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As far back as 1944 two scientists, Lillie and Wang, were taking bits of feather follicle (which is basically the same structure as a mammal hair follicle) and implanting them to chicken skin to induce new hair follicles to form. In the 1960's Cohen and Oliver showed the same could be done with rat follicles.


The Current Roadblocks with Hair Cloning

1 - Unreliable Quantities

While the principle of hair cloning is proven, turning it into a practical technique for clinical use is fraught with problems. First, the results of implantation can be very variable. Even if they inject the same quantity of cells, and even if the cells are from the same donor, the number of hair follicles produced in response is extremely unreliable. There have been unofficial reports from two sources (Aderans/Bosley, Dr Jerry Cooley) that they have successfully induced hair growth in humans by using cultured cells. Unfortunately the success rate stated by both sources was poor. Implantation of cultured cells to volunteers by Aderans/Bosley produced just 2 hairs in a single individual. Dr Jerry Cooley implanted cultured cells into himself at fifteen different sites but only managed to promote one hair follicle to grow.

2 - Unreliable Angles

Second, the new hair follicles induced in studies using rats or mice are usually disorientated. Natural hair follicles grow hair with a “grain”, so on your scalp your hair grows in whirl pattern (usually clockwise) about the vertex. On your lower legs your hair grows down towards your feet etc. With hair follicles induced in hair cloning studies on rodents, the follicles can grow hair at all sorts of angles. This gives a cosmetically “scruffy” appearance.

3 - Uneven Distribution / Patchy Growth

Third, natural hair follicles are evenly distributed over the skin, but in rodent studies hair follicles induced by hair cloning do not have an even distribution over the skin – there can be clumps of hair growth. Again, the cosmetic appearance of this clumpy growth is generally unacceptable.

For hair cloning to become a practical and popular treatment, all these problems must be overcome.


Is it Mom's Fault?

It’s an enduring and common misconception among patients that MPB is ‘inherited from the mother’s side’. Well, that statement is neither right nor wrong. Pattern baldness can be inherited from the mother’s side. But it can also be inherited from the father’s side. Despite the universal interest in the genetics of MPB, there is a surprisingly small number of scientific studies in regards to the genetics of MPB and there is only one known extensive family study on MPB. This study of hair growth patterns in 22 families concluded that common pattern baldness was an autosomal dominant phenotype in men and an autosomal recessive phenotype in women. However, the validity of these results are controversial because of a lack of details regarding examination methods and sampling errors of this study, which was published in 1916.

Despite the fact that the entire human genome, comprising approximately 30,000 genes in the human DNA, was completely mapped out as of April 2003, the gene or, more likely, genes responsible for MPB, have not been identified. Studies of the genes (on chromosome Xq11.2^q12) encoding the two 5alpha-reductase isoenzymes show that they are not the genes associated with male pattern baldness.


Maybe we can blame Dad?

A study examining 410 men with premature baldness found evidence of a genetic influence from the father’s side in only 236 cases. Hair loss similarities between father and son have also been observed in another study in regards to the frequency of MPB in brothers of men having prematurely bald fathers (66%) compared with brothers of men with unaffected fathers (46%). The relatively strong association of MPB between fathers and sons in this study was not consistent with a simple Mendelian autosomal or sex-linked dominant inheritance and suggested that several genes (a polygenic etiology) may be responsible for MPB. As further evidence against a single and/or X-linked gene being responsible for MPB is the observation that only 33% of the fathers of 18 women suffering from severe pattern baldness also had MPB. These findings suggest that other autosomal genes play an important role in the expression of MPB.

Considering the high proportion of men affected by MPB, its distribution in the general population, the increased risk of MPB as the number of affected close relatives increases, and the high risk of inheritance from either or both affected parents, one can support a strong argument in favor of a polygenic inheritance.

It seems ironic that with all the knowledge that has been accumulated in regards to MPB in the past several decades, we still do not know the exact genetic inheritance of MPB. What is known is that the genes are autosomal (not on the X or Y chromosomes), dominant (as opposed to recessive), and have variable penetrance (so it may not affect siblings of the same parents to the same degree).