In recent posts we explored the basis of pattern hair loss and touched on treatment methods used to blunt the onset and progression of the disorder. Among other things, we learned that, in common pattern hair loss, early treatment offers a better prognosis than attempts to reverse advanced baldness. In this post we will touch on the importance of hair cycle biodynamics -- and why this offers a potentially intriguing target for the development of advanced hair growth stimulants.
Human scalp hair growth differs from most other mammals in that most hair bearing animals shed in waves, nose to tail. This cephalocaudal (i.e. front to back) wave also explains why a dog loses far more hair in certain seasons and less in others. In contrast, humans display a mosaic pattern of hair growth, in that each and every scalp hair grows and sheds according to its own time clock. This means that we are constantly growing and shedding hair, typically in a ratio of 80% anagen (growth) & 20% catagen/telogen (shed/rest). A normal healthy scalp hair will grow for three to five years at a rate of approximately 1/2" per month. It will then cease growing and shed. For approximately 90 days the follicle will not produce a hair. At the 90 day point a new hair of equal caliber will grow and will reprise the three to five year growth pattern in about the same way.
In persons affected by AGA (androgenetic alopecia) the hair cycle becomes disturbed with more frequent resting cycles and shorter growing cycles. Also, with each hair shed, the replacement hair is thinner, finer and weaker. Morphologically, the growth stimulus centers in the hair follicle also display a negative cycle, with fewer dermal papilla cells and smaller structures throughout the organ.
In our lab and elsewhere, efforts are underway to better understand the genetic, epigenetic and biochemical factors which influence this process. To use an imperfect analogy, imagine that you had a beautiful deciduous tree in your front yard. The tree produced thick luxuriant leaves in early spring and shed them in the fall. Then, let's imagine that over time, your tree began producing leaves later and later in the spring and shedding them earlier in the fall. Also, let us suppose that the leaves produced were smaller and weaker. Eventually, the growing season would become so short and the leaves so diminutive that it would be as though the tree was in a permanent state of Winter sleep.
Common pattern baldness is a bit like this. One of the key goals of research thereby, is to comprehend the factors responsible for precipitating a negative modulation in AGA-affected scalp hair follicles. Some interesting clues have recently emerged. In our next installment we'll explore a few of these.
