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

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?

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.

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.

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.

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.

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.

2.

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

3.

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.

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.

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.

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.

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.

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.