Androgenetic alopecia: what really happens beneath the scalp

Summary

Androgenetic alopecia is by far the most common form of hair loss. It is not a disease of the hair itself. What changes is the behaviour of the follicle, the small factory sitting in the dermis, once it is exposed to a hormone it is genetically sensitive to. The hair that grows back is slightly finer, slightly shorter, slightly paler. Then one day it stops growing back at all.

This page covers the mechanism, what heredity actually means here, how a doctor reaches the diagnosis, and what the available treatments can reasonably deliver. If you are looking for the wider picture across every other type of shedding, the file on alopecia in the broad sense is a better starting point.

The mechanism, step by step

Hair does not grow continuously. It runs through a cycle: a growth phase called anagen, lasting two to five years, a brief transition phase known as catagen, of two to three weeks, then a resting phase called telogen, of two to four months, at the end of which the hair falls. The hair cycle then starts over. Shedding 50 to 100 hairs a day is therefore normal. Those are simply the ones reaching the end of their cycle, and they get replaced.

Infographic titled the hair cycle takes place in three phases, showing the anagen phase of hair growth over two to five years, the catagen phase where growth stops over two to three weeks, the telogen phase of hair loss over two to four months, then a new anagen phase

In androgenetic alopecia, one specific part of that machinery drifts. The growth phase gets shorter with every cycle. Two years, then one year, then a few months. Since the length of a hair depends directly on how long it has been growing, the consequence shows up quickly: the hair no longer has time to reach adult size. It comes through finer, less pigmented, and ends up looking like down.

This is what is meant by follicular miniaturisation. It is gradual and, early on, close to invisible. Nobody notices the hairs that are missing; what people notice is that their hair “does less” than it used to. Many patients first describe thinning hair long before they can point to a genuinely bare patch. After several years of this, the hair follicle atrophies and disappears. Past that point, no medicine will bring it back.

DHT, and why it only troubles certain follicles

The hormone responsible is dihydrotestosterone, or DHT. It is a derivative of testosterone, produced locally by an enzyme called 5-alpha-reductase, which is present in the scalp among other places. DHT and hair loss have been a well documented pair for decades.

Blood tube labelled DHT-Test held in a gloved hand above a laboratory request form

One thing deserves spelling out, because it is so often misread: the people affected do not have “too many hormones”. Their levels are usually perfectly normal. What differs is how sensitive the follicle is to that hormone, and that sensitivity is written into the genes. It is not spread evenly across the skull either. Follicles at the crown and at the front react to DHT. Those in the horseshoe at the back and along the sides ignore it. That difference in terrain, and nothing else, is why baldness draws such a recognisable outline. It is also what makes a transplant possible in the first place.

Heredity does not run through your mother’s father

Here is the most stubborn myth on the subject: “look at your mother’s father and you will know”. It is wrong. The androgen receptor gene does sit on the X chromosome, which comes from the mother, and that is where the legend was born. But it is one factor among a great many.

A large genetics study carried out on more than fifty thousand men identified 71 regions of the genome associated with male pattern baldness, accounting for roughly 38% of the total risk, and most of those regions are not on the X chromosome (Pirastu et al., 2017). More recent work counts more of them still. The practical conclusion is straightforward: androgenetic alopecia is polygenic, and the risk is passed down by both parents. A father with a receding hairline counts. A mother whose hair has thinned counts. A bald maternal grandfather counts too, no more than the rest.

That is precisely why a family tree gives no reliable forecast. It gives a direction, not a date. Two brothers, same parents, can follow very different paths. The question of hereditary baldness is worth studying closely, as long as nobody treats it as an oracle.

In men: a pattern you can spot from across the room

Progression in men is highly stereotyped. It almost always starts with the temporal recessions, those two angles above the temples, together with thinning at the vertex, the whorl at the top of the head. The two areas advance separately, then meet. The back band and the sides stay put.

Man parting his hair with both hands over an area of bare skin above the temple

That progression has been sorted into stages, which is the whole point of the Norwood-Hamilton scale. It gives patient and practitioner a shared language for pinning down a stage and anticipating what comes next.

The age at which it begins matters more than the stage reached today. Shedding that settles in at twenty does not point to the same trajectory as shedding that starts at forty-five. The earlier the onset, the larger the surface likely to be involved in the end, and the more the strategy has to be planned over the long run. Catching the first signs of baldness early genuinely changes which options remain on the table.

In women: same cause, different map

Infographic comparing the female cycle and the male cycle of hair loss and alopecia, each shown in five numbered stages

The mechanism is identical, the pattern is not, and that mismatch causes constant confusion. Women rarely lose their temporal recessions. The frontal line usually stays intact, sometimes only across a centimetre or two, but it stays. What happens instead is a widening of the parting and a diffuse drop in density across the whole top of the head. The scalp starts to show through, especially under harsh light.

Woman holding out both open palms filled with shed hair

Woman leaning forward and parting her hair over a thinning area on the top of her head

The grading used is therefore not the same one. The reference here is the Ludwig scale, in three stages.

Ludwig plate for stage 2, illustration of a woman's face beside a photograph of a widened parting on the top of the head

One point deserves particular attention in women. Onset or worsening in the forties, or after the menopause, is a classic pattern: as oestrogen levels fall, the androgenic influence becomes relatively stronger. The file devoted to androgenetic alopecia in women goes through the specifics of the work-up and the treatments.

How the diagnosis is actually made

There is no single test. The diagnosis is clinical, and it rests first on what the doctor sees and what the patient describes: how long it has been going on, how fast, which areas, and what the family history looks like.

The examination then moves to the dermatoscope, a lit magnifier placed against the scalp. It reveals what the naked eye cannot: thick hairs and fine hairs sitting side by side within the same patch. That variation in shaft diameter is the single most characteristic sign of androgenetic alopecia. In diffuse shedding of another origin, every hair keeps the same calibre.

Dr Cinik, in scrubs and mask, examining a patient's scalp with a red light device

What remains is to rule out anything that might be layered on top, because two causes can coexist and one of them is often reversible. Blood work is frequently requested to check ferritin, which reflects the body’s iron stores, along with thyroid function: a thyroid disorder will speed up shedding that is already under way without being its root cause. In women, the menstrual cycle and any signs of androgen excess are reviewed as well. Correcting a deficiency does not cure androgenetic alopecia. Ignoring that deficiency loses ground for nothing.

Wooden board laid out with spinach, broccoli, avocado, sweet potato, almonds, walnuts, sunflower seeds and vegetable oil

Minoxidil and finasteride: what they do, what they do not

Only two molecules have a solid scientific file behind them in this indication. Their limits are known and documented.

Minoxidil is applied to the scalp, as a solution or as a foam. It extends the growth phase and improves the blood supply around the follicle. It does not block DHT.

White and blue box showing the full chemical formula of the minoxidil molecule

Finasteride is taken orally and acts further upstream: it inhibits 5-alpha-reductase, so it reduces DHT production. Head to head comparisons between the two strategies show density gains of the same order, with a slight edge to 5-alpha-reductase inhibitors on hair count (Gupta et al., 2025).

Box of 28 film-coated finasteride tablets at a dose of 1 mg

Several things need to be settled before starting. Timing, first: nothing visible before three to six months, and the effect can only be judged seriously at twelve months. Dependence, next: these treatments slow the process down, they do not switch it off. Stop, and shedding resumes its course, with the ground gained lost again within months. This is a long term commitment. Side effects, finally: scalp irritation and unwanted facial hair growth with topical minoxidil, changes in libido and mood reported on finasteride. They are uncommon and reversible on stopping in the vast majority of cases, but they justify real medical follow-up rather than an order placed online. Finasteride is also contraindicated in women of childbearing age.

Above all, neither one regrows a follicle that has gone. They work on what is still alive.

The transplant: the most lasting treatment

Where the follicle no longer exists, one option restores hair: the transplant. It exploits exactly the peculiarity described earlier. Follicles harvested from the donor area, at the back and along the sides of the head, are genetically insensitive to DHT. Moved to the top, they keep that insensitivity. They grow, and they stay. It is the most lasting treatment for androgenetic alopecia, and the only one whose outcome does not depend on taking a product for life.

Top view of a shaved scalp during implantation, several gloved hands placing grafts with forceps

Close-up of a DHI implanter pen held in a gloved hand among freshly implanted hairs

One condition, though, is not up for negotiation: the shedding has to be stable. Operating on a scalp still in full evolution risks watching the native hair keep falling around the grafts, opening up a visible gap two or three years later. That is why medical treatment is often continued alongside, to protect what is left. The prior assessment, the quality of the donor area and the stage reached determine what can realistically be done. The starting point is knowing whether you are suitable for a hair transplant.

Smiling patient whose future frontal hairline has been drawn with a marker, standing in front of a wall of clinic logos

Key points

Androgenetic alopecia is not some vague inevitability. It is an identifiable process with a known hormone, a known genetic background and a known chronology. Acting early means preserving; acting late means rebuilding. The two approaches are not rivals, they complement each other, and the calendar counts as much as the method.

Dr Cinik’s team sees patients at every stage of this journey. A precise diagnosis remains the condition for any decision: it is what will say whether a hair transplant Turkey makes sense now, later, or not at all.

Sources

Piraccini, B. M., Gavazzoni Dias, M. F., Spagnol Abraham, L., & Rudnicka, L. (2026). Androgenetic alopecia: an international expert view on the aetiopathogenesis, quality of life and current and emerging therapeutic approaches. European Journal of Dermatology, 36(S1), 4-12. https://doi.org/10.1684/ejd.2026.4999

Gupta, A. K., Dennis, D. J., Economopoulos, V., & Piguet, V. (2026). The genetic landscape of androgenetic alopecia: current knowledge and future perspectives. Biology, 15(2), 192. https://doi.org/10.3390/biology15020192

Pirastu, N., Joshi, P. K., de Vries, P. S., Cornelis, M. C., et al. (2017). GWAS for male-pattern baldness identifies 71 susceptibility loci explaining 38% of the risk. Nature Communications, 8(1). https://doi.org/10.1038/s41467-017-01490-8

Gupta, A. K., Bamimore, M. A., Williams, G., & Talukder, M. (2025). Comparative efficacy of minoxidil and 5-alpha reductase inhibitors monotherapy for male pattern hair loss: network meta-analysis study of current empirical evidence. Journal of Cosmetic Dermatology, 24(7). https://doi.org/10.1111/jocd.70320

Henne, S. K., Nöthen, M. M., & Heilmann-Heimbach, S. (2023). Male-pattern hair loss: comprehensive identification of the associated genes as a basis for understanding pathophysiology. Medizinische Genetik, 35(1), 3-14. https://doi.org/10.1515/medgen-2023-2003