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

Research Reveals Inner Workings Of Immune System 'Thermostat'

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

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

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

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

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

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

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

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

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

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

The oxidative modification of low-density lipoprotein (LDL) may play an important role in atherogenesis. Our understanding of the mechanism of LDL oxidation and the factors that determine its susceptibility to oxidation is still incomplete. We have isolated LDL from 45 healthy individuals and studied the relationship between LDL fatty acid, vitamin E and beta-carotene composition, intrinsic phospholipase A2-like activity and parameters of LDL oxidation. LDL was exposed to a copper ion-dependent oxidising system and the kinetics of oxidation studied by monitoring formation of fatty acid conjugated dienes. The length of the lag phase of inhibited lipid peroxidation was measured as well as the rate of lipid peroxidation during the propagation phase. There was no significant correlation between LDL antioxidant vitamin or fatty acid composition and lag time to LDL oxidation. Oleic acid was negatively correlated with the rate of LDL oxidation (r = -0.41, P < 0.01) whilst linoleic acid was significantly correlated with the extent of LDL oxidation measured by the production of total dienes (r = 0.34, P < 0.05). Interestingly, LDL vitamin E content was positively correlated with both the rate (r = 0.28, P < 0.05) and extent of LDL oxidation (r = 0.43, P < 0.01). LDL isolated from this group of subjects showed significant intrinsic phospholipase-like activity. The phospholipase activity, whilst not correlated with lag time, was significantly correlated with both rate (r = 0.43, P < 0.01) and total diene production (r = 0.44, P < 0.01) of LDL oxidation. We conclude that antioxidant content, fatty acid composition and intrinsic phospholipase activity have little influence on the lag time of Cu-induced LDL oxidation. These components do however, significantly influence both the rate and extent of LDL oxidation, with increased vitamin E, linoleic acid content and phospholipase activity associated with faster and more extensive oxidation. The possible pro-oxidant effect of vitamin E has interesting implications for the postulated 'protective' effects of vitamin E on atherogenesis.

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

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

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

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

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

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

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

And a key point is made about this mechamism:

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

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

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

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

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

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

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

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

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

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

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

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