Because most “experts�?think dietary PUFAs are “essential,�?despite the fact that this was refuted in 1948, they never consider what things would be like if the diet did not contain these dangerous molecules, but some studies have “stumbled upon�?the benefits (without any deleterious effects) of this situation, for example:

“…Young cartilage is characterised by the presence of high levels of 20:9 w-9, Mead acid, indicating a relative deficiency of EFA. Skeletal muscle from the same subjects showed normal EFA levels, and no Mead acid. Age decreases the Mead acid level and increases the EFA level, with weight-bearing cartilage having more EFA and less Mead acid than costal tissues. Cartilage from osteoarthritis affected joints showed even lower Mead acid levels and even higher w-6 EFA levels, leading the authors to speculate that accumulation of w-6 EFAs in cartilage might predispose towards the development of OA, and that the presence of Mead acid might somehow be protective�?�?

Source: Poster Presentation at the Third International Conference on Essential Fatty Acids and Eicosanoids, Adelaide, Australia March 1 1992

In contrast, a group of researchers tried to apply evidence from test tubes to human “AIDS�?patients, and the results speak for themselves: “One study used dietary N-3 fatty acid (fish oil) supplementation in people with advanced AIDS. It has been shown in vitro that large doses of fish oil reduced production of TNF and IL-1 by monocytes and macrophages stimulated by endotoxin (bacterial infection). Another study showed that a fish oil based diet blocked IL-1 induced anorexia in rats. However, clinical trial results were disappointing as the fish oil supplementation was unable to prevent further weight loss in subjects who developed new AIDS complications.�?

Source: http://www.aegis.com/pubs/step/1995/STEP7107.html

This points out how important it is to try and understand the situation in “big picture�?terms, and not to seek to designate molecules as “good�?and “bad,�?depending upon how they fit into assumptions that have demonstrated themselves to be failures. TNF-alpha has a role in restoring health, and trying to inhibit it is a very dangerous proposition, for example:

"A new meta-analysis of many previous studies of TNF- (tumor necrosis factor) blocking antibodies for treatment of rheumatoid arthritis has confirmed a previously discovered increased risk for serious infection and has found that cancer also is a potential risk associated with the drugs."

Source: http://www.sciencedaily.com/releases/2006/05/060522093410.htm

The molecular level evidence is clear: with coconut oil as your main source of fatty acids, unlike fat sources high in polyunsaturated fatty acids, you get just the appropriate amount of TNF-alpha during "inflammation." As I have seen after ridding my body of AA in favor of the Mead acid, a cut will produce a strong (but not overwhelming) inflammatory response that lasts a short time.

The reason gets a bit technical, but it seems to depend upon where the TNF-alpha is coming from, for example: “Production of both cytokines by inflammatory M phis [macrophages] decreased with increasing unsaturation of the high fat diets, such that cells from FO [fish oil]-fed mice showed significantly decreased production of TNF-alpha and IL-1 beta compared to those from mice fed on each of the other diets. In contrast, resident M phis from mice fed FO showed increased TNF-alpha production compared to those from CO [coconut oil]-fed mice. Thus, FO feeding decreases production of TNF-alpha and IL-1 beta by inflammatory M phis and increases production of TNF-alpha by resident M phis…�?Source: Cytokine. 2000 Sep;12(9):1374-9.

And this finding is important because: "...inflammatory M psi [macrophages] normally emigrate rapidly from the peritoneal cavity during the resolution of inflammation, contrasting with resident M psi, which persist in the noninflamed peritoneum for weeks." Source: The Journal of Immunology, Vol 157, Issue 6 2577-2585, Copyright © 1996 by American Association of Immunologists.

The significance here is that an overload of omega 3 or omega 6 fatty acids means that severe damage from TNF-alpha is a good possibility, and then when doctors tell you to take certain drugs, which may or may not be effective, you may die of something worse and at an earlier age. Simply stated, we do not yet live in an age where drugs can solve such problems, yet an understanding of diet appears to be all this is required to avoid such "diseases."

Thus, there is evidence for an explanation of at least the overwhelming majority of "disease" down to the molecular level which can be directly connected to diet and agents that people are often exposed to, such as cigarette smoke. At this point, it would make sense to compare a group of animals fed a large amount of fish oil with a group of animals fed a large amount of coconut oil, and then simply wait and see which group lives longer. They should be exposed to common, but not highly toxic, stressors, to mimic stress they would encounter under natural conditions. The evidence that exists to date suggests that the fish oil-fed animals would live considerably shorter lives, but there is no reason not to do this kind of experiment �?it is simple, cheap, and “on point.�? And everyone would understand the significance of the results. Instead, we get a huge number of studies from the biomedical establishment about markers, endpoints, correlations, links, mathematical models, associations, etc., when there is no longer any need for most of them, since if one views the evidence as a whole, what is happening is obvious and easy to prevent, assuming the person is willing to do what is asked of him or her.

Furthermore, in science, one is supposed to investigate variables by isolating each one versus "controls," in order to determine if the "marker," "correlation," or whatever one calls the item one thinks is important is the cause or just an epiphenomon generated further down the pathway. If a scientist finds a "correlation," real or imagined, and then says, "this deserves further investigation," but then several years later all we see is that he/she keeps doing the same thing, we need to ask whether that person is being disingenuous (for any number of reasons) or is ignorant of the scientific method. In any case, as I have demonstrated above, there is enough evidence right now to know if a "marker," for example, has anything to do with the underlying, molecular-level cause or not. And while you may not always be able to avoid major cellular stressors, packing your body with saturated fatty acids and ridding it of omega 3 and 6 PUFAs will make it much more resistant and lessen damage that may occur, which eventually leads to symptoms of a "disease" (and at that point it may be too late to "cure" it simply and with little or no discomfort nor risk).

Note that the 1948 refutation of the 1929/1930 Burr & Burr experiment that established the ludicrous "essential fatty acid" notion (and is still cited as the major source in some of the professional literature, if anything is cited at all to support it) can be located in the Encyclopedia Britannica Book of the Year, 1948, 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..." Thus, on a fat-free diet, the rats were fine, so long as they were given proper vitamin supplementation (some truly essential vitamins were not known in 1930, and so they seem to have basically guessed that PUFAs were the vital substance).