Have you ever wondered why so few “experts�?and “journalists�?ask how it could be that something that is supposed to be “scientific�?fails over and over again? How many predictions have you heard about “outbreaks of infectious disease�?that never come to pass? How many “flu pandemics�?have been predicted in the last few decades? And let's not forget the "Mad Cow Disease" scare a few years back, which frightened many people I know. What about the massive death from “infectious diseases�?in the wake of the tsunami disaster and Hurricane Katrina that were predicted and never occurred? On the other hand, it is estimated that each year 90,000 hospital patients die of infections they acquired while in this supposedly “antiseptic�?environment in the USA alone. Something is very wrong here, and when something is this wrong, it is usually because the underlying assumptions are not accurate. Fortunately, some have investigated why the predominant notions about the “immune system�?and “inflammation�?do not seem to work in the “real world�?the way it is said that they operate in models presented in the major textbooks.

Nobody really knows what the “immune system�?is. New molecules and processes are being “discovered�?all the time, and basically what is known is based upon observations (often made under specific, “un-natural�?conditions) and assumptions derived from untested or partially tested models. What we do know is that it developed via evolutionary processes, but not that it was designed to be a “system,�?so it is important not to take anything for granted, or to assume that a “promising marker�?that was found upon preliminary investigations should be reified into textbook dogma (unfortunately, this situation is all too common in recent years). Because of the many problems with existing notions about the “immune system,�?some scientists have reevaluated the textbook notions, and today there is Matzinger’s “Danger Model�?and Cuniliffe’s “Morphotstatic�?one. Cunliffe’s is more “radical,�?but also more consistent with the notion that an inflammatory response that is too strong is very dangerous. Below, I will present a few passages from Cunliffe’s web site, along with my comments in brackets (the specific page is http://www.morphostasis.org.uk/Papers/Phlog199803.htm). After this, I will discuss a recent report which provides a common example of how this works in practice.

Here is Cunliffe’s view:

A morphostatic system works in a different way. "Ooopppss! Something's making a tissue mess. Better go tidy up the mess and fix any losses. While we're about it we'll take a snapshot of this mess. We'll remember the most unusual signature of it. Then, if we meet a similar mess in the future, we'll ramp up the accumulation of mess eaters and make these act more aggressively when they get there."�?

It is almost a scorched earth (scorched extracellular space) policy that sequesters away nutrients and metabolites from potential invaders. Invaders must dedicate genetic resources to ensuring the generation of supplies and other metabolites - or, alternatively, get themselves invited into the host's cells where there are more accessible resources. These conditions are, naturally, proinflammatory for phagocytes and APCs so the invading organisms are obliged to be proinflammatory (pathogenic) themselves.

[This does not need to be the case, but it is usually the case for those with AAOS (arachidonic acid overload syndrome). With Mead acid in the place of AA, “pathogens�?come in, find the environment to be rather placid (since cells are packed with saturated fatty acids and non-oxidized cholesterol) and do little reproducing and little harm. Some “pathogens,�?in fact, only become dangerous to people when they are placed under enormous stress, such as when bacteria often found in peoples�?GI tracts is exposed to the stresses of surgery. This is a major reason for the hospital deaths from normally benign bacteria. With “flu outbreaks�?of the common variety, people who are either not healthy or who are enduring a great deal of biochemical activity, for example, if they are doing manual labor for many hours a day, act as incubators because the “pathogen�?has the resources under these circumstances to adapt to the “immune system.�? They are still only deadly for a small number of people, however, and a personal story is illuminating in this context. Up until the time I decided to rid my body of AA, I used to experience at least two “colds�?a year, on average, and the symptoms were usually very uncomfortable and lasted for at least two weeks. Once I began avoiding dietary PUFAs, it took a few years before I “caught�?something at a family gathering. One relative was very ill for several days with pain in the throat and other nasty symptoms, and had to try two different antibiotics, then she developed another infection, while another relative was told by his doctor that he had “strep throat�?and was also prescribed antibiotics. I had a mildly uncomfortable sensation in my throat for several hours one day, then felt a bit tired the next, but there was little else �?a few sneezes and a bit of nose blowing over the course of a couple of days. What was the difference? They experienced a stronger inflammatory response than I did, which everyone agrees will occur with Mead acid instead of AA in one’s cells, but they also had problems containing the infection, while my body appears to have had no problem coming to some sort of “settlement�?with the “pathogen.�? Thus, without AA in your body, you basically have a different “immune system.”]

So, microbes have two distinct influences when encountered by phagocytes (including antigen presenting cells like dendritic cells). First they have features characteristic of microbes (in general) and the phagocyte remembers these, from its evolutionary roots, as potential food: an encounter with them up-regulates the phagocyte's activity (probably, in part, by TLRs). Second, microbes have mechanisms to generate extracellular debris (and this equates to pathogenicity). Little wonder, then, that a macerated wound (from a physical pathogen like, for example, excessive heat) is a breading haven for microbes.

Cells that die suddenly in trauma (e.g. heart attacks, burns) have not been preparing for apoptosis. Cells that die of viral infections or other intracellular nasties have probably moved somewhere along the path towards apoptosis. This means that cells that die by trauma do not spill much Il-1 whereas infected cells do. Spilt Il-1 is a strong contender to be one of the danger signals (eicosanoids, which are released after membrane perturbations, are another). Nevertheless, Dressler's syndrome is the occasional autoimmune sequel to a heart attack - so trauma does increase the risk of autoimmunity. Similarly, in burns and major trauma, autoimmune activity is easy to demonstrate. Indeed, it is the probable precipitant of the phagocytic anergy that precedes multiple organ failure. Any system that allows auto-rejection of normal cells must sport a failsafe cut off device to inhibit the piecemeal destruction of self (6).

[Another key point is contained here: since AA metabolites/eicosanoids are very strong in comparison to Mead acid metabolites/eicosanoids, “danger signals�?will have to be quite a bit of “danger�?for such signals to occur in a person who has Mead acid in place of AA, whereas the AAOS person’s “immune system�?will experience these danger signals in situations where there really is little, if any danger. And there is a price to be paid for these unnecessary danger signals; first, an inflammatory response that has self-destructive qualities, perhaps to the point of “autoimmune disease,�?and in some people, T-cell anergy and “AIDS�?like conditions.]

· Th1 cells evolve as an elaboration of the Tc cell system. Now, the cellular and cytoplasmic debris of leaking cells can be digested by APCs and then processed so that representative peptides can be presented on the APC's surface. Apoptosis of these APCs will favour tolerance to ClassII+peptide epitopes. But, when these APCs fail to contain the problem and start to rupture, Th1 aggression will be favoured. On any future encounter with a similarly caricatured APC (not of the pathogen nor of its native antigen), the inflammatory response can be quickly ramped up - bringing in copious aggressive phagocytes and Tnk cells. This is designed to give inflammation a memory. The newly immigrant phagocytes still have to sort healthy-self-cells from the rest but they are now stirred up into a frenzy of eagerness to get on with this job.

· Since extensive tissue destruction is undesirable, phagocytes must be inhibited when the Th1 cell amplification process becomes too intense. Phagocyte activity is consequently inhibited (as, e.g. in a boil) and this increases the amount of debris left to be cleaned up; the IgM free antibody system arose to act as a debris mop. (Macrophage derived cells (B-cells) have an immunoglulin receptor that internalises only targeted debris and processes this into peptide+ClassII epitopes. (Then, when a suitable CD4 T-cell receptor encounters this epitope, it triggers the respective B-cell to produce a sea of free IgM.) B-cells (cells that evolve from the macrophage line) have an immunoglulin receptor that internalises only targeted debris and processes this into peptide+ClassII epitopes. Then, when a suitable CD4 T-cell receptor encounters this epitope, it triggers the respective B-cell to differentiate into a plasma cell that then secretes free IgM. This then tags the debris and enhances its clearance. So, progression to Th2 activity is most likely to occur when cell-mediated auto-rejection is inhibited in the interests of inhibiting piecemeal self-destruction. But this inhibits the clean disposal of mess. The release of IgM is an attempt to compensate for this. All the other immunoglobulins have evolved as shells that envelop IgM (e.g. IgG, IgA, IgE).

[This kind of tissue destruction is what the “HIV�?protein band test detects. IgM tries to deal with the cellular “mess,�?but at some point this fails too, and then comes the anergy and “full-blown AIDS.�? Molecules like TNF-alpha and AA metabolites do great damage to cells, tissues, and organs, so cellular debris continues to accumulate (and tangential “syndromes�?develop, such as “AIDS dementia).�? At some point the body is so devastated that TNF-alpha and/or AA metabolites may begin to be generated in much smaller amounts, and this may be the “point of no return,�?when death in the near future is a certainty. Note that other effects of this process can be insufficient stomach acid and digestive enzyme production, which would cause an “AIDS wasting syndrome,�?along with multiple physiological failures. Without the ability to digest protein especially, thyroid hormone, for example, is going to be produced in insufficient quantities, leading to fatigue, etc.]

And now for the report I mentioned in the second paragraph:

"'Sepsis represents a patient's response to severe infection,' explains senior author William C. Aird, MD, Chief of the Division of Molecular Medicine and Associate Director of the Center for Vascular Biology at BIDMC. 'We know that antibiotics will take care of the primary infection, but 30 percent of patients with severe sepsis will die in spite of successful antibiotic therapy because the body's host response is out of control and turns on its bearer. Sepsis develops when the immune system becomes overactivated in response to an existing infection, setting in motion a cascade of dangerous inflammatory and coagulation responses throughout the body. A leading cause of organ failure and intensive care unit (ICU) hospitalizations, severe sepsis accounts for 200,000 deaths...'"

So the question is, why is there such an "out of control" response? "Experts" who recently examined records written by surgeons a couple of hundred years ago were surprised that these kinds of problems were very rare, with most people recovering from amputations of limbs with no such "out of control" response. Animals experiments have shown that if the animal is fed coconut oil, there is no such "out of control" response, but once again, we are dealing with the problem that comes with the extreme specialization that characterizes today's biomedical establishment.

Source for the passage above: http://www.sciencedaily.com/releases/2006/05/060519152635.htm

As the scientific literature on "viruses" makes clear, viruses can prompt a powerful inflammatory/"immune system" response, which in turn can do the actual damage, and which can also make the body susceptible to various "pathogens" that are not normally problematic. There is really no debate on this subject, though some "experts" seem to be blissfully unaware of it (and these people might be best be referred to as crude germ theory adherents). A "retrovirus" is not something that can do this (except perhaps when cells are subjected to un-natural laboratory conditions), but instead is activated by it (if one believes this phenomenon should be termed a "virus"). It may be that "retroviruses" evolved into "real viruses" (that is, agents capable of "infecting" cells), but the point is that in light of what is known, real damage cannot be done by a "retrovirus" to a person who is in good health - there is no known, nor plausible explanation for such a claim. The entire concept is illogical, because "retroviral" phenomenona is found in cells that are under great stresses, and while a person may appear healthy to others for a while, at some point the powerful stressors will cause what most people think of as "disease." Thus, the all-too-common mistake of concluding that effect was cause was made by many of the early "HIV/AIDS" investigators.

Not all of these investigators, however, have (consciously or otherwise) decided to accept the mainstream model of the "disease" and attempted to fit the evidence into the model, even when it is clearly contradictory. For example, one group's findings are consistent with Cunliffe's view:

"It is likely that suppression of cytotoxic T-lymphocyte function has evolved as a mechanism to control the immunopathological damage that can occur as a consequence of cytolytic killing by CD8+ T cells. For example, in the mouse model for hepatitis B infection CD8+ T cells exhibit virus control via gamma interferon and tumor necrosis factor alpha production without causing the liver tissue destruction that would result from active cytolysis (18). In human immunodeficiency virus infections, the down-regulation of perforin in virus-specific CD8+ T cells from gut-associated lymphoid tissue may be a mechanism to protect the integrity of the rectal mucosa from cytotoxic T-lymphocyte activity..."

Ironically, and sadly, the "medications" many "HIV/AIDS patients" are given result in just such damage - damage that the body possesses mechanisms to prevent in this situation.

Source: Journal of Virology, August 2005, p. 10619-10626, Vol. 79, No. 16

"CD8+ T-Cell Dysfunction due to Cytolytic Granule Deficiency in Persistent Friend Retrovirus Infection."

Gennadiy Zelinskyy,1 Shelly J. Robertson,2 Simone Schimmer,1 Ronald J. Messer,2 Kim J. Hasenkrug,2, and Ulf Dittmer1.