This is a page that I will be working on for a while. Basically, there are some quotations from reports or studies that show how most "experts" are "barking up the wrong tree," finding "germs" where the underlying cause is one or more known stressors. In the case of Hep C., for example, whether or not a "germ" is actually present appears to be beside the point; what determines whether illness manifests itself is the amount and kinds of stress (and also things that keep stress under control, such as antioxidants). The report about a possible connection between "prion disease" and "heart disease" is evidence that some scientists don't realize that they are mistaking effect for cause; damaged proteins will likely be found in all kinds of "diseases," but again, the stressors caused that damage, and the proteins are just an effect, not a cause.

While working at her clinic at the military hospital, Sjogren noted that at least half of her patients tested positive for the hepatitis C virus. She then started wondering about how servicemembers were faring with treatments and how the disease affected the quality of their lives. From the start, Sjogren wanted to answer specific questions for servicemembers who have Hepatitis C: What happens to these people over time? How does it affect their quality of life? What happens when you treat them? "We just don't know what the impact of hepatitis C is. The rate of hepatitis C has been studied in the military but not the outcomes," she said. "Nobody has talked to them as a research population ... and captured the story the way we do." Sjogren's research endeavors were funded by a grant from the DoD's Peer Reviewed Medical Research Program. Congress created the program in 1999 to promote research in health issues the military faces. Since its inception through 2005, the program has spent almost $300 million to fund nearly 200 projects in a range of medical topics, including combat casualty care and technology and infectious disease research like Sjogren's. Once members from any of the military services were diagnosed as positive for the hepatitis C virus, their doctors told them about Sjogren's study so they could learn more about joining it. If they decided to participate, Sjogren's team performed a liver biopsy, if one hadn't already been done, to see how advanced the disease was. At the end of four years, a second biopsy was taken. "It's the only way to establish the progression of the disease," Sjogren said. Her patients, ranging in age from 18 to the upper 50s, mostly come from the Northeast because of its proximity to Walter Reed. Thirty percent of the study volunteers had minimal liver disease, Sjogren said. Of the 70 percent with more advanced liver disease, 15 to 20 percent had cirrhosis, a condition in which scar tissue replaces healthy tissue, blocking the flow of blood through the organ and preventing it from working as it should. Cirrhosis is the twelfth leading cause of death by disease, killing about 26,000 people each year, according to The National Digestive Diseases Information Clearinghouse Web site. Sjogren's clinic provided treatment to "just about everybody unless they have very minimal disease or liver damage," she said. "We may not offer them treatment because chances are that person's disease may not progress." The standard treatment--24 to 48 weeks of a once-a-week injection with interferon and several pills of ribavirin each day--are what Sjogren speculated would cause a decrease in quality of the volunteers' lives. "The medications are tough to take," she said. On initial questionnaires, study volunteers reported that they were depressed; anxious about their health, families, and careers; and having trouble sleeping. Once treatment began, however, they reported that their quality of life had improved. "We've been very surprised. When we asked the patients why (they felt better), they said, 'I'm doing something for my infection,'" Sjogren said. Another factor that may have calmed study volunteers is the patient education Sjogren's staff offers. "Sometimes they don't fully understand hepatitis C, and the patients are very anxious. They think they have HIV or something that's going to kill them overnight," she said. "We like to talk to the patient and put them at ease, and say 'Look this is the story, let's work together.'"

http://www.sciencedaily.com/releases/2006/07/060707152257.htm

These findings raise the possibility that heart infection could be a new aspect of prion diseases, including those that affect humans and livestock, and that these diseases could travel through the blood�?"Until now, prion disease has been thought of as a chronic neurological condition," says Scripps Research Professor Michael B. Oldstone, M.D., who led the research. "Our study has shown, however, that it can have other manifestations, therefore expanding the types of conditions it could cause."

http://www.sciencedaily.com/releases/2006/07/060707151953.htm

A new study shows that statins, which are typically used as anti-cholesterol medications, can inhibit the replication of the hepatitis C virus (HCV). They could replace ribavirin in combination therapy with interferon. These findings are published in the July 2006 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD), published by John Wiley & Sons, Inc. Currently, 170 million people worldwide are infected with HCV. The standard treatment is a combination therapy of interferon and ribavirin, which is only effective in about 55 percent of patients. The remaining 45 percent face a threat of the disease progressing to cirrhosis and liver cancer. Based on recent reports that one statin, lovastatin, inhibits HCV replication, researchers led by Masanori Ikeda of Okayama University in Japan, tested other statins in search of a more effective anti-HCV therapy. Using the OR6 cell culture assay system, they evaluated the anti-HCV activities of five statins: atorvastatin, fluvastatin, lovastatin, pravastatin and simvastatin. When the statins were tested alone, all except pravastatin inhibited HCV replication. Fluvastatin had the strongest effect. Atorvastatin and simvastatin had moderate effects while lovastatin had a weak effect. While pravastatin exhibited no anti-HCV activity, it did work as an inhibitor for HMG-CoA reductase, suggesting that the anti-HCV activities of the other stains are not due to the direct inhibition of HMG-CoA. The researchers determined that the anti-HCV activities of statins were not related to cytotoxicity, meaning they did not kill the host cell. Additional experiments also suggested that, "the statins possess the ability to inhibit the replication of HCV RNA via a specific antiviral mechanism," the authors report. The researchers tested the theory that certain proteins are required for HCV RNA replication and that statins block the replication by inhibiting those proteins. In support of this theory, they found that the addition of both mevalonate and geranylgeraniol restored HCV RNA replication in the statin-treated cells. To evaluate statins as potential replacements for ribavirin in combination therapy, the researchers tested the anti-HCV activities of each one when combined with interferon. Each combination, except the one including pravastatin, had even stronger inhibitory effects on HCV RNA replication than when the statin was used alone. Again, fluvastatin plus interferon exhibited the strongest effect. "We clearly demonstrated that co-treatment of interferon and fluvastatin was an overwhelmingly effective treatment," the authors report. This combined therapy was more effective against HCV RNA replication than interferon alone and more effective than the standard combination therapy of interferon and ribavirin.

http://www.sciencedaily.com/releases/2006/07/060709125024.htm

Circulation Journal. 2005 Apr;69(4):475-80. Title: Fluvastatin ameliorates the hyperhomocysteinemia-induced endothelial dysfunction: the antioxidative properties of fluvastatin.

…CONCLUSIONS: Hyperhomocysteinemia, even mild to moderate, induces endothelial dysfunction through its oxidative effect. The antioxidant fluvastatin was able to cancel out the oxidative stress induced by hyperhomocysteinemia and ameliorate endothelial dysfunction.

Here is a recent report that shows how a virus actually does cause "disease."

Viral disease outbreak in Mauritius PORT LOUIS, Mauritius, July 15 [2006] (UPI) -- A rare mosquito-borne virus has killed at least 77 people on Mauritius and other Indian Ocean Islands this year.

The chikungunya virus causes fever, joint pain and other symptoms, the Times of London reported. Some tourists have been infected along with local inhabitants.

Most of the dead were elderly.

The outbreak was reported in The Lancet after researchers at the University of Lausanne reported finding the virus in a woman who had recently returned from Mauritius.

The disease usually makes itself felt within four to seven days after a person is bitten by an infected mosquito. About 12 percent of people with the infection continue to experience joint pain for at least three years.

The outbreak peaked in the first three months of the year, although health officials advise tourists in the area to take precautions against mosquito bites.

Copyright 2006 by United Press International. All Rights Reserved.

Note that the most of the deaths were among the elderly, and that the symptoms occurred within days, and are characteristic of a pronounced inflammatory response. In fact, many victims continued to have these symptoms for years, due to this "autoimmune" problem. Whether or not the diet of the people was a major factor was apparently not explored, as one would guess (after reading many such reports and studies). There was no direct cytopathic effect here, and this "deadly" virus killed a tiny percentage of the population that was exposed to it - the very weak in particular - just as evolutionary theory would predict. I would like to see one piece of evidence that demonstrates a direct cytopathic effect by any "germ" in a healthy, non-"geriatric," adult human. I have yet to find any. Please post the evidence of this in the general message board forum if you can find any. What is interesting is how "HIV/AIDS" is also said to be viral, and yet in this "condition," one can be asymptomatic for years, then all of a sudden one or more of several very different disorders might afflict you, and it does not matter how healthy you are. In a sense, "HIV/AIDS" is a charicature of a realistic understanding of how "germs" cause "infectious disease." In fact, what can do direct cytopathic damage to a tissue or organ are the kinds of drugs being given to the "HIV infected," which explains why so many of them now die of liver failure. At this point, the only interesting question to me is, will future historians regard the "virus hunters" of today in more or less the same light as the witch hunters of several hundred years ago?

Ane here's a report today about how molecules in cranberry juice prevent "infectious bacteria" from becoming a problem, by preventing the bacteria from becoming "clingly" (as one scientist phrased it):

QUOTE: Compounds in cranberry juice have the ability to change E. coli bacteria, a class of microorganisms responsible for a host of human illnesses (everything from kidney infections to gastroenteritis to tooth decay), in ways that render them unable to initiate an infection... The new results build on previously published work, in which Camesano and her team showed that cranberry juice causes tiny tendrils (known as fimbriae) on the surface of the type of E. coli bacteria responsible for the most serious types of UTIs to become compressed. Since the fimbriae make it possible for the bacteria to bind tightly to the lining of the urinary tract, the change in shape greatly reduces the ability of the bacteria to stay put long enough to initiate an infection. UNQUOTE.

Source: http://www.sciencedaily.com/releases/2006/09/060910142246.htm

And here's another good passage from a recent report:

"Bacteria use chemical signals to initiate the majority of human infections. When these signals reach a certain threshold (in a process known as quorum sensing), pathogenic bacteria will change their mode of growth and produce virulence factors that lead to infection. These chemical signals also trigger the bacteria to produce slimy biofilms that cloak the bacteria and make the colony physically resistant to antibiotics."

Source: http://www.sciencedaily.com/releases/2006/09/060911103419.htm