In the case of "mad cow" types of neurodegeneration, a damaged protein has been said to act as an infectious "germ" or sorts. If you have read the other essays, you can probably guess what my response is: it is certainly possible, but the inflammatory response to the proteins would be the cause of the damage, and inflammation can be attentuated, so that experiments should be done that control for possibly relevant factors that might render the "disease" negligible or non-existant. However, here are some facts that few people are aware of, which suggest that the supposedly dangerous prion proteins are an effect, not a cause. With this knowledge, it is obvious that those who have claimed that prions act as a sort of infectious agent have not followed the scientific method:

"High-manganese, low-copper environments can create prion diseases without the organophosphate catalyst, as seen in deer and elk herds in Colorado who eat manganese-rich pine needles."

Source: http://madcow.pamrotella.com/

QUOTE: Cambridge University prion biochemist, David R. Brown is dismissive of the science behind the infectious model of BSE. He terms it "a very limited amount of science by a few assumed -- reputable scientists." He insists there is "no evidence an infectious agent is present in either meat or milk." "Simple tests on udder walls of cows -- which could easily detect an infectious prion -- have not been done, why I don't understand."

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey. In December 1999, the same Dr. David Ray was appointed to the UK Veterinary Products Committee (VPC) -- a government body that licences animal medicines. Purdey has been consistently denied even exploratory funding to extend his privately supported research. Yet the Purdey chemical poisoning model matches with the epidemiological spread of CJD clusters in humans. It also predicts the incidence of BSE-type diseases in animals. The accepted infectious model fits neither. The question is rhetorical, and Purdey has an eye-opening answer. He argues that the prion molecule acts as a shock-adsorber of damaging energy from ultraviolet rays and other oxidizing agents. Once this prion defence system is rendered ineffective by organophosphates, these oxidizing effects have an unmediated impact on tissues.

UNQUOTE.

Source: http://www.cqs.com/opmadcow.htm

"Several US trials failed to invoke BSE in cattle after feeding or injecting them with massive doses of scrapie-contaminated brain tissue. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass-and-silage system without any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding."

Source: http://www.ourcivilisation.com/madcow/madcow.htm

And this comment by virologist Stefan Lanka suggests that the "deadliness" of a "germ," as demonstrated in a lab, may have little to do with the "germ:" QUOTE: These experiments have been used already since over 100 years back, in order to "prove" the existence of several "viruses" quite different from each other, for instance also that of the purported smallpox virus. In these experiments, extracts are being injected through the eggshell into the embryo. Depending on how much is injected and where in the embryo the supposedly "virus-infected" extract is injected, the embryo dies faster or more slowly. It would die from such injections in precisely the same manner too if the extracts were sterilized in ad- vance. This killing then is presented by those virologists, firstly, as direct proof of the existence of the respective virus, secondly as proof of the possibility of multiplying the virus, and thirdly and simultaneously as proof of the isolation of the virus. From hen embryos killed in this way, millions of which are dying silently each year at the vaccine manufacturers', various vaccine substances are being produced. Besides hen embryos, also cells are being killed in test-tubes in order to present the dying of these cells as proof of the existence, the multiplying and the isolation of a disease- causing virus. Nowhere however is a virus being isolated in this manner, photographed in an electron microscope and its component parts described in processes of the type called electrophoresis. UNQUOTE.

Source: http://www.gatago.com/misc/health/aids/2472802.html and: http://www.gnn.tv/A02138

The other thing you have likely heard about is that “defective genes�?cause various “diseases,�?but what you rarely hear is that oxidative stress (probably involving lipid peroxidation) and other stressors caused the genes to become defective in the first place, and thus the “disease�?is entirely preventable �?if one follows a correct diet and lifestyle. It is no mystery that so many “diseases�?have reached what we are told are “epidemic�?levels in recent years. The following is one of the few reports that includes a discussion of “inflammation�?and stressors along with the results that defective genes were detected:

Title: Genetic variation linked to age-related macular degeneration.

QUOTE: "...These data suggest that CFH Y402H [the gene in question] may be a causal factor in more than 50 percent of all AMD cases in the general population."

"Genetic predisposition to a malfunctioning CFH can only be of importance when the complement system is switched on," the authors write. "This is demonstrated by the significant interaction between chronic as well as acute inflammation and CFH Y402H."

"The effect of CFH is significantly influenced by environmental and genetic factors that determine the inflammatory response and activate the complement pathway." (JAMA. 2006;296:301-309. Available pre-embargo to the media at www.jamamedia.org). UNQUOTE.

Source: http://www.eurekalert.org/pub_releases/2006-07/jaaj-gvl071306.php

Note that this was a study of correlations, and not of direct molecular-level mechanisms. Here is a much better kind of study, discussing molecular-level mechanims, yet also presenting a comprehensive view of disease:

Eur Respir J. 2006 Jul;28(1):219-42.

Oxidative stress and redox regulation of lung inflammation in COPD.

Rahman I, Adcock IM.

Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (c-Jun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kappaB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kappaB-mediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kappaB-alpha kinase or the enhanced recruitment and activation of transcriptional co-activators. Enhanced NF-kappaB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression. Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity. The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/quercetin and reserveratol), specific spin traps, such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kappaB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells. Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.

Another group of researchers has reached similar conclusions: QUOTE: ...the research team studied what precedes inflammation - the injury of hepatocytes caused by toxic chemicals, which sets in motion the inflammation process....  We now understand development of liver cancer in mice. 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..." UNQUOTE.  Source: http://health.ucsd.edu/news/2006/06_21_Karin.htm.

And here's the latest point about free radical damage/oxidative stress being the root cause of "infectious disease:"

QUOTE: Dr. Howard Taylor Ricketts, who eventually died of typhus, identified rickettsia in the late 1800s. Sahni's research group first began investigating the rickettsia bacteria as a model to study the biological changes that occur in the lining of the blood vessels (endothelium) as the bacteria travels through the blood stream. Initially they were looking at what types of cellular changes occur in response to the infection. They discovered that cells undergo oxidative stress and produce harmful free radicals, causing inflammation and other complications.

Researchers hypothesized that antioxidants might serve as useful therapies after examining the damage to infected cells, as seen by electron microscopy, and through biochemical evidence proving oxidative stress (OS), a term used to describe a level of damage in cells, tissue and organs. Antioxidants can generally neutralize free radicals and reduce oxidative damage. Earlier experiments in which scientists infected cells with rickettsia bacteria and then treated the cells with alpha-lipoic acid, a powerful antioxidant, showed that the infected cells did, indeed, marshal a defense against the bacteria. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/08/060809232944.htm

And here's a study that supports the connection between "infectious diseases" and damage from free radicals:

J Am Coll Cardiol. 2006 Jun 20;47(12):2436-43. Oxidized low-density lipoprotein autoantibodies, chronic infections, and carotid atherosclerosis in a population-based study. Mayr, M., et al. OBJECTIVES: We investigated whether associations exist between immune reactions to oxidized low-density lipoproteins (OxLDLs), chronic infections, and carotid atherosclerosis as quantified by ultrasound. BACKGROUND: Atherosclerosis is a chronic immuno-inflammatory disease wherein both oxidized lipids and infectious agents are incriminated as possible contributors. METHODS: We measured immunoglobulin (Ig)G and IgM autoantibody titers to copper-oxidized-LDL and malondialdehyde-LDL (OxLDL-AB), IgG and IgM apolipoprotein B-100-immune complexes (ApoB-IC), and titers of antibodies to Escherichia coli and chlamydial lipopolysaccharide (LPS), mycobacterial heat shock protein 65 (mHSP65), Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus and evaluated their relationship to cardiovascular risk factors, chronic infections, and incident/progressive carotid atherosclerosis in the Bruneck study. RESULTS: The OxLDL-AB and ApoB-IC levels remained stable over time as indicated by strong correlations between 1995 and 2000 measurements (p < 0.001 each). Significant associations existed between all OxLDL markers and antibody titers to pathogens, especially to E. coli-LPS and mHSP65. Both OxLDL-AB and ApoB-IC levels showed a rise with increasing pathogen burden. Notably, OxLDL-ABs were also elevated in subjects with chronic infection as defined by clinical criteria. Titers of IgG, but not IgM, OxLDL-AB, or ApoB-IC inversely correlated with total cholesterol, LDL cholesterol, and apoB concentrations. The IgG OxLDL markers were positively and IgM markers were inversely associated with incident and progressive carotid atherosclerosis in univariate analyses but were not independent predictors in multivariate analyses. CONCLUSIONS: Our study provides evidence for an association between human oxLDL markers and chronic infections. Moreover, in this population-based study, neither IgG nor IgM OxLDL autoantibodies were independently predictive of atherosclerosis progression in the carotid arteries.

Though I've debunked several claims often seen in nutritional and biomedical textbooks (as have others before me), I think my most important "discovery" is that the "immune system" can only work optimally with Mead acid in your cells (rather than arachidonic acid or an omega 3 PUFA).  The reason is that with the Mead acid in your cells, if there is an insult that triggers the immune system, you will get a short burst of "inflammation," then it will recede and allow the humoral immune system (antibodies) to do its job.  With arachidonic acid in your cells, the inflammatory response will last too long, and may do tremendous damage.  If the inflammatory response with AA does become chronic, you run a great risk of having vital biomolecules getting damaged and becoming dysfunction or being attacked by the immune system become they now appear to be "foreign," due to modifcation by free radicals.  And if this continues, at a certain point the body will produce so many antibodies that everything appears foreing; it is then that the Th1 to Th2 shift occurs, leading to "AIDS" (the "opportunistic infections"), because the body needs to prevent self-destruction.  In some cases, this fails and "autoimmune diseases" occur instead.  With the fatty acids from fish oil in your cells, the situation appears to be even worse, which may be what led some "experts" to suggest that one needs to "balance" omega 3s and 6s.  It's not clear that this is possible, because when cells are stressed, one fatty acid must predominate, in terms of being metabolized into inflammatory molecules.  In any case, the Mead acid appears to be clearly the best choice in the microscopic "Goldie Locks" story.