Background & Context
Androgenetic alopecia (AGA), also known as pattern hair loss, affects more than sixty million men in America and more than forty million women. Interestingly, rather than actual loss, it is now known that AGA is really a process of miniaturization — wherein the affected hair follicles and accompanying structures become smaller and less robust with the passage of time.
From a biochemical standpoint, a key feature of AGA is the conversion of the androgen hormone testosterone (T) to its more pathological metabolite dihydrotestosterone (DHT) via the triggering enzyme 5-alpha reductase. Recently, a number of other triggers have been identified, including certain forms of tissue inflammation.
The Triggers
Three things need to occur in order for a person to suffer from AGA. First: genetics — i.e., choosing one's parents poorly. The more profound the degree of hair loss in your parents and grandparents, the more likely you are to recapitulate the problem yourself.
The disorder manifests in adulthood — six-year-old children do not suffer from AGA — and is considered a progressive process in that the zone of hair loss worsens over time. In men, the age of onset often occurs in the mid-to-late 20s, whereas in women female pattern hair loss may not become apparent until the late 30s to early 40s.
Treatment Options That Actually Work
Until recently, there were no viable treatment options against AGA. In the 1980s and 1990s two drugs became readily available: minoxidil (Rogaine™) and finasteride (Propecia™). While each drug showed positive benefits in slowing the rate of hair loss, both also demonstrated significant negative side effects.
Interestingly, in its etiology, a disorder known as benign prostatic hyperplasia (BPH) shares a striking degree of similarity to AGA. This becomes relevant as naturally based compounds useful against BPH were successfully tested against AGA.
Why No Actual "Cure"?
One of the difficulties in progressing toward an actual cure for AGA has been the fact that no animal model exists for the disorder. This tends to limit the tools available to interrogate putative therapeutic targets. However, progress is occurring on several fronts.
Because AGA is known as a complex-trait disorder (i.e., caused by a number of genetic and epigenetic factors), the first effort involves developing a cocktail mix of naturally-based compounds with an eye toward creating a therapeutic synergy.
The next option is based on modifying the causative genes — in effect, stimulating those "hair-growing genes" which have become silenced and down-regulating those which are contributing to the onset and progression of AGA.
The last option involves recapitulating the entire human scalp hair follicle in vitro — in other words, growing hair in the lab. Here, progress is occurring, and the endpoint should be the ability to take one or two hairs and grow enough new hair to fill in a denuded scalp. As progress occurs in each of these areas, we will update you as we are able.
References available on request and via the National Library of Medicine (PubMed).