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It has been noted that the main cause of the pattern baldness or the balding in men is a combination of genetic predisposition and androgens that are sufficiently circulated in the human system. The stance of genetic predisposition on pattern baldness remains debatable on the areas of genetics since the genes that cause pattern baldness are still unmarked. Although the advancement of the study of alopecia in men is nearing its conclusion, the reason for alopecia in women remains vague.

The current theory widely pursued by researches nowadays is that the same genes are responsible for the production of androgen, androgen conversion to dihydrotestosterone (DHT), the activity of the androgen receptor, and the cause of alopecia. The importance of understanding the genetic signature that triggers alopecia lay in the potential treatment modules that can be devised once the mechanism is fully understood.

Is Androgenetic Alopecia an Autosomal Dominant Disorder?

Non-sex determining chromosomes are called autosomal chromosomes. An autosomal dominant gene is one of the autosomal chromosomes in our genetic make up. Since these autosomal genes are dominant, these genes only need to exist in the chromosomes of one of the parent in order to cause diseases. In the study of alopecia, it was generally assumed that a person inherited baldness from the maternal grandfather in the mode of inheritance. However, the mode of inheritance was well documented in the science as autosomal dominant, implying that the inheritance of only one autosomal gene can be a full blown genetic predisposition.

A study in 1916 by Dorothy Osborn led to the proposition that balding in men and in women is due to a single gene with two alleles, B (balding) and b (non-balding). She suggested that balding in men occurs whichever combination of the alleles present, that is whether the alleles are homozygous/same (BB) or heterozygous (Bb). Balding in women only occurs when these alleles are homozygous. Simply put, a single autosomal gene, termed “B,” could account for genetic predisposition to baldness, acting in an autosomal dominant fashion in men and in an autosomal recessive manner in women. In simpler words, men are predisposed to baldness if they inherit either “BB” or “Bb”; women are only predisposed if they inherit “BB.”

The Polygenic Hypothesis

A study in 1984 done by Kuster and Happle re-evaluated the inheritance of pattern baldness. They found out that there is a need for a more complex mode of inheritance needed for pattern baldness to occur. A polygenic trait is a trait controlled by many genes and whose trait is the summary of the values of each individual genes, defining a degree with which the traits are expressed.

The authors argued that a Gaussian curve of normal distribution that represents the full range of phenotypes -from fully developed baldness to no hair loss at all – was followed by the pattern baldness distribution. In addition, Kuster and Happle argued that it would be highly improbable for the hereditary traits to be determined by a single gene with the low value of 0.1 percent. Along with this, there is much difficulty in determining the exact figure of men with alopecia although an estimate runs of 40% to 60% which further supports the pervasive mode of inheritance.

Father-to-Son Transmission

Advances in the research for alopecia suggests that the mode of inheritance for pattern baldness involves a very complex process which engage many genes that could involve a gene or genes transmitted from father to son. Sexual dimorphism in the androgen-estrogen balance modulates the phenotypic expression of pattern baldness. However, one scientist, Hoffman, argued against this since the androgen receptor gene is located on the X-chromosome, which does not explain the father-to-son inheritance.

Androgen Receptor

The main function of the androgen receptor is to regulate the response of the androgen. Some recent researchers believe that the gene encoding in the androgen receptor possibly plays a role in the regulation of androgen potency that is available in their hair follicles – which could be a factor in the predisposition of pattern baldness. However, the same suggestion offered by Hoffman hinders the advancement of this thought since the androgen receptor gene is located on the X-chromosome.

Nonetheless, it is not impossible for a gene on the X chromosome to be involved in a polygenic predisposition. Researches propose the idea of a gene on the X chromosome causes an increase in androgen receptor expression and increase in potent androgen dihydrotestosterone (DHT). DHT is also assumed to cause shortening of the anagen phase, production of progressively finer pseudo-vellus hairs, and the cause of the miniaturization of the follicles, at the same time decreasing the level of the enzyme that converts androgens to estrogens, aromatase, that could be detected in balding scalps.

Polycystic Ovary Syndrome and Female Pattern Baldness

Sex hormone binding globulin (SHBG) binds to testosterone, making the testosterone unable to convert androgens to dihydrotestosterone (DHT). The hypersecretion of the androgen hormones and the below normal production of sex hormone binding globulin (SHBG) indicates a Polycystic Ovary Syndrome. Once a person has Polycystic Ovary Syndrome, the insulin levels are increased, affecting the production of hormones and SHBG. Researches suggest that a single gene causes the human body’s vulnerability to Polycystic Ovary Syndrome and the same gene may affect the production and the effects of androgen on the body. This gene that causes Polycystic Ovary Syndrome on women, when passed down from the man’s side of the family could be a possible culprit to the balding in women.

However, not every woman with Polycystic Ovary Syndrome develops pattern baldness. Estrogen is an indirect antagonist of testosterone, and the high levels of estrogen in the syndrome may block the androgen activity to some degree.

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