Male, or female, pattern baldness, known medically as androgenic alopecia, is a genetic condition that presents in men as a receding hairline and thinning at the crown that can eventually lead to partial or complete baldness. It differs in women as hair loss is usually all over and rarely leads to total baldness.
Understanding Genetic Hair Loss
Although environmental factors can play a role in androgentic alopecia, it has been proved in recent years that this form of hair loss is related to the androgen hormone and in particular dihydrotestosterone.
Dihydrotestosterone, known as DHT, basically wants your hair follicles to die. It binds to the receptors in the scalp follicles, shrinking them so the hair is unable to survive. Although these androgens are known as male hormones, women have a small level of male hormones and the levels can rise, for example through the menopause.
Up till now, it was thought that the gene that might be at fault as such is the AR gene. This gene instructs the body to make a protein called an androgen receptor and this allows the body to deal, in the normal way, with dihydrotestosterone as well as other androgens.
New Research into Genetic Hair Loss
A new study in the medical journal Plos Genetics has furthered understanding of the genetic cause of hair loss. MicroRNAs are short strands of ribonucleic acid and they regulate how your genes are expressed and play a role in the pathways of male or female pattern baldness.
An excess of one particular microRNA – miR-22 – was found to send the hair growth cycle into the resting phrase prematurely and prevent the replication of hair stem cells. Over time this results in permanent hair loss.
The scientists behind the study increased activity of miR-22 in mouse hair follicles and found it halted the active growth stage of the follicles, by reducing the activity of over 50 separate keratin genes.
New genetic discoveries are likely to lead to the hair loss treatments of the future as treatments that inhibit the actions of miR-22 could be developed.