The mysterious disappearance of investigation of the role of infection in atherosclerosis is noted in the review by F. Javier Nieto, "Infections and atherosclerosis: New clues from an old hypothesis?" (Am J Epidemiology 1998;148(10):937-948; no abstract available online):
"The inability of 'traditional' risk factors such as hypercholesterolemia, hypertension, and smoking to completely explain the incidence and trends in cardiovascular diseases has resulted in repeated calls for a search for 'new risk factors.' Recently, infections have been placed among these new putative risk factors. This commentary reviews the historical antecedents of the infectious hypothesis, which is actually one of the oldest etiologic theories of atherosclerosis. Because inflammation may mediate the putative atherogenic role of infections, the historical antecedents that have discussed a possible role of inflammation in atherogenesis are also briefly reviewed. [Comment: It is not just that the so-called traditional risk factors fail to "completely" explain heart disease rates; it is that some 40% or more of heart attack victims have none of those supposed risk factors whatsoever -cast.]
"This review demonstrates that inflammation and infection were considered as possibly atherogenic more than a century ago. However, these hypotheses were all but completely abandoned early in the present century, coinciding with a shift in paradigms in the pathogenetic theories of atherogenesis, i.e., with the development of the multifactorial model of causation of chronic ('non-infectious') diseases. [Comment: the so-called "shift in paradigms" consisted of the Lasker Lobby taking over our health establishment and deliberately suppressing research on the role of infection, in order to ram their health fascist ideology down the public's throats, e.g., How the Public Was Brainwashed About Heart Disease -cast]
"Striking resemblances are apparent between current research on the putative atherogenic role of infections and research on the topic that was conducted up to one century ago. The synthesis of past and current evidence reviewed here suggests the following hypotheses and clues for further studies: 1) that the study of a possible atherogenic role of infections should be extended to infectious agents other than the three that have been the focus of research in recent years (herpesvirus - mainly cytomegalovirus (CMV), Chlamydia pneumoniae, and Helicobacter pylori); 2) that the introduction of antibiotic therapies in the 1940s and 1950s may have contributed to the decline in coronary heart disease incidence and mortality observed in the Western hemisphere in the last three decades; 3) that infections could be one of the mediating factors in the association between low socioeconomic status (SES) and coronary disease; and 4) that infections in childhood could also be one of the confounding factors that explain the alleged association between birth/childhood weight and coronary disease in adulthood."
He has failed to mention 5) that infection, in combination with smokers' lower socioeconomic status, could be the confounding factor that explains the alleged association between smoking and cardiovascular disease, and also 6) that infection, in combination with passive smokers' lower socioeconomic status, could be the confounding factor that explains the alleged association between passive smoking and cardiovascular disease. Remember: the autopsy study by Davidson et al. found an odds ratio of 10 for antibodies to Chlamydia pneumoniae versus development of atherosclerosis, in young persons in whom the precipitating causes have not been obscured by age. An odds ratio of this magnitude is fully capable of producing spurious risks by confounding, as Phillips & Smith (1994) demonstrated. But this is typical of the dishonesty with which the subject is treated by the health establishment.
This article was written to provide historical background for the recent intense interest about infection in cardiovascular disease. Dr. Jonathan Samet, the anti-smokers' star perjuror at the Minnesota tobacco trial, was one of Nieto's fellow editors at the American Journal of Epidemiology, and would have been aware of this development as well. In the "Acknowledgements" at the end of the article, Nieto thanks Samet and others for reading and criticizing previous drafts of his manuscript. Although it was submitted in June, a few months after Samet's testimony in February, this 11-page paper with 137 references must have taken considerable time to prepare. The old references in particular cannot be found by a search of Medline, whose listings don't begin until around 1965, so they would have had to be tracked down via later citations. Yet despite having sworn under oath that he had conducted an "extensive review" on the topic of smoking and health, Samet mentioned not a word about infection in his testimony about the risk factors for coronary heart disease or stroke. Nor did the tobacco industry's awesomely incompetent counsel, Mr. Garnick, ever broach the subject during his cross-examination of Samet. And so the anti-smokers' single largest health claim against smoking (not to mention the source of about 94% of pretended secondhand smoke deaths) was allowed to pass without challenge.
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