Hormones
What DHT actually is, and why it picks on the temples
You will have seen the letters. DHT is on the shampoo bottle, the supplement label, the advert, usually with the word “blocker”. It is genuinely the central character in pattern thinning, in women as well as men. Here is what it is without the marketing.
Where it comes from
Every woman makes testosterone — from the ovaries and the adrenal glands, in small amounts, all her life. In certain tissues an enzyme called 5-alpha reductase converts some of that testosterone into dihydrotestosterone, DHT, which is several times more potent. The scalp is one of those tissues. So is skin generally, which is why DHT is also behind acne and unwanted facial hair.
What it does to a follicle
DHT binds to androgen receptors inside the follicle, and in follicles that are sensitive to it, the binding sends a signal to shorten the growing phase and shrink. Each cycle after that is a little shorter and the hair a little finer — the miniaturisation described in the hair cycle article. Follicles on the face and body respond to the same hormone in the opposite direction, growing thicker hair, which is why women with high androgens get both a thinning parting and a chin hair.
Why the temples and the crown
Because that is where the receptors are. The follicles at the corners of the hairline, the crown and along the parting carry far more androgen receptors and more of the converting enzyme than the follicles at the back and sides, and this is decided genetically before you are born. It is why pattern loss has a pattern, why the hair at the nape is never affected and can be used for transplants, and why two sisters with the same hormones can have different hair: they inherited different receptor maps.
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Oestrogen protects. It lengthens the growing phase directly, and it competes with DHT at the follicle. While oestrogen is high, DHT-sensitive follicles are shielded. Pregnancy is the highest oestrogen a woman ever has; the drop after the birth removes the shield abruptly, and the slow decline of the late thirties and forties removes it gradually. The DHT was always there. What changed is what was standing between it and the follicle. That is the whole mechanism of thinning after children, and it explains why the pattern is so predictable.
“DHT blockers”
There are three real ways to interfere with DHT, and most products do none of them.
Stop it being made. Finasteride and dutasteride block the converting enzyme and are the standard treatment in men. In women they are used off-label, by specialists, only in women who cannot become pregnant, because they harm a male foetus. Saw palmetto does the same thing weakly.
Stop it binding. Spironolactone blocks the androgen receptor and is the most common prescription anti-androgen for female pattern loss in the UK. Some contraceptive progestogens do the same. Both need a prescriber.
Change the follicle’s response. This is where the peptide and growth-factor approach sits: rather than lowering DHT, it restores the growth signals that DHT has switched off, improves supply, and reduces the inflammation that accompanies miniaturisation. It works at the follicle, does not change hormone levels elsewhere in the body, and is the category we match women to through the quiz.
A shampoo, a gummy or a tea that says “DHT blocker” is usually doing none of these in any dose that matters. This article explains why.
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