Quote: "The results do not mean that high cholesterol, smoking, obesity and hypertension are not important factors in heart disease, said Dr. Paul Ridker of the Harvard Medical School. Rather, the findings add one more risk factor to the constellation of health problems that lead to heart attacks." (Scientists prove link in study. Bacteria infection tied to heart disease. By THOMAS H. MAUGH, Los Angeles Times. Friday, Feb. 26, 1999 Houston Chronicle 19A.)

In fact, the new evidence that Chlamydia pneumoniae proteins trigger cardiovascular damage via attack by the immune system does help demolish their claim that "smoking causes heart disease." They will probably lose it completely, as Helicobacter pylori did with ulcers and stomach cancer, and human papillomavirus did with cervical cancer.

They are lying to us when they pretend that infection could not be the root cause of their smoking claim in particular, which unlike the others has been accused of causing heart disease by way of inflammation.

They are lying to us when they continue to pretend that smoking is "a proven risk factor." All of their old evidence must be re-evaluated in light of the fact that it did not consider the effect of CP or other infections. Their "mountain of evidence" is now just a pile of landfill.

And, it demonstrates the anti-smoker capacity for self-deception that Ridker still clings to dogma, despite admitting that his own earlier study disproves it.

Earlier work by Ridker:

Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. NEJM 1997 Apr 3;336(14):973-979. Physicians Health Study 543 case + 543 controls. Effects of high levels of C-reactive protein same in smokers & non- smokers. P977 "Finally, there was no significant association for venous thromboembolism, suggesting that the relation of inflammation to vascular risk may be limited to the arterial circulation." [Remember my old article, "Cover up: Non-smoking is a risk for thromboembolism," 1993. The evidence shows that smokers are actually at less risk of venous thromboembolism than non-smokers, so whatever causes excess risk of heart disease is in the arterial circulation only.] P978 "The mechanism that relates the level of C-reactive protein to atherothrombosis is unclear.

Previous infection with Chlamydia pneumoniae, Helicobacter pylori, herpes simplex virus, or cytomegalovirus may be a source of the chronic inflammation detected by C-reactive protein. It is also possible that C-reactive protein is a surrogate for interleukin-6, a cellular cytokine associated with the recruitment of macrophages and monocytes into atherosclerotic plaques. In addition, C-reactive protein can induce monocytes to express tissue factor, a membrane glycoprotein important in initiating coagulation.

FINALLY, IT HAD BEEN HYPOTHESIZED THAT BRONCHIAL INFLAMMATION DUE TO SMOKING WAS RESPONSIBLE FOR ASSOCIATIONS SEEN IN PREVIOUS STUDIES RELATING C-REACTIVE PROTEIN TO VASCULAR RISK [Kuller 1996, in MRFIT]. IN THIS REGARD, OUR OBSERVATION THAT THE EFFECT OF C-REACTIVE PROTEIN IS PRESENT AMONG NONSMOKERS MAKES BRONCHIAL INFLAMMATION A LESS LIKELY MECHANISM." [emphasis added.] Greatest aspirin benefit with highest levels. [Funded by NIH & AHA].

Carol Thompson 3-3-99
Smokers' Rights Action Group
P.O. Box 259575
Madison, WI 53725-9575
71334.3541@compuserve.com