Substance families

Aromatizes to estradiol

Built on the testosterone skeleton. Most convert to estradiol via aromatase, which is why estrogen management is a topic here — water retention, gynecomastia risk, and the option of an aromatase inhibitor.

No aromatization, finasteride does not apply

Derived from dihydrotestosterone. They do not convert to estradiol, so no water retention — but also no estrogen of their own. Finasteride is useless against their hair loss, because they are already past the step it blocks. Hardest on the lipid profile.

Progestogenic, raises prolactin

Testosterone missing the carbon at position 19. They carry progestogenic activity and raise prolactin, which is why nipple and libido symptoms here need prolactin measured rather than an aromatase inhibitor. Suppression outlasts most other classes.

Same receptor, tissue-selective — still suppressive

Non-steroidal compounds binding the same androgen receptor as testosterone, but favouring muscle and bone over prostate and hair. The selectivity is real; the suppression of the body's own production is not avoided by it. None is approved anywhere.

Works over months, costs insulin sensitivity

Growth hormone itself and the peptides that prompt the body to release it. Effects build over months rather than weeks, and reduced insulin sensitivity is what limits duration.

Appetite suppression, muscle loss alongside fat

Gut hormone analogues that suppress appetite. Highly effective for fat loss, with the consistent caveat that a substantial share of the weight lost is lean mass unless protein and training compensate.

Mechanism plausible, human evidence thin

Peptides used for tendon, gut and skin repair. Mechanisms are described and animal data exists; controlled human trials for these applications largely do not.

Blocks the estrogen receptor selectively

Selective estrogen receptor modulators. They block the receptor in some tissues while leaving it active in others — which is why they restart the hormonal axis and protect breast tissue without lowering estradiol itself.

Lowers estradiol production

They block the enzyme that converts androgens to estrogens. The recurring error is using them without measuring — estradiol that is too low causes symptoms confusingly similar to estradiol that is too high.

Mechanism decides whether it applies

Which one works depends entirely on the cause. 5-alpha-reductase inhibitors block a conversion; receptor blockers block the receptor; minoxidil acts on the growth cycle regardless of androgens.

Applied where the problem sits

Acne under androgens is driven from the inside, but most of what works against it is applied from the outside. The exception is isotretinoin, which acts on the sebaceous gland itself — and is the only one of these that needs medical supervision.

Raises energy expenditure, loads the heart

They increase metabolic rate or mobilise fat through adrenergic and thermogenic mechanisms. Cardiac load is the shared limiting factor, and it adds up when they are combined.

Corrects what other substances damage

Medications for blood pressure, lipids and glucose. They appear here because these are exactly the markers most anabolic compounds push in the wrong direction.

Corrects deficiency, does not add on top

Vitamins, minerals, amino acids and enzymes. The recurring pattern: correcting an actual deficiency helps, supplementing beyond a normal level generally does not.