QUOTE FROM ARTICLE: The presence of a bacteria that commonly causes lung inflammation also may signal a risk of repeat heart attacks, a study concludes. Treating the bacterial infection with a common antibiotic seems to reduce the risk of a second heart attack, British researchers said in a report published in Monday's edition of the American Heart Association journal Circulation. Dr. Sandeep Gupta and his colleagues at St. George's Hospital Medical School in London measured levels of antibodies to an organism called Chlamydia pneumoniae in 213 patients who had had heart attacks.

COMMENT: The first version of this story contained only comments by Gupta, with no mention of smoking. But in the second version, the author rounded up an anti-smoker, with no particular expertise on the subject of Chlamydia pneumoniae, to provide the Politically Correct spin:

QUOTE FROM ARTICLE: Fuster said the findings "may open a door to a new understanding" about how infection could combine with other risk factors to contribute to heart attacks. It is possible, he said, that further study could show that the bacterium is as important a trigger for heart attacks as cigarette smoking. COMMENT: With that phrase, "as important a trigger for heart attacks as cigarette smoking," Fuster deceives the public that the claim that "smoking causes heart disease" is unchallengable, even though none of the studies upon which it is based considered the effects of CP.

In fact, it can be presumed that the anti-smokers blame smoking for heart attacks and heart disease actually caused by CP. We already know that numerous kinds of infections are more common in poorer people than richer ones, and that smokers are generally less wealthy than non-smokers. We already know from experience with Helicobacter pylori, where infection almost always begins in childhood before people begin smoking, and thus is not "caused" by smoking, that their efforts to "control for social class" were not successful.

By the same means that they falsely blame active smoking for heart disease, the anti-smokers have cooked up the claim that passive smoking causes 50,000 deaths in non-smokers, who, like the smokers they are exposed to, are more likely to be from a lower socioeconomic background than non-exposed non-smokers.

And, we know from animal experiments that CP "caused plaque...to develop in the blood vessels of rabbits that had no other risk factors for the plaque.... Symptoms of atheroclerosis began to develop after as little as a month. Rabbits that were not exposed to the infection did not develop atherosclerosis." ("Bacterial infection produces blockage that can hurt heart." The Washington Times 1996 Sun Dec 22, p D8.)

This is in contrast to the highly publicized propaganda of Stanton Glantz and his ilk, purporting to link cigarette smoke to atherosclerosis. In these studies, experimental animals were fed high-cholesterol diets to induce heart disease, then it was claimed that the differences between exposed and non-exposed animals were (barely) statistically significant, not unequivocal as with CP.

Furthermore, there is a study, funded by the British Heart Foundation, showing that HP and CP cause heart attacks by raising fibrinogen levels, which the anti-smokers implicate as an important mechanism by which smoking causes heart attacks.

"Seropositivity to both infections was independently associated with raised fibrinogen even after controlling for possible confounding factors related to either infection or fibrinogen.... Individually, the effects of H pylori and C pneumoniae on fibrinogen were equivalent to 66% and 80%, respectively, of the SD [standard deviation] in this population. Although the age-adjusted effect of smoking on fibrinogen was of the same order of magnitude as that reported elsewhere, this was diminished by controlling for H pylori and C pneumoniae." Smoking became non-significant, p> 0.5. (Patel P et al. Fibrinogen: a link between chronic infection and coronary heart disease. Lancet 1994 Jun 25;343(8913):1634-1635.)

There is also work showing that "Gram-negative septic infections have for a long time been known to induce elevated triglyceridemia and lower high density lipoprotein (HDL) values. These lipid alterations are astonishingly striking in C. pneumoniae, despite their low mortality and benign outcome. The lipid pattern is similar to a typical risk factor for CHD. There is even a possibility that this lipid pattern is partly a marker of chronic inflammation associated with coronary arteriosclerosis as proposed by some researchers." (Saikku P. Chlamydia pneumoniae infection as a risk factor in acute myocardial infarction. Eur Heart J 1993 Dec;14(suppl K):62-65.

This is further evidence that it is not that other factors "combine" with smoking, but that the anti-smokers falsely blamed smoking for heart disease caused by HP and CP. And they cannot deny it on the basis of their studies, because those studies considered neither infection. So, they have no right to keep pretending, as Fuster does, that the claim that "smoking causes heart disease" is written in stone.

The legitimate presumption is now not just that THEY WERE WRONG, but also that for years, they have misdirected their research and caused unnecessary deaths in order to further their social engineering goal of eliminating smoking. They have made false promises about the benefits of quitting smoking (smoking quitters tend to be of higher socioeconomic background than continuers), and they are committing scientific fraud by justifying smoking bans under the pretense that ETS causes heart disease in passive smokers, as well.

P.S., also note that the media use the words "virus" and "bacteria" as if they are interchangable, when they are not. CP and HP have been determined to be bacteria.

Counterpoint by

Carol Thompson
Smokers' Rights Action Group
P.O. Box 259575
Madison, WI 53725-9575
Phone: 608-249-4568