See how the AHA's Gordon Fung submitted to the California EPA ETS report authors, an unsupported speculation by prominent anti-smoker Neal Benowitz that "ETS exposure produces chronic inflammation in the lungs, which itself may have promoting effects on atherosclerosis."

Yet even before the public comment period on the report was over, an analysis of the Physicians Health Study, funded by the AHA itself, and referred to in this very press release, discredited the hypothesis that chronic inflammation in the lungs, even of active smokers, causes cardiovascular disease (Ridker PM et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. NEJM 1997 Apr 3;336(14):973-979). "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. In this regard, our observation that the effect of C-reactive protein is present among nonsmokers makes bronchial inflammation a less likely mechanism."

The AHA is deliberately deceiving the public with its statement that "If future research shows that high blood levels of Cp characterize individuals who have heart disease but have not yet had a heart attack, Cp may be placed on a par with cigarette smoking as a lurking `trigger' for heart attack." They are pretending that their claim that "smoking causes heart disease" has been written in stone, and that their entire vaunted "mountain of evidence" in support of this claim will not have to be discounted and re-evaluated for confounding by Chlamydia pneumoniae infection.

Furthermore, CP must be properly re-evaluated, with due regard for exposure to the main disease vectors, namely children (especially ages 7-13), in whom CP infection is particularly common, probably due to exposure to each others' hygeine in school. They bring the infection home to their families, which also suggests that, rather than smokers causing heart disease in children, children cause heart disease in adults.

The AHA has also refused to address the associations with heart disease of another bacterium, Helicobacter pylori. The HP-heart disease link is very threatening to the anti-smokers' claim, because nearly all infection occurs in early childhood, before people become smokers, and is associated with lower socioeconomic class. Smokers are more likely to be of lower socioeconomic class than non-smokers, and passive smokers would share this class attribute with the smokers to whom they are exposed.

So, the anti-smokers' "mountain of evidence" blaming smoking for heart disease must also be re-evaluated for confounding by HP. HP infects the stomach, causing gastritis and ulcers, so a likely fruitful avenue of investigation is the connection between a flare-up of symptoms and the ironic clinical observation that "Half the patients with indigestion think they're having a heart attack, and half the patients with heart attack think they have indigestion."

The effects of HP gastritis-caused malnutrition on homocysteine levels should be investigated as well. Thus, even past research on other risks which are trumpeted in AHA's press release, such as depression and diet, will have to be re-evaluated as well, since the reported findings may also be confounded by CP and HP.

Courtesy of Carol Thompson 08/23/93
Smokers' Rights Action Group
P.O. Box 259575
Madison, WI 53725-9575
Phone: 608-249-4568