AAS – CNS Effects

[Michael Scally MD]

Chantal Y, Bernache-Assollant I, Schiano-Lomoriello S. Examining a negative halo effect to anabolic steroids users through perceived achievement goals, sportspersonship orientations, and aggressive tendencies. Scand J Psychol. Examining a negative halo effect to anabolic steroids users through perceived achievement goals, sportspersonship orientations, and aggressive tendencies - CHANTAL - 2013 - Scandinavian Journal of Psychology - Wiley Online Library

We investigated the social image of anabolic steroids (AS) users grounding our analysis on the achievement goal theory of Nicholls. Our main goal was to explore how an athlete's acceptance of AS use would impact on the way that athlete will be perceived by others. Non-AS-using participants reacted to one of two scenarios portraying a male athlete either accepting or refusing to engage in drug use behavior. The results suggested that the acceptance of anabolic steroids yielded an unfavorable social image - perceivers inferred a predominant ego orientation to characterize the AS-user's motivation as well as weaker sportspersonship and a stronger proclivity for reactive aggression than instrumental aggression. Moreover, the analyses did not yield significant gender or interaction effects. Finally, those findings are commented in view of methodological shortcomings and of the perspectives that they may offer for future research concerning the motivational aspects of the social perceptions of drug use in sport.

 

[Michael Scally MD]

GMAFB - Where are all of these so-called men with AAS dependency? Ironically, the authors do not even recognize the contradictions of their “study.” Amazingly, they cite an AAS dependency prevalence of ~25-35% with roughly 1 MILLION having experienced AAS dependence. BUT, in ALL of the studies published the total equals far less than a few hundred.

This is a JOKE. However, this is a possible good estimate for those that have experience Androgen Induced Hypogonadism (AIH).

AAS dependency is no more than a myth and fantasy of a handful of “researchers” who have their life’s work dependent upon this false fact.


Pope HG, Jr., Kanayama G, Athey A, Ryan E, Hudson JI, Baggish A. The lifetime prevalence of anabolic-androgenic steroid use and dependence in Americans: Current best estimates. Am J Addict. The lifetime prevalence of anabolic-androgenic steroid use and dependence in Americans: Current best estimates - Pope - 2013 - The American Journal on Addictions - Wiley Online Library

BACKGROUND AND OBJECTIVES: Although various surveys have tracked the prevalence of anabolic-androgenic steroid (AAS) use in American teenagers and young adults, no recent surveys have assessed the lifetime prevalence of AAS use in Americans overall. We therefore analyzed serial youth-survey data to derive estimates of the lifetime prevalence of AAS use in the current American general population.

METHODS: We first determined the distribution of age of onset of AAS use, based on pooled data from nine studies. Using this distribution, we then developed equations to project the eventual lifetime prevalence of AAS use among young survey respondents, once they aged and completed the period of risk for initiating AAS. We similarly calculated the denominator of lifetimes of risk for AAS use in the total American population. We next applied these equations to four independent national youth datasets to derive current American general-population estimates for lifetime AAS use. Finally, using data from 10 pooled studies, we estimated the lifetime prevalence of AAS dependence among AAS users.

RESULTS: Age-of-onset studies consistently showed that AAS use begins later than most drugs, with only 22% of users (95% confidence interval: 19-25%) starting before age 20. Applying the age-of-onset findings to national youth datasets, we estimated that among Americans currently age 13-50 years, 2.9-4.0 million have used AAS. Within this group, roughly 1 million may have experienced AAS dependence.

CONCLUSIONS AND SCIENTIFIC SIGNIFICANCE: Although subject to various limitations, our estimation techniques suggest a surprisinigly high prevalence of AAS use and dependence among Americans.

 

[CensoredBoardsSuck]

AAS dependency is no more than a myth and fantasy of a handful of “researchers” who have their life’s work dependent upon this false fact.


Applying the age-of-onset findings to national youth datasets, we estimated that among Americans currently age 13-50 years, 2.9-4.0 million have used AAS. Within this group, roughly 1 million may have experienced AAS dependence.

Wow! The prevalence of users who become dependant on AAS is higher than cocaine and heroin and rivals that of tobacco. Why isn't this stuff banned?

I think the authors need to redefine their definition of dependancy because the current one makes their bias too obvious.

 

[TheHamburglar]

We're not dependent on juice, we're dependent on being awesome.

 

[Millard]

Wow! The prevalence of users who become dependant on AAS is higher than cocaine and heroin and rivals that of tobacco. Why isn't this stuff banned?

I think the authors need to redefine their definition of dependancy because the current one makes their bias too obvious.

I believe some of the same researchers have been working to change the official DSM definition to accomodate their bias.

 

[Michael Scally MD]

Cornford CS, Kean J, Nash A. Anabolic-androgenic steroids and heroin use: A qualitative study exploring the connection. Int J Drug Policy. http://www.ijdp.org/article/S0955-3959(14)00149-2/abstract

BACKGROUND: Anabolic-androgenic steroids (AAS) are commonly used drugs by young males. There are known associations with other drugs, including heroin. Current explanations for the association with heroin include evidence that both heroin and AAS users come from similar social groups and that both heroin and AAS have similar effects on certain neurochemical pathways.

The purpose of this study was to determine what additional socio-cultural explanations might account for the association between AAS and heroin use.

METHODS: The study was conducted with eight focus groups of 30 individuals including both heroin and non-heroin users, and individual semi-structured interviews with two key informants.

RESULTS: AAS were used to reverse the weight loss associated with heroin use. Because of the stigma, hiding weight loss from heroin, or demonstrating recovery by increased size, were important both for the heroin user himself and for reassurance to others. Increased size and increased muscularity and strength were important in intimidating others for roles such as drug dealing.

CONCLUSION: The need to demonstrate weight gain in recovery from heroin use, and the advantages of increased muscularity for intimidation purposes, provide further explanations for the link between heroin and AAS use.

 

[TheGuy85]

Cornford CS, Kean J, Nash A. Anabolic-androgenic steroids and heroin use: A qualitative study exploring the connection. Int J Drug Policy. http://www.ijdp.org/article/S0955-3959(14)00149-2/abstract

BACKGROUND: Anabolic-androgenic steroids (AAS) are commonly used drugs by young males. There are known associations with other drugs, including heroin. Current explanations for the association with heroin include evidence that both heroin and AAS users come from similar social groups and that both heroin and AAS have similar effects on certain neurochemical pathways.

The purpose of this study was to determine what additional socio-cultural explanations might account for the association between AAS and heroin use.

METHODS: The study was conducted with eight focus groups of 30 individuals including both heroin and non-heroin users, and individual semi-structured interviews with two key informants.

RESULTS: AAS were used to reverse the weight loss associated with heroin use. Because of the stigma, hiding weight loss from heroin, or demonstrating recovery by increased size, were important both for the heroin user himself and for reassurance to others. Increased size and increased muscularity and strength were important in intimidating others for roles such as drug dealing.

CONCLUSION: The need to demonstrate weight gain in recovery from heroin use, and the advantages of increased muscularity for intimidation purposes, provide further explanations for the link between heroin and AAS use.

I've been around A LOT of heroin users and drug users in general. I know of one that I can think of who started using AAS. Now he maintains a steady life style free of drugs except for AAS. AAS and weightlifting has changed his life and may even have saved it. Though I have never seen one active heroin addict pick up AAS and weightlifting as a hobby in order to intimidate people for the purpose of drug dealing. Guns are way better tools of intimidation and all the muscle and strength and the world is going to stop bullets .

A lot of the guys who sober up in prison and pick up weight lifting don't carry on with it when they are released.

 

[devildog93]

Actually that isn't totally true. Muscle is a low class kevlar vest. Of course we would have to be comparing extremes off both edges of the spectrum, like a 100 pount guys with no muscle versus a worlds strongest man competitor, but yea i think there is a difference.

I don't see the comparison between other drug addictions and this supposed aas addiction. I know quite a few aas users, but i can't say that i think any of them are addicts. Some of them are hopelessly tied to their body fat% or something along those lines, but i don't think that is the aas use.

 

[Michael Scally MD]

[I have said repeatedly there is no such thing as AAS Addiction/Dependency. There Is ASIH.]

Most of Us Still Don’t Get It: Addiction Is a Learning Disorder
http://www.substance.com/most-of-us-still-dont-get-it-addiction-is-a-learning-disorder/9176/

Addiction is not about our brains being "hijacked" by drugs or experiences—it's about learned patterns of behavior. Our inability to understand this leads to no end of absurdities.

Sex, food, shopping, the Internet, video games—all of these activities are being studied by neuroscientists, which frequently leads to headlines like “Oreos May Be As Addictive As Cocaine” and “Brain Activity of Sex Addicts Similar to That of Drug Addicts.”

These stories carry the very strange implication that our brains have areas “for” drug addiction that can be “hijacked” by experiences like sex, junk food and MILF porn.

Shockingly, kids today with their Tinder and Grindr and nomophobia are misusing the regions nature gave us to allow us to get hooked on wholesome pleasures like heroin, cocaine and methamphetamine.

Of course, put that way, these claims sound completely absurd.

Evolution didn’t provide us with brain circuitry dedicated to alcoholism and other drug addictions—it gave us brain networks that motivate us to seek pleasure and avoid pain in ways that promote survival and reproduction.

To understand addiction, we’ve got to stop falling for arguments that obscure this truth and make unsound claims about brain changes that cannot tell us anything about its real nature.

This means that any study that says it shows that something is addictive because the stuff “lights up” the same brain areas seen in addiction is tautological. Anything that provides pleasure or certain types of stress relief will activate these regions. If it doesn’t activate these areas, it can’t be perceived as pleasant, desirable or comforting.

In fact, despite hundreds of millions of dollars spent on neuroimaging research, we still don’t have a scan that can reliably separate addicted people from casual drug users or accurately predict relapse.

Some studies have suggested that this may be possible but none have found a replicable diagnostic scan, even though some clinicians market the use of scanners in treatment.

 

[Michael Scally MD]

Hildebrandt T, Langenbucher JW, Flores A, Harty S, Berlin HA. The Influence of Age of Onset and Acute Anabolic Steroid Exposure on Cognitive Performance, Impulsivity, and Aggression in Men. Psychol Addict Behav. http://psycnet.apa.org/index.cfm?fa=search.displayRecord&uid=2014-20547-001

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) x 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.

 

[Michael Scally MD]

Highlights
· Anabolic-androgenic steroids (AAS) cause psychiatric and cognitive abnormalities.
· We conducted the first systematic brain imaging study of human long-term AAS users.
· AAS users had larger right amygdalas and reduced right amygdala fMRI connectivity.
· AAS users also had dorsal anterior cingulate cortex neurochemical abnormalities.
· AAS use causes brain changes that may underlie psychiatric and cognitive changes.

Kaufman MJ, Janes AC, Hudson JI, Brennan BP, Kanayama G, et al. Brain and cognition abnormalities in long-term anabolic-androgenic steroid users. Drug Alcohol Depend. https://www.sciencedirect.com/science/article/pii/S0376871615002197

BACKGROUND: Anabolic-androgenic steroid (AAS) use is associated with psychiatric symptoms including increased aggression as well as with cognitive dysfunction. The brain effects of long-term AAS use have not been assessed in humans.

METHODS: This multimodal magnetic resonance imaging study of the brain compared 10 male weightlifters reporting long-term AAS use with 10 age-matched weightlifters reporting no AAS exposure. Participants were administered visuospatial memory tests and underwent neuroimaging. Brain volumetric analyses were performed; resting-state fMRI functional connectivity (rsFC) was evaluated using a region-of-interest analysis focused on the amygdala; and dorsal anterior cingulate cortex (dACC) metabolites were quantified by proton magnetic resonance spectroscopy (MRS).

RESULTS: AAS users had larger right amygdala volumes than nonusers (P=0.002) and reduced rsFC between right amygdala and frontal, striatal, limbic, hippocampal, and visual cortical areas. Left amygdala volumes were slightly larger in AAS users (P=0.061) but few group differences were detected in left amygdala rsFC. AAS users also had lower dACC scyllo-inositol levels (P=0.004) and higher glutamine/glutamate ratios (P=0.028), possibly reflecting increased glutamate turnover. On a visuospatial cognitive task, AAS users performed more poorly than nonusers, with the difference approaching significance (P=0.053).

CONCLUSIONS: Long-term AAS use is associated with right amygdala enlargement and reduced right amygdala rsFC with brain areas involved in cognitive control and spatial memory, which could contribute to the psychiatric effects and cognitive dysfunction associated with AAS use. The MRS abnormalities we detected could reflect enhanced glutamate turnover and increased vulnerability to neurotoxic or neurodegenerative processes, which could contribute to AAS-associated cognitive dysfunction.

 

[Sworder]

[I have said repeatedly there is no such thing as AAS Addiction/Dependency. There Is ASIH.]

Most of Us Still Don’t Get It: Addiction Is a Learning Disorder
http://www.substance.com/most-of-us-still-dont-get-it-addiction-is-a-learning-disorder/9176/

Addiction is not about our brains being "hijacked" by drugs or experiences—it's about learned patterns of behavior. Our inability to understand this leads to no end of absurdities.

Sex, food, shopping, the Internet, video games—all of these activities are being studied by neuroscientists, which frequently leads to headlines like “Oreos May Be As Addictive As Cocaine” and “Brain Activity of Sex Addicts Similar to That of Drug Addicts.”

These stories carry the very strange implication that our brains have areas “for” drug addiction that can be “hijacked” by experiences like sex, junk food and MILF porn.

Shockingly, kids today with their Tinder and Grindr and nomophobia are misusing the regions nature gave us to allow us to get hooked on wholesome pleasures like heroin, cocaine and methamphetamine.

Of course, put that way, these claims sound completely absurd.

Evolution didn’t provide us with brain circuitry dedicated to alcoholism and other drug addictions—it gave us brain networks that motivate us to seek pleasure and avoid pain in ways that promote survival and reproduction.

To understand addiction, we’ve got to stop falling for arguments that obscure this truth and make unsound claims about brain changes that cannot tell us anything about its real nature.

This means that any study that says it shows that something is addictive because the stuff “lights up” the same brain areas seen in addiction is tautological. Anything that provides pleasure or certain types of stress relief will activate these regions. If it doesn’t activate these areas, it can’t be perceived as pleasant, desirable or comforting.

In fact, despite hundreds of millions of dollars spent on neuroimaging research, we still don’t have a scan that can reliably separate addicted people from casual drug users or accurately predict relapse.

Some studies have suggested that this may be possible but none have found a replicable diagnostic scan, even though some clinicians market the use of scanners in treatment.

Highlights
· Anabolic-androgenic steroids (AAS) cause psychiatric and cognitive abnormalities.
· We conducted the first systematic brain imaging study of human long-term AAS users.
· AAS users had larger right amygdalas and reduced right amygdala fMRI connectivity.
· AAS users also had dorsal anterior cingulate cortex neurochemical abnormalities.
· AAS use causes brain changes that may underlie psychiatric and cognitive changes.

Kaufman MJ, Janes AC, Hudson JI, Brennan BP, Kanayama G, et al. Brain and cognition abnormalities in long-term anabolic-androgenic steroid users. Drug Alcohol Depend. https://www.sciencedirect.com/science/article/pii/S0376871615002197

BACKGROUND: Anabolic-androgenic steroid (AAS) use is associated with psychiatric symptoms including increased aggression as well as with cognitive dysfunction. The brain effects of long-term AAS use have not been assessed in humans.

METHODS: This multimodal magnetic resonance imaging study of the brain compared 10 male weightlifters reporting long-term AAS use with 10 age-matched weightlifters reporting no AAS exposure. Participants were administered visuospatial memory tests and underwent neuroimaging. Brain volumetric analyses were performed; resting-state fMRI functional connectivity (rsFC) was evaluated using a region-of-interest analysis focused on the amygdala; and dorsal anterior cingulate cortex (dACC) metabolites were quantified by proton magnetic resonance spectroscopy (MRS).

RESULTS: AAS users had larger right amygdala volumes than nonusers (P=0.002) and reduced rsFC between right amygdala and frontal, striatal, limbic, hippocampal, and visual cortical areas. Left amygdala volumes were slightly larger in AAS users (P=0.061) but few group differences were detected in left amygdala rsFC. AAS users also had lower dACC scyllo-inositol levels (P=0.004) and higher glutamine/glutamate ratios (P=0.028), possibly reflecting increased glutamate turnover. On a visuospatial cognitive task, AAS users performed more poorly than nonusers, with the difference approaching significance (P=0.053).

CONCLUSIONS: Long-term AAS use is associated with right amygdala enlargement and reduced right amygdala rsFC with brain areas involved in cognitive control and spatial memory, which could contribute to the psychiatric effects and cognitive dysfunction associated with AAS use. The MRS abnormalities we detected could reflect enhanced glutamate turnover and increased vulnerability to neurotoxic or neurodegenerative processes, which could contribute to AAS-associated cognitive dysfunction.

Nice post.

 

[Michael Scally MD]

The Dopamine Theory of Addiction: 40 Years of Highs and Lows

The dopamine theory of reward and addiction, which states that dopamine release mediates reward and thus leads to addiction, has had huge traction. However, it became accepted as a ‘universal’ theory without properly accounting for findings from studies in different drug addictions that did not support the theory.

Tellingly, the dopamine theory has not led to any new treatments for addiction. We suggest that the role of dopamine in addiction is more complicated than the role proposed in the dopamine theory of reward. We propose that dopamine has a central role in addiction to stimulant drugs, which act directly via the dopamine system, but that it has a less important role, if any, in mediating addiction to other drugs, particularly opiates and cannabis.

Addiction is a complex mixture of behaviours and attitudes that vary from drug to drug and from user to user, and it is unlikely that a single neurotransmitter could explain every aspect of addiction. We foresee that addiction will be conceptualized as a multiple-neurotransmitter disorder in which the dopamine system is central to stimulant addiction but in which other neurotransmitter systems, such as the endogenous opiate or GABA systems, have important roles in other drug addictions.

In conclusion, this account of the rise and fall of the universal dopamine theory of addiction serves as a lesson in neuroscience research. Unifying theories, although intrinsically appealing, should be subject to careful scrutiny just like other theories — and perhaps even more so because they can lead the field into directions that ultimately prove to be unfruitful.

Nutt DJ, Lingford-Hughes A, Erritzoe D, Stokes PRA. The dopamine theory of addiction: 40 years of highs and lows. Nat Rev Neurosci. 2015;16(5):305-12. http://www.nature.com/nrn/journal/v16/n5/full/nrn3939.html

For several decades, addiction has come to be viewed as a disorder of the dopamine neurotransmitter system; however, this view has not led to new treatments.

In this Opinion article, we review the origins of the dopamine theory of addiction and discuss the ability of addictive drugs to elicit the release of dopamine in the human striatum.

There is robust evidence that stimulants increase striatal dopamine levels and some evidence that alcohol may have such an effect, but little evidence, if any, that cannabis and opiates increase dopamine levels.

Moreover, there is good evidence that striatal dopamine receptor availability and dopamine release are diminished in individuals with stimulant or alcohol dependence but not in individuals with opiate, nicotine or cannabis dependence.

These observations have implications for understanding reward and treatment responses in various addictions.

 

[Big_paul]

I'm a drug addict, an alcoholic and a degenerate gambler. There is no comparison between substance abuse and the use of AAS.

Anyone ever die from AAS withdrawal? Not that I have heard of. We just admire admire ourselves more than before.

 

[Michael Scally MD]

Resetting the Addictive Brain
Researchers have begun to pinpoint the detailed circuitry that governs addiction. By rewiring those connections, they just might serve up a cure.
http://discovermagazine.com/2015/may/17-resetting-the-addictive-brain

 

[Michael Scally MD]

[OA & BS] Pomara C, Neri M, Bello S, Fiore C, Riezzo I, et al. Neurotoxicity by Synthetic Androgen Steroids: Oxidative Stress, Apoptosis, and Neuropathology: A Review. Curr Neuropharmacol. 2015;13(1):132-45. http://www.eurekaselect.com/126863/article

Anabolic-androgenic steroids (AAS) are synthetic substances derived from testosterone that are largely employed due to their trophic effect on muscle tissue of athletes at all levels.

Since a great number of organs and systems are a target of AAS, their adverse effects are primarily on the following systems: reproductive, hepatic, musculoskeletal, endocrine, renal, immunological, infectious, cardiovascular, cerebrovascular, and hematological.

Neuropsychiatric and behavioral effects as a result of AAS abuse are well known and described in the literature. Mounting evidence exists suggesting that in addition to psychiatric and behavioral effects, non-medical use of AAS carries neurodegenerative potential.

Although, the nature of this association remains largely unexplored, recent animal studies have shown the recurrence of this AAS effect, ranging from neurotrophin unbalance to increased neuronal susceptibility to apoptotic stimuli.

Experimental and animal studies strongly suggest that apoptotic mechanisms are at least in part involved in AAS-induced neurotoxicity.

Furthermore, a great body of evidence is emerging suggesting that increased susceptibility to cellular oxidative stress could play a pivotal role in the pathogenesis of many neurodegenerative disorders and cognitive impairment.

As in other drug-evoked encephalopathies, the key mechanisms involved in AAS - induced neuropathology could represent a target for future neuroprotective strategies.

Progress in the understanding of these mechanisms will provide important insights into the complex pathophysiology of AAS-induced neurodegeneration, and will pave the way for forthcoming studies.

Supplementary to abandoning the drug abuse that represents the first step in reducing the possibility of irreversible brain damage in AAS abusers, neuroprotective strategies have to be developed and implemented in future.

 

[Michael Scally MD]

[OA & BS] Busardo FP, Frati P, Sanzo MD, Napoletano S, Pinchi E, et al. The Impact of Nandrolone Decanoate on the Central Nervous System. Curr Neuropharmacol. 2015;13(1):122-31. http://www.eurekaselect.com/126871/article

Nandrolone is included in the class II of anabolic androgenic steroids (AAS) which is composed of 19-nor-testosterone-derivates.

In general, AAS is a broad and rapidly increasing group of synthetic androgens used both clinically and illicitly.

AAS in general and nandrolone decanoate (ND) in particular have been associated with several behavioral disorders.

The purpose of this review is to summarize the literature concerning studies dealing with ND exposure on animal models, mostly rats that mimic human abuse systems (i.e. supraphysiological doses).

We have focused in particular on researches that have investigated how ND alters the function and expression of neuronal signaling molecules that underlie behavior, anxiety, aggression, learning and memory, reproductive behaviors, locomotion and reward.

 

[Michael Scally MD]

[OA & BS] Piacentino D, Kotzalidis GD, Del Casale A, Aromatario MR, Pomara C, et al. Anabolic-androgenic Steroid use and Psychopathology in Athletes. A Systematic Review. Curr Neuropharmacol. 2015;13(1):101-21. http://www.eurekaselect.com/126866/article

The use of anabolic-androgenic steroids (AASs) by professional and recreational athletes is increasing worldwide. The underlying motivations are mainly performance enhancement and body image improvement.

AAS abuse and dependence, which are specifically classified and coded by the DSM-5, are not uncommon. AAS-using athletes are frequently present with psychiatric symptoms and disorders, mainly somatoform and eating, but also mood, and schizophrenia-related disorders. Some psychiatric disorders are typical of athletes, like muscle dysmorphia.

This raises the issue of whether AAS use causes these disorders in athletes, by determining neuroadaptive changes in the reward neural circuit or by exacerbating stress vulnerability, or rather these are athletes with premorbid abnormal personalities or a history of psychiatric disorders who are attracted to AAS use, prompted by the desire to improve their appearance and control their weights.

This may predispose to eating disorders, but AASs also show mood destabilizing effects, with longterm use inducing depression and short-term hypomania; withdrawal/discontinuation may be accompanied by depression.

The effects of AASs on anxiety behavior are unclear and studies are inconsistent. AASs are also linked to psychotic behavior.

The psychological characteristics that could prompt athletes to use AASs have not been elucidated.

 

[Michael Scally MD]

Hallgren M, Pope HG, Jr., Kanayama G, Hudson JI, Lundin A, et al. Anti-Social Behaviors Associated with Anabolic-Androgenic Steroid Use among Male Adolescents. Eur Addict Res. 2015;21(6):321-6. http://www.karger.com/Article/Abstract/433580

Anabolic-androgenic steroids (AAS) have been linked to a range of problematic behaviors, but AAS use is still sometimes portrayed as more benign than other forms of classical drug abuse. To address this issue, we compared the prevalence of anti-social behaviors among adolescent AAS users, non-AAS illicit drug users, and drug non-users. We examined 3 waves (2004, 2008, and 2012) of self-reported cross-sectional data from a secondary school survey conducted in Stockholm, Sweden (total n = 19,773; response percentage, 79.6%). Across all survey years, the risk ratios for virtually all measured anti-social behaviors were significantly higher among AAS users compared to non-AAS illicit drug users and to drug non-users.

 

[Michael Scally MD]

Cross-Sensitization between Testosterone and Cocaine [Load Of Crap Study]

Highlights
· Repeated testosterone increased cocaine-induced hyperlocomotion in adolescent rats.
· Acute testosterone did not change the locomotor response to cocaine.
· Cross-sensitization between testosterone and cocaine in adolescent rats.

Engi SA, Cruz FC, Crestani CC, Planeta CS. Cross-sensitization between testosterone and cocaine in adolescent and adult rats. Int J Dev Neurosci. https://www.sciencedirect.com/science/article/pii/S0736574815004323

Cocaine and anabolic-androgenic steroids are substances commonly co-abused. The use of anabolic steroids and cocaine has increased among adolescents. However, few studies investigated the consequences of the interaction between anabolic-androgenic steroids in animals' model of adolescence.

We examined the effects of acute and repeated testosterone administration on cocaine-induced locomotor activity in adult and adolescent rats.

Rats received TEN once-daily subcutaneous (s.c.) injections of testosterone (10mg/Kg) or vehicle. Three days after the last testosterone or vehicle injections rats received an intraperitoneal (i.p.) challenge injection of either saline or cocaine (10mg/Kg).

A different subset of rats was treated with a single injection of testosterone (10mg/Kg) or vehicle and three days later was challenged with cocaine (10mg/Kg, i.p.) or saline.

Immediately after cocaine or saline injections the locomotor activity was recorded during forty minutes.

Our results demonstrated that repeated testosterone induced locomotor sensitization to cocaine in adolescent but not adult rats.