Rather than write up more essays, which, in a sense, are variations on the same theme, I think it might be best for you to read the other essays, then come to this page, where I will post evidence as it is published. If there was new evidence that appeared to contradict the points I've made in the other essays, and did not seem to be flawed (and also if the data was made public so that all could examine it, which is not always the case) then I would write up a new essay for it.

The points I've made about TNF-alpha (being released when cells are stressed), free radical damage, and "inflammation" are supported by new calorie-restriction experiments. Here is a passage from one report:

"The researchers also found that calorie restriction (CR) decreases the circulating concentration of a powerful inflammatory molecule called tumor necrosis factor alpha (TNF). They say the combination of lower T3 levels and reduced inflammation may slow the aging process by reducing the body's metabolic rate as well as oxidative damage to cells and tissues."

Source: http://www.sciencedaily.com/releases/2006/05/060531164818.htm

I would add that the issue is stress, not calories consumed, unless one eats so much that it in itself becomes stressful. Most likely, people on calorie-restricted diets ate a lot less unsaturated fatty acids. As I suggested in the essay about doing experiments, all one needs to do is the substitute fresh coconut oil for the usual fat sources in lab animal diets and see what the results are. If this was done, the results would be similar to calorie restriction, if not better, assuming the animals were not being fed much more food than is necessary.

This is suggested by their statement: "The thyroid gland produces critical hormones that play an indispensable role in cell growth and development as well as in lipid and carbohydrate metabolism. T4 is the main product secreted by the cells of the thyroid gland, but most actions of thyroid hormone are initiated by T3."

In other words, if the T3 levels are higher, there is more lipid metabolism, and that means more AA metabolites around to do damage.

In a study just published, the point I've made about my argument about "inflammation" is stated explicityly:

"Blockade of cytokines, particularly of tumour necrosis factor alpha (TNF-alpha), in immuno-inflammatory diseases, has led to the greatest advances in medicine of recent years... TNF-alpha is of crucial importance in the development of antigen-dependent and antigen-independent models of inflammation, and that these results correlate well with clinical success..."

The only thing not mentioned is the role fatty acids play, again, probably due to the excessive specialization in today's biomedical establishment.

Source: Springer Semin Immunopathol. 2006 Jun;27(4):391-408.

Title: "Inhibition of IL-1, IL-6, and TNF-alpha in immune-mediated inflammatory diseases."

Moller B, Villiger PM.

Today, there was a report about a study showing the long-term effects of surgery, something that few if any patients are told:

"'The first insight we take away from this is that when bad things happen down the road, months, maybe even years later, that we cannot, as we have in the past, just attribute it to the natural course of illness.'"

But what is this mostly due to? Again, we are back to "inflammation," macrophages, etc:

"Inflammation is a player in most major diseases, from cardiovascular disease to cancer. A heart patient, for example, already has chronic inflammation and the coronary bypass surgery he needs, ironically, may accelerate it. ...research is showing the impact of even a small infection [common after even minor surgery] in the face of chronic inflammation. Using an animal model of sickle cell disease, a disease marked by systemic inflammation, he’s studying the host’s defense to microbial products such as lipopolysaccharide. He’s found a resulting transformation of macrophages, which typically work like garbage collectors for the immune system, into large, pro-inflammatory cytokine-spewing cells."

This is similar to the oxidized cholesterol role in "heart disease." The only thing missing, as usual, is an understanding of the role fatty acids play, which explains why certain common "diseases" of today were not at all common a hundred years ago, when people's cells were not overloaded with arachidonic acid.

Source: http://www.sciencedaily.com/releases/2006/06/060605155505.htm

You may have heard that recently a scientist "infected" himself with H. pylori, giving himself an ulcer and "proving" that this was the "cause" of ulcers - a bacterial infection. However, it is undeniably true that not everyone who has been exposed to H. pylori develops an ulcer. Thus, this claim of "causation" appears to violate the scientific method. A recent experimental study shows what is really going on in this "disease," and guess what? Arachidonic acid metabolites appear to be what causes the "disease:"

"Our findings are the first to demonstrate that the detrimental consequences of H. pylori LPS on gastric mucin synthesis involve ERK-dependent cPLA2 activation that leads to up-regulation in PAF generation and ET-1 production..."

Source: IUBMB Life. 2006 Apr;58(4):217-23.

As in other "diseases," a stressor compels cells to release AA, which is made into particular molecules (such as LTB4), which cause some bacteria to become "clingly," prompting the body to attack it with molecules (such as TNF-alpha) that do terrible damage if cells are chronically exposed to it, and leading to what people perceive as "disease."

For more on this, see the essay, "The AA connection to today's common 'diseases.'" Now here is something recent that makes some important points:

"Just as immune cells recognize and attack foreign invaders in the human body to protect against harmful infections, single-cell organisms have a protein called H-NS that recognizes foreign DNA and prevents it from becoming active, the researchers discovered. But bacteria can also benefit from foreign DNA. When Salmonella is infecting an animal or person, for instance, many proteins the bacteria need to cause disease are encoded by DNA acquired from other bacteria. The researchers found that when the bacteria is infecting a host, other molecules can compete with the H-NS protein, allowing the disease-causing genes to be expressed. When the bacteria are in the environment, H-NS turns these genes off to avoid detrimental consequences if all the disease-causing genes were to be expressed at once. These findings give scientists new insight into how bacteria can protect themselves from an invasion by foreign DNA, yet still take in genetic information from diverse sources that makes them more virulent. 'By harnessing foreign DNA, bacteria that cause typhoid, dysentery, cholera and plague have evolved from harmless organisms into feared pathogens...'"

Source: http://www.sciencedaily.com/releases/2006/06/060608225847.htm

Note how it is mentioned that certain proteins and also biochemical activity are needed for "disease" to occur (meaning that a damaging inflammatory response will be provoked). My argument is that the evidence, when viewed as a whole, suggests that there is a "ramping up" of "the war" between the "immune system" and the "pathogens" that is not necessary and that does the person more harm than good. The proper diet and lifestyle can largely prevent this from occurring (in almost all practical situations).

And here is something very interesting about multiple sclerosis:

QUOTE: It may sound like a case of blame the victim, but researchers at Washington University School of Medicine in St. Louis have shown that cells in the central nervous system can sometimes send out signals that invite hostile immune system attacks. In mice the researchers studied, this invitation resulted in damage to the protective covering of nerves, causing a disease resembling multiple sclerosis.

Eliminating a molecular beacon can help protect a neuron (shown here) from destructive immune system cells. (Image courtesy of Washington University School of Medicine)Ads by Google Advertise on this site

"It's been clear for quite a while that our own lymphocytes (white blood cells) have the ability to enter the central nervous system and react with the cells there," says John Russell, Ph.D., professor of molecular biology and pharmacology. "Under normal circumstances, the brain and the immune system cooperate to keep out those cells that might harm the brain. But in people with multiple sclerosis, they get in."

The researchers found that they could prevent destructive immune cells from entering nervous system tissue by eliminating a molecular switch that sends "come here" messages to immune cells. Ordinarily, flipping that switch would cause immune cells to rush to the vicinity of the cells that sent the signals and destroy whatever they consider a danger �?including nerve cell coatings.

But in the mice in which the switch was removed, the researchers saw that immune cells previously primed by the scientists to attack the central nervous system (CNS) did not enter the CNS, and the mice stayed healthy. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/06/060616125632.htm

So once again we see that a terrible "disease" is caused by the body attacking itself because of some cellular-level stressor. If you read the other essays, you know that just through diet alone this "attack" might be prevented, with no inhibition to the "immune system." The evidence is now clear - none of these ideas originate with me. Every day, it seems, the evidence, which is consistent down to the molecular level, mounts, for example:

"Hepatocellular carcinoma (HCC), the most common form of liver cancer, is the third leading cause of cancer deaths worldwide. Its major risk factors are persistent infection with hepatitis B and C viruses, and exposure to toxic chemicals, including alcohol, all of which cause chronic liver injury and inflammation... 'Since inflammation drives both damage and regeneration in liver tissue, it is the repeating cycle of damage, inflammation and regeneration that leads to liver cancer,' said [Michael] Karin."

Source: http://www.sciencedaily.com/releases/2006/06/060623001538.htm

I would just add that excess polyunsaturated fatty acids in the diet have the potential to be toxic in the same way, as is clear from the literature. Here's a less technical explanation:

"...when highly unsaturated vegetable oils are heated at frying temperature (365 F) for extended periods--or even for half an hour--a highly toxic compound, HNE (4-hydroxy-trans-2-nonenal) forms in the oil... Csallany's work underscores the risk of repeated heating, or reusing, highly unsaturated oils for frying because HNE accumulates with each heating cycle. In future studies, Csallany and her colleagues plan to determine how long polyunsaturated oil must be heated at lower temperatures in order to form HNE and its related compounds."

Source: http://www.medicalnewstoday.com/medicalnews.php?newsid=23733