HIV Infection and Premature Heart Disease May be Due to Low DHEA
James Michael Howard, www.anthropogeny.com
Re:American Heart Journal 2004; 147: 55-9 "Acute myocardial infarction in patients infected with
human immunodeficiency virus"
In 1985, I first suggested low DHEA may result in HIV infection based on my primary hypothesis that
low DHEA adversely affects all tissues. The first report of low DHEA in AIDS appeared in 1989.
Later, based on my same primary hypothesis, I decided the "symptoms" of AIDS actually occur because
of loss of DHEA. Since I think the natural loss of DHEA in old age results in the symptoms of old
age, I suggest AIDS is HIV-induced loss of DHEA or premature old age. Therefore, I was not surprised
by the findings of Varriale, et al., which make a case for "premature heart disease." In support,
read the abstract of Varriale, et al., just below and the abstract of "Evidence for an association
between dehydroepiandrosterone sulfate and nonfatal, premature myocardial infarction in males." just
below that. I suggest the loss of DHEA of HIV infection is the cause of premature heart disease.
American Heart Journal 2004 Jan; 147(1): 55-9. Acute myocardial infarction in patients infected with
human immunodeficiency virus.
Varriale P, Saravi G, Hernandez E, Carbon F.
Cabrini Medical Center, New York, NY, USA.
BACKGROUND: Recent clinical and post-mortem reports suggests that human immunodeficiency virus (HIV)
infection may participate in the process of atherosclerosis independent of other coronary risk
factors. In this prospective and observational study, we investigated whether an associative link
exists between HIV infection and coronary artery disease. METHODS: Of 690 patients admitted to our
hospital in a 3-year period, 29 patients (28 men and 1 woman) with a mean age of 46 +/- 10 years had
an acute myocardial infarction (AMI) on the basis of acute prolonged chest pain, ischemic
electrocardiogram abnormalities, and elevated serum markers of myocardial necrosis at presentation.
RESULTS: ST-segment elevation MI was present in 15 patients, and non-ST-segment elevation MI was
present in 14 patients. Twenty-two patients (76%) were <55 years; 17 of these patients had no or 1
coronary risk factor, and 5 patients had 2 or 3 risk factors. Five patients >55 years had 1 coronary
risk factor, and 2 patients had 2 risk factors. Thirteen patients underwent a myocardial
revascularization procedure, and 1 patient died during hospitalization. CONCLUSIONS: HIV infection,
as a cause of endothelial injury, may initiate the inflammatory process of early atherosclerosis and
participate in the evolution of the atherothrombotic lesion responsible for AMI. This study suggests
that the association of HIV infection and acute coronary syndrome may be more common than previously
reported and underscores the need for further clinical studies.
Circulation. 1994 Jan; 89(1): 89-93. Evidence for an association between dehydroepiandrosterone
sulfate and nonfatal, premature myocardial infarction in males.
Mitchell LE, Sprecher DL, Borecki IB, Rice T, Laskarzewski PM, Rao DC.
Division of Biostatistics, Washington University School of Medicine, St Louis,
Mo. 63110.
BACKGROUND: Several studies indicate that endogenous hormones play a role in the etiology of
coronary artery disease, either as independent risk factors or indirectly, via an effect on lipids,
lipoproteins, or other heart disease risk factors. METHODS AND RESULTS: The relation between
endogenous hormone levels and premature (< 56-year-old patients) myocardial infarction was assessed
in a retrospective study involving 49 male survivors of premature myocardial infarction and 49 age-
matched, volunteer male controls. Serum samples were obtained for each subject the morning after a >
or = 12-hour fast and frozen at -70 degrees C for subsequent hormonal analysis. Among the male
patients, the average duration between the most recent myocardial infarction and blood sampling was
3.4 years (range, 0.7 to 19.2 years). Individuals reporting the use of any medications with the
potential to alter lipid, lipoprotein, or hormone levels were excluded from these analyses.
Dehydroepiandrosterone sulfate levels were significantly lower in the patients than in the control
subjects. This association remained statistically significant even after accounting for the effects
of total cholesterol, triglycerides, the ratio of total to high-density lipoprotein (HDL)
cholesterol, HDL, apolipoprotein A-I, apolipoprotein A-II, apolipoprotein B, and body mass index.
There were no significant differences in the levels of estradiol, testosterone, or free testosterone
or the ratio of estradiol to testosterone between patients and control subjects. CONCLUSIONS: Our
conclusions are limited by the retrospective nature of this study. However, these data indicate that
serum dehydroepiandrosterone sulfate levels are inversely related to premature myocardial infarction
in males and that this association is independent of the effects of several known risk factors for
premature myocardial infarction.