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Life extesnsions rebuttal to recent JAMA study.  There was several significant flaws in that study and thus limited evidence can be gained by that study.  In fact, I find no useful clinical information from that study. In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity.  But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men.  Age, stress, and weight are primary causes of increases estrogen production in these men.  These would be why likely high estrogen production occurred and less than optimal serum T resulted.   And, increased E2 will cause an increase in CRP which can precipitate CVD events.

Study looked at aromatase activity in androgen production in older men.  The study found that aromatase inhibition with arimidex increased Testosterone production.  PSA was also monitored and PSA increased in the smaller dose group versus the high dose group.

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Fructose intake increases MetS and hypertension.  The high fructose intake upregulates phosphofructokinase which increases triglyceride production, bypassing central regulation.  This results in ATP depletion with reduced capacity to recover.  Thus attempts by the cells to increase ATP through AMP deaminase results in uric acid production.

Adiponectin is negatively associated with LH, FSH production at the level of the pituitary and Testosterone at the level of the testicle.  Meaning: a risking adiponectin, as found in obesity, is associated with a down regulated HPA stimulation and Testosterone production.  This study, however, found a local autocrine/paracrine effect on sperm that was quite the opposite.

Glyophosate found to be increased in the urine of animals and humans eating GMO food products.  Interesting association that "ill" humans had higher urinary glyophosate levels.  What is defined as "ill" is left to be determined. But clearly, glyophosate is not the innocent product that we have told it was.

ADT therapy with abiraterone inhibits androgen production from both testicular and adrenal origins.  This study finds that a decrease in androgen production through ADT did not always equal a decrease in PSA, indicating other mechanisms of prostate cancer profession.

Study looked at inflammatory markers in RA.  The authors point to high aromatase activity, low androgens, and elevated estrone in synovial fluid as an indicator of a link between aromatase activity and inflammation production through E1 production.  The authors also point to the 16 alpha metabolite pathway as pro-inflammatory as well.  One very interesting point made by the authors is that vitamin D down regulates aromatase activity.  In addition to NK-kappaB inhibition, this may be another mechanism by which vitamin D reduces inflammation.

Might the enzymes be more important than the hormones themselves?  The number is important i.e. progesterone, but how the number came to be is more important as it points to the underlying etiology.  Here, the balance of enzymes are found to direct cell line tumor potential.  The enzyme 5alpha-reductase increased production of the 5alpha-pregnanes which increased tumor potential.  In contrast, the enzymes 20alpha-hydrosteroid oxidoreductase and 3alpha-hydroxysteroid oxidoreductase increase production of the 4alpha-pregnanes, which decreased tumor potential.

Cholecalciferol (vitamin D3) was found to increase male Testosterone production in cell culture model.  This fits with other data that low vitamin D and low T often go hand in hand.  This study actually shows improved D levels increase Testicular Testosterone production, though in cell culture.

Increased visceral adiposity results in increased 11beta-HSD that results in increased cortisone to cortisol production preference.  Cortisol production doesn't just come from the adrenals--it is also produced and metabolized in peripheral and visceral fat.

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Fascinating study on how the addition of Lactobacillus reuteri increased Testicular size, prevented testicular atrophy, increased serum Testosterone production and protected against diet-induced/obesity-induced hypogonadism.  This was a mouse model

full article to previous abstract:  fecal transplant from male mice to female mice resulted in an increase in Testosterone production in the female mice revealing a link between the gut microbial population, diversity and Testosterone production.

Bisphenol A shown to disrupt ovarian estrogen production from exposure in adults.  The point of this that is important is that BPA, a xenoestrogen, can infact disrupt physiologic hormone production in adults, and contribute to ovarian failure.  BPA, itself, is 1,000 fold weaker than E2, yet it disrupts ovarian function.

BPA as endocrine disruptor and as immune disruptor

small cohort with low serum Total Testosterone improved T:E2 ratio with clomid.  Clomid restores the HPA through inhibition of the negative feedback of Estradiol on the Hypothalamus and Pituitary in men.  This allows for an increase in gonadotropin production and thus increase in testosterone production.  Aromatase inhibition therapy would likely still prove beneficial in this situation.

This article, here only abstract available, points to low Testosterone as the effect and not the cause.  The cause being obesity.  An interesting association between leptin and low T is found.  Leptin is a hormone produced from adipocytes, this study found leptin receptors in the leydig cells of testes.  Thus, increased leptin production from increased abdominal adiposity can result in a decrease in 17,20 lyase activity and thus a direct inhibition of leydig cell Testosterone production.

study points to a modest decrease in dopamine and serotonin production in heroic users.  There appears to be a decrease in dopamine production, which could be via a down regulation of tyrosine hydroxylase enzyme and thus release.  Decreased homovanillate also noted.  Other studies have pointed to a decrease/downregulation of D2/D3 receptors.