Androgenic anabolic steroid (AAS) interventions with effects that are unclear if meaningful
Androstenidone (testosterone precursor) at 300 mg a day for 7 days increased total T by 34%, and total estradiol by 24% on average, in young men (Leder et al., 2000).
A 2007 review on testosterone DHEA, androstenedione, and androstenediol concluded that “ Studies have demonstrated repeatedly that acute and long-term administration of these oral testosterone precursors does not effectively increase serum testosterone levels and fails to produce any significant changes in lean body mass, muscle strength, or performance improvement compared with placebo.” (10.1016/j.pcl.2007.05.002).
Interventions with no meaningful effects
DHEA 100mg/day for 28 days was found to have no effect on exercise performance in athletic women (doi: 10.1055/a-0631-3008).
DHEA 100mg/day for 28 days in young athletic men had no effect on body composition or BMI (https://www.ncbi.nlm.nih.gov/pubmed/21789881)
60 mg prednisone a day for 1 week in young men had no effect on exercise performance (doi: 10.1016/j.steroids.2014.04.008).
General risks to the androgenic steroid class (not all these apply to each drug within the class): copied from 10.4085/1062-6050-47.5.08.
- 11. Supraphysiologic AAS dosing may occasionally be associated with hypomanic or manic syndromes that are often characterized by irritable or aggressive behavior.21,54,67–78 Episodes of major depression may be associated with AAS withdrawal.79–81 Abusers of AAS may develop a dependence syndrome related to both myoactive and psychoactive effects82–89 and may exhibit other forms of drug dependence, such as opioids.83,90–93 Evidence Category: B
- 12. The cardiovascular effects of therapeutic AAS remain unclear. Substantial research findings now suggest that AAS abuse negatively influences the cardiovascular system.25,67,94–103 The best evidence indicates that nontherapeutic AAS-related conditions include cardiomyopathy96,97,99,100and the potential for atherosclerotic vascular disease caused by detrimental lipid changes, which may adversely affect one's risk for coronary artery disease.25,102,103 Evidence Category: B
- 14. Exogenous AAS abuse inhibits the hypothalamic-pituitary-gonadal axis, reducing the production of endogenous testosterone, luteinizing hormone, and follicle-stimulating hormone.7,11–14,22,51 It can also alter thyroid function11,12,22 and negatively affect glucose tolerance.12,22,105 Evidence Category: B
- 15. Abuse of AAS directly affects the male reproductive system, with possible side effects including hypogonadism, decreased spermatogenesis, decreased sperm motility, erectile dysfunction, impotence, gynecomastia, and male-pattern baldness.7,11–14,22,51,55 Many of these conditions are reversible with cessation of AAS, although breast tissue changes and hair loss often require additional treatments, including surgery.7,11–13,22,51,55 Evidence Category: B
- 16. Reproductive changes to females who abuse AAS generally involve virilization, including voice deepening, hirsutism, clitoral hypertrophy, breast reduction, libido changes, menstrual dysfunction, male-pattern baldness, and acne.11–14,22,51 Unlike the side effects in males, many of these changes are permanent in females.12,14,22 Evidence Category: B
- 17. Skeletally immature AAS abusers might experience premature epiphyseal closure of the long bones, resulting in shortened stature.11,12,14,22,51 Other negative effects of AAS abuse on the musculoskeletal system may include tendinopathies (including possible rupture).7,11–13,22,51 Little evidence supports the therapeutic use of AAS for musculotendinous injury recovery.7,106 Evidence Category: C
- 19. High-dose AAS abuse