Jama Commits Scientific Fraud

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RE: Cigarette smoking and progression of atherosclerosis, the Atherosclerosis Risk in Communities (ARIC) Study. By George Howard, DrPh; Lynne E Wagenknecht, DrPh; Gregory L Burke, MD, MS; Ana Diez-Roux, PhD; Gregory W Evans, MS; Paul McGovern, PhD; F Javier Nieto, MD, PhD; Gretna S Tell, PhD; for the ARIC investigators. Journal of the American Medical Association 1998 Jan 14;279(2):119-124.

 AND: What's so passive about passive smoking" Secondhand smoke as a cause of atherosclerotic disease. (Editorial re Howard et al). By Rachel M Werner and Thomas A Pearson, MD, PhD. Journal of the American Medical Association 1998 Jan 14;279(2):157-158.

ALSO MEDIA ACCOUNTS OF THE ABOVE: Study Probes Second-Hand Smoke. By Lindsey Tanner, AP - Chicago. AP 13-Jan-1998 20:19 EST REF5582.
Ex-Smokers May Have Irreversible Damage to Arteries, Wake Forest Study Shows. By Robert Conn, Mark Wright & Jim Steele, Wake Forest University Baptist Medical Center. PR Newswire 1998 Jan 13, 1737.
AHA Says Study on Secondhand Smoke Supports ... U.S. Newswire 1998 OTC 01/14 0002.
Scary evidence of smoking's danger. Study finds damage to arteries never heals. By Brigid Schulte, Knight-Ridder Newspapers. Wisconsin State Journal 1998 Wed Jan 14, p A2.

"Cigarette smoking and exposure to secondhand smoke both significantly hasten hardening of the arteries, and the damage may be permanent, a new study suggests. An estimated 30,000 to 60,000 annual deaths in the United States can be attributed to secondhand smoking, wrote the authors, led by epidemiologist George Howard at Wake Forest University in Winston-Salem, N.C.," the Associated Press screamed.

 But this study is fraudulent, because the authors knowingly left out the risk factors that really cause excess heart disease in smokers and in passive smokers. Howard's boast to the media that "We threw the kitchen sink at the data, and still couldn't make it go away," (Knight-Ridder) is an outright lie. The media, as usual, left it unchallenged. They never ask the key questions, "What about Helicobacter pylori, Chlamydia pneumoniae, and homocysteine" Why weren't these considered" Or even mentioned""

 The anti-smoking demagogues have produced an endless stream of deceitful and misleading statements on smoking, ETS and heart disease. It has been known since the Seven Countries studies of the 1960s that smoking rates do not correlate with the wide variations in heart disease rates between different countries. "Differences in the all-causes mortality or coronary death rate or the coronary incidence rates of the cohorts could not be shown to be related to any measure of the smoking habits of the cohorts -- the proportion of the men who were nonsmokers, the proportion who were heavy smokers, the average cigarettes per day, and so on." (Seven Countries: A multivariate analysis of death and coronary heart disease, by Ancel Keys, p. 325).

 Smokers in countries with low rates of cardiovascular disease have lower rates than non-smokers in countries with high rates. Therefore, the study's leadoff claim that "Smoking is a powerful risk factor for incident heart disease and stroke," when it does not account for those differences, is an outright lie as well.

 Thanks to recent research, we now know that those varying rates of heart disease in different countries DO correlate with plasma homocysteine levels (Plasma homocysteine and cardiovascular disease mortality. G Alfthan, A Aro, KF Gey. The Lancet 1997 Feb 8;349:397). But this study, as well as the accompanying editorial, fail to mention homocysteine even once.

 And when the health establishment does mention it, they try to trump up the supposed role of smoking instead, by admitting only that homocysteine might play "perhaps as large a role as smoking," (Newsweek 1997 August 11, "The Heart Attackers," by Geoffrey Cowley). Yet homocysteine accounts for drastic differences in cardiovascular disease rates, while smoking does not.

 This study and the editorial also fail to mention Helicobacter pylori and Chlamydia pneumoniae infection, which many studies have linked to cardiovascular disease. Nor is there mention of C-reactive protein, a general marker of inflammation. These anti-smoker bunko artists and their media confederates just brazenly ignore these important risk factors, and base their hysterical accusations on defective studies with incomplete, inadequate, and out-of-date selections of risk factors, and misrepresent them as complete.

 It is known that HP infection occurs in early childhood, before smoking begins, and infection at older ages is extremely rare. The infection persists throughout life, unless treated by a unique combination of drugs. There may also be a link between Helicobacter pylori, homocysteine and heart disease, in that patients with HP-caused gastritis suffer malabsorption of cobalamin, an essential cofactor for methionine synthetase.

 HP infection is more common in the lower socioeconomic classes, and in blacks, as is smoking, and HP is thus more common among both smokers and passive smokers, who share smokers' socioeconomic characteristics. Because of this, the anti-smokers have blamed smoking for heart disease caused by HP.

 In this study, the socioeconomic and racial differences by smoking and ETS status are clearly shown by the proxy variable of educational level. It compares a group more likely to be white female college graduate not exposed never smokers, versus white male college grad not exposed ex-smokers, versus current smokers who are more likely than the former to be black high school dropouts. By ETS exposure, groups most likely to be college grads are compared with groups most likely to be high school grads.

 Howard et al. admitted that the socioeconomic differences were "dramatic." Those differences were supposedly adjusted for, but the use of proxy variables instead of true risk factors is known to be insufficient to control for the effect of true risks, and often false ones are implicated. Anti-smokers have pulled this trick on us before to blame smoking for ulcers actually caused by HP, so there is no reason to trust them.

 In fact, the raw average progression was the same between smokers and ETS-exposed never or ex-smokers (37 fm), who also shared the characteristic of most likely being high school grads, nor was it much different between non-exposed never or ex-smokers (31 & 32 fm), who shared the characteristic of most likely being college grads.

 The ostensible differences within those educational groupings, which they attributed to smoke exposure, were entirely artificially produced. So it is far more accurate to say that Howard et al. threw the kitchen sink at the data to fabricate those claims, not to make them go away. Isn't epidemiology a marvelous science"

 Chlamydia pneumoniae infection has been linked to atherosclerosis, heart attack and stroke. Even the AHA has been forced to grudgingly acknowledge the evidence (Press release. American Heart Association's Top Research Advances.... U.S. Newswire OTC 12/31 1410). Gupta showed that heart attack patients with high antibody levels to CP who were given antibiotics had no more risk of a second heart attack than uninfected patients (Gupta S et al. Elevated Chlamydia pneumoniae antibodies, cardiovascular events, and azithromycin in male survivors of myocardial infarction. Circulation 1997 Jul 15;96(2):404-407).

 The media embellished this story with an anti-smoker mouthpiece, Dr. Valentin Fuster, who was not even associated with Gupta's study, to dissemble to us that "It is possible," he said, "that further study could show that the bacterium is as important a trigger for heart attacks as cigarette smoking," to encourage the false belief that it is not necessary to inquire whether CP is actually responsible for supposed smoking risks (Infection May Predict Heart Attack. AP 15-Jul-1997 10:30 EDT REF5251).

 Re Howard, The AP told us, "Dr. Stanton A. Glantz, a secondhand smoke expert at the University of California-San Francisco, said the study `provides a real important bridge' between studies that have found that cigarette smoke causes deteriorating arteries and studies showing that passive smokers have an increased risk of fatal heart attacks. `This fills in that missing link,' Glantz said." Except that all of those studies committed the same epidemiologic malpractice.

 Glantz's claim to fame is his trumpeting of animal studies of ETS exposure and atherosclerosis. These studies induced atherosclerosis with unnatural high-fat diets, and then contended that there was a statistically significant difference between the exposed and non-exposed. We are expected to consider these as conclusive as an animal study showing that infection with Chlamydia pneumoniae alone caused artherosclerosis, in the absence of any other risk factors (Fong IW et al. Rabbit model for Chlamydia pneumoniae infection.J Clin Microbiol 1997 Jan;35(1):48-52).

 And, Glantz's speculations purporting a role for PAHs are discredited by the high levels of PAHs in food, which overwhelm any possible contribution from ETS (HA Hattemer-Frey, CC Travis. Benzo-a-pyrene: Environmental partitioning and human exposure. Toxicology and Industrial Health 1991;7(3): 141-157).

 "Previous studies have shown that secondhand smoke, like active smoking, can kill by causing more acute but reversible problems, such as thickening of the blood," the AP told us. Except that the real cause of such "thickening of the blood" could very well be HP, CP, or other infection (IY Bova et al. Acute infection as a risk factor for ischemic stroke. Stroke 1996;27:2204-2206). And until studies properly evaluate this risk, they should desist from all such pronouncements about both secondhand smoke and active smoking.

 The American Heart Association resorted to the most despicable demagoguery of all, by exploiting children: "This study provides more evidence that in order to protect the health of all non-smokers, particularly children, smoking must be banned in all public places, including restaurants" (AHA press release).

 In fact, the main vectors of CP infection are children, especially ages 7-13. CP infection is particularly common in them, probably due to exposure to each others' hygiene in school. They bring the infection home to their families. This indicates that, rather than smokers causing heart disease in children, children cause heart disease in adults. And the most important public measures would be getting them to wash their hands and keep their fingers out of their noses. But the AHA couldn't care less when there are smokers to attack.

 "Hardening of the arteries, or atherosclerosis, is responsible for more deaths in the United States than any other single cause," the media dutifully informed us (Knight-Ridder). So, see how the anti-smoker research establishment diverts attention and funding from investigating the real causes of disease into persecuting smoking instead.

 The anti-smoker health establishment refuses to design or analyze studies to determine whether these important new risk factors explain the alleged risks of smoking. They want no data released to the public which could be usable by smoking defenders.

 Then, their demagogues have the gall to accuse the tobacco industry of supposedly concealing data, not one example of which is ever put forth, because none exist; and of "misdirecting" research toward defending smoking, instead of witch hunting for bogus "smoking dangers" as the anti-smoking crowd prefers. If only this were true, we all would have been better off.

 The tobacco industry's response is pathetic, as usual: "Tom Lauria, a spokesman for The Tobacco Institute, which is funded by the tobacco industry, said advocates there had not yet evaluated the study". But he noted: "The majority of studies do not show any increased risk for nonsmokers. We consider the science to be inconclusive" (AP). The tobacco industry has yet to utter a peep about the evidence casting doubt upon the anti-smokers' claims.

 The only truthful statement Howard made is that the magnitude of their claimed ETS risk is "unbelievable." It certainly is unbelievable, and informed people find it far more credible that the damage is due to the risk factors they left out of the study, not to ETS. But the uninformed are intended to take the word "unbelievable" as a recommendation for its credibility, and use it to steal away more of our freedom.

 The American Heart Association chimed in on this vicious deceit. "`If a non-smoker is around a person who smokes a pack of cigarettes during the day, the non-smoker's exposure is so great that it's almost comparable to his or her smoking half of that pack of cigarettes,' said Aubrey Taylor, Ph.D., an AHA spokesperson and lead author of an American Heart Association statement on environmental tobacco smoke" (AHA press release).

 In fact, the study found that "there was no evidence of a dose-response relationship between increasing weekly hours of ETS exposure and increased progression rates among those exposed to ETS" (which failed to come out in the media). This gives weight to the idea that the purported ETS risk is really due to the risk factors they left out. It also shows that the AHA feels free to dispense with the requirement for a dose-response at will.

 The Journal of the American Medical Association placed its official seal of approval on scientific fraud: "Not much is passive about 'passive smoke,"' wrote the editorial authors, Rachel Werner and Dr. Thomas Pearson of the University of Rochester School of Medicine in Rochester, N.Y. "What is passive is our lack of recognition of the importance of passive smoke as a cardiovascular disease risk factor, our oversight in not asking patients about this exposure, and our lack of advocacy for clean air as a way to help prevent chronic disease," they wrote (AP). Their indifference to the real risk factors and to scientific integrity can be characterized a lot more harshly than merely "passive."


 Carol Thompson 1-19-98
Smokers' Rights Action Group
P.O. Box 259575
Madison, WI 53725-9575

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