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Hormones

DHT (Dihydrotestosterone)

DHT, dihydrotestosterone

Dihydrotestosterone (DHT) is a non-aromatizable androgen that Ray Peat considered the safest and most preferred steroid for therapeutic use, primarily because it cannot convert into estrogen and acts as an aromatase inhibitor itself. The special difference between testosterone…

11 passages
2 authors
2015–2023
Most-cited: Georgi Dinkov

Dihydrotestosterone (DHT) is a non-aromatizable androgen that Ray Peat considered the safest and most preferred steroid for therapeutic use, primarily because it cannot convert into estrogen and acts as an aromatase inhibitor itself. The special difference between testosterone and DHT is that testosterone is easily aromatized into estrogen, a process DHT completely avoids, making its cardiovascular and androgenic effects distinct. Peat argued that correcting underlying metabolic issues with thyroid, vitamin D, DHEA, and pregnenolone will usually bring DHT up to where it should be, and that direct supplementation is generally not to be messed with unless there is a very specific knowledge of a deficiency.

Mainstream medicine has vilified DHT for decades, blaming it for pathologies including baldness, prostate enlargement, and prostate cancer, which led to the development of 5-alpha-reductase inhibitors like finasteride. Georgi Dinkov has written extensively that the evidence for DHT causing these conditions is correlational and misinterpreted; biopsies showing elevated DHT in balding scalps likely represent an adaptive, protective response, as DHT applied to scalp cells actually increases hair growth. Furthermore, Dinkov notes that DHT is approved as a cream in France for treating prostate diseases, and injection of testosterone (which converts to DHT) into the prostate has been shown to stop terminal prostate cancer, directly contradicting the androgen hypothesis. The inhibition of DHT synthesis via finasteride causes severe hypothyroidism, with elevated prolactin, cortisol, and cholesterol, which explains the debilitating symptoms of post-finasteride syndrome.

DHT exerts its therapeutic effects through multiple mechanisms. It is a powerful inhibitor of both aromatase and 11β-HSD1, meaning its primary effects in physiological doses are to inhibit estrogen and cortisol synthesis. Dinkov has emphasized that DHT is a much stronger stimulant of DNA and RNA synthesis and muscle protein synthesis than testosterone, and its anabolic effect is roughly 80% opposition to cortisol. Clinically, synthetic DHT derivatives like Masteron (2-alpha-methyl-DHT) have been approved since the 1960s for treating estrogen-positive breast cancer, with older studies reporting sudden and complete regression of metastatic disease within one week. Large-scale studies show that declining levels of DHT and other steroids in aging correlate with rising cholesterol and degenerative diseases, and administration of these hormones has strong therapeutic effects.

Regarding practical use, Peat suggested that if DHT is warranted in cases like breast or prostate cancer, a dose of one milligram daily dissolved in tocopherol or fat is appropriate, but only after everything else is in place. Dinkov has stated that physiological doses up to 25 mg daily are probably safe, with Peat considering even 3–5 mg daily sufficient for pronounced benefits. DHT is a paracrine steroid synthesized in peripheral tissues as needed from precursors including testosterone, DHEA, and progesterone, and in reasonable doses it can stimulate endogenous androgen synthesis rather than causing suppression. Dinkov notes that DHT is also approved in several countries as a treatment for micropenis, where topical application leverages the high expression of 5-alpha reductase in penile skin to stimulate development.

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