Anabolic-Androgenic Steroids and Performance Enhancing Drugs in general, including CNS stimulants, diuretics, growth hormones, and anti-estrogens, have several different pharmacokinetics in various systems. When a subject uses the particular substance above the recommended medical dose, side effects can begin to occur. These side effects are listed below, and may have a negative impact on the following organs, tissues and internal regulatory systems:
- CNS (Central Nervous System)
-AAS: Increase in systolic blood pressure (>140mm Hg)=>atherosclerosis=>rupture of cerebral aneurysms=>hemoragic stroke
-Fluoxymesterone: has a high androgenic index (800) and it is responsible for headaches, nausea.
-Clenbuterol HCL, Ephedrine HCL, Thyroxine: Increase in systolic blood pressure (>140mm Hg)=>nose bleeding, temporal headache, blurred vision=>acute hypertensive episode=>cerebral hemorrhagic stroke. Moreover, insomnia, manic episodes, neurosis.
-T3, T4: short term moderate doses=>hyperthyroidism (TSH drops). In case of T3, T4 abuse=>hyporthyroidism (TSH elevates)-HGH: decrease in FT3=>modulation of the thyroid gland: During HGH abuse, the thyroid gland develops nodulation due to hyperthyroidism (TSH elevation). This also reflects for those who suffer from hypophyseal adenoma and gigantism occurs.
-AAS: decrease in HDL, elevation in LDL=>risk for CVD. LVH=>Chronic heart failure & hypertension. Increase in sodium and calcium retention, leading to calcification of endothelium and heart arrhythmia (1)(2).
-HGH: Cardiomegaly=>Chronic heart failure
-Diuretics: i) Hypovolemic shock=>colapsus due to hypotension. ii) Muscle spasms due to electrolyte imbalance. iii) Heart arrhythmia due to hyperkalemia (in the case of spironolactone).
-Stimulants: Heart arrhythmias (ventricular tachycardia, atrial fibrillation). Hypertensive episode due to an increase in systolic blood pressure=>hemoragic stroke. The most common causes of death among competitive bodybuilders are i) ventricular fibrillation from hyperkalemia (spironolactone) or ventricular tachycardia (b2 agonists) ii) AMI due to vasoconstriction of coronary arteries coming from CNS stimulants, or due to poor atheromatic index from AAS abuse iii) Chronic heart failure coming from somatotropin abuse that leads to cardiomegaly.
-AAS: i) rise in hepatic enzymes-transaminitis (ALT-SGOT,AST-SGPT)=>pharmaceutical hepatitis, ii) cholestasis (ALP,GGT,BIL)=>jaundince, iii) hepatic peliosis (3).
Most hepatotoxicity -AAS: methyltrienolone, methandienone, oxymetholone, oxandrolone, stanozolol (17 alkylated per oss)
- GASTROINTESTINAL (Stomach)
-AAS: Irritation of gastric mucose=>gastritis=>vomiting=>ulcer
- UROGENITAL (Kidneys-Prostate-Gonads)
-AAS: i) Increase in urea serum level-azotemia (>80mgol/Dl) & Creatinine (>1.5mg/Dl) due to positive nitrogen retention. Especially during pre-contest session-ketosis, when animal protein consumption is high (3gr/kg)=>increase in ammonia (NH3) & in ketone bodies (HMB). ii.) During overtraining-rhabdomyolysis effect=>microscopic hematuria in urine (RBCs), that turns urine to pinkish. Rise of CPK>500 in serum=>myoglobin release that is toxic to renal glomeruli. iii) Increase in calcium concentration=>hypercalcemia=>renal stones in ureters. iv) hypertrophy of prostate (PSA>5) v) Hypogonadism-LH, which leads to testicular shrinkage and oligospermia-FSH (<20 million/Dl), erectile disfunction-low libido, gynecomastia (>E2), peripheral edema (4).
-Stimulants: Irritation of prostatic gland (perineum). The combination of Clenbuterol HCL & ephedrine HCL=>hypertension that affects renal tubules.
-AAS: i) Increase in hematocrit=>increase in blood viscosity=>risk for thrombotic stroke & raise in blood pressure=>atherosclerosis=>rupture of cerebral aneurism,nose bleeding. ii) Prolonged coagulation time (PT, APTT, INR)=>inadequate hemostatic ability (5).
-HGH: chronic abuse>8iu=>IGF1 raise is related to oncogenesis.
Worst AAS for increased hemopoiesis-erythrocytosis: Testosterone, Trenbolone, Oxymetholone, Boldenone.
Worst PEDs for tumors: HGH, IGF1, GHRH peptides
-AAS: rupture of tendons, rhabdomyolysis.
-HGH: Acromegaly, enlargement of soft tissues (lips, tongue, nose), skeletal deformation (maxilla, mandible, elbows, zygomatic bones)
-CNS Stimulants: Trembling, muscle spasms.
-AAS: Irritability, aggressiveness, mood swings (emotional instability), insomnia.
-CNS Stimulants: Irritability, insomnia, restlessness.
Worst AAS for mental disorder: Trenbolone, Fluoxymesterone
-HGH: Non-insulin-dependent diabetes mellitus type 2
-IGF1: Negative feedback for HGH (somatotropin) release from the adenohypophysis, through GHRIH (somatostatin) release from the pancreas.
-Insulin: Severe hypoglycemia=>coma (blood sugar<50mg/dl). Trembling, cold sweating, irritability, tachycardia, fainting, loss of consciousness, even death.
Worst peptides for hypoglycemic coma: Insulin, IGF1-Peptide C
-AAS: i) Acne in face and body, due to increased activity of sebaceous glands. ii) Water-based injectable AAS (suspensions): Intramuscular edema that leads to abscess due to bacterial infection. Treatment with antibiotics, surgical opening if not treated. In the case of abscess in the gluteal region, sciatic nerve neuropathy=>severe pain during flexing hip joint due to stretching of the sciatic nerve.
Worst AAS for acne: Trenbolone, Fluoxymesterone, Oxymetholone, Methandienone, Stanozolol.
Worst AAS for intramuscular infections: Testosterone suspension, Stanozolol Suspension, Trenbolone suspension. Water-based injectables are more easily contaminated than oil-based injectables.
-AAS: during prolonged abuse, overtraining and dieting=>shrinkage of thymus gland=>decrease in T-lymphocytes production. Raise in TNF & IL1 cytokines & drop in IGA, IGD, IGE, IGG, IGM.
-AAS & HGH: Hypertrophy of throat & soft tissues (epiglottis,pharynx)=>shortening of upper airways=>snoring & Obstructive Sleep Apnea=>peripheral hypoxemia=>respiratory acidosis (raise in CO2).
-AAS, HGH, IGF1: Hepatocellular carcinoma, prostatic hyperplasia, renal tumor.
Somatotropin abuse & insulin hypersecretion=>IGF1 hypersecretion from liver=>chronic inflammations & oncogenesis (proto-oncogenes+mutations=>oncogenes)
- Peter J Angell, Neil Chester, et al. Performance enhancing drug abuse and cardiovascular risk in athletes: implications for the clinician. Br J Sports Med 2012; 46: i78-i84
- Manu Kaushik, Siva P. Sontineni, et al . Cardiovascular disease and androgens: A review. International Journal of Cardiology 2010; 142: 8–14 H Kuipers, et al.
- Chitturi S, Farrell GC. Adverse effects of hormones and hormone antagonists on the liver. In, Kaplowitz N, DeLeve LD, eds. Drug-induced liver disease. 3rd ed. Amsterdam: Elsevier, 2013, pp. 605-20. (Review of hepatotoxicity of androgenic steroids including cholestasis, vascular disorders, benign tumors and hepatocellular carcinoma).
- Safa E. Almukhtar, Alaa A. Abbas, et al. Acute kidney injury associated with androgenic steroids and nutritional supplements in bodybuilders. Clinical Kidney Journal, 2015; 8 (4): 415
- Shahani, M. Braga-Basaria, et al. Androgens and erythropoiesis: past and present. Journal of Endocrinological Investigation 2009; (32):704–716
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