If you've read the other essays, you are familiar with the evidence for the cause of "disease" as we perceive it today being rooted in the inflammatory response (and TNF-alpha in particular), and not just the response of several hundred years ago, but one that is greatly enhanced by the "modern" diet (rich in omega 6 PUFAs). Here is evidence for the role of an AA metabolite in producing a common symptom of "disease:"

Am J Physiol Regul Integr Comp Physiol. 2006 May;290(5):R1262-70. Epub 2006 Jan 12.

Kupffer cell-generated PGE2 triggers the febrile response of guinea pigs to intravenously injected LPS.

Li Z, Perlik V, Feleder C, Tang Y, Blatteis CM.

Dept. of Physiology, Univ. of Tennessee Health Science Center, 894 Union Ave., Memphis, TN 38163. [email protected]). Because the onset of fever induced by intravenously (iv) injected bacterial endotoxic lipopolysaccharides (LPS) precedes the appearance in the bloodstream of pyrogenic cytokines, the presumptive peripheral triggers of the febrile response, we have postulated previously that, in their stead, PGE(2) could be the peripheral fever trigger because it appears in blood coincidentally with the initial body core temperature (T(c)) rise. To test this hypothesis, we injected Salmonella enteritidis LPS (2 mug/kg body wt iv) into conscious guinea pigs and measured their plasma levels of LPS, PGE(2), TNF-alpha, IL-1beta, and IL-6 before and 15, 30, 60, 90, and 120 min after LPS administration; T(c) was monitored continuously. The animals were untreated or Kupffer cell (KC) depleted; the essential involvement of KCs in LPS fever was shown previously. LPS very promptly (<10 min) induced a rise of T(c) that was temporally correlated with the elevation of plasma PGE(2). KC depletion prevented the T(c) and plasma PGE(2) rises and slowed the clearance of LPS from the blood. TNF-alpha was not detectable in plasma until 30 min and in IL-1beta and IL-6 until 60 min after LPS injection. KC depletion did not alter the times of appearance or magnitudes of rises of these cytokines, except TNF-alpha, the maximal level of which was increased approximately twofold in the KC-depleted animals. In a follow-up experiment, PGE(2) antiserum administered iv 10 min before LPS significantly attenuated the febrile response to LPS. Together, these results support the view that, in guinea pigs, PGE(2) rather than pyrogenic cytokines is generated by KCs in immediate response to iv LPS and triggers the febrile response.

Arachidonic acid by itself is highly unstable and toxic, for example:

"We conclude that lethal injuries sustained by cells during short exposures to AA were caused by the fatty acid itself and were not mediated by the AA-induced influx of Ca2+/cations. Moreover, direct physical effects of AA on the plasma membrane (changes in membrane fluidity or detergent-like action) were also excluded."

Source: Biochem Pharmacol. 2004 Mar 1;67(5):903-9.

AA metabolites are even more potent, which suggests that what appear to be "diseases" are really just the epiphenomena of AA overload, which becomes manifest when a stressor is applied to cells. However, the amount and length of exposure to the stressor plays a major role in the kind of damage the "inflammation" will do (especially when one's cells contain omega 3 and 6 PUFAs), for example:

Infect Immun. 2003 May;71(5):2674-83.

Title: "The levels and patterns of cytokines produced by CD4 T lymphocytes of BALB/c mice infected with Leishmania major by inoculation into the ear dermis depend on the infectiousness and size of the inoculum."

"Diseases" are not necessarily caused by "germs," even when they are present and appear to be the "obvious" cause, for example:

"The bacteria [H. pylori] are found everywhere in the world, but are especially prevalent in developing countries, where up to 80% of children and 90% of adults can have laboratory evidence of an H. pylori infection--usually without having any symptoms."

What does cause "disease?"

"The vast majority of H. pylori in colonized hosts are free-living, but approximately 20% bind to gastric epithelial cells. This binding induces an immune response..." which can lead to "...peptic ulcer disease, gastric adenocarcinoma, and non-Hodgkins lymphoma of the stomach."

In the other essays, I showed how having the wrong fatty acids in your cells increases your chances of a chronic inflammatory condition significantly, and this is the case with H. pylori in the context of a typical "modern" diet:

"The means through which H. pylori causes gastric cancer are more complex but likely involve alterations in gastric epithelial cell responses that are perturbed within the context of a chronic gastric inflammatory infiltrate, which can persist for decades."

So far, so good, but then, as is so often the case, the interpreation of the findings is illogical:

"'Our results indicate that H. pylori can co-opt a host protein as a receptor and that it can increase expression of this receptor in gastric epithelial cells,' says Peek. 'Further, absence of this receptor abolishes the inflammatory response that H. pylori induces in infected mice, suggesting that this receptor mediates H. pylori-induced injury in the stomach.'"

Another group of researchers found that "disease" occurred only when cellular stress was present, though this has been known for some time (for instance, it was found that a common bacterium in the GI tract only became dangerous - possibly life-threatening - when subjected to stressors produced during surgery):

"The researchers discovered a new function for these glycolipids--they are cleaved in response to cell stress caused by changes in osmotic pressure and relative acidity or alkalinity... 'We found that putting these cells under stress similar to that initially encountered by the trypanosome inside the fly caused the parasites to cleave free GPIs...'"

Source: http://www.sciencedaily.com/releases/2006/05/060509174333.htm

Source for the above quotations about H. pylori "infection:"

http://www.sciencedaily.com/releases/2006/05/060506103846.htm

It is this "clinging" action when subjected to stressors that appears to make many "pathogens" dangerous to the "host." After "clinging," the body invokes the "inflammatory" process (the exact nature of which is determined by the fatty acids present), which then could do the actual damage that results in symptoms of a "diseases." Here's another example of this in "infections" common in the West:

"UTIs [urinary tract infections] begin when bacteria gain a foothold on cells lining the kidney or bladder and grow into colonies. They latch onto cells using tiny fibers known as pili. Similar fibers also are produced by bacteria responsible for a variety of gastric, respiratory and other infections."

Source:

http://www.sciencedaily.com/releases/2002/11/021115070154.htm

The key point in all of this is that arachidonic acid is very unstable and toxic, and is released from cells upon the most minor of stressors. Then it can stress the "germs," which cause "disease" by the "clinging" action, provoking the "inflammatory" process, which is too potent and sustained in people with arachidonic acid in their cells (and it appears to also be the case for people with long chain omega 3s as well), and then the damage that is called one "disease" or another eventually appears. Note that it would be very easy to confirm this idea by feeding one group of animals fresh coconut oil as their only fat source (at 30% of total caloric intake) while another group would be fed something like corn oil, canola oil, fish oil, or some combination of oils rich in omega 6s and/or omega 3s. The animals would then be exposed to knwon "pathogens" that cause "disease" in that species. The animals fed the high PUFA diet should not be given antioxidants, so that the fatty acids would cause the stress that would then allow the "pathgen" to become dangerous in the manner described above.

Another point I'll make here, though perhaps in the future I'll write up a new essay on it, has to do with "co-factors." If you read through studies concerning "chronic disease" you find iron, for example, to be "implicated" in many conditions. The evidence suggests that while iron may indeed by a co-factor that enhances various "disease," it can be neutralized by diet. For instance, it has been found that though Asians have high iron level (in general) they do not have the "disease" Western "experts" thought they should: "'The finding that Asians and Pacific Islanders have high levels of iron in the blood is surprising because they also have the lowest prevalence of the particular gene mutation that is found in Caucasians with the typical form of hemochromatosis,' he said. 'This may mean that the Asians and Pacific Islanders have a different genetic mutation that has not yet been discovered, or that they do not, for some reason, develop hemochromatosis/iron overload despite their high blood levels of iron.'"

Source: http://www.sciencedaily.com/releases/2005/04/050430222454.htm

Here again, the "experts" don't realize that having your cells packed with more stable fatty acids neutralizes this potential problem, and instead they go on to speculate about the role undiscovered genes may be playing, rather than examining the literature as a whole to see if there is an explanation already "in the books."

An excellent abstract that explains the role iron does play (in those overloaded with omega 6 PUFAs at least) is the following:

Med Hypotheses. 2003 Jan;60(1):69-83. Are lipid peroxidation processes induced by changes in the cell wall structure and how are these processes connected with diseases? Spiteller G. Lehrstuhl Organische Chemie, Universitatsstrasse 30, Bayreuth, Germany. [email protected]

Apparently nature uses the unique sensitivity of polyunsaturated fatty acids (PUFAs) versus oxygen to generate chemical signals if the surface of a cell is influenced by an outside or inside event... It seems that mammalian and plant cells respond equally to such changes in their structures by transformation of polyunsaturated fatty acids localized in the phospholipid layer of the cell wall to lipidhydroperoxides (LOOHs). These lipid peroxidation (LPO) processes involve all PUFAs, not only arachidonic acid.Slight physiological changes of the cell wall for instance by proliferation seem to activate enzymes, e.g., phospholipases and lipoxygenases (LOX). When an outside impact (for instance by attack of microorganisms) exceeds a certain level LOX commit suicide and liberate iron ions. These start a nonenzymatic LPO. Enzymatic and nonenzymatic LPO distinguish fundamentally which has not been recognized in the past. In the enzymatic LPO processes peroxyl radicals generated as intermediates cannot leave the enzyme complex. In contrast in a nonenzymatic LPO process peroxyl radicals are not trapped. They attack nearly any kind of biological molecules, for instance proteins. Thus only the amount of an outside impact decides if proliferation, apoptosis, or necrosis is started... After consumption of food rich in linoleic acid its LPO products become increased in low density lipoprotein (LDL). This LDL is able to enter endothelial cells and damage cells from inside, long before an inflammatory response is detectable.

And this brings me to the topic of "HIV/AIDS." Various attempts at discovering the "pathogenesis" of the "virus" have been attempted, and all have failed, leading the "experts" to argue that there is enough circumstantial-type evidence to establish "causation" and thus the pathogenesis issue can be put on the proverbial back burner with no threat to public health. Therefore, at this point, there is little effort being put into trying to figure out exactly how "HIV" (assuming it exists, of course) can cause death by numerous means (including some cases of cervical cancer) several years after "infection."

But after reading through the essays on this forum, and of course what is written above, I hope that you now realize that in order for a virus to kill someone many years after infection and after several years of apparent good health, something has to be going on in the body that is doing damage. "HIV" could be doing something similar to what the researchers discovered about H. pylori, but if that were the case, this would have been uncovered long ago. Instead, the "experts" posit "models" of "pathogenesis" and are more or less content to do other things. What this demonstrates clearly is that they don't understand that if an "infectious disease" has the characteristics of "HIV/AIDS" it must have an "inflammatory" component, meaning that molecules like TNF-alpha, PGE2, and LTB4 are doing the damage, though it's also possible that the biochemical signals or free radicals generated by the "inflammatory" activity cause the changes seen not just in "HIV/AIDS," but also in "aging" and other "diseases."

The most common model of "HIV/AIDS" that one hears about in the mainstream media is that, over time, "HIV" destroys enough CD4 cells to cause "immune system collapse." However, the body can adapt to a small loss of cells, and if there was a large loss of cells, symptoms and death would occur much sooner, as was common in the early days of the "AIDS epidemic." Thus, what started out as a reasonable assumption that was consistent with the evidence (though, again, from what is known now the first thing that should be investigated in such a phenomenon is "inflammation") became reified into a cult-like belief system that is about as inconsistent with the evidence and what is known as an explanation could possibly be.

A similar thing has happened in the "nutritional science" field. For example, in the "early days" it was reasonable to classify fatty acids into broad categories: saturated, monounsaturated, and polyunsaturated. Yet now it is known that each kind of fatty acid has distinct biochemical and physiological effects. As science journalist Gary Taubes has noted, some saturated fatty acids tend to raise serum cholesterol levels while others tend to lower them. Despite calls from some experts in this field to reconsider this abstract system, which, over time, appears less and less consistent with the scientific reality, change comes at a pace that would make a snail appear to be an Olympic sprinter.

My proposal to deal with this situation is to approach the problem in two ways: at the molecular-level, where "hard science" prevails, and at the practical level, where researchers can focus on results, rather than on attempting to fit square evidence pegs into their round abstract, unverified model holes. For example, in "HIV/AIDS," why not follow around as many "AIDS patients" who will allow such an intrusion and record everything they do (and also try to get them to be honest about their pasts), while also measuring various markers, especially ones related to "inflammation" and free radical damage? After several years of gathering such information, researchers could then try to "connect the dots." Instead, the dots got connected before the black points were printed on the page, due to the preconceptions held or asserted by the authorities in charge. In nutrition, why not determine exactly what people are eating, here and in countries with very different diets and rates of "disease," as well as other lifestyle elements that may be relevant, and then compare this information database with what is known at the molecular-level.