Androgenetic Alopecia

What is Androgenetic Alopecia?

Androgenetic alopecia (AGA) ranks among the most prevalent hair disorders worldwide. Estimates suggest that around half of all men experience a cosmetically noticeable degree by age 50, with the proportion rising to approximately 80% among those over 70. ^[1] Women can also be affected, though the presentation often differs.

Despite being commonly referred to as a condition, androgenetic alopecia is more accurately described as a natural variation in which hair follicles respond more sensitively to hormonal signals than in other individuals. The progression is chronic and typically advances without intervention. The characteristic pattern-based course has given rise to the term "pattern hair loss."

Recognizing the Symptoms

Presentation in Men

In men, androgenetic alopecia typically manifests as a gradual recession of the hairline at the temples. This creates the familiar M-shaped frontal hairline, commonly referred to as a receding hairline. Concurrently or subsequently, hair often thins at the crown, where a circular area of thinning develops – dermatologists call this vertex baldness or tonsure. In advanced stages, these areas may merge, leaving only a horseshoe-shaped ring of hair along the sides and back of the head. The Norwood-Hamilton scale classifies this progression into seven stages.

Presentation in Women

In women, hair loss tends to follow a more diffuse pattern. Rather than a retreating hairline, there is typically an even thinning across the crown while the frontal hairline remains intact. Some women develop what is called a "Christmas tree pattern," where the thinning tapers from the forehead toward the back of the head. The Ludwig scale categorizes these presentations. ^[5]

Changes at the Individual Hair Level

The hallmark feature is hair follicle miniaturization. With each successive hair cycle, the regrowing hair emerges slightly thinner and shorter than its predecessor. Robust terminal hairs gradually transform into fine, barely visible vellus hairs. This shrinkage does not occur while the hair is growing but rather at the moment of regeneration, when a new hair forms after the previous one has shed. ^[2]

In healthy hair, approximately 85 to 90% of follicles are in the growth phase (anagen) at any given time, with only 10 to 15% in the resting phase before shedding (telogen). In affected scalp areas, this ratio can shift to 60 to 40 or worse. Additionally, the growth phase shortens from the typical two to seven years to just a few months, which explains why some hairs never grow beyond a certain length. ^[2]

Understanding the Causes

The Interplay of Genes and Hormones

Androgenetic alopecia arises from an interaction between genetic predisposition and hormonal activity. Both components are necessary; neither alone is sufficient. For a detailed overview, read our article Hair Loss Causes.

Genetic Component

Studies indicate that men whose fathers experience hair loss carry roughly a 2.5-fold increased risk. However, the maternal line also plays a role, as the gene encoding the androgen receptor sits on the X chromosome, which men inherit from their mothers. Unlike single-gene disorders, there is no single "hair loss gene." Rather, numerous genetic variants contribute (polygenic inheritance), accounting for the considerable individual variation. ^[4]

Interestingly, studies of identical twins reveal that despite sharing the same genetic makeup, the progression can differ between siblings. This suggests that environmental factors or individual circumstances may also influence outcomes.

The Role of DHT

Dihydrotestosterone (DHT) occupies a central position in the pathophysiology of androgenetic alopecia. DHT forms when testosterone is converted by the enzyme 5-alpha reductase. In the scalp, the type II variant of this enzyme is particularly active. ^[3]

Several observations underscore DHT's pivotal role: men who cannot produce DHT due to a genetic deficiency do not develop androgenetic alopecia. Balding scalp regions show higher DHT concentrations than hair-bearing zones. Medications that inhibit DHT formation halt hair loss in the majority of those treated. ^[3]

DHT binds to androgen receptors within hair follicle cells. In genetically susceptible follicles, this binding triggers a cascade leading to miniaturization. Crucially, the absolute testosterone level in the bloodstream is not the determining factor; rather, what matters is how sensitively the local follicles respond to DHT – and that is genetically determined.

Changes in Surrounding Tissue

Miniaturization affects more than just the hair follicle itself. The surrounding dermal tissue undergoes structural changes. The collagen bundles around affected follicles thicken, a phenomenon termed dermal sheath thickening. In advanced stages, this can progress to perifollicular fibrosis – scarring of the tissue surrounding the follicle. These structural alterations limit the space available for follicle regeneration and partly explain why fully reversing the process proves so challenging. ^[6]

Open Questions in Research

Despite decades of study, several aspects of androgenetic alopecia remain puzzling. Why does DHT cause hair loss on the scalp while simultaneously promoting beard and body hair growth? Beard cells actually exhibit three to five times greater 5-alpha reductase activity than scalp cells. Why does hair loss follow such a characteristic pattern while the sides and back of the head remain unaffected? And what initially triggers the increase in DHT activity in certain scalp regions? These questions remain subjects of ongoing investigation. ^[3]

Emerging Research Directions

The Wnt-Beta-Catenin Signaling Pathway

Hair regeneration depends on stem cells activated through the Wnt-beta-catenin signaling pathway. Recent research shows that DHT, via the secretion of the protein DKK-1, inhibits this pathway. This impairs stem cell activity and reduces the follicle's regenerative capacity. Encouragingly, animal studies suggest that even prolonged inhibition may be potentially reversible. ^[3]

Mechanical Tension and the Galea

The galea aponeurotica is a taut layer of connective tissue stretching across the top of the head. Intriguingly, the typical pattern of hair loss corresponds quite closely to the areas of highest tension in this layer. Some researchers hypothesize that mechanical pull on follicles could promote oxidative stress and chronic inflammatory processes, which in turn amplify androgen activity. This hypothesis is not yet conclusively proven but offers a compelling explanatory framework for the characteristic pattern. ^[3]

Olfactory Receptors

A surprising discovery emerged in 2018: hair follicles possess smell receptors, particularly the receptor OR2AT4. Activation of this receptor by certain scent compounds extended the hair growth phase in laboratory experiments. Whether and how these findings can be translated into therapeutic applications is currently under investigation. ^[7]

Risk Factors

What Increases Risk

Family history stands as the strongest predictor. If your father, grandfather, or uncles are affected, your own risk rises significantly. Age also plays a role, with likelihood increasing with each passing decade. Ethnicity has an influence as well, with men of Caucasian descent statistically more commonly affected than men of Asian or African heritage.

What Does Not Significantly Matter

Many widespread assumptions do not hold up to scientific scrutiny. Frequent hair washing, wearing headwear, sexual activity level, or hairstyle (except for chronic strong tension that can lead to traction alopecia) do not meaningfully influence androgenetic alopecia.

Diagnosis

Clinical Assessment

In most cases, a visual examination by a dermatologist suffices. The physician looks at the distribution pattern and often employs standardized scales for classification. Questions about family history provide important clues.

Supplementary Examinations

Using a dermatoscope, a specialized magnification instrument, the physician can examine the follicles more closely and assess the extent of miniaturization. In the pull test, 20 to 60 hairs are gently tugged: if more than 10% come loose, this indicates an elevated shedding rate. For atypical presentations, blood tests may be useful to rule out thyroid dysfunction, iron deficiency, or other causes.

Is a Formal Diagnosis Necessary?

Not always. If the pattern is clear and you wish to begin treatment, extensive diagnostics are often unnecessary. However, a medical evaluation can help exclude other causes and identify the optimal strategy.

Treatment

Can Hair Return?

With available treatments, hair loss can be halted in the majority of cases. Some treated individuals even experience thickening or regrowth, with results generally better the earlier treatment begins. Complete restoration of the original hair state, however, remains uncommon.

Medication Options

Minoxidil is available over the counter as a solution or foam. The exact mechanism of action is not fully understood, but the active ingredient extends the growth phase and improves scalp circulation. In studies, approximately 85% of users report positive effects after twelve months. Application must continue indefinitely, as hair loss resumes upon discontinuation. Read more about minoxidil application.

Finasteride is a prescription medication taken as a tablet. It inhibits the type II 5-alpha reductase enzyme and reduces scalp DHT concentration by 50 to 70%. Progression of hair loss is halted in 80 to 90% of treated men. Learn more in our article Finasteride: Efficacy & Studies. For prescription information, see Finasteride Prescription Switzerland.

The combination of both agents shows the best results in studies, as they work through different mechanisms.

Additional Approaches

Low-level laser therapy (LLLT) uses red light to extend the anagen phase. The evidence is promising but not yet as extensive as for medication options. PRP (platelet-rich plasma) is an autologous blood therapy in which enriched platelets are injected into the scalp. Studies show positive effects on extending the growth phase. Hair transplantation offers a permanent solution for advanced stages, relocating DHT-resistant hairs from the sides and back of the head to balding areas.

Realistic Expectations

Among men who treat consistently, progression can be halted in the majority. Thickening occurs in approximately 60 to 70%. Treatments generally must be continued indefinitely, as hair loss resumes after discontinuation.

Prevention

Act Early

Genetic predisposition cannot be changed, but the timing of treatment initiation can. The earlier you respond, the more hair can be preserved. Do not wait until hair loss becomes clearly visible. Start your online consultation now or learn more about our treatment options.

Scalp Care

Gentle, sulfate-free shampoos and regular cleansing can help remove excess sebum and DHT from the scalp. Shampoos containing ketoconazole are sometimes recommended as a complement.

General Lifestyle

A balanced diet with adequate protein, iron, and zinc supports hair growth. Chronic stress can negatively influence progression, even if it is not the primary cause. Sufficient sleep and stress management can therefore be beneficial.

Monitor Changes

Regular photos of the hairline and crown help detect changes early and document progress under treatment.

Key Takeaways

Androgenetic alopecia is a common, genetically determined form of hair loss arising from increased sensitivity of hair follicles to the hormone DHT. The progression is chronic and advances over time but can be halted with available treatments in most cases. The two most effective options are minoxidil (over the counter) and finasteride (prescription), with the combination yielding the best results. The earlier treatment begins, the more hair can be preserved. A complete cure does not currently exist, but research continues on new approaches that go beyond DHT inhibition alone.