the benefit of testosterone supplementation therapy exceeds the correction of symptoms of androgen deficiency and also includes glucose homeostasis and metabolic control.
I love this abstract. I am going to try and find the full print. As it relates to metabolic dysfunction, elevated Testosterone provides a similar functional picture in women as low Testosterone does in men.
Opiates and prescription meds are a common cause of low T in men. In this study with men with metabolic dysfunction and opiate induced low T, Testosterone therapy did not worsen inflammatory/metabolic markers. Of note, this study did not find improvement in the metabolic and inflammatory markers as other studies have shown.
low Testosterone associated with insulin resistance, type II diabetes, metabolic syndrome, and increased fat. These will all translate to increased mortality.
Testosterone levels, measured as total, bioavailable and free, found to be associated with age and central (not visceral) obesity in those men with type I and II Diabetes. Weakly with symptoms of low T and ED.
low Testosterone linked to insulin resistance, type II Diabetes, and increased metabolic syndrome. Low T is linked to increased visceral fat in this study.
This study found that low T was clearly associated with "pre diabetes" independent of weight and MetS. All men that are overweight, obese, with metabolic syndrome, "pre diabetic" need evaluation of hormones, not just Testosterone.
the age trend in free T was more substantial (−1.3% per annum)
The core hormonal pattern with increasing age is suggestive of incipient primary testicular dysfunction with maintained total T and progressively blunted free T associated with higher LH.
Obesity was associated with progressively lower total and free T independent of the simultaneous decrease in SHBG.
our data highlight the fact that LH was unchanged or even lower in older men in the face of lower T in obesity, suggesting that there may be a failure at the hypothalamic-pituitary level.
a change in BMI from nonobese to obese may be equivalent to a 15 yr fall in T.
This pattern supports the hypothesis that different underlying mechanisms influence the functions of the HPT axis: age predominantly affects testicular function, whereas obesity impairs hypothalamic/pituitary function.
the effects of aging on testicular function can be moderated by increased LH compensation for many decades
obesity impairs hypothalamic/pituitary function independent of age, arguably an adaptive response for which there should be no compensatory mechanism.
the concurrent but opposite (and separate) effects of obesity and age on SHBG
SHBG was negatively associated with increasing strata of obesity
Obesity is associated with insulin resistance (28), and the increased circulating insulin inhibits hepatic SHBG synthesis
the SHBG increase with age may be related to relative IGF-I deficiency (27), although this has not been directly proven.
Obesity is associated with peripheral and central insulin resistance (30) and proinflammatory cytokine production (TNFα and IL-6) from adipocytes (31) and central nervous system endocannibinoid release (32), all of which are potential candidates for abrogating hypothalamic endocrine and downstream reproductive axis functions.
The HPA axis effect may be the result of inflammation.
The relationship between obesity and T can be bidirectional: low T may be the cause rather than consequence of obesity
chronic alcohol abuse is known to suppress LH (40), our data showed no significant association among the three hormones or SHBG and alcohol intake.
increase in total T in smokers occurs through a primary increase in SHBG with a compensatory rise in LH
the effects of obesity (BMI or waist circumference) was by far the most important determinant of variance in total T, whereas age per se was important for SHBG, LH, and free T with comorbidity and smoking being comparatively minor contributors
It is noteworthy that these predisposing lifestyle and health factors are modifiable. This implies that the apparent age-related decline in T may constitute a barometer of health and thus be potentially preventable and/or reversible.
Age induced decline in Testosterone is more associated with a decline in leydig cell function and thus elevated LH will be associated. In contrast, obesity is more of a HPA axis disruption and thus LH may be normal to low. The pulse amplitude is decrease. No change in pulse frequency is noted.
With obesity, a decline in TT and fT was independent of SHBG.
Aging is associated with a greater decrease in fT versus TT.
small study of men post prostate cancer radiotherapy: only 1 of the 5 had a transient rise in PSA, though the level was still below the 1.5 ng/ml threshold. This fits within the saturation theory concept. F/u in this study was 14.5 months. Abstract only available here.
This study assumes a 13% low T prevalence. Probably too low. This will only grow. Low T contributes to many disease states in men. This study showed a cost of 190-525$ billion in cost from these disease states over a 20 year time period.
Study of men with hepatitis C and interferon therapy found decrease in free and total Testosterone levels in men. The study results suggest a non-HPA effect, which suggests more of a peripheral effect at the level of the TEsticles.