The androgen-related, hereditary hair loss (medically also called androgenetic alopecia) is the well-known hair loss without disease value, which ultimately affects about 80 percent of all men of European descent to a greater or lesser extent and leads to the development of receding hairline and baldness.
The time at which the first changes are noticed varies, as does the speed at which the hair loss progresses. In every third man, the symptoms appear before his 30th birthday, every second man shows visible hair loss at 50, and by his 80th birthday only about one in five is spared hair loss. On average, it takes 15 to 25 years for the process to reach its end point – but some men also lose all their hair within just five years. Periods of accelerated hair loss can alternate with longer periods of relative stabilization. Often only the increasing thinning of the hair is noticeable, but some men also notice a phased increase in the number of lost hairs when combing or washing.
Symptoms of androgenetic alopecia
Androgenetic alopecia leads to a characteristic pattern of hair loss: At first, the hairline on both temples retracts largely symmetrically, forming the so-called receding hairline. This is followed by a diffuse thinning of the hair in the area of the vertex. Over time, a round bald spot develops and grows there. If the receding hairline becomes open to this involuntary toning, a small island of hair is often spared in the front area. With the further enlargement of the hairless areas, this also disappears, a semicircle of hair in the lower side areas and at the back of the head now surrounds the classic bald patch. The latter is often in less of a hurry to disappear, but may eventually also thin out and be lost. The successive stages of hair loss are today usually classified according to the so-called Hamilton-Norwood scale and are designated Norwood I to Norwood VII.
Regardless of this typical course, there are individual variations: Sometimes the bald spot on the parting shows up even before the receding hairline, or the entire hairline retracts dramatically, while the hair on the parting remains dense for a long time.
What are the causes of androgen-related hair loss?
The name androgen-related hair loss already indicates this: Hair loss is a direct result of the quite natural hormonal situation. Healthy men with androgen-induced hair loss generally do not show any pathological changes in their androgen levels. (Women with androgen-induced hair loss, on the other hand, sometimes – but not necessarily – have too high androgen levels).
For men, hormone levels that prevent hair loss are more likely to be worthy of illness or at least clearly deviate from the norm: In men who have very low levels of testosterone and/or dihydrotestosterone due to congenital enzymatic defects, long-term treatment with antiandrogens (e.g. in prostate cancer) or as a result of testicular removal, hair loss does not occur or the hair loss already manifest before the treatment/intervention does not progress.
But of course, even though this is not the case in the majority of men in Europe, you can have normal androgen levels and still keep your hair. What exactly is going wrong in the hair follicles of men affected by androgenetic alopecia is actually still not known exactly. The only thing that is clear is that the disorder is hereditary (the vast majority of men of European descent seem to be “burdened” accordingly). However, it is not inherited by a single gene, but rather multifactorially. Not much is yet known about the genes involved, only certain changes in the gene for the androgen receptor have so far been clearly associated with a tendency to hair loss .
The current state of knowledge about the concrete causes of androgenetic alopecia can be summarized in this way: The cause is the hormone dihydrotestosterone (DHT), which is produced from testosterone in the cells of the hair follicles, among other things. There is nothing pathological about this either. At least one of the three types of the enzyme 5α reductase, which is responsible for conversion, is part of the basic equipment of many cells in the body. Incidentally, the DHT level in men with hair loss is not necessarily elevated above the normal level – and elevated DHT levels do not necessarily cause hair loss. The trigger for hair loss is therefore most likely the reaction of the cells of the hair follicle to DHT. But why DHT causes the follicles of the scalp hair to atrophy, while body hair and beard hair generally continue to grow unchallenged – nobody can explain this to you today. One thing is clear: without DHT there is no hair loss.
But let us stress once again: 5α reductases are found in the skin, brain and nervous system, muscles, mammary glands, in almost all internal organs, in men and testicles and prostate and in women in the ovaries and cervix. In addition to the conversion of testosterone into DHT, these enzymes catalyze further conversion reactions of the body’s own messenger substances, about whose role there are still many, many open questions. Even though DHT is more negative than positive in the adult organism (the hormone is directly associated with benign prostate enlargement in addition to androgenetic hair loss): It would be naive to assume that on the one hand DHT and on the other hand the 5α reductases have no positive functions in the body.
Connection with the metabolic syndrome
The metabolic syndrome is a disease of civilisation that is very widespread in affluent countries: this is the name given to the complex of symptoms consisting of obesity, elevated blood fat and blood sugar levels, diabetes or its precursor stage of insulin resistance, arteriosclerosis and high blood pressure, which, due to nutritional and lifestyle factors, already plagues more than half of all adults in this country.
A connection between androgenetic hair loss and metabolic syndrome has been and is suspected in various cases – after all, the metabolic syndrome also has a complex effect on the body’s hormone balance. The question of whether the metabolic syndrome occurs significantly more frequently in groups of men with androgenetic alopecia than in control groups without hair loss has now been answered positively rather than negatively by more studies  – such a correlation therefore exists with some probability. Nevertheless, it can be assumed that the hereditary component of androgenetic alopecia dominates and that the presence or absence of the metabolic syndrome only influences the occurrence or absence of hair loss or its severity in a minority of men.
What happens in androgenetic alopecia?
In androgen-induced hair loss, there is an increasing miniaturisation of the hair follicles in the affected areas of the scalp and at the same time changes in the cycle of these follicles: The follicles change from terminal hair-producing organs to vellus hair-producing organs .
The anagen phase (the growth phase of the hair) shortens from cycle to cycle – consequently not only thinner but also shorter hairs grow from the shrunken follicle, whose pigment content also decreases due to the parallel decrease in the number of melanocytes in the follicle. In return, the telogen phase (the resting phase of the follicle) is extended. Accordingly, the probability of hair spontaneously falling out during the telogen phase or falling victim to mechanical stress during combing or washing increases: Since there are now many follicles in the telogen phase at any given time, this leads to thinning of the hair counted per unit area. In the final stage of hair loss, the anagen phase is so short that the hair produced in its course may no longer protrude above the scalp. Even if the hair follicles are by no means “dead” (the number of living follicles per unit area remains constant!), the impression of hairlessness is still created.
Can women also get androgenetic alopecia?
Since women also have different amounts of testosterone and correspondingly also dihydrotestosterone in their bodies, androgen-related hair loss can indeed also occur in the female sex. However, the pattern of hair loss is less clear than in men. The hair loss takes its typical course in a line that runs along the entire upper skull and becomes broader over time, often especially towards the hairline. In this context, the Christmas Tree pattern is often mentioned: here the thinning of the hair begins as a triangle with its tip pointing away from the forehead. Other patterns are possible, especially mixed forms of male and female alopecia. In most cases, however, the hair remains clearly thinned, and complete baldness – even in places – is rare. As in men, female androgenetic alopecia usually does not affect hair growth at the back of the head.
Since there are no generally binding diagnostic criteria for female androgenetic hair loss, there is some uncertainty about the frequency of its occurrence. In rare severe cases, the first signs of hair loss are already noticed in puberty. Figures for the frequency in the third decade of life are between 3 and 13 percent. The prevalence increases with menopause and is in the order of 30 to 50 percent for women of European descent in the seventh and eighth decades of life .
Female androgenetic hair loss also has a strong direct hereditary component. There is also a clear association with metabolic disorders: Women with androgenetic hair loss are also more frequently affected by the metabolic syndrome  and/or polycystic ovary syndrome  than women without hair loss. Polycystic ovary syndrome is a hormonal imbalance disorder that occurs in 4 to 12 percent of women of European descent (often, but by no means always, in connection with the metabolic syndrome) and whose symptoms develop around elevated androgen levels.
Treatment of androgenetic hair loss
The standard treatment for androgenetic hair loss in men, in accordance with the guidelines of medical societies, is now minoxidil ,finasteride or a combination of both drugs. Additional relatively well studied treatment options that may increase the effectiveness of the standard treatment include microneedling, platelet-rich blood plasma or laser therapy.
Not yet approved for the treatment of androgenetic alopecia are dutasteride, a finasteride-related active ingredient, which has been shown in studies to be much more effective, but also to have more side effects, and latanoprost, a prostaglandin F2α analogue, which already stimulates eyelash growth as a component of eyelash serums. Dutasteride can be prescribed by dermatologists at their own risk in off-label use. For the time being, the large-scale application of Latanoprost is strongly discouraged in view of the unclear side effect profile – incidentally, it would also be a very expensive pleasure. No or insufficiently published study results are available for other alternative therapies in order to be able to assess their efficacy. We have dedicated separate sections to each of these methods.
The standard treatment for androgenetic hair loss in women is minoxidil. Microneedling, platelet-rich blood plasma and laser therapy also play a role as additional treatment options. In women, androgen receptor antagonists can also be used for drug therapy of androgenetic alopecia.
Androgenetic alopecia is the most common reason for hair transplantation.