Male baldness related to genes and male sex hormones affects almost 80% of men under the age of 70 and may influence their self-esteem. Recently, however, it has also been suggested that it may be related to other androgen-related conditions.
This type of baldness is also known as male, androgenetic or androgenic alopecia. Androgens affect various skin functions, such as sebaceous gland growth and differentiation, hair growth, epidermal barrier and wound healing, mainly through a multistep signaling pathway. Although human hair growth is also affected by thyroid hormones and glucocorticoids, androgens are the most important regulators as they can stimulate, leave unaltered or inhibit hair growth depending on the body site. Androgens can increase the size of hair follicles in androgen-dependent areas (beard, axillary hair and pubic hair) but, in turn, in the scalp follicles of susceptible men, they suppress hair growth and promote miniaturization and hair shortening. Since the follicles are exposed to the same circulating hormones, this differential response would be the result of variations in androgen gene expression in different areas of the body, generally regulated at different mediators depending on the part of the body where the hair grows.
Each hair strand lies in a corresponding hair cavity in the skin called a follicle. In general, in the balding process the hair follicle shrinks over time, producing shorter and thinner hair, until it finally fails to form a new hair. However, the follicle remains viable, indicating that it would be possible for hair to grow back. A circular area usually appears at the back of the head known as the crown of the head that gradually becomes thinner and increases in size over time. Eventually, the hair becomes thinner, finer and shorter and creates a horseshoe-shaped pattern of hair around the sides of the head and a bald area at the back of the head.
Additionally, through the same androgenic link, male alopecia appears to have been linked to prostate cancer risk and its early onset has been postulated as a strong predictor of early onset of severe coronary heart disease and metabolic syndrome.
13.5 million variants
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