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Commonly, testosterone
replacement improves cardiovascular and metabolic functions (Ruige et al., 2011; Hyde et al., 2012). In addition, a prospective observational study with men aged 70–96 years demonstrated
that low testosterone in men, independent of pre-existing health conditions, and other risk factors, is associated with increased
mortality risk (Fukai et al., 2011).
Experimental
data demonstrate that testosterone induces relaxation of many vascular beds, including coronary, mesenteric, iliac, renal,
and femoral arteries in several animal species such as rabbit, dog, rat, pig, both in
vivo and in vitro conditions [lowers blood pressure]. In general, most studies indicate that the relaxation
induced by testosterone involves endothelium-independent mechanisms, potassium channel-opening actions and calcium antagonistic
effects (Yue et al., 1995; Chou et al., 1996; Crews and Khalil, 1999; Murphy and Khalil, 1999; English et al., 2000, 2002; Deenadayalu et al., 2001)…. Using endothelial cell cultures these authors demonstrated that testosterone enhances
NO production by directly acting in the endothelial cells via PKC- and MAPK-dependent pathways. Testosterone also significantly
increased DNA synthesis indicating that androgens may also modulate vascular endothelial cell growth (Campelo et al., 2012). In addition, testosterone, at physiological concentrations and via androgen receptor activation,
induces proliferation, migration, and colony formation activity of EPCs (Foresta et al., 2008), indicating that the release of EPCs by bone marrow may be an additional mechanism by which
testosterone modulates endothelial function (Foresta et al., 2006)…. Testosterone also stimulates thromboxane synthase as well as COX-1 and COX-2, which
are key enzymes in the synthesis of prostaglandins (Cheuk et al., 2000; Song et al., 2004). Accordingly, the aging-associated decrease in testosterone levels may interfere with vascular
function via changes in the thromboxane/COX pathway (Figure 1).
Hypogonadism is a condition
associated with endothelial dysfunction (Akishita et al., 2007; Foresta et al., 2008). A study where male patients were submitted to examination of vasomotor function of the brachial
artery and intima-media thickness (IMT) of the carotid artery, showed that low levels of testosterone are associated with
endothelial dysfunction, independent of age, body mass index, hypertension, hyperlipidemia, diabetes mellitus, or current
smoking, suggesting a protective effect of testosterone on endothelial function (Akishita et al., 2007). Likewise, testosterone has been shown to improve
hemodynamic parameters in patients and animal models of heart failure, especially via a reduction in peripheral vascular resistance
and increased coronary blood flow through vasodilation and via direct effects in the cardiac tissue (e.g., by inhibition of
cardiac cAMP-phosphodiesterases; Bordallo et al., 2011; Nguyen et al., 2011)…. Transdermal testosterone replacement therapy increased androgen bioavailability and
decreased pulse wave velocity, indicating that testosterone replacement can diminish arterial stiffness associated with male
hypogonadism (Yaron et al., 2009). [The use of transdermal or other prepackaged testosterone products are designed to only increase
the level from low to normal for the elderly Far
greater benefits are obtained by increasing the dose by two to 3 fold so as to obtain a high youthful level. Two positives examples are Jk and Dr. Paul Thompson of Cenegenics who is seen on television and in magazines. They are two examples. The higher level is necessary
to counter the reduce bioactivity that occurs with aging. Remember that pharma
is in the business of treating illness, thus they oppose the use of effective dose of testosterone—their normal business
practice.]
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Of course similar, though greater benefits are true for natural hormone replacement therapy for women, see HRT. And of course pharma has used the worse formulation Prempro
and the NIH’s WHI study (2002) to limit HRT usage. Note A century ago men
lived longer than women, mainly because of the risks of delivering children and the drain of going through over a half-dozen
pregnancies. Men are still subjected to greater environmental hazards in the
work place, a factor contributing to the difference in death rate. I would also
include the earlier decline in testosterone which is about 50 percent when compared to a study done in 1916 and 6 subsequent
studies confirming the progressive decline in testosterone levels through to 2004, at http://healthfully.org/malehormones/id26.html bottom of page for graphs. I suspect that estrogen mimic,
possible from the increase in soya bean products whose usage by food manufacturers has steadily increased and more recent
sources such as BPA (bisphenol A).
http://sageke.sciencemag.org/cgi/content/abstract/2005/23/pe17 Sci. Aging Knowl. Environ., 8 June 2005
Vol. 2005, Issue 23, p. pe17
Why Females Live Longer
Than Males: Control of Longevity by Sex Hormones
Abstract:
Females live longer than males in many species, including humans. We have traced a possible explanation for this
phenomenon to the beneficial action of estrogens, which bind to estrogen receptors
and increase the expression of longevity-associated genes, including those encoding
the antioxidant enzymes superoxide dismutase and glutathione peroxidase. As a result, mitochondria from females produce fewer reactive oxygen species than those from males.
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