DHT and the follicle: which androgens the scalp actually hears

DHT is dihydrotestosterone, what you get when 5α-reductase takes testosterone and reduces the double bond in the A ring. The product binds the androgen receptor harder than testosterone does, and it lets go more slowly. Skin, the prostate, and the beard use this conversion on purpose. So does the hair follicle on a scalp that is going to thin. James Hamilton showed, in the 1940s, that men castrated before puberty did not develop male-pattern baldness, and that giving them testosterone later only produced it if they were genetically susceptible. The hormone is the signal. The follicle's genes decide whether the signal miniaturises the hair. That split has not been improved on. A man can have a high DHT and a full head, and a man can thin on an ordinary one, because the papilla is the variable.

In short. DHT is testosterone after an enzyme edit, and it grips the androgen receptor harder. It only miniaturises hairs that are genetically set up to listen. Hamilton showed that eighty years ago.

There are two enzymes worth naming. SRD5A2, type 2, is the one in prostate and in the follicle that finasteride blocks. SRD5A1, type 1, is more widely spread, including skin and liver, and dutasteride blocks both. The follicle that miniaturises shortens its growth phase, anagen, and the shaft that emerges is finer, until the pore is making a colourless wisp. That is androgenetic alopecia: miniaturisation, a change in the organ, unlike shock loss or the telogen effluvium after fever, which comes back at the same thickness. The hair you see in the shower from a seasonal shed is a different count.

In short. Type-2 5α-reductase is the follicle enzyme finasteride blocks. Dutasteride blocks type 1 as well. The follicle shortens its growth phase and the hair gets finer. A seasonal shed is a different event.

Testosterone is a substrate. A share of it becomes DHT in the scalp, which is why injectable testosterone can thin a susceptible hairline even though the injection never touched the skin. Nandrolone is the awkward one. 5α-reductase converts it to dihydronandrolone, and DHN is a weaker androgen than nandrolone. In the scalp and the prostate, the enzyme softens nandrolone rather than sharpening it. Blocking the enzyme with finasteride, while nandrolone is the androgen on board, removes that softening and leaves the stronger parent molecule in the tissue. That is enzyme logic, and it is the opposite of what finasteride does to testosterone. Trenbolone is barely a substrate at all. It does not need the enzyme to be androgenic, so blocking the enzyme does not disarm it. Drostanolone, mesterolone and the other DHT-derived drugs are already reduced. They arrive as the potent form. There is no upstream enzyme left to inhibit.

In short. Testosterone becomes DHT in the scalp. Nandrolone becomes a weaker androgen there, so blocking the enzyme can make nandrolone harsher, not kinder. Tren and the DHT-derived drugs do not need the enzyme.

Finasteride at one milligram a day is the trial Kaufman published in 1999: more hair counted on the vertex, and the frontal scalp moved less dramatically, over a year and beyond. Dutasteride suppresses serum DHT further because both enzymes are shut. Both drugs also lower DHT in the prostate, which is why the five-milligram finasteride dose exists for urinary symptoms, and why a young man should know he is taking a prostate drug for a hair. Sexual side effects are real in a minority and, in a smaller minority, are reported to linger. The mechanism of the lingering ones is still argued. The existence of the complaint is not a reason to pretend the enzyme is optional in every tissue. Brain, penis and prostate all see androgens. You are choosing a tissue when you block the conversion, not deleting a waste product.

In short. Finasteride at the hair dose regrows vertex hair in the trials. It is still a hormone drug. A minority get sexual side effects, and some say those linger. You are changing DHT in every tissue that used the enzyme, not only the scalp.

Minoxidil is a different door. It is a potassium-channel opener that lengthens anagen and does not block 5α-reductase. It can thicken a hair while DHT is still sitting on the papilla, which is why the two are stacked in clinics, and why stopping minoxidil returns the hair to the clock the androgens set. A topical anti-androgen stays local only to the extent it does not go systemic. Many of them do, a little. Creatine's one rugby paper on DHT has not turned creatine into a baldness drug; the creatine essay already said so, and nothing since has made that paper larger. The variables that do the work are genetic susceptibility, how much testosterone you are offering the enzyme, and whether the androgen you added is a substrate, a softened substrate, or an already-reduced DHT analogue.

In short. Minoxidil keeps a hair growing without blocking DHT. Stop it and the follicle goes back to the androgen clock. Creatine is not a hair-loss drug on the strength of one small study.

A scalp hair spends years in anagen, the growth phase, then a few weeks in catagen, the retreat, then a few months in telogen, resting, before it sheds and the next shaft starts. Androgenetic miniaturisation shortens anagen and lengthens the relative time spent resting. The pore that used to deliver a thick hair for six years starts delivering a thin one for a few months. You notice the shed because telogen hairs fall, and you miss the real change, which is that the replacement is thinner than the hair it replaced. Count the hairs in the drain and you are counting a normal telogen quota plus whatever extra the shortened cycle is throwing. Look at the calibre of the hair still in the skin and you are looking at the disease. A seasonal shed, or the shed after a fever, empties telogen early and the next hair comes back the same thickness. Miniaturisation does not give the thickness back unless the androgen signal at that papilla is reduced for long enough that a later cycle builds a thicker shaft.

In short. Balding shortens the years a hair grows and the next hair comes in thinner. Hairs in the shower can just be a seasonal shed, which grows back the same. Thickness, not the number in the drain, is the thing that matters.

The beard and the scalp are the same hormone doing opposite jobs. DHT makes many beards thicker and, in susceptible scalps, makes the hair finer. The difference is the dermal papilla's programme, not a different molecule. Wnt signalling, the local growth conversation in the follicle, is pushed one way in the beard and the other way on a balding crown. That is why a man can grow a denser beard on testosterone and watch his temples go at the same time, and why blocking 5α-reductase can thicken the scalp and slightly thin the beard or the body hair in some men. You are turning down one signal that two tissues read differently. Finasteride does not know you only meant the mirror.

In short. The same DHT thickens a beard and thins a susceptible scalp, because the follicles are programmed differently. Blocking the enzyme can help the scalp and slightly soften beard and body hair. It cannot do only one of those.

Oral finasteride at the one-milligram hair dose lowers serum DHT by about seventy percent. Dutasteride, blocking both enzymes, lowers it by about ninety-five. More suppression is not automatically a better cosmetic result for every man, and it is a more complete removal of DHT from prostate, skin, and anywhere else type-1 enzyme was working. Topical finasteride still reaches the blood. 'Local' is a hope about the amount, not a guarantee of zero systemic effect. Sexual side effects remain a minority event and a real one. Saw palmetto is sold as a natural 5α-reductase inhibitor. Whatever it does in a test tube, it is not in the same league as finasteride, and the hair trials are modest. A plant extract that weakly leans on an enzyme is not a small dose of the drug that has hair-count data. The androgen you are offering the enzyme still decides more than the shampoo.

In short. Finasteride cuts DHT by about seventy percent. Dutasteride cuts it by about ninety-five, and it is a bigger change in every tissue, not a stronger shampoo. Saw palmetto is not a mild finasteride. Topical finasteride still gets into the blood.