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  1. #1
    johnsomebody's Avatar
    johnsomebody is offline Senior Member
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    May 2002

    AAS PERMANENTLY lower serotonin in adolescents

    I've been doing research on the affect of AAS on serotonin levels in adults (i.e. me) and kept coming up with this annoying study that applies only to adolescents, who shouldn't even be ON AR in the first place.

    But since plenty of them are and are even asking for cycle advice (which is insane IMO) here's yet another reason NOT to do gear til you're at LEAST 21 -and who knows if your brain has fully developed by then or not. From what I was like at 21 I'd say NOT!!

    Note that the hypothesis that AAS PERMANENTLY lowers serotonin in adolescents was confirmed. Note also that lower serotonin levels are associated with depression -Prozac works by elevating serotonin, for example.

    There's always room for more research and I don't have the abstract where it was confirmed so I can't comment on the methodology but it should be easy to find.

    Anabolic steroids may lead to violence
    Friday, 21-Nov-2003 11:40AM PST

    Story from United Press International
    Copyright 2003 by nited Press International (via ClariNet)

    BOSTON, Nov. 21 (UPI) -- Anabolic steroids may have long-term effects on players' behavior and aggression long after they stop abusing the performance enhancing drugs.
    NewsVantage – Just all the news you want, with all the depth you need.

    Northeastern University psychology professor Richard Melloni, with funding from the National Institutes of Health, recently found evidence that long after steroid use ends it can produce long-term aggression, the university said Friday.

    Melloni has been studying how steroids used during adolescence may permanently alter the brain's ability to produce serotonin. Adolescent Syrian hamsters, given their similar brain circuitry to human adolescents, were administered doses of anabolic steroids and then measured for aggressiveness over certain periods of time.

    The researchers initially hypothesized steroid use during adolescence might permanently alter the brain's chemistry and a person's tendency toward aggression long after use has stopped.

    Their most recent findings, published this week in Hormones and Behavior, enabled them to confirm this hypothesis and conclude there is indeed a lengthy price -- namely long-term aggression -- to pay for drug abuse even after the ingestion of steroids ceases.

    "We know testosterone or steroids affect the development of serotonin nerve cells, which, in turn, decreases serotonin availability in the brain," Melloni says.
    Last edited by johnsomebody; 03-16-2004 at 11:12 AM.

  2. #2
    daem's Avatar
    daem is offline Anabolic Member
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    Oct 2002
    glad more research is finding conclusive evidence that teens should NOT take these drugs, as the live and learn advice never works.

    just one more piece of hard evidence that scientifically shows that AAS during adolescence causes permanent damage to the body...

  3. #3
    monstercojones's Avatar
    monstercojones is offline The Anabolic Assassin
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    Dec 2002
    ill give this a bump.....

    for anyone that doesnt know my situation,,, i got pushed into using AS at a young age (16)...e ven though ultimately it was my own mistake...

    and i can vouch for lower seratonin levels, i have some pretty heady depression issues...

    please younger lifters contemplating AS use, take this as a warning...

  4. #4
    Ex_banana-eater's Avatar
    Ex_banana-eater is offline Junior Member
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    Jun 2002
    Here's the study

    Serotonin modulates offensive attack in adolescent anabolic steroid -treated hamsters.

    Grimes JM, Melloni RH Jr.

    Behavioral Neuroscience Program, Department of Psychology, 125 Nightingale Hall, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.

    Chronic anabolic-androgenic steroid (AAS) treatment during adolescence facilitates offensive aggression in male Syrian hamsters (Mesocricetus auratus). The current study assessed whether adolescent AAS-facilitated offensive attack was modulated by serotonin (5-HT) and if AAS exposure during this developmental period influenced 5-HT innervation to areas of hamster brain implicated in aggressive behavior. In a first experiment, hamsters were administered high-dose AAS throughout adolescence, and then scored for offensive attack following the systemic administration of saline or fluoxetine, a selective 5-HT reuptake inhibitor. Saline-treated hamsters showed high levels of offensive attack, while treatment with fluoxetine attenuated the AAS-facilitated aggressive response. In a second experiment,were administered high-dose AAS or sesame oil throughout adolescence, tested for offensive attack and then examined for differences in 5-HT innervation to areas of the hamster brain important for aggression. Aggressive AAS-treated hamsters showed significant reductions in the number of 5-HT immunoreactive (5-HT-ir) varicosities and fibers in several of these areas, most notably the anterior hypothalamus (AH), ventrolateral hypothalamus (VLH) and medial amygdala (MeA). However, no differences in 5-HT afferent innervation were found in other aggression areas, such as the bed nucleus of the stria terminalis (BNST) and lateral septum (LS). Together, these results support a role for altered 5-HT innervation and function in adolescent AAS-facilitated offensive aggression.
    From this we can tell that high doses of steroids increase agressive response in rats, and an SSRI (selective serotonin reuptake inhibitor) prevents these effects. Since they were introducing an SSRI during adolescence you can hardly say that steroids would cause imbalances in seratonin when they are actually introducing something that directly disrupts serotonin.
    As well, they obviously had to kill the rats to check their levels after adolescence, which means they did not look at the long term effects, just hypothesized.

    Here is another study usually quoted by people

    Repeated anabolic-androgenic steroid treatment during adolescence increases vasopressin V(1A) receptor binding in Syrian hamsters: correlation with offensive aggression.

    DeLeon KR, Grimes JM, Melloni RH Jr.

    Behavioral Neuroscience Program, Department of Psychology, Northeastern University, Boston, Massachusetts 02115, USA.

    Repeated anabolic-androgenic steroid treatment during adolescence increases hypothalamic vasopressin and facilitates offensive aggression in male Syrian hamsters (Mesocricetus auratus). The current study investigated whether anabolic-androgenic steroid exposure during this developmental period influenced vasopressin V(1A) receptor binding activity in the hypothalamus and several other brain areas implicated in aggressive behavior in hamsters. To test this, adolescent male hamsters were administered anabolic steroids or sesame oil throughout adolescence, tested for offensive aggression, and examined for differences in vasopressin V(1A) receptor binding using in situ autoradiography. When compared with control animals, aggressive, adolescent anabolic steroid-treated hamsters showed significant increases (20-200%) in the intensity of vasopressin V(1A) receptor labeling in several aggression areas, including the ventrolateral hypothalamus, bed nucleus of the stria terminalis, and lateral septum. However, no significant differences in vasopressin V(1A) receptor labeling were found in other brain regions implicated in aggressive responding, most notably the lateral zone from the medial preoptic area to anterior hypothalamus and the corticomedial amygdala. These data suggest that adolescent anabolic steroid exposure may facilitate offensive aggression by increasing vasopressin V(1A) receptor binding in several key areas of the hamster brain. Copyright 2002 Elsevier Science (USA)

    PMID: 12367571 [PubMed - indexed for MEDLINE]
    This is discussed here:

    Take note that it is discussed AFTER the original post. The original post shows that superphysiological testosterone for long periods does not adversely effect adolescents moreso than an adult. It also lead to increased height rather than stunted growth in human adolescent males.

    Here was my reply:

    BTW Shpongled, how do you come to the conclusion that agressive behavior later in life would actually happen? The only thing the study showed was that Vasopressin receptor binding in the hypothalamus was greater. They were probably disected at the point of being administered androgens, thus this indicates not later in life, but while using. Many users report slight increases in agression while using, and then the agression goes away when discontinueing. Also, there were no markers of agression measured, just the V1a in the hypothalamus, which means it may have been an indicator yet we can't conlude a strong "will" produce agression. This study in the citation says nothing about long term, so I don't know how you can verify the later in life thing.
    Patrick Arnold (Ergopharm, Chemist) chimes in on the rat studies regarding behavior saying:

    Who knows why? Maybe its because the administration of androgens during that time gives the hamster a physical boost that then makes him stronger than other hamsters. As a result, in their social order he learns to take on a dominant and aggressive role. After that, he might become psychologically imprinted as an alpha hamster and continue that behaviour even after androgen administration ceases

    OTOH, human social settings are much more complex. It is not the person with the most testosterone or muscle that necessarily becomes dominant in our society. IN our society, interpersonal skills, intelligence, financial advantage, and many other things are much more important.

    My point I guess is that we should not automatically extrapolate unto humans the results from such animal studies
    Here is the first study for people who don't want to sign up for avant labs. It does not relate to behavior. It shows superphysiological doses of androgens are equally as safe in adolescents as adults though. It also shows 500mg of testosterone enanthate per week for long periods actually causes an increase in height:

    Therapy was started at a BA of 14 yr or older, adult final height significantly exceeded height prognosis at the time of start of treatment. This suggests that treatment had resulted in induction rather than reduction of growth -- this was treatment of constitutionally tall stature (CTS) children with androgen therapy (Testosterone Enanthate at 500mg/wk).

    __________________________________________________ _________________

    High doses of T induce suppression of the hypothalamo-pituitary-gonadal axis (113, 136). Contraceptive studies in adult men have shown that androgen-induced suppression of gonadotropins and of spermatogenesis is reversible (137, 138). However, extrapolation of these data to the management of tall stature in pubertal boys must be viewed with caution since factors that regulate spermatogenesis in normally functioning adult testes may not be the same as during puberty (139). Androgen therapy in tall boys is usually initiated at the first signs of puberty, and it is in this peripubertal period that important maturational changes take place in the testis (139, 140, 141, 142, 143, 144). Influenced by complex hormonal actions, these maturational processes eventually lead to initiation of spermatogenesis. Onset of spermatogenesis (spermarche) as detected by urine analysis (spermuria) appears to be an early pubertal event: the median age of spermarche has been estimated to be 13–14 yr (145, 146, 147, 148). In addition, it is noteworthy that administration of T esters at high doses may cause morphological and cytological changes, as shown in rat and human adult testes (149, 150, 151).

    1. Plasma hormone levels: High T levels are obtained during treatment with supraphysiological doses of androgens suppressing the hypothalamo-pituitary-gonadal axis (152).

    Zachmann, Prader, and co-workers (98, 113) reported a slow recovery of pituitary gonadotropins during LHRH-stimulation tests after discontinuation of T therapy. Brämswig et al. (136) demonstrated normalization of gonadotropin levels in 100 tall boys after discontinuation of treatment with follow-up periods up to 48 months, although transient hypergonadotropic LH- and FSH- secretory patterns were observed. In a recently published study by the same group (153), hormonal levels and testicular function were evaluated after a follow-up period of approximately 10 yr and compared with normal volunteers. Mean values of LH, FSH, PRL, T, estradiol, and sex hormone-binding globulin were in the normal range in both groups. T was lower and FSH was higher in treated tall men compared with volunteers, but the only statistically significant difference was for T. We observed different levels of gonadotropins in previously treated tall men compared with controls (tall and ‘normal’ men) (154). Androgen-treated tall men had significantly higher FSH levels compared with controls. Levels of plasma hormones were not significantly correlated with parameters of sperm quality; however, we observed significant negative correlations between plasma FSH levels and sperm concentration as well as the age at start of therapy in the androgen-treated men. We speculate that the higher levels of FSH may reflect intratesticular changes due to androgen treatment received during a period of testicular maturation especially during the earlier pubertal stages (155). These increased FSH levels may compensate for partially disturbed germinal function to maintain normal sperm quality (156). In a subgroup of previously treated and untreated men, we also measured inhibin B, which probably is a more direct marker of spermatogenesis than FSH (157). We found similar levels, well within the normal range (F. H. De Jong and W. J. De Waal, unpublished results). On the other hand, the difference in gonadotropin levels may also reflect a change in responsiveness at the hypothalamo-pituitary level (136).

    2. Testicular volume: Treatment with high doses of androgens induces reduction in testicular volume in adult men (158) as well as in tall adolescent boys (98, 99, 113). This implies major intratesticular changes during therapy such as a decrease in seminiferous tubule size (149, 150). These processes are likely to be reversible since testicular volume normalizes after discontinuation of therapy as shown in several studies (98, 99, 113, 158). This is in contrast to the observations of Willig et al. (159, 160), who reported significantly smaller testicular sizes in previously treated men. In contrast, in our studies at a mean follow-up period of 8 yr after cessation of treatment, there was no difference in mean testicular volume between treated and untreated tall men (154).

    3. Sperm quality: When sperm quality is evaluated, one must be aware of the normal distribution in the population as well as of confounding factors interfering with parameters of sperm quality. It is well established that varicocele (161, 162, 163, 164), smoking (165), sexually transmitted disease (166), and cryptorchidism (167) are likely to affect sperm quality and/or plasma hormone levels. Semen analysis in our study of previously androgen-treated men showed that sperm quality was comparable with a control group of untreated tall men, even after correction for the above mentioned possible interfering conditions, after a mean follow-up period of 8 yr. These findings are in agreement with the experiences reported by Zachmann and Prader and co-workers (98, 113). In contrast, Willig and co-workers (159, 160) found significantly reduced sperm concentrations in previously treated tall men compared with controls. Their control group, however, showed a relative high mean value of sperm concentration of 120.2 x 10'6/ml, almost twice as high as values found in the normal population at present (168, 169). Their treated group showed a mean sperm concentration of 63.4 x 10'6/ml, which is comparable with values found in our study (154). It is possible that differences in patient selection, semen analysis methodology, and treatment regimens may account for the observed differences. In addition, the extent to which interfering conditions are present may cause important bias as well. In a recent report Lemcke and co-workers (153) showed that 10 yr after T treatment, none of the tall men had azoospermia, and the mean ejaculate parameters were in the normal range or only slightly subnormal. Overall, seminal parameters of T-treated tall men were slightly, but not significantly, lower compared with normal statured volunteers. Interestingly, they found a significantly higher prevalence of varicocele and maldescended testes in the tall men compared with their control group of normal volunteers (153). They surmised that varicocele and maldescended testes, rather than T treatment, caused the somewhat lower semen quality in the tall men. In our studies in treated and untreated tall men, we observed an overall prevalence of varicocele of 42% (12% subclinical and 30% clinical) (154). This would suggest that varicocele occurs more often than reported in the normal population (12.4–25.8%) (170, 171, 172). A relationship to androgen treatment is unlikely since no difference in the prevalence of varicocele was observed between androgen-treated men and controls. One could speculate on the impact of stature on the pathogenesis of varicocele (153, 154).

    4. Pregnancy/paternity: Thus far, only casuistic and exclusive female data have been available on successful pregnancies after height-reductive therapy. At the time of our follow-up studies five of the 43 androgen-treated men and six of the 30 untreated tall men had fathered one or more children (154). All 11 men reported that pregnancy had occurred in their partners after less than 1 yr of unprotected coitus. Two other pregnancies, fathered by a previously treated man and a control, respectively, ended in spontaneous abortion. These very limited numbers do not allow any further conclusions.

    Other clinical effects
    Many patients experience side effects during therapy (98, 99, 113, 132, 173, 174). Most of these, however, are mild and transient (see Table 7). In some patients, slight to moderate edema, notably in the pretibial or malleolar area, was associated with marked weight gain during the first 6 months of treatment. This indicates that the early gain in weight is not only due to protein anabolism but also to water retention (98). Acne was by far the most reported side effect (98, 99, 175). Occasionally acne fulminans has been reported and necessitated discontinuation of therapy (173, 176). A causal relationship with androgen therapy is likely as shown by Fyrand et al. (177). Hinkel et al. (178) investigated the effects of high doses of androgens on lipoproteins during and after the cessation of therapy. Although during treatment a significant fall of triglycerides and HDL was observed, all values normalized after the end of treatment (178). In our studies, gynecomastia occurred in 13% of the cases. Since gynecomastia is rather prevalent in population studies in pubertal boys (179), it is difficult to say whether the condition had increased. One would expect that treatment would have effects on sexuality (sex interest, masturbation). Although in one study a marked increase of sexuality in younger, but not in older patients, was noted, it never exceeded the normal range seen in adolescence (98). Treatment with supraphysiological doses of T were not shown to provoke aggressive behavior in adolescents or young adults (180, 181).
    Last edited by Ex_banana-eater; 03-16-2004 at 01:42 PM.

  5. #5
    johnsomebody's Avatar
    johnsomebody is offline Senior Member
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    Maybe I'm missing something but I don't get the above response at all.

    The first study involves hamsters not rats -are you referring to some other study? I also can't imagine why you'd say "you can hardly say that steroids would cause imbalances in serotonin" when the conclusion is the opposite of what you say - "these results support a role for altered 5-HT innervation and function in adolescent AAS-facilitated offensive aggression". 5-HT is another term for serotonin. Fluoxetine (aka Prozac) is used to treat imbalances in serotonin, and the adolscent hamsters lost their AAS-induced aggression when given it. The study looks to me like it was done to try to determine the cause of increased agression in AAS administered hamsters.

    It also showed definite alterations in brain structure in those hamsters treated with AAS.

    The height thing is another issue altogether and not what this thread is about.

    In fact the thread at avantlabs you posted refers to a study that has nothing to do with serotonin or brain development as you say yourself:
    Posted: Dec 14 2003, 03:39 PM
    "This dosnt adress any brain developemental issues which is unfortunate"

    You then say "Anyway I still wouldn't recommend AAS to teenagers like myself since we're all too immature and would end up killing ourselves."

    I think that says it all, thank you.
    Last edited by johnsomebody; 03-16-2004 at 03:01 PM.

  6. #6
    johnsomebody's Avatar
    johnsomebody is offline Senior Member
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    Actually I don't want to be unnecessarily alarmist here. Without seeing the Hormones and Behavior article (which I can't find - the one I do find is undated and may not be the one referred to at top) it's not possible to determine exactly what "permanent" may mean here, though from the terminology used in the article one can assume "life-long".
    Last edited by johnsomebody; 03-16-2004 at 03:00 PM.

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