Androgenetic alopecia: causes, symptoms and treatments

What exactly is androgenetic alopecia?

It is a chronic and progressive form of non-scarring alopecia that affects genetically predisposed individuals.

In susceptible follicles, hormonal signals related to androgens play a role in a progressive modification of the hair cycle.

The growth phase shortens and the follicle miniaturizes.

The result is straightforward to understand: each new generation of hair can be finer than the previous one.

That is why, in the early stages, the patient still has hair. They simply have less volume and hairs of varying thicknesses.

Follicular miniaturization is precisely one of the fundamental characteristics of this condition.

Is the cause having too much testosterone?

Not necessarily.

This is one of the concepts that causes the most confusion.

A man can have completely normal hormone levels and still develop androgenetic alopecia.

The problem does not simply consist of 'having too much testosterone'.

In the genetically predisposed male, certain follicles display a particular sensitivity to androgenic signals. The enzyme 5-alpha-reductase converts testosterone into dihydrotestosterone, or DHT, which plays an important role in the miniaturization of those susceptible follicles.

Therefore: genetics + follicular sensitivity + androgenic signalling are far more important than looking at a testosterone value in isolation.

Is it hereditary?

There is a strong genetic predisposition.

But it doesn't work in such a simple way as: 'My father is bald, therefore I will be bald.'

Androgenetic alopecia is genetically complex and numerous genes are involved. A 2025 review in Nature Reviews Disease Primers notes that genomic studies have identified more than 380 loci associated with this condition.

We can therefore have a family history across different branches of the family.

And we can also develop androgenetic alopecia even if we cannot recall any close relative with an identical pattern of hair loss.

How does it manifest in men?

In male androgenetic alopecia, the classic pattern usually begins with progressive loss in the frontotemporal regions — the well-known receding temples — and/or a reduction in density at the crown.

Over time, the affected areas can continue to expand.

But again, what happens at the microscopic level is not that all the follicles disappear immediately. They miniaturize progressively.

That is why diagnosing the condition when a good population of miniaturized follicles still exists offers us more therapeutic options than waiting until very advanced stages.

And in women?

Female androgenetic alopecia tends to present differently.

Many women retain the frontal hairline, but notice a progressive reduction in density across the upper part of the scalp.

A very characteristic sign can be: 'My parting keeps getting wider.'

They may also notice that their ponytail has less volume, or that the scalp becomes more visible under certain types of lighting.

Female androgenetic alopecia should not be automatically interpreted as evidence of an excess of male hormones.

In fact, the pathophysiology of female-pattern hair loss is more complex and is still not fully understood.

When should hormones be studied in a woman?

Not all female patients with hair loss require an exhaustive hormonal workup.

But if, alongside hair loss, we find signs such as hirsutism, significant acne, or menstrual irregularities, the clinical history may justify a targeted endocrinological evaluation.

We must also consider other diagnoses that can cause or worsen diffuse hair loss.

Because a woman may simultaneously present with androgenetic alopecia and telogen effluvium.

And when both processes coincide, the loss of density can become evident much more rapidly.

How is it diagnosed?

In many patients, the diagnosis is fundamentally clinical.

We observe the distribution pattern, the progression, and the patient's history.

But a particularly useful tool is trichoscopy.

Using magnification, we can observe differences in hair shaft diameter and other characteristic signs of miniaturization that assist with both diagnosis and follow-up.

Trichoscopy is routinely used to differentiate androgenetic alopecia from other causes of hair loss and to assess its progression.

Do we need blood work?

Not necessarily.

In a man with a completely typical pattern, the diagnosis can often be established clinically.

In other patients, especially when shedding is diffuse or there are findings suggesting another cause, we may carry out targeted investigations.

For example, depending on the clinical history, it may be reasonable to assess iron levels, thyroid function, or other parameters.

Blood tests alone do not diagnose androgenetic alopecia.

They are primarily used to look for other conditions that may coexist with it or mimic it.

Can androgenetic alopecia be treated?

Yes.

But we need to understand what the goal is.

At present, we can slow or halt progression, preserve follicles, and, in certain patients, achieve an improvement in density.

What we cannot promise is to indefinitely rebuild follicles that have been severely miniaturized for years or that are no longer functional.

That is why, in this condition, timing matters.

Minoxidil

Minoxidil is one of the cornerstone treatments for androgenetic alopecia, and we have already dedicated a specific article to it in The Doctor Explains.

It can promote growth and help maintain density in appropriately selected patients.

We have topical formulations available, and in current dermatological practice, low-dose oral minoxidil is also used in certain patients, although its oral use for alopecia is off-label.

Treatments take time: clinically appreciable improvements typically require several months.

Finasteride and dutasteride

In certain patients, we can also act on the 5-alpha-reductase pathway, reducing the conversion of testosterone into DHT.

Two well-known medications appear here: finasteride and dutasteride.

Finasteride has solid evidence and approval for male androgenetic alopecia in certain markets. Dutasteride more broadly inhibits 5-alpha-reductase and is also used in trichology, although its regulatory status for alopecia depends on the country and the indication.

An interesting piece of data from Spain: a study published in 2026 on the prescribing habits of Spanish physicians in dermatology found that oral dutasteride had become the most widely used antiandrogen among participants for male androgenetic alopecia, even though its use for this indication is off-label.

That does not mean it is automatically the right treatment for every patient.

The choice must be individualized.

What about women?

Here we must be even more careful.

The treatment of female androgenetic alopecia depends on age, clinical characteristics, hormonal status, and the possibility of pregnancy, among other factors.

Minoxidil is one of the therapeutic cornerstones.

In selected patients, antiandrogen treatments such as spironolactone or other medications may be considered, but there are important reproductive and safety considerations that make it essential to individualize the prescription.

There is therefore no single prescription for all women with androgenetic alopecia.

What about PRP, laser, or supplements?

Complementary treatments may exist.

The problem arises when we confuse complementary with fundamental.

The evidence for some adjuvant therapies is promising or shows modest benefits, while for many others it remains limited or heterogeneous. A 2026 clinical review emphasizes precisely that numerous supplements and treatments marketed for alopecia still lack sufficiently robust data.

That is why we must not replace a well-established medical strategy with an accumulation of commercial treatments.

Does it need to be treated forever?

Androgenetic alopecia is a chronic, progressive condition.

This means that treatments which maintain their effect while we use them tend to gradually lose that benefit once we stop.

We should not think of it as: 'I follow a treatment for three months and I am cured.'

The approach is more like maintenance: preserving, for as long as possible, the follicles and the density we still have.

When will we see results?

Patience.

The hair cycle is slow.

Improvement usually takes several months, and many strategies require at least around six months before a reasonable clinical assessment can be made.

That is why standardised photographs and trichoscopy are particularly useful in the consultation.

Visual memory is unreliable. Comparable photographs are far more reliable.

Does a hair transplant solve the problem?

A hair transplant can be an excellent option for certain patients.

But there is something we need to understand: transplanting hair does not eliminate the predisposition of the non-transplanted follicles to continue miniaturising.

That is why good hair planning must consider not only where to place hair, but also how the existing hair will evolve over the years.

What I want you to remember

Androgenetic alopecia does not simply mean: "my hair is falling out."

It means that certain follicles are undergoing a progressive process of miniaturization.

And here is the fundamental idea: the earlier we recognize miniaturization, the more hair we still have left to try to preserve.

We do not necessarily wait until an area is completely bare.

We diagnose. We assess the pattern. We observe the follicles using trichoscopy when indicated. And we choose a strategy tailored to the patient.

Because in androgenetic alopecia, the goal is not solely to try to recover hair. It is also to preserve the hair we still have.