:

"...researchers have found that blood levels of the oxidized form of low density lipoprotein (LDL) are directly related to the severity of heart disease, according to a report in today's Circulation: Journal of the American Heart Association. In the two-part study, Japanese researchers also found that oxidized LDL was higher in the plaques of individuals with unstable angina than those with stable angina. Oxidized LDL (ox-LDL) is a form of LDL that has combined with oxygen. It is considered more dangerous than LDL because it promotes clogging of blood vessels." Article: "Form Of Cholesterol Singled Out As Cause Of Chest Pain, Heart Attack."

Source: http://www.scienceblog.com/community/older/2001/A/200110575.html

Anything that provokes and inflammatory response can cause a "disease," and with AA in your cells symptoms are greatly enhanced, for example:

Am Rev Respir Dis. 1985 Apr;131(4):624-32.

Production of arachidonic acid metabolites by macrophages exposed in vitro to asbestos, carbonyl iron particles, or calcium ionophore.

Kouzan S, Brody AR, Nettesheim P, Eling T.

"Consequent to asbestos deposition, alveolar macrophages (AM) accumulate at alveolar duct bifurcations where they phagocytize fibers. Because phagocytosis can stimulate the release of arachidonic acid (AA) metabolites, the possibility that secretion of these powerful mediators of inflammation might be induced by chrysotile asbestos was investigated in vitro. Rat AM were treated in vitro with chrysotile asbestos, and the cyclooxygenase products--prostaglandins, thromboxane B2 (TXB2), 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT)--and lipoxygenase products--leukotrienes (LT), hydroxyeicosatetraenoic acids (HETE)--secreted in the medium were isolated by high-performance liquid chromatography. Composition of the AA metabolites released was compared with that from those stimulated by the calcium ionophore A 23187 (20 microM) and by another particulate phagocytic stimulus, i.e., carbonyl iron beads. Calcium ionophore stimulation induced a marked release of various AA metabolites in the medium from both the cyclooxygenase pathway (HHT, TXB2, and PGE2, in decreasing quantities, respectively) and the lipoxygenase pathway (LTB4, 5-HETE, 12-HETE, and LTC4). The major product was LTB4. Treatment of the macrophages with asbestos fibers induced the release of a similar array of AA metabolites, although there were smaller amounts of LTC4 and 12-HETE, but increased quantities of PGF2 alpha. A time course study showed a steady increase in metabolite production for 1 h, followed by a plateau. In addition, the amount of metabolites released was dependent on asbestos concentrations. Phagocytosis of iron beads induced the secretion of the same metabolites as asbestos stimulation, but in larger quantities, probably reflecting the lack of cytotoxicity of the particle..."

Note that LTB4 seems to be doing most of the damage in this "disease," and that Mead acid cannot be made into LTB4.