Androgenic anabolic steroid exposure during adolescence: ramifications for brain development and behavior.
Cunningham RL1, Lumia AR, McGinnis MY.
Horm Behav. 2013 Jul;64(2):350-6. doi: 10.1016/j.yhbeh.2012.12.009. Epub 2012 Dec 26.
This article is part of a Special Issue "Puberty and Adolescence". Puberty is a critical period for brain maturation that is highly dependent on gonadal sex hormones. Modifications in the gonadal steroid environment, via the use of anabolic androgenic steroids (AAS), have been shown to affect brain development and behavior. Studies in both humans and animal models indicate that AAS exposure during adolescence alters normal brain remodeling, including structural changes and neurotransmitter function. The most commonly reported behavioral effect is an increase in aggression. Evidence has been presented to identify factors that influence the effect of AAS on the expression of aggression. The chemical composition of the AAS plays a major role in determining whether aggression is displayed, with testosterone being the most effective. The hormonal context, the environmental context, physical provocation and the perceived threat during the social encounter have all been found to influence the expression of aggression and sexual behavior. All of these factors point toward an altered behavioral state that includes an increased readiness to respond to a social encounter with heightened vigilance and enhanced motivation. This AAS-induced state may be defined as emboldenment. The evidence suggests that the use of AAS during this critical period of development may increase the risk for maladaptive behaviors along with neurological disorders.
High-dose testosterone treatment is applied during puberty to reduce the predicted adult height in excessively tall boys. To date it has remained unclear whether this therapy produces any long-term effects on reproductive functions of the patients. To clarify this question, we performed a follow-up study in 47 tall men, determining seminal and hormonal parameters 10.6 +/- 2.5 years (mean +/- SD) after cessation of therapy. The tall men treated were compared with 123 normal men attending the Institute of Reproductive Medicine as volunteers for various clinical studies. Clinical examination revealed a significantly higher prevalence of varicoceles and history of maldescended testes in the testosterone-treated tall men compared with the controls. Semen analysis revealed significantly lower progressive motility in the tall men compared with the normal men (49.2 +/- 13.4 vs. 54.3 +/- 12.8%). A nonsignificant tendency towards lower sperm concentration (43.8 +/- 35.4 vs. 57.8 +/- 45.6 mL/mL), lower total sperm count (184.4 +/- 158.0 vs. 225.4 +/- 277.5 mL/ejaculate), and reduced normal sperm morphology (27.6 +/- 12.5 vs. 30.9 +/- 13.1%) was evident in the testosterone-treated tall men. Although there was no difference in testicular volume and FSH between the groups, testosterone was lower in the testosterone-treated tall men (19.9 +/- 7.4 vs. 23.9 +/- 7.0 nmol/L). Statistical analysis of the subgroups of testosterone-treated tall men and control men without varicocele and cryptorchidism revealed no differences in any ejaculate parameter. The small difference in semen variables may be explained by a higher prevalence of varicocele and maldescended testes in the testosterone-treated tall men.
At a mean follow-up of 21 yr after high-dose androgen treatment, we conclude that fatherhood and semen quality in tall treated men are not affected. Serum testosterone levels, however, are reduced in androgen-treated men. Future research is required to determine whether declining testosterone levels may become clinically relevant for these men as they age.
Using AAS without any medical basis is abuse.