AAS usage and serotonin levels (Bill, Dr.Scally)

Discussion in 'Steroid Forum' started by Reinheart, Oct 14, 2011.

  1. Reinheart

    Reinheart Member

    Can steroids lower serotonin levels to the point where one will get depressed and maybe even get a panic attack? We are talking about healthy men over the age of 21, not adolescents.

    Thank you.
     
  2. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Are you asking while on or off AAS?
     
  3. Reinheart

    Reinheart Member

    Both please. Can steroids have a long term effect on serotonin levels?
     
  4. dfein

    dfein Junior Member

    It seems the testosterone-derived androgens are capable of causing anxiety and paranoia, particularly equipoise. I have not heard of anyone complaining of mental issues from plain testosterone (except when the levels are very low which will cause depression).
     
  5. quenca333

    quenca333 Junior Member

    hm. I dont think so
     
  6. quenca333

    quenca333 Junior Member

    not while on


    Endocrinology. 2011 May;152(5):2001-10. Epub 2011 Mar 8.
    Androgenic influence on serotonergic activation of the HPA stress axis.
    Goel N, Plyler KS, Daniels D, Bale TL.
    Source

    Department of Animal Biology, University of Pennsylvania, School of Veterinary Medicine, Philadelphia, Pennsylvania 19104, USA.
    Abstract

    The higher incidence of stress-mediated affective disorders in women may be a function of gonadal hormone influence on complex interactions between serotonin and neural circuits that mediate the hypothalamic-pituitary-adrenal (HPA) stress axis. The paraventricular nucleus of the hypothalamus (PVN) receives serotonergic innervation, and selective serotonin reuptake inhibitors such as citalopram activate the HPA axis independent of stress. We have previously demonstrated that the magnitude of this serotonergic activation was greater in females and was attenuated by testosterone administration; however, the potential central sites of action where androgens reduce these serotonergic effects have not been determined. Therefore, we examined a time course of corticosterone production and used central c-Fos protein levels to assay neuronal activation in stress-related brain regions in female, male, and gonadectomized male mice after an acute citalopram injection (15 mg/kg). In the hippocampus, c-Fos-immunoreactivity was greater in males than in females or gonadectomized males. This same pattern emerged in the lateral septum after vehicle and gonadectomy reversed the effect of citalopram. These regions are important for inhibitory influences on the PVN, and accordingly, hippocampal c-Fos levels were negatively correlated with corticosterone production. No sex differences in c-Fos were detected in the PVN, cingulate cortex, or paraventricular thalamus in response to vehicle or citalopram. These data support brain region-specific regulation of the HPA axis where sex differences may be mediated partly through androgen enhancement of signaling in inhibitory regions.

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    J Psychopharmacol. 2009 Sep;23(7):841-53. Epub 2008 Jun 18.
    Is there a neuroendocrinological rationale for testosterone as a therapeutic option in depression?
    Ebinger M, Sievers C, Ivan D, Schneider HJ, Stalla GK.
    Source

    Department of Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany. martin.ebinger@mh.org.au
    Abstract

    Depression is a disease of growing incidence and economic burden worldwide. In view of increasing treatment resistance, new therapeutic approaches are urgently needed. In addition to its gonadal functions, testosterone has many effects on the central nervous system. An association between testosterone levels and depressive symptoms has been proposed. Many hormones and neurotransmitters are involved in the aetiology and the course of depression including serotonin, dopamine, noradrenaline, vasopressin and cortisol. Testosterone is known to interact with them. Preclinical data suggest that testosterone has antidepressant potential. However, the data from clinical studies have been inconsistent. This review provides a critical overview on the currently available preclinical and clinical literature and concludes with clinical recommendations.

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    J Clin Psychopharmacol. 2005 Dec;25(6):584-8.
    Intramuscular testosterone supplementation to selective serotonin reuptake inhibitor in treatment-resistant depressed men: randomized placebo-controlled clinical trial.
    Seidman SN, Miyazaki M, Roose SP.
    Source

    Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA. sns5@columbia.edu
    Abstract
    BACKGROUND:

    Treatment-resistant depression is a persistent clinical problem. Exogenous testosterone therapy has psychotropic effects and has been proposed as an antidepressant supplement, although this strategy has received limited systematic study.
    OBJECTIVE:

    The aim of the study was to examine the mood effects of testosterone supplementation to a serotonergic antidepressant in men with treatment-resistant depression.
    METHOD:

    Twenty-six healthy adult men with major depressive disorder, partial or nonresponse to 2 adequate antidepressant trials during the current episode, and currently using a selective serotonin reuptake inhibitor were randomized under double-blind conditions to receive intramuscular injections of escalating doses of testosterone or placebo, in addition to their existing selective serotonin reuptake inhibitor regimen, for 6 weeks. The main outcome measure was the Hamilton Rating Scale for Depression score.
    RESULTS:

    The mean age was 46.4 +/- 10.8 years; mean total testosterone level, 417.5 +/- 197 ng/dL; mean baseline Hamilton Rating Scale for Depression score, 22.2 +/- 5.2; and median duration of the current depressive episode, 6.3 +/- 10.6 years. Hamilton Rating Scale for Depression scores decreased significantly in both testosterone (8.4) and placebo (7.4) groups. Antidepressant response, defined as a 50% decline in Hamilton Rating Scale for Depression score, was achieved by 53.8% (7/13) in the testosterone group and 23.1% (3/13) in the placebo group (P = 0.226).
    CONCLUSION:

    Both injectable testosterone and placebo supplementation to selective serotonin reuptake inhibitor were associated with improvement in mood; group differences were not distinguishable in this small sample of predominantly eugonadal men with treatment-resistant depression.
     
    Last edited: Oct 16, 2011
  7. quenca333

    quenca333 Junior Member

    J Steroid Biochem Mol Biol. 2005 Mar;94(4):369-73. Epub 2005 Jan 28.
    Effect of testosterone and steroids homologues on indolamines and lipid peroxidation in rat brain.
    Guzmán DC, Mejía GB, Vázquez IE, García EH, del Angel DS, Olguín HJ.
    Source

    Laboratorio de Neuroquímica, Instituto Nacional de Pediatría, Avenida Imán No. 1, 3er piso, Colonia Cuicuilco, CP 04530 México City, Mexico.
    Abstract

    The purpose of the present study was to evaluate the effect of 4-pregnen-17-hydroxy-3-one (A) and two steroids homologues: 3beta-acetoxy-5,16-pregnadien-20-one (B) and 3beta-acetoxy-16alpha-17alpha-epoxy-4-pregnen-20-one (C). Male Wistar rats were treated with o-cresol combined (A, B or C) steroids. Lipid peroxidation status as result of measurement reactive substances to thiobarbituric acid (TBARS) as well as serotonin (5-HT) and its precursor 5-hydroxytryptophan (5-HTP) were measured. The prostate glands were weighed, the 5alpha-reductase activity was determined. The animals treated with A, B, and C steroids showed a slight increase in both 5alpha-reductase activity and prostate size. 5-HT and 5-HTP levels did not change significantly, and TBARS showed an increase in the group treated with B steroid and a decrease in the A steroid group with significant differences in both groups (p<0.05) versus control group. Results suggest that A steroid reduces TBARS in rat brain, perhaps as a result of the interaction between the testosterone unsaturated carbons and OH(-) groups with free radicals.

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    on the other side..


    Med Sci Monit. 2005 Apr;11(4):RA136-45. Epub 2005 Mar 24.
    Testosterone and aggressiveness.
    Giammanco M, Tabacchi G, Giammanco S, Di Majo D, La Guardia M.
    Source

    Institute of Physiology and Human Nutrition, University of Palermo, 90127 Palermo, Italy. giammanco@unipa.it
    Abstract

    Aggressiveness is an ancestral behavior common to all animal species. Its neurophysiological mechanisms are similar in all vertebrates. Males are generally more aggressive than females. In this review, aggressive behavior in rodents, monkeys, and man and the role of testosterone and brain serotonin levels have been considered. Interspecific aggressiveness in rats has been studied considering the mouse-killing behavior; the neonatal androgenization of females increases adult mouse-killing as does the administration of testosterone in adults. Intraspecific aggressiveness was studied by putting two or more male rats (or mice) in the same cage; the condition of subjection or dominance is influenced by testosterone. In monkeys, testosterone is related to aggressiveness and dominance and, during the mating season, increases in testosterone levels and aggressive attitude are observed. In men, higher testosterone levels were obtained in perpetrators of violent crimes, in men from the army with antisocial behaviors, in subjects with impulsive behaviors, alcoholics and suicidals, in athletes using steroids, and during competitions. Aggressive and dominant behavior are distinguished. Testosterone influences both of these, even if man is usually inclined to affirm his power without causing physical damage. Testosterone receptors are mainly in some hypothalamic neurons, where it is aromatized into estrogens, which determine the increase in aggressiveness. A relation between testosterone levels and diencephalic serotonin has been shown: in fact, the lack of serotonin increases aggressive behaviors both in animals and man. Testosterone also increases ADH levels in the medial amygdala, lateral hypothalamus, and preoptical medial area, involved in aggressive behaviors.