X-Message-Number: 26260
Date: Sun, 29 May 2005 23:09:55 -0700 (PDT)
From: Doug Skrecky <>
Subject: antiaging effects of testosterone

[Reduces murine lipofuscin, and may reduce cardiovascular disease.]

Reproduction. 2004 Mar;127(3):359-66.
Age-induced apoptosis in the male genital tract of the mouse.
  We have examined the effects of ageing on the increase in
apoptotic cells numbers in the male genital tract of the house
mouse (Mus musculus). We have found that not all organs have the
same response. There is an induction of apoptosis in both the
epididymis and ventral prostate. However, seminal vesicles and
other prostatic lobes remain unaffected. Apoptosis was assessed by
several methods: TUNEL, detection of the active fragment of
caspase-3 and the pattern of DNA fragmentation on agarose gels.
This increase in apoptosis is related to the fall in testosterone
levels, although there is only a partial decrease in androgen
receptor (AR). AR is still present in all tissues and only
moderately reduced in the epididymis and ventral prostate. A more
intense increase of lipofuscin granules, which may be indicative of
oxidative stress, occurred in these tissues. Finally, testosterone
supplementation reverses the changes (both in apoptosis and
lipofuscin content in the tissue), suggesting a role of androgens
in these processes.

Am J Cardiovasc Drugs. 2005;5(3):141-54
Testosterone and atherosclerosis in aging men : purported
association and clinical implications.
  Two of the strongest independent risk factors for coronary heart
disease (CHD) are increasing age and male sex. Despite a wide
variance in CHD mortality between countries, men are consistently
twice as likely to die from CHD than their female counterparts.
This sex difference has been attributed to a protective effect of
female sex hormones, and a deleterious effect of male sex hormones,
upon the cardiovascular system. However, little evidence suggests
that testosterone exerts cardiovascular harm. In fact, serum levels
of testosterone decline with age, and low testosterone is
positively associated with other cardiovascular risk factors.
Furthermore, testosterone exhibits a number of potential
cardioprotective actions. For example, testosterone treatment is
reported to reduce serum levels of the pro-inflammatory cytokines
interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha, and
to increase levels of the anti-inflammatory cytokine IL-10; to
reduce vascular cell adhesion molecule (VCAM)-1 expression in
aortic endothelial cells; to promote vascular smooth muscle and
endothelial cell proliferation; to induce vasodilatation and to
improve vascular reactivity, to reduce serum levels of the
pro-thrombotic factors plasminogen activator inhibitor (PAI)-1 and
fibrinogen; to reduce low-density lipoprotein-cholesterol (LDL-C);
to improve insulin sensitivity; and to reduce body mass index and
visceral fat mass. These actions of testosterone may confer
cardiovascular benefit since testosterone therapy reduces atheroma
formation in cholesterol-fed animal models, and reduces myocardial
ischemia in men with CHD. Consequently, an alternative hypothesis
is that an age-related decline in testosterone contributes to the
atherosclerotic process. This is supported by recent findings,
which suggest that as many as one in four men with CHD have serum
levels of testosterone within the clinically hypogonadal range.
Consequently, restoration of serum levels of testosterone via
testosterone replacement therapy could offer cardiovascular, as
well as other, clinical advantages to these individuals.

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