Anabolic steroids (often shortened to "anabolics") are synthetic substances that mimic the action of the male sex hormone testosterone in the body.
"Anabolic" refers to their ability to build up tissues—most commonly muscle—but they can also act on bone, fat, and other organs.
"Steroid" denotes the chemical structure: a four‑ring core that is common to many hormones (e.g., cortisol, estrogen).
Because of this mimicry, anabolic steroids are used in medicine to treat conditions such as delayed puberty, muscle wasting disorders, and certain hormonal deficiencies. However, athletes often take them off‑label for performance enhancement.
2. How Anabolic Steroids Work on the Body
Step Process What Happens
1 Absorption Oral steroids are absorbed through the digestive tract; injectable forms bypass digestion and enter directly into circulation.
2 Transport to Target Cells Steroids circulate bound mainly to sex‑hormone‑binding globulin (SHBG) and albumin; only free molecules can penetrate cells.
3 Receptor Binding Inside the cell, steroids bind to intracellular receptors (androgen or estrogen). This complex then translocates to the nucleus.
4 Gene Expression Modulation The steroid–receptor complex acts as a transcription factor, binding to hormone response elements on DNA and influencing the transcription of specific genes—either up‑regulating anabolic proteins (e.g., creatine kinase) or down‑regulating catabolic pathways.
5 Physiological Outcomes Resultant changes include increased protein synthesis, reduced proteolysis, enhanced glycogen storage, altered water retention, and modifications in lipid metabolism. These biochemical shifts manifest as improved strength, endurance, recovery, and muscle hypertrophy.
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3. Commonly Used Performance‑Enhancing Supplements
A 35‑year‑old female, BMI = 27, sedentary, mild hypertension, normal glucose tolerance High visceral adiposity; elevated waist circumference (≥88 cm). No overt diabetes. Lifestyle: diet (Mediterranean pattern), aerobic exercise (150 min/wk). Consider metformin if insulin resistance is evident.
B 55‑year‑old male, BMI = 32, impaired fasting glucose, dyslipidemia, smoking history Visceral fat correlates with atherosclerosis risk; smoking exacerbates endothelial dysfunction. Smoking cessation, statin therapy, intensive lifestyle changes, potential low-dose aspirin for secondary prevention.
C 45‑year‑old female, BMI = 28, PCOS phenotype, hirsutism, menstrual irregularity Excess visceral fat contributes to hyperandrogenism; insulin sensitizers beneficial. Low‑dose oral contraceptives + metformin or thiazolidinedione if metformin ineffective; lifestyle interventions.
D 60‑year‑old male, BMI = 26, history of myocardial infarction, hypertension, dyslipidemia Visceral fat increases cardiovascular risk; requires comprehensive management. Statin therapy, ACE inhibitor or ARB for blood pressure control, weight loss program targeting visceral reduction.
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Summary
BMI is a quick screening tool but cannot distinguish body composition.
Waist circumference/waist‑hip ratio, and body fat percentage (via DXA) are the most reliable metrics for assessing risk related to excess body fat, especially visceral fat.
For clinical practice, measuring waist circumference or using DXA scans when available provides actionable information about health risks beyond BMI alone.
Feel free to let me know if you’d like more detailed guidance on how to perform these measurements or interpret results!
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