This attachment has tons of ALPHA on E. From obesity to diabetes, fertility and etc, you will find that Estrogen, not Free T, DHT is what they highlight as the reason for fat loss, and fertility and so much more.
Areas of interest with snippets below.
(page 300-303)
Only over the past few years have clinical intervention studies begun to confirm preclinical evidence that estradiol contributes to body weight regulation and meta- bolic health in men. One small study examined the effects of testosterone replace- ment in obese men with low-normal baseline serum testosterone concentrations. Whereas treatment with testosterone gel led to significant reductions in adiposity, these changes were not seen when testosterone was co-administered with an aroma- tase inhibitor (Juang et al. 2014). In a larger study of healthy men, two subject cohorts were administered the GnRH analogue goserelin acetate to suppress endog- enous sex steroid production. Simultaneously, subjects in the first cohort received either placebo gel or variable doses of add-back testosterone gel, and the second cohort of subjects received either placebo gel or testosterone gel with an aromatase inhibitor. Strikingly, whereas androgen exposure appeared to mediate changes in lean mass, estradiol rather than testosterone was found to be the primary determi- nant of changes in fat mass (Finkelstein et al. 2013). Subsequently, another clinical study similarly enrolled healthy, eugonadal men and rendered them medically cas- trate through use of the GnRH antagonist acyline. Subjects in this study variably received placebo gel, low-dose or full replacement dose testosterone gel, or full replacement dose testosterone gel with an aromatase inhibitor. In all three treatment groups rendered sex steroid deficient, significant increases in body fat mass were evident within only 4 weeks of drug treatment (Chao et al. 2016). Again, estradiol rather than testosterone deprivation exhibited a stronger correlation with the observed increases in adiposity.
Page 303
Another population for whom the metabolic effects of estradiol could prove highly relevant are men with prostate cancer. In the USA, prostate cancer affects 2 million men, and up to 50% of these men will undergo androgen deprivation therapy (ADT) at some point in their treatment course (Meng et al. 2002). The most com- mon form of ADT involves GnRH analogues that confer central hypogonadism, and over the past decade, clinical evidence has compellingly demonstrated the men undergoing ADT are at substantially higher risk of increased adiposity, insulin resis- tance, T2DM, and cardiovascular disease than age-matched controls with or without prostate cancer
Finally, as efforts continue to develop an effective form of hormonal contracep- tion for men (Ayoub et al. 2016; Zitzmann et al. 2017), these findings collectively underscore the need to carefully assess changes in estradiol exposure consequent to different contraceptive regimens. Thus, mounting evidence suggests that estradiol replacement is a pivotal facet of the treatment of male hypogonadism and, by corol- lary, states of estradiol deprivation – whether consequent to physiologic hypogo- nadism, androgen deprivation therapy, or hormonal forms of contraception – must be avoided as possible to optimize metabolic health in men.
Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity
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