The “medical/biological establishment�?(MBE) has failed to live up to the rigorous standards of the scientific method. Instead, assumptions and “models�?that appeared to be accurate when viewed in a superficial have failed over and over again to be demonstrably correct (examples: “vaccine for HIV/AIDS,�?“war on cancer won by 1980,�?“flu pandemic�?predictions, “miracle cures�?via “genetic engineering�?. The public is told that if only some more money was spent on “research,�?a “cure�?would soon be forthcoming. Some “experts�?have recently predicted an end to “all diseases�?within the next ten to fifteen years. If I could, I would bet every asset available to me that this will not be the case twenty years from now (unless my advice is followed, rather than the vaccines, genetic engineering, etc.). In fact, the data indicates higher rates of “chronic diseases�?in nearly all “modern�?Western nations, not less. Where did it all go so wrong?

Basically, the research has been done and is conclusive. There is little need for much further research, except perhaps in very rare and disabling conditions, and in cases of severe traumatic injury (such as what happened to actor Christopher Reeve). Below, I will examine just a tiny number of passages from the scientific literature in an attempt to show that the problem is not a lack of evidence, but a faulty interpretation of the evidence. It may be useful here to talk about inductive versus deductive reasoning, and how exclusive reliance on one can cloud one’s judgment. At this point in history, the MBE is trapped in a deductive mode, that is, they assume that their assumptions and models are correct, and thus they ignore evidence that contradicts these assumptions and models. In some cases, they totally misinterpret the data, insisting that it actually does support their notions. In these kinds of cases, one can build a logical argument and allow those with “an open mind�?to judge for themselves, but the problem in this field is that there is technical language that can be used to confuse or mislead the “average person.�? To be clear, I am not suggesting that most people in the MBE are doing this consciously, and none actually may be doing it, but it’s getting done all the same. In an inductive process, which is what the fictional Sherlock Holmes was noted for (despite Watson’s talk of “deduction�?, one looks at various pieces of evidence that may appear unrelated to each other and considers how a “big picture�?can be formed from these items.

This is what I have done over the last several years in an attempt to understand “disease�?comprehensively. With this approach, it’s important to put your preconceptions aside. Of course, you probably should have at least one tentative hypothesis in the “back of your mind,�?but you should keep it there until you can understand all the evidence in the context of that hypothesis. This is something that today’s MBE does not do. Instead, you will find them constantly saying that they are “puzzled�?or that a virus is “wiley�?or that the “war�?against a particular “disease�?needs to be “fought harder�?or that the results of a particular study are “baffling�?or “paradoxical.�? Now it is certainly true that some studies are not designed well or are flawed or are generating data that is not relevant, but these are the exceptions, whereas if you listen to the MBE “experts�?it seems to be the rule. If you don’t believe me, I invite you to do your own research, at pubmed.com, for example. If you do, you will see that the studies I cite and discuss below are the proverbial “tip of the iceberg,�?and that the evidence as a whole points in one direction �?a direction that is very different from the one presented to the public by most MBE spokesmen.

In “medicine,�?clinical syndromes, which are just aids for scientists, have been ossified into unquestioned “reality,�?and the result is that doctors and researchers no longer have to think. If the markers are present for such a syndrome and if the symptoms seem to fit, a scientific reality is affirmed without any thought of the scientific method. In the case of “HIV/AIDS,�?the situation is even more egregious, because people with no symptoms of any “disease�?are often told that they do in fact have one �?a deadly one �?simply because certain markers are present. The idea that one should look for actual damage being done by a stressor, and then remove the stressor before it can do permanent damage or render it harmless, is never considered, even though the molecular level evidence is clear and consistent: only a stressor can cause “disease�?and having the wrong fatty acid as the predominant stressor induced fatty acid (PSIFA) amplifies the problem greatly.

Now, I’ll discuss something you may have heard of recently. It is being claimed that fish oil supplements are “good�?because they are “anti-inflammatory.�? Some “experts�?realize that arachidonic acid (AA) has “pro-inflammatory�?effects (Dr. Nicholas Perricone has talked about this on his PBS show about “curing�?wrinkles, for example). But other “experts�?talk about “boosting the immune system�?as being a goal all should seek to acheive. Since most Americans, for example, are overloaded with AA, wouldn’t it be the case that their “immune systems�?are optimal? I used to get at least two colds a year while in the AA overloaded condition (AAO), but I have only had one very minor bout of cold-like symptoms since ridding my cells of AA, for example. How is this possible? Excessive inflammation, while harsh on “pathogens,�?is “overkill.�? It damages more than it heals, at least compared to the inflammation one generates when Mead acid is present instead of omega 6 PUFAs. And it damages the overall effect of the “immune system,�?in direct and indirect ways. The question the “experts�?rarely if ever seem to ask is, “if I take the fish oil supplements, am I doing more harm than good, and if so, is there a better way?�

The answer is yes to both, for example: “Dietary fish oil increased secretion of the proinflammatory cytokine, TNF, but decreased secretion of the anti-inflammatory cytokine, IL-10�?fish oil has an overall pro-inflammatory effect.�? Source: J Nutr. 2002 Dec;132(12):3740-3.

And: “…high consumption of fish oils, by virtue of their high content of omega-3 polyunsaturated fatty acids, can lead to an exaggerated production of mediators of inflammation with potentially adverse consequences on the outcome and severity of infectious diseases.�?Source: Immunol Lett. 1992 Sep;34(1):13-7.

And: “…the anti-inflammatory effects of FO may be explained in part by a shift in the Th1/Th2 balance, due to the direct suppression of Th1 development…�? Source: J Nutr. 2005 Jul;135(7):1745-51.

This last passage is very significant, because the Th1 to Th2 shift is characteristic of many “AIDS patients�?(again, the problem of putting the clinical syndrome cart before the molecular evidence cart makes it difficult to say how often this is the case), and is a toxic effect. It is not a “beneficial�?effect, but again, if someone is suffering from the AAOS, it might appear to help in the short term. In the long term, it is highly unlikely that this could be viewed by any reasonable person as “beneficial,�?if one looks beyond the markers and “surrogate endpoints,�?and at overall mortality, but fish oil has even been found to cause a worsening of the “inflammatory�?symptoms so many “experts�?are now claiming it lessens, for example:

�?7 RA patients took part in a 12 week prospective, double blind study. 17 had a high pufa /low saturated fat diet with added MaxEPA (10g/d). 20 acted as controls,and had a normal diet with less pufa, together with placebo capsules. At 12 weeks the trial group had less morning stiffness, and fewer tender joints (6.4v9.0). At follow up 4-8 weeks later,the MaxEPA group were significantly worse than the control group for pain and overall condition. The control group was better for morning stiffness & tender joints on follow up…� Source: The Lancet,1985 Jan 26:i, 184-7.

And the dangerous The Th1 to Th2 shift is directly related to the PUFAs in one’s body, for example: “PUFAs act to inhibit production of Th1-type cytokines with little effect on Th2-type cytokines; n-3 PUFAs are particularly potent.�

Source: J Leukoc Biol. 2001 Mar;69(3):449-57 How can the “experts�?be so wrong? It appears that the reason is that they became focused on the effects of AAO and considered this to be a “pro-inflammatory�?state. In reality, AA metabolites can have “pro�?or “anti-inflammatory�?effects, whereas fish oil does not have the anti-inflammatory effects (at the molecular level), for example: “…prostaglandin E(2)(PGE(2)) and leukotriene B(4)(LTB(4)) which inhibit and stimulate, respectively, tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) production…�? Source: Cytokine. 2000 Sep;12(9):1374-9.

PGE2 is considered “anti-inflammatory,�?but it is very dangerous because: “Prostaglandin E2 (PGE2) favors T helper type 2 (Th2)-like cytokine secretion profiles in murine and human CD4+ T cells by inhibiting the production of the Th1-associated cytokines interleukin-2 (IL-2).�? Source: Eur J Immunol. 1995 Jan;25(1):59-63.

PGE2 is rich in human semen and “receptive�?anal intercourse is strongly associated with dying of “AIDS.�? Everything makes sense �?the molecules simply don’t lie!

Fish oil does, however, interfere with the AA metabolites (both genesis and potency), and since AAO “diseases�?(what I call AAO syndrome, or AAOS) are consistent with what is considered “inflammation�?in various textbooks, the effects are fish oil are thus viewed as “anti-inflammatory.�? What is needed now is a description of exactly what is occurring at the molecular level, not what fits a textbook model, but what one finds is that even when there is a promising finding on the molecular level, researchers cannot “think outside the box,�?for example:

“The correlation of persistent tumor necrosis factor-alpha (TNF-alpha) activation with disease progression in patients infected with human immunodeficiency virus type 1 (HIV-1), suggests a role for TNF-alpha in the pathogenesis of HIV-1 infection�?The pattern of abnormalities seen in AIDS patients suggests a role for persistent activation of the TNF system in the accelerated CD4+ lymphocyte destruction, the enhanced HIV-1 replication, and the markedly impaired antimicrobial defense in advanced HIV-1-related disease.�? Source: Blood. 1997 Oct 1;90(7):2670-9. But this problem is a general one, and not confined to a small number of people who expose themselves to tremendous stressors, for example: “The underlying hypothesis that links these pathologies can be summarized as follows: Initial injury, whether initiated by an infectious, chemical, or environmental agent, produces focal tissue necrosis in a target organ through any one of several toxic mechanisms (e.g., lipid peroxidation, mitochondrial damage). As a result of this damage, tissue-fixed macrophages and circulating monocytes migrate to the damaged site, become activated, and secrete products that cause additional cell damage or induction of inflammatory products. Some of these products are short-lived, such as reactive oxygen species and the nitrogen-centered radical nitric oxide (NO.). Other products, such as arachidonic acid and proinflammatory cytokines, regulate the production of additional inflammatory mediators and thus amplify as well as propagate these responses. The overall effect is a chronic inflammatory response resulting in tissue damage that can lead to fibrotic changes.

Although many factors contribute to the inflammatory response, arguably tumor necrosis factor (TNF) plays the major role in regulating this process. The cellular effects of TNF include physiologic, cytotoxic, and inflammatory processes…�? Source: Environmental Health Perspectives Volume 106, Number 9, September 1998.

Notice how the author points out that the initiating stressor can lead to lipid peroxidation and then to TNF-alpha production and AA metabolization, resulting in a vicious cycle occurring: “tumor necrosis factor stimulates prostaglandin synthesis and greatly amplifies prostaglandin synthesis…�? Source: J Cell Physiol. 1989 Oct;141(1):85-9.

This is why I tell people to pack their cells with saturated fatty acids, and to let their bodies make unsaturated fatty acid as they see it, because saturated fatty acids are not subject to lipid peroxidation, and the whole “disease�?process may be dependent upong this, or enhanced greatly. As I’ve said to many people, I wish the argument I am making is totally original, and that I am the first to make it, but that is not the case. I am merely trying to point out how strong the evidence is for this position, and how weak it is for all others. “AIDS researchers,�?for example, instead of saying to themselves, “perhaps TNF-alpha is causing the problems, and not a virus which is supposed to be present �?let’s see if we can recreate a similar “disease�?with just the TNF-alpha,�?assume that somehow a virus that cannot be detected is causing the TNF-alpha release. This is so far removed from reality that it could not be used for the basis of a science fiction novel, because the author would realize that the readers would ask how a substance that is generated upon stress is said to be generated by something that is undetectable, especially considering that TNF-alpha will not be generated in large amounts �?amounts needed to do serious damage �?if large amounts of a continuous stressors are absent.

Most “disease�?occurs because the body is exposed to too much TNF-alpha (which is true of “HIV/AIDS�?as well as “non-infectious�?disease �?there is never any difference, and the exceptions are so rare �?if they really exist - that they deserve to be relegated to a few specialists, who might encounter them once or twice in a lifetime), along with the metabolites of AA, such as LTB4 and PGE2. Other “events�?occur “downstream,�?including things like glutatione depletion, and other things, like having too much iron in one’s body, may enhance the process significantly. This leads some “experts�?to claim that a specific antioxidant supplement may be a “cure,�?but there is no way to know whether this will be effective in the long term, assuming it is effective for the overwhelming majority in the short term, and the logical approach is to remove the dandelion weed at the root, not petal by petal.

Even “chronic diseases�?that most people associate with the elderly are caused by this process, for example: “The proinflammatory cytokines IL-1 and TNF-α are reported to play important roles in cartilage and bone degradation, with TNF- α occupying a primary position in the cytokine cascade…� Source: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000400002