No, there are physiologic reasons that may be of concern with the introduction of AAS at a relatively young age i.e. adolescence/early adulthood. For example, the brain doesn't fully mature until the early 20s. Androgens are known to have a major influence on the brain during this developmental period. It seems like a fundamentally bad idea to introduce large supraphysiologic dosages of testosterone and synthetic AAS. Could it permanently alter the organization of the brain during this important developmental period? That's the question. I'd rather individuals err on the side of caution.
Psychol Addict Behav. 2014 May 19.
The Influence of Age of Onset and Acute Anabolic Steroid Exposure on Cognitive Performance, Impulsivity, and Aggression in Men.
Hildebrandt T,
Langenbucher JW,
Flores A,
Harty S,
Berlin HA.
Abstract
[Correction Notice: An Erratum for this article was reported online in Psychology of Addictive Behaviors on Oct 27 2014 (see record 2014-44847-001). The name of author Heather Berlin omitted a middle initial in the byline and author note and should appear as Heather A. Berlin.] A growing translational literature suggests that adolescent exposure to anabolic-androgenic steroids (AASs) leads to increased aggression and impulsivity. However, little is known about the cognitive effects of AASs among AAS users or the differences between adolescent- and adult-onset users. This study provides a test of the effects of acute naturalistic AAS use and age of onset (adolescent vs. adult) on measures of inhibitory control, planning and attention, and decision making. Seventy-one active adult male AAS users completed self-report measures of impulsivity and aggression, and a subsample (11 adolescent onset vs. 11 adult onset) matched on current age were administered 4 computerized tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB) (Cambridge Cognition, 2002) and the Iowa Gambling Task (Stanton, Liening, & Schultheiss, 2011). Multiple regression analyses and a series of 2 (adolescent vs. adult) × 2 (on-cycle vs. off-cycle) analyses of variance (ANOVAs) were used to examine the differential effects of age of onset and acute drug use on cognition and behavior.
Regression analyses revealed larger on-cycle effects for adolescent users than adult users. Subsample analyses indicated that on-cycle users performed less well on cognitive measures of inhibitory control and attention, but not on tests of planning or decision making.
Adolescent onset was associated with greater impulsivity and more acute sensitivity to AAS effects on attention. These preliminary findings suggest the possibility that acute AAS use is associated with some differences in inhibitory control and impulsivity and to a lesser degree, aggression. These effects may be more potent for those initiating AAS use in adolescence. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
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Edit: Doc posted this one earlier today]
Peper JS, de Reus MA, van den Heuvel MP, Schutter DJ. Short fused? associations between white matter connections, sex steroids, and aggression across adolescence. Hum Brain Mapp. http://onlinelibrary.wiley.com/doi/10.1002/hbm.22684/abstract
Functional neuroimaging studies in adults show that aggression involves reduced brain communication between subcortical and cortical areas dedicated to motivation and control, respectively. Prior research indicates that sex steroid hormone production during adolescence negatively influences the rapid development of white matter connectivity between subcortical and cortical areas during adolescence and may potentiate aggression.
Here, we tested this hypothesis in 258 participants between 8 and 25 years of age by using Diffusion Weighted Imaging to examine the microstructure of white matter connections within the fronto-temporal-subcortical network. Trait aggression was measured using the Buss Perry Aggression Questionnaire and
testosterone and estradiol levels were measured in saliva.
Results indicated that higher levels of testosterone were associated with less white matter integrity within the fronto-temporal-subcortical network (i.e., higher mean diffusivity [MD] longitudinal [LD], and radial diffusivity [RD]).
Furthermore, lower fractional anisotropy and higher MD, LD, and RD values within this network increased expressive forms of aggression and reduced inhibited forms of aggression (hostility). Our study indicates higher levels of testosterone relating to lower quality of structural cortical-subcortical connectivity, arguably resulting in a shift from inhibited towards expressive forms of aggression.
Our data adds evidence to the idea that aggressive tendencies are subcortically driven, but individuals with relatively high testosterone might have lower structural connectivity within cortical control areas, resulting in a stronger tendency to act on these aggressive tendencies.
Horm Behav. 2013 Jul;64(2):350-6.
Androgenic anabolic steroid exposure during adolescence: ramifications for brain development and behavior.
Cunningham RL1,
Lumia AR,
McGinnis MY.
Abstract
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.
Drug Alcohol Depend. 2013 Jun 1;130(1-3):208-14.
Cognitive deficits in long-term anabolic-androgenic steroid users.
Kanayama G1,
Kean J,
Hudson JI,
Pope HG Jr.
Abstract
BACKGROUND:
Millions of individuals worldwide have used anabolic-androgenic steroids (AAS) to gain muscle or improve athletic performance. Recently, in vitro investigations have suggested that supraphysiologic AAS doses cause apoptosis of neuronal cells. These findings raise the possibility, apparently still untested, that humans using high-dose AAS might eventually develop cognitive deficits.
METHODS:
We administered five cognitive tests from the computerized CANTAB battery (Pattern Recognition Memory, Verbal Recognition Memory, Paired Associates Learning, Choice Reaction Time, and Rapid Visual Information Processing) to 31 male AAS users and 13 non-AAS-using weightlifters age 29-55, recruited and studied in May 2012 in Middlesbrough, UK. Testers were blinded to participants' AAS status and other historical data.
RESULTS:
Long-term AAS users showed no significant differences from nonusers on measures of response speed, sustained attention, and verbal memory.
On visuospatial memory, however, AAS users performed significantly more poorly than nonusers, and within the user group, visuospatial performance showed a significant negative correlation with total lifetime AAS dose. These were large effects: on Pattern Recognition Memory, long-term AAS users underperformed nonusers by almost one standard deviation, based on normative population scores (adjusted mean difference in z-scores=0.89; p=0.036), and performance on this test declined markedly with increasing lifetime AAS dose (adjusted change in z-score=-0.13 per 100g of lifetime AAS dose; p=0.002). These results remained stable in sensitivity analyses addressing potential confounding factors.
CONCLUSIONS:
These preliminary findings raise the ominous possibility that long-term high-dose AAS exposure may cause cognitive deficits, notably in visuospatial memory.