I will try to respond to the 3 claims:
✖ cause male reproductive pathologies [1] - even when exposure is to environmental estrogens, far less potent than E2 and in very low concentrations
Refutation:
The study discusses synthetic or environment disruption by xenoestrogens. This doesn’t support the argument that identical exogenous estrogen is harmful. From the study:
“ As a result, low doses of xenoestrogens can interfere with natural estrogen actions, even in the presence of higher circulating E2 concentrations.”
✖cause an increase in IGFBP-1, decreasing IGF-I bioavailability [3]
Refutation:
This is true. More HGH may be needed to get the same IGF1 response especially when using oral E2 (first pass effect):
A Switch from Oral (2 mg/Day) to Transdermal (50 mg/Day) 17b-Estradiol Therapy Increases Serum Insulin-Like Growth Factor-I Levels in Recombinant Human Growth Hormone (GH)-Substituted Women with GH Deficiency
https://sci-hub.se/https://doi.org/10.1210/jcem.85.1.6311
“Serum IGF-I levels significantly increased after the switch from oral to transdermal estrogen therapy “
✖cause a dramatic increase in SHBG (reducing T bioavailability) [4]
Refutation:
This is true but the study was on men with normal testosterone levels. It follows reasoning that men on exogenous testosterone would have lower levels of SHBG and the effect won’t be as dramatic.
Counter evidence:
- Higher levels of estrogen are associated with reduced mortality and endothelial function
- Man with aromatase deficiency was treated with exogenous estradiol improving various health markers (bone, lipids etc) with exogenous estrogen treatment
- Higher E2 is associated with better lipid profiles, lower atherosclerosis and lower cardiovascular risk. Benefits are independent of testosterone level.
Endogenous estrogen levels are associated with endothelial function in males independently of lipid levels
DOI 10.1007/s12020-010-9307-7
“Flow-mediated dilatation (FMD) and intima-media thickness (IMT) of the common carotid artery were evaluated. Obesity parameters were recorded; estradiol, testosterone, SHBG, free testosterone, insulin, as well as glucose and lipid levels were measured. FMD was positively correlated with estradiol (r = 0.201, P = 0.041) and negatively with total cholesterol (r = -0.205, P = 0.022), low density lipoproteins (r = -0.232, P = 0.009), and triglyceride levels (r = -0.179, P = 0.046). In multivariate analysis, the association of FMD with estrogen was independent of BMI and lipid levels. No significant association between FMD and testosterone levels was found.”
EFFECT OF TESTOSTERONE AND ESTRADIOL IN A MAN WITH AROMATASE DEFICIENCY
https://sci-hub.se/10.1056/NEJM199707103370204
“Estrogen treatment induced substantial decreases in the ratio of serum LDL cholesterol to serum HDL cholesterol and in serum triglycerides in our patient (Table 1). Although this effect may depend at least in part on reduced concentrations of serum testosterone, it is clear that the abnormal lipid profile in an aromatase-deficient subject can be modified with estrogen treatment.17”
“With estrogen treatment spinal bone mineral density increased, and complete epiphyseal closure was achieved after nine months. The increases in bone mineral density, serum levels of alkaline phosphatase and osteocalcin, and urinary excretion of pyridinoline were similar to those that occur during normal skeletal maturation during puberty.13,14”
Endogenous Sex Hormones and Cardiovascular Disease in Men
“Estradiol was found to be associated with apolipoprotein E (15).”
“Peripheral arterial disease To our knowledge, only one study (104) has been published on the association between endogenous sex hormones and peripheral arterial disease. The Edinburgh Artery Study, a large-scale prospective survey, found that after 5 yr of follow-up, 40 men had developed peripheral arterial disease. In a nested case-control study, total T, SHBG, and estradiol appeared to have a protective effect, whereas estrone appeared to have an adverse effect.”
“In male-tofemale transsexuals, long-term estrogen supplementation improves vascular function, compared with men [(mean se) 11.5 1.3% vs. 5.2 1.0%, respectively, P 0.005] (121). The effect of high-dose conjugated estrogen (5 mg/d) was studied in the Coronary Drug Project, but estrogen treatment was discontinued because it nearly doubled the incidence of nonfatal MI in the treatment group (122). It may be stated that estrogen as well as T administration had both beneficial and deleterious effects on cardiovascular functioning, depending on dose, population, and end point.”
Conclusion:
Exogenous supplementation in men of E2 provides the same benefits are E2 produced by aromatisation. Higher levels have been shown to be harmful (last quote).
I don't know what qualifies as "high" but maybe getting into the female reference range would be ok.
I think Type-2x is AFK, I sent him a message asking him about ROS and synthetic androgens but he didn't respond. So I'm posting it here not on the original thread.
I will defer to someone with a formal education (not myself).