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Speaking of steroids
- Thread starter armygas
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These drugs are out there and can be bought on the INTERNET or imported from other countries.
If that guy didn't prescribe the drugs they would have gotten them from other sources and they would have still died, maybe quicker though!
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speaking of steroids anyone know if there is any adrenal suppression in patients who have received epidural steroid injections ? Asked a couple of pain docs and they said they were not sure.
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It does occur, but is uncommon. However, with repeated injections on a frequent basis, the risk is probably higher. Hence the sanctity of the rule of "3" epidural steroid injections. A rule that is completely non-evidenced based...
Rev Rhum Engl Ed. 1995 Jun;62(6):429-32.
Systemic effects of epidural dexamethasone injections.Maillefert JF, Aho S, Huguenin MC, Chatard C, Peere T, Marquignon MF, Lucas B, Tavernier C.
Department of Rheumatology, General Hospital, Dijon, France.
OBJECTIVES: to evaluate potential systemic effects of a single epidural injection of dexamethasone. PATIENTS AND METHODS: each of nine patients (five males and four females, mean age 47 +/- 11.8 years) admitted for sciatica was given a single epidural injection of 15 mg dexamethasone acetate. Before the injection (D0) and two (D2), seven (D7) and 21 (D21) days after the injection, the following laboratory tests were performed: serum cortisol and ACTH in the morning after an overnight fast, free cortisol in a 24-hour urine collection, fasting serum levels of glucose, triglycerides and cholesterol, serum levels of sodium and potassium. Blood pressure was measured on D0, D2, and D7. RESULTS: Serum cortisol, ACTH and urinary cortisol were profoundly decreased on D2 and D7 but normal on D21. There were no changes in fasting serum glucose, triglycerides, cholesterol, sodium or potassium levels. CONCLUSION: a single epidural injection of 15 mg dexamethasone acetate is associated with transient adrenal suppression, denoting passage of the steroid into the systemic bloodstream. However, evidence of hypercorticism is usually lacking.
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Wait, I'm pretty sure the article refers to steroids of the anabolic/andrenergic persuassion. Not some glucocorticoid (synthetic or not).
Regardless, I suppose there could be some adrenal suppression of the zona reticularis (not sure though) as a result of exogenous testosterone (or derivitive of) administration.
Anyone ever hear of clomid (FSH analog)? Also hCG (LH analog)has been used for post cycle testicular recovery. Anyone familiar with this, or have any knowledge of such?? (first hand or otherwise)
Regardless, I suppose there could be some adrenal suppression of the zona reticularis (not sure though) as a result of exogenous testosterone (or derivitive of) administration.
Anyone ever hear of clomid (FSH analog)? Also hCG (LH analog)has been used for post cycle testicular recovery. Anyone familiar with this, or have any knowledge of such?? (first hand or otherwise)
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Thank You🙁
there is a difference.
And the article may be new but the story is very old.
The steriods may have contributed but the guy was not all together at all. Roid Rage is a phenomenon we all know about but it tal=kes more than roids to make someone do this IMHO.
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I do know this, chronic elevation of steroid levels will cause atrophy of structures within the limbic system (i.e. the hippocampus and amygdala) and there is a very strong link b/w elevated steroid levels (either exogenous or endogenous) and major depression. Did they cause his episode...... maybe not, but if he was using them then it certainly did not help his problem.
Also, the adrenal suppression from anabolic steroids is severe and there really is no difference (steroids are steroids and will suppress CRF and ACTH), in fact it may be worse..... why do you think wrestlers are dying so young?
[SIZE=+1]The effect of anabolic steroids on the gastrointestinal system, kidneys, and adrenal glands.[/SIZE]
Modlinski R, Fields KB.
Moses Cone Family Medicine Residency, Greensboro, NC 27401, USA.
Over the past several decades we have seen an increase in the prevalence of anabolic steroid use by athletes. Because use of anabolic steroids is illicit, much of our knowledge of their side effects is derived from case reports, retrospective studies, or comparisons with studies in other similar patient groups. It has been shown that high-dose anabolic steroids have an effect on lowering high-density lipoprotein, increasing low-density lipoprotein, and increasing the atherogenic-promoting apolipoprotein A. Steroid abuse can also be hepatotoxic, promoting disturbances such as biliary stasis, peliosis hepatis, and even hepatomas, which are all usually reversible upon discontinuation. Suppression of the hypothalamic adrenal axis can also lead to profound adrenal changes that are also reversible with time. Although rare, renal side effects have also been documented, leading to acute renal failure and even Wilms' tumors in isolated cases. Much of our knowledge of these potentially severe but usually limited side effects is confounded by use of combinations of different steroid preparations and by the concomitant use with other substances. Physicians must target their efforts at counseling adolescents and other athletes about the potential harms of androgenic anabolic steroids and the legal options to improve strength and performance.
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Anabolic steroids are Androgens and Androgen derivatives, they do not have negative feedback on ACTH or CRF, they could suppress FSH and cause secondary suppression of endogenous Androgens and infertility.
These are two separate systems.
The study you are quoting did not say that anabolic steroids suppress the adrenal/pituitary/hypothalamic system and if they did they would be WRONG.
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Really? no suppression? Your telling me adrenal androgens have no direct suppression?
This is a adrenal cell assay showing direct suppression of cortisol synthesis. It doesn't matter if there is short loop or long loop negative feedback, the point is that there is direct adrenal suppression and thus the HPS axis is disrupted/suppressed
J Anim Sci. 1993 Jul;71(7):1771-7.Related Articles, Testosterone, dihydrotestosterone, trenbolone acetate, and zeranol alter the synthesis of cortisol in bovine adrenocortical cells.[/SIZE]
Isaacson WK, Jones SJ, Krueger RJ.
Department of Animal Science, University of Nebraska, Lincoln 68583-0908.
The objective of this study was to examine the effect of anabolic steroids (testosterone, T; dihydrotestosterone, D; trenbolone acetate, B; and zeranol, Z) on cortisol synthesis by cultured bovine adrenocortical cells. Adrenal glands were obtained from slaughter-aged steers (n = 4). Cortical cells were isolated and their steroidogenic capacity was examined. They were plated in multiwell culture plates. At confluence, cells were treated with T, D, B, or Z at 0, 10, 50, 125, or 500 ng/mL (eight wells per treatment). Twenty-four hours after treatment, one-half of each treatment concentration was stimulated with 10(-9) M ACTH. After 8 h of incubation, cortisol concentration in the media was measured using RIA. Cortical cells were removed from the plates using 1 mM EDTA and analyzed for DNA content. Data were subjected to rank transformation and analyzed by randomized complete block design. Adrenocorticotropic hormone stimulated (P < .01) the release of cortisol by more than threefold. Cortisol synthesis was lower (P < .05) in the presence of T, D, and B. Testosterone caused a greater (P < .05) suppression in cortisol production at 50 and 125 ng/mL than did D. The suppression of cortisol synthesis did not differ between B and T or between B and D. Cortisol synthesis was lowered (P < .05) by the presence of T, D, and B in both ACTH-stimulated and nonstimulated cells but was only suppressed in ACTH-stimulated cells of Z-treated cells.(ABSTRACT TRUNCATED AT 250 WORDS)
The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-adrenal response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD, Hinds LR, Handa RJ. J Neurosci. 2006 Feb 1;26(5):1448-56.
Department of Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA. [email protected]
Estrogen receptor beta (ERbeta) and androgen receptor (AR) are found in high levels within populations of neurons in the hypothalamus. To determine whether AR or ERbeta plays a role in regulating hypothalamo-pituitary-adrenal (HPA) axis function by direct action on these neurons, we examined the effects of central implants of 17beta-estradiol (E2), 5alpha-dihydrotestosterone (DHT), the DHT metabolite 5alpha-androstan-3beta, 17beta-diol (3beta-diol), and several ER subtype-selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress. In addition, activation of neurons in the paraventricular nucleus (PVN) was monitored by examining c-fos mRNA expression. Pellets containing these compounds were stereotaxically implanted near the PVN of gonadectomized male rats. Seven days later, animals were killed directly from their home cage (nonstressed) or were restrained for 30 min (stressed) before they were killed. Compared with controls, E2 and the ERalpha-selective agonists moxestrol and propyl-pyrazole-triol significantly increased the stress induced release of corticosterone and ACTH. In contrast, central administration of DHT, 3beta-diol, and the ERbeta-selective compound diarylpropionitrile significantly decreased the corticosterone and ACTH response to immobilization. Cotreatment with the ER antagonist tamoxifen completely blocked the effects of 3beta-diol and partially blocked the effect of DHT, whereas the AR antagonist flutamide had no effect. Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN. Together, these studies indicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conversion to 3beta-diol and subsequent binding to ERbeta.
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Since the adrenal glands produce DHEA(dehydroepiandtrostenedione) and androstenedione, I don't see a direct negative feedback from endogenous or exogenous testosterone on the adrenals (zona reticularis).
However, hypercortisolemia (from exogenous admin of corticosteriods) could suppress ACTH at the anterior pituitary. And since ACTH is the major stimulator of adrenal function (stimulates cholesterol desmolase, which is the rate limiting?/first step in all 3 reaction products of the adrenals....aldosterone, cortisol, and DHEA/androstendione).
THUS, in females hypercortisolemia could negatively feedback on androgen production. In males, we still have the testes, which would not be effected, and may even be enhanced given that our own adrenal androgen production may be decreased due to the above.
Thoughts??
However, hypercortisolemia (from exogenous admin of corticosteriods) could suppress ACTH at the anterior pituitary. And since ACTH is the major stimulator of adrenal function (stimulates cholesterol desmolase, which is the rate limiting?/first step in all 3 reaction products of the adrenals....aldosterone, cortisol, and DHEA/androstendione).
THUS, in females hypercortisolemia could negatively feedback on androgen production. In males, we still have the testes, which would not be effected, and may even be enhanced given that our own adrenal androgen production may be decreased due to the above.
Thoughts??
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I am not aware of any clinical study in humans where testosterone derivatives where shown to suppress the hypothalamus /pituitary/ adrenal system, are you aware of such study?
not on isolated pig adrenal cells?
and even if I agree with your logic and accept that study, it does not show an effect on ACTH/ CRF as you claimed initially, it attempts to show a direct effect on isolated pig adrenal cells.
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You know as well as I do that mammalian cellular responses are very universal, if they weren't then why do we get funding to perform studies if animal models did not translate into clinical use?
Your just going to argue to argue, androgens can work at all points along the HPA axis and suppress it, I could keep posting studies but that gets old.
You did see the androgen study I posted right? about androgens acting on ER-beta in the hypothalamus to suppress activity?
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No, I think when you issue statements with certain generalizations on a forum like this one, you need to be able to show convincing evidence to prove your point and not get defensive and evasive when your point is scrutinized.
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I am still waiting for a clinical study in humans that shows testosterone derivatives supressing CRF/ACTH/Cortisol axis.
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Neuropsychopharmacology. 2005 Oct;30(10):1906-12. Related Articles, Links
Testosterone suppression of CRH-stimulated cortisol in men.
Rubinow DR, Roca CA, Schmidt PJ, Danaceau MA, Putnam K, Cizza G, Chrousos G, Nieman L.
Behavioral Endocrinology Branch, National Institute of Mental Health, Building 10-CRC, 10 Center Drive MSC 1276, Bethesda, MD 20892-1276, USA. [email protected]
Despite observations of age-dependent sexual dimorphisms in hypothalamic-pituitary-adrenal (HPA) axis activity, the role of androgens in the regulation of HPA axis activity in men has not been examined. We assessed this role by performing CRH stimulation tests in 10 men (ages 18-45 years) during gonadal suppression with leuprolide acetate and during testosterone addition to leuprolide. CRH-stimulated cortisol levels as well as peak cortisol and greatest cortisol excursion were significantly lower (p<0.05, 0.005, and 0.01, respectively) during testosterone replacement compared with the induced hypogonadal condition (leuprolide plus placebo); cortisol area under the curve was lower at a trend level (p<0.1). Paradoxically, CRH-stimulated corticotropin (ACTH) was increased significantly during testosterone replacement (p<0.05). The cortisol : ACTH ratio, a measure of adrenal sensitivity, was lower during testosterone replacement (p<0.1). A mixed effects regression model showed that testosterone but not estradiol or CBG significantly contributed to the variance of cortisol. These data demonstrate that testosterone regulates CRH-stimulated HPA axis activity in men, with the divergent effects on ACTH and cortisol suggesting a peripheral (adrenal) locus for the suppressive effects on cortisol. Our results further demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone.
Their conclusion:
In conclusion, we have shown that testosterone regulates CRH-stimulated HPA axis activity in men. Similar to findings in animal studies, CRH-stimulated cortisol was decreased during testosterone-replaced compared with hypogonadal conditions. The concomitant increase in ACTH suggests that the decrease in stimulated cortisol levels by testosterone or its metabolites is mediated at the level of the adrenal gland. While provocative, these results must be viewed with caution. Notwithstanding the value of the repeated measures design, the sample size is small, and the differences observed across hormonal conditions, while significant, are small in magnitude (particularly the ACTH results) and of unclear clinical significance. Nonetheless, our findings complement our earlier demonstration of the regulatory role of progesterone on the HPA axis in women (Roca et al, 2003) and suggest that, as in animals, the reproductive axis actively participates in the regulation of the stress axis and is not merely acted on by it. While the effects observed in this study are quite modest, they demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone. Finally, the potential health implications of the removal of restraint on stress-stimulated cortisol secretion during the hypogonadism of aging deserve examination.
Testosterone suppression of CRH-stimulated cortisol in men.
Rubinow DR, Roca CA, Schmidt PJ, Danaceau MA, Putnam K, Cizza G, Chrousos G, Nieman L.
Behavioral Endocrinology Branch, National Institute of Mental Health, Building 10-CRC, 10 Center Drive MSC 1276, Bethesda, MD 20892-1276, USA. [email protected]
Despite observations of age-dependent sexual dimorphisms in hypothalamic-pituitary-adrenal (HPA) axis activity, the role of androgens in the regulation of HPA axis activity in men has not been examined. We assessed this role by performing CRH stimulation tests in 10 men (ages 18-45 years) during gonadal suppression with leuprolide acetate and during testosterone addition to leuprolide. CRH-stimulated cortisol levels as well as peak cortisol and greatest cortisol excursion were significantly lower (p<0.05, 0.005, and 0.01, respectively) during testosterone replacement compared with the induced hypogonadal condition (leuprolide plus placebo); cortisol area under the curve was lower at a trend level (p<0.1). Paradoxically, CRH-stimulated corticotropin (ACTH) was increased significantly during testosterone replacement (p<0.05). The cortisol : ACTH ratio, a measure of adrenal sensitivity, was lower during testosterone replacement (p<0.1). A mixed effects regression model showed that testosterone but not estradiol or CBG significantly contributed to the variance of cortisol. These data demonstrate that testosterone regulates CRH-stimulated HPA axis activity in men, with the divergent effects on ACTH and cortisol suggesting a peripheral (adrenal) locus for the suppressive effects on cortisol. Our results further demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone.
Their conclusion:
In conclusion, we have shown that testosterone regulates CRH-stimulated HPA axis activity in men. Similar to findings in animal studies, CRH-stimulated cortisol was decreased during testosterone-replaced compared with hypogonadal conditions. The concomitant increase in ACTH suggests that the decrease in stimulated cortisol levels by testosterone or its metabolites is mediated at the level of the adrenal gland. While provocative, these results must be viewed with caution. Notwithstanding the value of the repeated measures design, the sample size is small, and the differences observed across hormonal conditions, while significant, are small in magnitude (particularly the ACTH results) and of unclear clinical significance. Nonetheless, our findings complement our earlier demonstration of the regulatory role of progesterone on the HPA axis in women (Roca et al, 2003) and suggest that, as in animals, the reproductive axis actively participates in the regulation of the stress axis and is not merely acted on by it. While the effects observed in this study are quite modest, they demonstrate that the enhanced stimulated HPA axis activity previously described in young men compared with young women cannot be ascribed to an activational upregulation of the axis by testosterone. Finally, the potential health implications of the removal of restraint on stress-stimulated cortisol secretion during the hypogonadism of aging deserve examination.
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So there is animal and human data that implicate androgen involvement in the HPA axis.
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Back to steroids and aggression................
Biol Psychiatry. 2007 Feb 1;61(3):405-11. Epub 2006 Sep 1.Related Articles, Links
[SIZE=+1]Cortisol moderates the relationship between testosterone and aggression in delinquent male adolescents.[/SIZE]
Popma A, Vermeiren R, Geluk CA, Rinne T, van den Brink W, Knol DL, Jansen LM, van Engeland H, Doreleijers TA.
Departments of Child and Adolescent Psychiatry, VU University Medical Center, Amsterdam. [email protected]
BACKGROUND: In animals, strong evidence exists for an association between testosterone and aggression. In humans, and particularly in children and adolescents, findings have been less consistent. Previous research has suggested that this may partly be due to moderating effects of other factors, e.g., hormones. This study aims to investigate the moderating effect of cortisol on the relationship between testosterone and subtypes of aggression in delinquent male adolescents. METHODS: Participants were 103 boys (mean age 13.7) referred to a delinquency diversion program. Testosterone and cortisol levels were determined from saliva samples collected during resting conditions and related to self-report scores on overt and covert aggression. RESULTS: Linear regression analyses revealed a significant interaction between cortisol and testosterone in relation to overt aggression, with a significant positive relationship between testosterone and overt aggression in subjects with low cortisol levels but not in subjects with high cortisol levels. Using the same model for covert aggression, no significant effects of testosterone, cortisol, or testosterone x cortisol interaction were found. CONCLUSIONS: These results indicate a moderating effect of cortisol on the relationship between testosterone and overt aggression in delinquent male adolescents. Implications and directions for future research are discussed.
So with this recent study, one could pose an argument that steroids may alter the HPA, decrease cortisol in some people and create aggressive tendencies.
Biol Psychiatry. 2007 Feb 1;61(3):405-11. Epub 2006 Sep 1.Related Articles, Links
[SIZE=+1]Cortisol moderates the relationship between testosterone and aggression in delinquent male adolescents.[/SIZE]
Popma A, Vermeiren R, Geluk CA, Rinne T, van den Brink W, Knol DL, Jansen LM, van Engeland H, Doreleijers TA.
Departments of Child and Adolescent Psychiatry, VU University Medical Center, Amsterdam. [email protected]
BACKGROUND: In animals, strong evidence exists for an association between testosterone and aggression. In humans, and particularly in children and adolescents, findings have been less consistent. Previous research has suggested that this may partly be due to moderating effects of other factors, e.g., hormones. This study aims to investigate the moderating effect of cortisol on the relationship between testosterone and subtypes of aggression in delinquent male adolescents. METHODS: Participants were 103 boys (mean age 13.7) referred to a delinquency diversion program. Testosterone and cortisol levels were determined from saliva samples collected during resting conditions and related to self-report scores on overt and covert aggression. RESULTS: Linear regression analyses revealed a significant interaction between cortisol and testosterone in relation to overt aggression, with a significant positive relationship between testosterone and overt aggression in subjects with low cortisol levels but not in subjects with high cortisol levels. Using the same model for covert aggression, no significant effects of testosterone, cortisol, or testosterone x cortisol interaction were found. CONCLUSIONS: These results indicate a moderating effect of cortisol on the relationship between testosterone and overt aggression in delinquent male adolescents. Implications and directions for future research are discussed.
So with this recent study, one could pose an argument that steroids may alter the HPA, decrease cortisol in some people and create aggressive tendencies.
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ok,
that's a better study, at least they had 10 people as a specimen not isolated pig cells.
This remains an area for debate and further study as the authors mentioned.
I would like to remind you of the certainty you used claiming that all steroids are the same and that adrenal suppression might be (even worse) with androgens than with corticosteroids.
Do you see this kind of certainty in this study? or in any study?
reffering to: Rubinow DR, Roca CA, Schmidt PJ, Danaceau MA, Putnam K, Cizza G, Chrousos G, Nieman L.
that's a better study, at least they had 10 people as a specimen not isolated pig cells.
This remains an area for debate and further study as the authors mentioned.
I would like to remind you of the certainty you used claiming that all steroids are the same and that adrenal suppression might be (even worse) with androgens than with corticosteroids.
Do you see this kind of certainty in this study? or in any study?
reffering to: Rubinow DR, Roca CA, Schmidt PJ, Danaceau MA, Putnam K, Cizza G, Chrousos G, Nieman L.
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Your conclusion is completely unrelated to the context of this study.
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Well, I would compare WWE wrestler mortality with a control population. I would bet that would be quite a significant difference.
I have been perusing PubMed and it must be a valid research area as (depending on the keywords) there are b/w 1100-2200 articles on this topic.
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It is definitly a valid research area, and we will know more about it in the future.
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Agreed
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Not really, there is a large steroid receptor density within the limbic system but I agree that the research is lacking but that is the point of good peer-reviewed research....to provoke thought and future directions.
Again, do I think steroids "caused" all these problems....no. But, I do think that they negatively affected pre-existing conditions.
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Fair enough.
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Do you know what part of the limbic system? hippocampus? amygdala? basal forebrain?
One would think the amygdala as it's most specific to perception of threats and fear.
Anyone?
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I can definitely say for certain that the hippocampus is one spot: here is an excerpt from a manuscript I wrote for one of my written qualification questions.
The hallmark of stressful experiences is a rise in adrenal corticosteroid levels (Warner-Schmidt and Duman, 2006). Corticosteroids enter the systemic circulation, pass through the blood brain barrier and bind to mineralcorticoid receptors (MR) and glucocorticoid receptors (GR) in the brain. In the hippocampus, both MR and GR exist (de Kloet et al., 1999). The GR receptor has been implicated in the pathology of depression as characterized by dexamethasone during in vivo binding studies (Pariante and Miller, 2001). GR belongs to the superfamily of nuclear receptors that function as ligand-dependent transcription factors (Beato et al., 1995; Bamberger et al., 1996). After ligand binding, GR phosphorylation and dissociation for the steroid/GR complex occurs. Translocation of the complex to the nucleus proceeds and results in the binding of DNA response elements, activation of transcriptional factors, and other cellular processes (Beato and Pacheco, 1996; Reichardt, et al., 1998). After exposure to a marked stressor, activation of GR in conjunction with MR enhances calcium influx and amplifies the response of biogenic amines (Joels, M. and de Kloet, 1989; Kerr et al., 1989; Joels et al., 1991; Beck et al., 1994; Joels and de Kloet, 1993). This altered response secondary to marked GR receptor activation could begin the previously described cycle of excitotoxic hippocampal degradation.
Here is another part of my manuscript where I present a theory from Egger (2007) which could account for the amygdala atrophy associated with hippocampal dysfunction:
It has recently been suggested that the circuit of emotion begins and ends in the hippocampus. Depression requires a person to sense a feeling of loss (Eggers, 2007). This entails placing and maintaining a valence on experience and self-worth. Thus, functional communication between the hippocampus and structures of the limbic system, most notably the amygdala, must exist. Disruption of this bidirectional communication could explain atrophy of the amygdala that accompanies many findings of hippocampal atrophy in human studies. This is important as the amygdala is thought to be the hub of sensing emotional value. Egger (2007) proposed an adjustment of the Papez' theory of emotion which could directly affect mood states. The adjustment infers that a cyclical circuit begins in the hippocampus, extends to the amygdala, to serotonergic pacemaker cells in the Dorsal raphe nucleus (DRN), and then back to the dentate gyrus of the hippocampus along two paths. The first relay is the DRN directly to the dentate gyrus with a second longer relay traveling from the DRN to the entorhinal cortex and back to the hippocampus. The DRN-Hippocampus relay promotes neurogenesis and the DRN-entorhinal cortex-hippocampus relay imprints ongoing moments of consciousness. Moreover, all structures have branches that project directly to the hypothalamus to participate in coordinating hormonal response to emotion. In turn, hormones can feedback and regulate activity of the hippocampus.
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So, what I discern from the bold is that high cortisol levels that would be seen in response to a stressor, actually facilitates hippocampal response to biogenic amines (dopamine, and catecholamines ??). Thus, in steroid abusers, which we've determined there could be negative feedback on the HPA axis, there would be lower levels of cortisol, and thereby DECREASING hippocampal sensitivity to biologic amines (dopamine), and hence the depressive effects seen in some steroid abusers????
Nice contribution, by the way! But, please tell me if I'm reading this correctly.
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Well that's a good question, this thing I had to write was for a related topic but was concerning stress, the hippocampus, and depression.
But by altering the stress response, either positively or negatively through the use of exogenous steroids could lead to an overstimulation or understimulation of GRs and MRs on limbic structures (have to remember they are all interconnected and have reciprocal communications) and either lead to excitotoxic atrophy or dendritic withdrawal/neuronal apoptosis secondary to understimulation/desensitization.
Not saying it absolutely positively happens, but it must be a consideration.
