What DHT Is
Dihydrotestosterone (DHT) is a metabolite of testosterone produced by the enzyme 5-alpha reductase. It binds the androgen receptor considerably more avidly than testosterone does, which is why comparatively small local quantities produce large biological effects in tissues that express the enzyme — scalp follicles and the prostate among them.
Where It Is Actually Produced
The important point is that much of the DHT relevant to a scalp follicle is generated inside or immediately adjacent to that follicle, not delivered from the bloodstream. Local, intracrine production means the concentration a follicle experiences is set largely by its own enzymatic activity.
This has a direct consequence: circulating hormone levels can look entirely normal in a person with advancing androgenetic alopecia. Serum testosterone is a poor predictor of follicular outcome, which is why testing it rarely resolves the question.
Why DHT Damages Susceptible Follicles
DHT does not attack the follicle. It reprograms its cycle. In a genetically susceptible follicle, androgen receptor signaling shortens the anagen (growth) phase and lengthens the interval before regrowth. Each cycle produces a slightly smaller follicle and a slightly finer shaft. Repeated over years, this is miniaturization.
Two follicles millimetres apart can respond very differently, because susceptibility is set by local receptor density and enzyme expression. That is why pattern loss is patterned rather than uniform.
The Two Isoforms
5-alpha reductase exists in more than one isoform, with different tissue distributions. Pharmacological inhibitors differ in which isoforms they suppress and how systemically they act — and systemic androgen suppression carries a recognized side-effect profile, which is the principal reason many people discontinue treatment.
The Case for Local, Multi-Point Intervention
If the pathological conversion is largely local, the rational target is local. Continuum's research has focused on modulating the follicular environment — inhibiting pathological DHT synthesis at the site where it occurs, while simultaneously addressing the inflammatory signaling that accompanies it.
TrichoCyte™ was developed on that logic: botanically derived 5-alpha reductase inhibition and anti-inflammatory phytochemicals paired with a beta-cyclodextrin delivery vector, so the active material reaches the follicular compartment rather than remaining on the surface. Delivery is not a detail — an active that cannot reach its target is pharmacologically inert regardless of its in-vitro potency.
What DHT Does Not Explain
DHT is not the whole disease. Follicular senescence, loss of immune privilege, stem-cell exhaustion, and estrogen-curve destabilization in women all contribute independently. A person can suppress androgen conversion and still lose ground if another mechanism is active. This is why single-target strategies commonly plateau after the first year.
The Practical Conclusion
DHT is necessary to the pathology in most men and many women, but it is not sufficient to explain it. Address the conversion locally, address the inflammation that accompanies it, and expect that a durable result requires holding more than one control point at once.
References available on request and via the National Library of Medicine (PubMed). This page is educational and is not a substitute for individual medical advice.