Because “germ theory�?assumptions are so central to the many recent failures (both to cure and predict) of the biomedical establishment over the last few decades, I will post new information about why the “germ theory�?is not correct, though in the certain situations uncommon during most of human evolutionary history, it undeniably can appear to be correct. That is, if everyone, or the vast majority of a society’s population is engaging in activities that cause certain bacteria to become “pathogenic�?then the use of toxic “medicines�?may seem to be a godsend (though they may cause some of the symptoms of the “disease,�?not to mention long-term adverse effects). Of course, most “experts�?blame the bacteria, as if they were the direct and sole cause, instead of blaming themselves for not emphasizing exactly how “bugs�?cause “disease.�

As I have pointed out in some of the other essays here, the "bugs" basically act according to conditions, that is, some become "pathogenic" when there is too much stress present (often oxidative). Under such circumstances, they become "clingy" and prompt an inflammatory response. If the stress is continual, the clinging continues, and the inflammatory response does serious damage (and fatty acids in your body seem to play a major role at this point, in terms of keeping the dangerous inflammation going longer than it should). In the case of viruses, the case is even weaker, and claims made by various "experts" are contradictory (or absent), as I've demonstrated in some of the other essays.

First, below, I will quote from the book, “The Secret Life of Germs,�?by Philip M. Tierno.

Page 15: “An apparently spotless glass at the bar in an exclusive Upper East Side hotel was actually spotted, invisibly, with group D strep, another of the many germs passed in feces; no doubt, a bartender or busboy handled the glass improperly. Pseudomonas aeruginosa, a common environmental organism which can produce a whopping eye infection, thrived on a nail dryer at an exclusive beauty salon and in the shower at a fashionable sports club. The sports-club shower also contained Klebiesella penumoniae; as its name indicates, this germ, which is found naturally in the human intestine, can cause pneumonia if it manages to get into the lungs. Finally, among other germ-ridden locales, consider a public phone at Madison Avenue and Seventy-first Street. Lingering on the handset were S. aureus and beta-hemolytic strep group A, a flesh-eating bacterium. These are the sorts of germs we run into every day�?if enough of them get into the wrong part of the body, serious illness, even death, can result. For example, if S. aureus infects an open sore or cut and goes untreated, it could lead to a minor infection or possibly to something as potentially lethal as toxic shock syndrome�?Fortunately, people with healthy immune systems usually beat off most germs pretty easily, including some of the nastier ones.�

The only thing to add here is that it is often the “inflammatory�?response that does damage; the minor cellular-level damage that some “bugs�?do can be repaired promptly. A quick and potent inflammatory response is what is needed, but due to the cellular-level stress people subject themselves to on a regular basis (such as from foods that act as oxidizing agents), the "bugs" get "clingy," and then, duet to the fatty acids in the cells in many people these days, the inflammatory response is too potent. I will post more interesting quotations from this book, including ones that do discuss the role of the inflammatory response, in the near future.

Page 40: “At least two billion people around the world harbor the toxoplasmosis parasite; most don’t know they have it and will never be troubled by it. Almost one hundred percent of the French population, for example, has contracted taxoplasmosis…�

In general, the reason Americans in particular have seen so much “disease�?is because they are engaged in activities that prompt powerful inflammatory responses to various “pathogen�?that have caused few problems in other populations, and at other times in history.

Page 41: “…there is often a fine line between mutualism and parasitism. For example, the bacterium Streptococus pneumoniae can give people pneumonia if it gets a foothold in their lungs. Yet the same germ resides benignly, elsewhere in the respiratory tract, in fifteen percent of the population�?Another good example is Staphylococcus aureus, a mutualistic component of most people’s normal skin flora. But if S. aureus gets into an open wound site, as can happen to patients after surgery, an infectious illness could occur and the germ would then become parastic…�

If you’ve read the other essays, you know that what happens is that the “germ�?prompts and inflammatory response, which then does the real damage, so calling it a “parasite�?needs to be clarified. It may indeed become “clingly,�?but it is just trying to survive. Under less stressful conditions, it lives inside a person without becoming clingly and prompting an inflammatory response, but when your body is subjected to certain kinds and amounts of stress, the “germ�?can become clingly, resulting in what we perceive as “disease.�

Page 140: “…scientists have discovered that animals may develop a subclinical form of prion disease [such as “Mad Cow disease”]. Although they carry lethal levels of prions in their brains, they have no symptoms. Yet prions from their bodies can produce a lethal form of the disease in other animals.�

Again, the only reasonable explanation is an inflammatory response to something perceived as a threat. I would also point out that calling something a “disease�?when no symptoms are present makes little sense, and obfuscates more than it illuminates an attempt to understand the basic mechanisms involved.

Page 204: “The immune system detects the presence of [H. pylori] and repeatedly sends T cells to wipe them out, but the T cells are stymied by the mucous coating and they accumulate futilely on one side of it, along with other immune-system cells. Eventually, they die, spilling their cell killing contents onto the stomach lining instead of H. pylori and initiating an inflammatory process�?The inflammatory immune response and the growth of H. pylori reinforce each other�?which can lead to the formation of ulcers.�

Page 214: “Quantitative changes in the gut flora can often trigger an inflammatory process�?a person may pick up a toxin-producing strain of a germ that is usually beneficial, like Shingella-bearing E. coli 0157:H7. In this connection, immunological responses may also have an impact."

Page 218: “…in people infected with Coxsackie virus, the immune system can send antibodies that will attack both the virus and the pancreatic cells it resembles.�

And as I’ve pointed out in some of the other essays, the fatty acids most Americans now have in their cells can make the situation much worse.

Below are passages from a recent sciencedaily.com report:

“Probiotics can help prevent and treat disease through a number of mechanisms. One way is by interacting directly with the disease-causing microbes, making it harder for them to cause disease... ‘Exposure to commensal organisms is necessary for the appropriate development of both the innate and acquired immune systems. Once established, probiotic organisms interact with these immune defenses, possibly changing the nature of the immune response to other antigens, including commensal and pathogenic organisms…’�

Source: http://www.sciencedaily.com/releases/2006/06/060610225845.htm

Note the vague language of the reporter �?this is why it is difficult to understand exactly what is occurring. I found that when I began to ask this question, and also tried to visualize the molecular-level situation, it helped a great deal. In any case, when it is said that “probiotic�?bacteria make things more difficult for “pathogenic�?bacteria, this likely means that the “bad bugs�?can’t become “clingy�?because the probiotic bacteria basically beat them to it. The probiotic bacteria, however, does not prompt an inflammatory response, and this is what is implied when the author states that the probiotic bacteria may change the nature of the immune response. The point is that “germs�?do no cause “disease;�?it is always contextual and contingent upon several factors, as would be the virulence, duration, etc., of the “disease,�?should what we perceive as disease result.

Note that many "experts" have suggested that a bacteria or virus is the cause of the "heart disease epidemic," and some still do, even though the molecular-level cause is now known. While "pathogens" may "take advantage" of damage in the body, they rarely, if ever, do much damage directly, and one also has to take into account how humans are trying to do things that have never been done before by other species, such as to have millions living in close quarters and subjected to powerful stressors, such as pesticides and estrogenic substances, on a continual basis.

Studies such as the following demonstrate what the scientific reality is regarding common "diseases," because they focus on molecular-level events:

Free Radic Biol Med. 2002 Jan 1;32(1):38-45.

Lipid peroxidation contributes to immune reactions associated with alcoholic liver disease.

Mottaran E, Stewart SF, Rolla R, Vay D, Cipriani V, Moretti M, Vidali M, Sartori M, Rigamonti C, Day CP, Albano E.

Increasing evidence indicates the involvement of immune reactions in the pathogenesis of alcoholic liver disease. We have investigated whether ethanol-induced oxidative stress might contribute to immune response in alcoholics. Antibodies against human serum albumin modified by reaction with malondialdehyde (MDA), 4-hydroxynonenal (HNE), 2-hexenal, acrolein, methylglyoxal, and oxidized arachidonic and linoleic acids were measured by ELISA in 78 patients with alcoholic cirrhosis and/or hepatitis, 50 patients with nonalcoholic cirrhosis, 23 heavy drinkers with fatty liver, and 80 controls. Titers of IgG-recognizing epitopes derived from MDA, HNE, and oxidized fatty acids were significantly higher in alcoholic as compared to nonalcoholic cirrhotics or healthy controls. No differences were instead observed in the titers of IgG-recognizing acrolein-, 2-hexenal-, and methylglyoxal-modified albumin. Alcoholics showing high IgG titers to one adduct tended to have high titers to all the others. However, competition experiments showed that the antigens recognized were structurally unrelated. Anti-MDA and anti-HNE antibodies were significantly higher in cirrhotics with more severe disease as well as in heavy drinkers with cirrhosis or extensive fibrosis than in those with fatty liver only. We conclude that antigens derived from lipid peroxidation contribute to the development of immune responses associated with alcoholic liver disease.

The above study is excellent, in that it shows how stress and too much polyunsaturated fatty acid content in your diet can lead to the body essentially destroying itself. This mechanism also seems to be the cause of at least many "AIDS" cases. In stark contrast:

"The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known..."

Source: Hepatology. 2005 Sep;42(3):568-77.

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice.

You M, Considine RV, Leone TC, Kelly DP, Crabb DW.

And:

"Rats fed a saturated fat diet are protected from experimentally induced alcoholic liver disease... Increases in dietary saturated fat increased liver membrane resistance to oxidative stress..."

Source: J Nutr. 2004 Apr;134(4):904-12.

Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition.

Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.

And here is something that ties everything together nicely:

"Bacteria and parasites often use special toxins to perforate the membranes of target cells. These pore-forming toxins are a key weapon in the attack arsenal of some common and virulent bacteria, such as Staphylococcus aureus, well-known for its role in hospital-acquired infections, Streptococcus pneumonie, responsible for middle ear infections and pneumonia, and Helicobacter pylori, implicated in ulcers. Pore-forming toxins compose about a quarter of all known protein toxins that increase the infectivity and severity of bacterial diseases.

Once the toxin perforates the host membrane, ions begin to leak out of the cell. Sensing a drop in its potassium concentration, the cell reacts by forming a multi-protein complex known as an inflammasome. Scientists know that inflammasomes act like a sort of roving security force inside the cell, detecting a variety of danger signals such as bacterial RNA or bits of bacterial flagellin. The inflammasomes join together and activate a protein, caspase-1, that in turn triggers an inflammatory response."

Most likely, the cell would be much more resistant to various "germs" if there were significantly less unsaturated fatty acids at the cell surface. Simple experiments could determine this.

Source: http://www.sciencedaily.com/releases/2006/09/060922093757.htm