Anabolic-Androgenic Steroid Misuse: Mechanisms, Patterns of Misuse, User Typology, and Adverse Effects

Table 4

Commonly encountered side effects in the “postcycle” period.

Side effect	Examples of self-initiated therapies	Possible mechanisms	Important findings
Gynecomastia [49]	SERMS (tamoxifen); AIs (anastrozole, letrozole, exemestane); Dopamine agonists (cabergoline and bromocriptine) for galactorrhea	SERMs inhibit pituitary E2 receptors, and therefore stimulate pituitary gonadotropin release and subsequent endogenous testosterone secretion; Aromatase inhibitors reduce the conversion of testosterone to estrogens, which exert powerful negative feedback on the HPT axis	Tamoxifen may effectively treat acute gynecomastia [51]; Chronic gynecomastia may only respond to surgical treatment; AAS users are also known to prophylactically administer SERMS and AIs to avoid developing gynecomastia
ASIH causing testicular atrophy, infertility, and low endogenous testosterone levels [46][	hCG injections (on-cycle); hCG injections (postcycle); SERMs (clomiphene, raloxifene); AIs (anastrozole, letrozole, exemestane)	The human placenta normally produces hCG, although synthetic forms are also available for exogenous administration; hCG and LH bind to the same LH receptor [52]; Serum and intratesticular testosterone levels can rise following hCG injections [53]	There is limited case report data demonstrating efficacy in accelerating return to endogenous testosterone production and spermatogenesis [54, 55]
Sexual dysfunction (low libido, erectile dysfunction) [49]	PDE-5 inhibitors (sildenafil, tadalafil); SSRI (dapoxetine); Herbal remedies; Dopamine agonists (cabergoline)		Commentators have suggested PDE-5 inhibitors as the first-line treatment and discouraged herbal remedies and dapoxetine use [45]