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
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
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,
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.