Androgens and male skin: one signal, several contradictory outcomes

The most persistent misunderstanding in men's skin is that androgen effects can be read off a blood test. They cannot. Circulating testosterone tells you very little about what any individual follicle or sebaceous gland is doing, because the action happens locally, at the receptor, and the local machinery differs by site and by genotype.

1. The pathway, briefly

Testosterone circulates, mostly bound to carrier proteins, with a small free fraction available to tissues. Within the skin, the enzyme 5-alpha reductase converts testosterone into dihydrotestosterone, commonly abbreviated to DHT. DHT binds the androgen receptor with substantially greater affinity than testosterone does, so tissues rich in 5-alpha reductase experience a much stronger androgen signal than the blood concentration alone would suggest.

Two isoenzymes matter. Type 1 is concentrated in sebaceous glands. Type 2 is concentrated in hair follicles, including scalp follicles. This is the anatomical basis for why a drug that inhibits one isoenzyme affects hair without much affecting oil, and why targeting the pathway at different points produces different clinical effects. The licensed treatments that exploit this are set out in male pattern hair loss.

2. What androgens do to sebaceous glands

Sebaceous glands enlarge under androgen stimulation and increase their output of sebum. That is the mechanism behind the timing of adolescent acne, and behind the persistence of oily skin in adult men. It also explains why acne is frequently one of the first visible signs in conditions or treatments that raise androgen exposure.

Crucially, sebum output is not the whole of acne. Follicular hyperkeratinisation, the behaviour of Cutibacterium acnes within the follicle, and the inflammatory response all contribute. Androgens raise the substrate; they do not by themselves determine who gets inflammatory lesions. This is why two men with similar oiliness can have entirely different skin. The clinical picture is in adult male acne, and the sebum story in sebum and oil in male skin.

3. What androgens do to facial follicles

Before puberty, the face carries fine, short, unpigmented vellus hair. Androgen signalling converts susceptible follicles to terminal follicles: larger, deeper, producing a thicker pigmented shaft with a longer growth phase. The distribution of susceptible follicles is genetically determined, which is why beard density and pattern run in families and vary substantially between populations.

Terminal conversion continues into the late twenties and sometimes beyond, which is why beard density often increases through a man's twenties and thirties without any change in circulating hormones. It also means the shaving problem gets harder before it gets easier.

4. The paradox: growth here, loss there

In androgenetic alopecia, susceptible scalp follicles respond to the same DHT signal in the opposite direction. Each successive growth cycle is shorter, and the follicle progressively miniaturises, producing a finer, shorter, less pigmented shaft until it produces effectively nothing. The pattern of susceptibility is inherited and follows a characteristic distribution across the temples, hairline and vertex, leaving the occipital region largely spared, which is the anatomical fact that makes hair transplantation possible at all.

So the paradox is only a paradox at the level of the bloodstream. At the level of the follicle, different genetic programmes are reading the same chemical message and executing different instructions. A man with very high beard density and early crown loss is not hormonally unusual. He has two independently inherited sensitivities pointing in opposite directions.

5. Why testosterone testing is rarely the answer

Men with hair loss, acne or oily skin frequently ask for a testosterone test on the assumption that a high result would explain things. In the absence of other clinical features, it usually does not. Androgenetic alopecia and adult acne occur across the normal range of circulating androgens; the variable is tissue sensitivity, not supply.

There are exceptions where investigation is appropriate: rapid onset of severe acne with other features, signs suggesting an endocrine disorder, or the use of anabolic androgenic steroids. Anabolic steroid use in particular produces a recognisable dermatological picture, often severe truncal acne with rapid onset, and it is substantially under-declared in consultations. A clinician who does not ask will frequently not be told.

6. Interfering with the pathway

Because the pathway is well characterised, it is druggable, and the UK licensed options act at defined points. Oral 5-alpha reductase inhibition reduces scalp DHT and is licensed for male pattern hair loss. Topical minoxidil acts by a different mechanism entirely and is available without prescription. Isotretinoin, used for severe acne, dramatically reduces sebaceous gland activity and is a hospital initiated, specialist supervised treatment in the UK with a defined monitoring framework.

All of these carry recognised adverse effect profiles that belong in a consultation rather than an article. The relevant point for this piece is mechanistic: they work because they interrupt a specific step in a known pathway, which is exactly what a supplement claiming to block DHT is not demonstrated to do at the tissue level.

7. How to read androgen claims

A great deal of men's grooming marketing invokes testosterone as a general explanatory principle. Three questions cut through most of it. Which tissue is the claim about, because the same signal does different things in different places. Which step in the pathway is being altered, because "blocks DHT" is not a mechanism unless it names where. And has the effect been shown at the tissue, because a laboratory assay showing enzyme inhibition in a dish is a long way from a measurable change in a scalp.