An enzyme called 5-alpha reductase converts testosterone into dihydrotestosterone (DHT). This conversion happens inside specific tissues throughout your body, and roughly 10% of your circulating testosterone gets converted to DHT each day. The process is straightforward: 5-alpha reductase strips a double bond from the testosterone molecule, producing a more potent androgen that drives everything from prostate growth to hair loss.
How 5-Alpha Reductase Works
Testosterone circulates through your bloodstream, but the conversion to DHT doesn’t happen there. It happens locally, inside the cells of target tissues like the prostate, skin, and hair follicles. When testosterone enters these cells, 5-alpha reductase uses a helper molecule called NADPH to chemically reduce it, removing a double bond and creating DHT.
The result is a significantly stronger androgen. DHT binds to the same androgen receptor as testosterone, but it triggers roughly twice the receptor activity. That’s because DHT creates stronger interactions between the receptor and the internal signaling molecules that switch on gene activity. Testosterone can activate the same receptor, but the signal it produces is weaker. This difference in potency is why DHT, not testosterone, is the primary driver behind certain androgenic effects like prostate growth and scalp hair loss.
Three Versions of the Enzyme
There isn’t just one 5-alpha reductase. Your body produces three distinct versions (called isoforms), each concentrated in different tissues and playing slightly different roles.
- Type 1 is widespread. It’s found in skin across your entire body, including hair follicles, sebaceous (oil) glands, sweat glands, and the liver. It’s also present in the brain, kidneys, colon, lungs, and pancreas. This version accounts for much of the DHT production in skin.
- Type 2 is more concentrated in reproductive tissues. It’s the dominant form in the prostate, seminal vesicles, and epididymis. It also appears in hair follicles and skin, particularly in the inner layers closest to the hair root. Type 2 is the version most directly linked to prostate enlargement.
- Type 3 is found virtually everywhere. It shows up at high levels in the kidneys, liver, pancreas, skeletal muscle, and skin. Its exact role in DHT production is less well characterized than the other two, but its expression levels are actually higher than types 1 and 2 across most tissues.
The distribution of these enzymes explains why DHT-related conditions show up in specific parts of the body. Your scalp and prostate are rich in 5-alpha reductase activity, so they’re especially sensitive to DHT’s effects.
What DHT Does in the Body
DHT is essential during fetal development. It drives the formation of male external genitalia. After puberty, it continues to play a role in body hair growth, oil production in the skin, and prostate function. But in excess, or in genetically susceptible tissues, it causes problems.
In hair follicles on the scalp, DHT binds to androgen receptors in the dermal papilla cells at the base of the follicle. Over time, this shrinks the follicle in a process called miniaturization. Each hair growth cycle becomes shorter, and the follicle produces thinner, finer hairs until it eventually stops producing visible hair altogether. This is the core mechanism behind male pattern hair loss.
In the prostate, DHT activates androgen receptors that promote cell proliferation. Over decades, this contributes to benign prostatic hyperplasia (BPH), the gradual enlargement of the prostate that affects most men as they age. Some researchers consider androgen receptor activation the decisive factor in BPH development.
Normal DHT Levels
In adult men under 60, typical circulating DHT falls somewhere in the range of 14 to 77 ng/dL, though community-based studies have reported ranges as wide as 23 to 102 ng/dL. A major commercial laboratory lists the normal range at 11 to 95 ng/dL. The variation across studies reflects differences in testing methods and populations.
Women produce DHT too, but at much lower levels. Premenopausal women average around 9 ng/dL, while postmenopausal women average closer to 3 ng/dL.
How DHT Production Gets Blocked
Because 5-alpha reductase is the bottleneck in DHT production, blocking it is the primary strategy for reducing DHT levels. Two prescription medications target this enzyme directly. Finasteride primarily blocks the type 2 isoform. Dutasteride blocks both type 1 and type 2, with roughly 100 times stronger inhibition of the type 1 enzyme and about three times stronger inhibition of the type 2 enzyme compared to finasteride. Both are used for BPH, and finasteride is widely prescribed for hair loss.
On the supplement side, saw palmetto is the most studied natural option. It acts as a competitive inhibitor of both isoforms of 5-alpha reductase, and lab studies show it can reduce DHT binding to androgen receptors by nearly 50%. Its fatty acid components appear to directly interfere with enzyme activity and alter the enzyme’s shape in ways that limit its access to the molecules it needs to function. Clinical results for hair loss are mixed but generally more modest than prescription options.
Your body’s rate of DHT conversion isn’t fixed. It varies with age, genetics, and hormone levels. Some people produce more 5-alpha reductase in certain tissues, which is part of why hair loss and prostate enlargement run in families. The enzyme itself is genetically determined, so the amount of DHT your body produces from a given level of testosterone is largely written into your DNA.