Recovery from Anabolic Steroid Hypogonadism

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madman

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Abstract

Hypogonadism can result following anabolic steroid abuse. The duration and degree of recovery from anabolic steroid-induced hypogonadism (ASIH) is immensely variable, and there is a paucity of prospective controlled data characterising the trajectory of natural recovery following cessation. This poses difficulties for users trying to stop androgen abuse, and clinicians wanting to assist them.

The objective of this paper was to synthesise evidence on the physical, psychological, and biochemical patterns of ASIH recovery. We present the pathophysiology of ASIH through a literature review of hypothalamic-pituitary-testosterone axis recovery in supraphysiological testosterone exposure. This is followed by a scoping review of relevant observational and interventional studies published on PubMed and finally, a conclusion that is an easy reference for clinicians helping patients that are recovering from AAS abuse.

Results indicate that ASIH recovery depends on age and degree of androgen abuse, with physical changes like testicular atrophy expected to have near full recovery over months to years; spermatogenesis expected to achieve full recover over months to year/s; libido returning to baseline over several months (typically less potent than during AAS use); and recovery from gynaecomastia being unlikely. For psychological recovery, data is insufficient and conflicting, indicating a transient withdrawal period which may be followed by persisting longer-term milder symptoms. For biochemical recovery, near complete recovery of testosterone is seen over months, and complete gonadotropin recovery is expected over 3-6 months. Further prospective studies are indicated to more closely describe patterns of recovery.





*Pathophysiology of ASIH


*Scoping Review of Recovery from ASIH


*Physical Changes

-Testicular volume
-Gynaecomastia
-Libido / Erectile dysfunction
-Spermatogenesis
-Psychological changes



*Biochemical changes
-Testosterone
-Gonadotropins





Conclusion

Amongst those who abuse AAS, cessation often results in the wide-ranging sequelae of anabolic steroid-induced hypogonadism. These sequelae encompass physical, psychological, and biochemical changes, which in some cases may be irreversible. In this scoping review, we found that recovery from the sequelae of ASIH was immensely variable, depending on the type of AAS used (‘stacking’ if multiple); the dosages used; the duration of use; the patterns (‘cycles’) of use; and comorbid conditions. Our scoping review demonstrated broad conclusions across some of the changes associated with ASIH, as summarised in Table 4. Recovery usually does occur in relation to gonadotropin levels while testosterone has near to complete recovery over the weeks to months of follow up depending on duration and dose of AAS abuse. Spermatogenesis is usually completely recovered over months to years with sperm concentration typically recovering first, followed by sperm motility, then sperm morphology, with fertility rates eventually normalising over years.

Similar to recovery of spermatogenesis, the recovery of testicular volume takes months to years; however, the volume difference is still present up to a year, be it minimal in reduction in AAS abusers. Gynaecomastia is more common in AAS abusers and can persist despite years of follow up, potentially warranting surgical intervention.

Owing to the paucity of data, the recovery patterns for libido and erectile dysfunction, and psychological changes remain less clear. There is an initial increase in depressive and anxious symptoms with recovery seen over months to years, however, some studies do not find any significant differences. The variability in duration of recovery and depth of symptoms ranging from mild to potential suicidality warrants further study in terms of helping patients avoid these dire outcomes, and helping those that are willing to abstain from returning to AAS abuse.

The secrecy, stigma, and illegality associated with AAS abuse has long made recruitment for research a challenge prone to selection bias. Nonetheless, there is a need for controlled prospective studies and quantification of the abused regimes used rather than just considering the cohort homogenously. In the absence of these fine-grained studies, the evidence base for managing abusers of AAS will continue to be challenging.
 

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Defy Medical TRT clinic doctor
Figure 1: Reinitiation of GnRH pulse by KNDy neurons and its regulation Schematic representation of the signalling pathway responsible for the generation of gonadotropin releasing hormone (GnRH) pulses. KNDy neurons (containing the neuropeptides kisspeptin, neurokinin B (NKB) and dynorphin (Dyn) in the arcuate nucleus (ARC) of the hypothalamus receive autoregulatory input from NKB and Dyn, forming a local circuit. Kisspeptin release is enhanced by NKB and reduced by Dyn and this net effect increases GnRH pulses. The resultant production of sex steroids will feedback to KNDy neurons to facilitate homeostatic regulation of GnRH pulses. Higher neuronal centres, such as the supra-chiasmatic nucleus as well as proopiomelanocortin (POMC) and neuropeptide Y (NPY) / Agouti-related protein (AgRP) feed into this circuitry. Peripheral hormones and potentially anabolic-androgenic steroids also regulate this system to govern fertility.
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