Up to 95 percent of permanent hair loss is due to androgenetic alopecia, a hereditary condition that affects millions of men, women and children. This condition is characterized by what we call pattern baldness. Male pattern baldness generally starts with a receding hairline at the front or thinning of the crown hair and gradually progresses until, in extreme cases, only a thin horseshoe-shaped rim of hair remains at the back and sides of the head. Female pattern baldness, which has received more attention in recent years, refers to general thinning of hair all over the scalp, usually beginning at around age 30 and becoming more noticeable after 40 and particularly after menopause.
Along with advancing age and an inherited tendency to bald early (a more complex link than researchers originally thought), androgenetic alopecia is sped up by an over-abundance of the male hormone dihydrotestosterone (DHT) within the hair follicle. DHT is a highly active form of testosterone, which influences certain aspects of masculine behavior, from aggression to sex drive.
Testosterone is converted to DHT by an enzyme called 5-alpha reductase, which is produced in the prostate, the scalp and various adrenal glands. Over time, DHT causes hair follicles to degrade and shortens their anagen, or active, phase.
Technically, the follicle is still alive and connected to a good blood supply (that’s why it can nurture a transplanted follicle that is immune to the effects of DHT), but it will grow smaller and smaller. Some follicles will die, but most will simply shrink in size and produce weaker hairs. The progressively shorter anagen growing cycle means more hairs are shed and remaining hairs become so thin that they cannot survive daily wear and tear, experts say. Hairs in balding areas gradually change from long, coarse, thick, colored hairs into fine, unpigmented, fuzzy hairs.
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