FORCES - HEART DISEASE

BRIEF EDITORIAL Applause to Niemel et al and Whincup et al for recognizing the potential for confusion from adjusting for so-called established risk factors without thinking. All too often this is not the case. Some researchers clearly don't think at all about their ingrained presumptions, since it ought to dawn on them, for instance, that social class, by itself, does not cause any diseases. Yet they adjust for it like robots when analyzing risk factors which may actually be the cause of those socio-economic differences.

Especially in regard to smoking, this bias is displayed over and over in the literature: Upon finding a new risk factor for CHD, the investigators automatically go, "Aha! Perhaps this is the mechanism we've been searching for all these decades, to explain how smoking causes heart disease!" And never is it proposed that "Perhaps this is a mechanism by which smoking has been falsely blamed for heart disease."

Like automatons, they control their analyses of Helicobacter pylori and Chlamydia pneumoniae bacteria (HP and CP) for social class and smoking, heedless of the fact that HP & CP may well account for those social class and smoking differences, and thus they should not be controlled for because this obliterates the truly key facts! This is the iron tyranny that has stifled scientific thought for 30+ years.

The unfortunate result of this mindset has been to devote countless dollars and research hours into "proving" that smoking causes various maladies, when real research on actual potential causes has fallen by the wayside.

Still, there are rigorous scientists who understand the importance of performing honest and unbiased research. Following are several excellent examples.

Juvonen J, Juvonen T, Laurila A, Alakrpp H, Lounatmaa K, Surcel H-M, Leinonen M, Kairaluoma MI, Saikku P. Demonstration of Chlamydia pneumoniae in the walls of abdominal aortic aneurisms. J Vasc Surg 1997 Mar;25(3):499-505.

12 AA pts, 3 accident victims, 9 coronary artery bypass pts. P 503 "Immuno-histochemical examination demonstrated chlamydial lipopolysaccharide-antigen in large amounts in the macrophages of the atherosclerotic plaques in all 12 aneurism specimens." All cultures negative. In past studies, only half of atherectomy tissue CP+ v ALL aneurisms CP+. P 504 "Despite direct evidence on the presence of C pneumoniae in all 12 patients with abdominal aortic aneurisms, one patient had no C pneumoniae antibodies, and two had only low titers present in the sera. A similar finding was reported earlier; only 60% of the autopsy sera obtained from persons with atherosclerotic lesions positive for C pneumoniae contained demonstrable antibodies to C pneumoniae." May be bound & sequestered.

THIS IS AN IMPORTANT STUDY: IT SHOWS THAT NOT ALL CASES OF CP INFECTION ARE DETECTED BY BLOOD TESTS. IN STUDIES, THIS WILL MAKE THE RISKS FROM CP LOOK SMALLER THAN THEY REALLY ARE.

Moazed TC, Kuo C, Grayston JT, Campbell LA. Murine models of Chlamydia pneumoniae infection and atherosclerosis. J Infect Dis 1997 Apr;175(4):883-890. 68 Apo-E deficient transgenic mice, 74m C57BL/6J mice. AE mice get athero from abnormal lipid levels. Single innoc's at ages 8 & 16 wks in AE, 8 wks in C57; multiple at 8, 10 & 12 wks in AE. Lung & kidney lesions in AE with mouse hepatitis virus but not without it. P888 "The long-term persistence of C pneumoniae in the aortas of apo-E-deficient mice within the developing lesion but not in C57BL/6J mice suggests that C pneumoniae have a predilection for atheromatous lesions." "Also consistent with the predilection of C pneumoniae for infection of atheromas was the finding that the percentage of mice infected was higher when they were infected at a higher age or at multiple times."

Niemel S, Karttunen T, Korhonen T, Lr E, Karttunen R, Ikheimo M, Kesniemi YA. Could Helicobacter pylori infection increase the risk of coronary heart disease by modifying serum lipid concentrations? Heart 1996;75:573-575. 116 elective angio CHD, 116 age & sex matched controls (54 v 52 y old). "In our study the similar trend observed both in the CHD patients and in the controls suggests that H pylori may modify serum lipid concentrations [HDL down, triglycerides up]. If this is true and the effect of H pylori infection on the risk of CHD is mediated by HDL cholesterol and triglyceride concentrations, then these lipid variables should not be adjusted when the effect of H pylori on the disease is assessed." Adjustment for age & sex only, all chd 1.48 (0.9-2.5); 2-3 vessel 1.86 (1.0-3.5).

Whincup PH, Mendall MA, Perry IJ, Strachan DP, Walker M. Prospective relations between Helicobacter pylori infection, coronary heart disease, and stroke in middle aged men. Heart 1996;75:568-572. 135 MI, 137 stroke, 136 controls; Brit Regional Heart Study. HP+ & MI not adj 1.84 (1.08-3.14), age adj only 1.83 (1.07-3.12); stroke 1.72 (1.00-2.97), 1.69 (0.98-2.93). "The interpretation of the associations between H pylori infection and cardiovascular risk factors (whether causal or not) is crucial, because this will determine whether adjustment for these factors is appropriate."

Whincup PH, Mendall MA, Perry IJ, Strachan DP, Walker M. (letter re: Prospective relations between Helicobacter pylori infection, coronary heart disease, and stroke in middle aged men). Heart 1996 Mar;77(3):294. Underrepresentation of pre-existing heart disease in controls does not affect results of the study.

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