1. Basic science
1.1. Endocrine system
1.1.1. Structures
1.1.1.1. adrenal glands
1.1.1.2. gonads
1.1.2. Steroid hormones
1.2. Anabolic androgenic steroids
1.2.1. What is this?
1.2.1.1. synthetic substances
1.2.2. Mechanism of action
1.2.2.1. promote protein synthesis by
1.2.2.1.1. increased transcription
1.2.2.1.2. glucocorticoid antagonist
1.2.2.2. stimulate human growth hormone synthesis
1.2.2.2.1. by the liver?
1.2.2.3. stimulate insulin growth factor I synthesis
1.2.2.3.1. by the pituitary gland
2. Therapeutic AAS use
2.1. male hypogonadism
2.2. (certain) anemias
2.3. anticatabolism for wasting syndrome
3. Nontherapeutic AAS use
3.1. much greater than therapeutic level
3.2. stack
3.3. 6-12 weeks cycle
4. AAS efficacy
4.1. limited research
4.1.1. ethical issues
4.2. as the dose increases
4.2.1. lean body mass increases also
5. AAS abuse health effects
5.1. syndrome
5.1.1. hypomanic syndrome
5.1.1.1. irritable or aggressive
5.1.2. manic syndrome
5.1.2.1. irritable or aggressive
5.1.3. AAS withdrawal
5.1.3.1. major depression
5.1.3.1.1. S&S review
5.1.4. dependence syndrome
5.1.4.1. opioids
5.2. cardiovascular
5.2.1. cardiomyopathy
5.2.2. atherosclerosis
5.2.2.1. coronary artery disease
5.3. liver
5.3.1. cholestatic jaundice
5.3.1.1. oral C17a-alkylated group of AAS
5.4. kidney
5.4.1. damage often w/
5.4.1.1. NSAID
5.4.1.2. high protein diet
5.4.1.3. dehydration
5.5. hypothalamic-pituitary-gonadal axis
5.5.1. reduce
5.5.1.1. testosterone
5.5.1.2. luteinizing hormone
5.5.1.3. follicle-stimulating hormone
5.6. male reproductive system
5.6.1. hypogonadism
5.6.1.1. often temporaliry
5.6.2. breast tissue changes
5.7. female reproductive system
5.7.1. virilization
5.7.1.1. voice deepening
5.7.1.2. hirsutism
5.7.1.3. breast reduction
5.7.1.4. libido changes
5.7.2. permanent changes
5.8. skeletal system
5.8.1. skeletally immature
5.8.1.1. premature epiphyseal closure
5.8.2. tendinopathies
5.9. immunosuppressant effect
5.9.1. hepatitis
5.9.2. human immunodeficiency virus
5.10. dermatologic conditions
5.10.1. acne