Here is a reply that I was asked to post from ALR author of "Building the Perfect Beast".
1. oestrogen suppression is the cause of loss of libido. Its quite common for those on cycle taking a gram of test a week to get libido loss when using letrozole (why? oestrogen suppression)
This has become a very common assumption by many normally based upon the errors of ATD research. Odd that the same and extensive additional research shows the opposite as well, yet most ATD sellers only quote the part that best fits their needs. This is of course why this and the potential class action law suit against its vendors has been so well supported by consumer reports and credited research references.
However, in one of many studies the lack of estrogen seems to lead to a sexual preference change due to ATD use. This is a good thing?
Horm Behav. 1991 Sep;25(3):323-41. Related Articles, Links
Adult partner preference and sexual behavior of male rats affected by perinatal endocrine manipulations.
Brand T, Kroonen J, Mos J, Slob AK.
Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands.
Intact adult male rats, in which aromatization of testosterone to estradiol was prevented pre- and/or neonatally by ATD (1,4,6-androstatriene-3,17-dione), were repeatedly tested for partner preference behavior (choice: estrous female vs active male). In consecutive tests increasing preference scores for the female were found. Neonatal ATD males showed significantly lower preference scores for an estrous female than controls or prenatal ATD males. Prenatal ATD caused preference scores only slightly lower than those of controls. Ejaculation frequencies were markedly reduced or even absent in neonatal ATD males. Prenatal ATD treatment only had no or a moderately lowering effect on ejaculation frequency. Lordosis behavior of adult intact males was more facilitated following neonatal ATD treatment than following prenatal ATD treatment. In a number of tests the serotonergic drug 8-OH-DPAT was injected prior to testing for sexual partner preference and copulatory behavior. DPAT significantly increased preference for an estrous female in all groups of males when interaction was possible, but had no effect when sexual interaction was prevented by wire mesh. DPAT was able to increase the number of ejaculators in nonejaculating groups (i.e., perinatally ATD-treated males). "Premature ejaculations," i.e., ejaculations with the first intromission, were frequently observed with DPAT treatment in all groups of males. In conclusion, the availability of neonatal estrogen (derived from testosterone) organizes, at least partially, the preference for an estrous female normally shown by adult male rats. The lack of neonatal estrogen causes males to be less masculinized, both in partner preference behavior and ejaculatory behavior, and less defeminized in lordosis behavior.
2. mainly because they are getting gynecomastia from compounds that do not aromatize, like superdrol, m1t, ergomax, 1test, etc... as a note taking an aromatase inhibitor with a compound like this (or one like winstrol, tren, alone) will destroy your lipids and libido.
This is certainly true (though progestins like trenbolone have their own libido issues totally unrelated to estrogens) but more who are non-androgen/ATD users, than those who are androgen/ATD users, report gyno.