Elsevier

Medical Hypotheses

Volume 72, Issue 1, January 2009, Pages 23-28
Medical Hypotheses

Big head? Bald head! Skull expansion: alternative model for the primary mechanism of AGA

https://doi.org/10.1016/j.mehy.2008.07.048Get rights and content

Summary

Currently, the predominant hypothesis explains androgenetic alopecia (AGA) as a process reliant upon affected follicles being individually programmed to accumulate dihydrotestosterone (DHT), which then causes progressive follicular miniaturisation. The goal of this paper is to suggest that such miniaturisation may result from an exaggeration of the bone remodelling process causing a reduction in blood supply to the capillary network within the affected region.

The bones of the human skull continue to grow during adulthood and observations made of those with AGA suggest that such growth may be responsible for the development of this condition. Studies of human cranial anatomy indicate that frontal and parietal bone growth can account for the development of the male pattern baldness (MPB) profile and the variations that can occur in the rate and location of hair loss. Steroid hormones such as DHT promote facial and body hair growth. Logically, this suggests that DHT should stimulate hair growth within the MPB region and not hair loss. However, DHT also has an anabolic effect on bone formation, and it is hypothesised that this stimulation of bone growth will overwhelm the hair growth promoting effects of DHT. Androgen receptor sites, 5-alpha-reductase (5α-R) and DHT have all been associated with AGA, but they also exist within numerous types of bone cells. DHT will stimulate the proliferation of osteoblast cells and the formation of new bone.

Verification of this hypothesis would imply that DHT is primarily involved with AGA through its stimulation of the skull expansion process rather than through interaction with individual follicles. Also, increased androgen receptor gene expression, 5α-R activity and subsequent production of DHT within the MPB region of balding individuals, may simply represent the body’s attempt to compensate for the skull expansion expression of hair follicle miniaturisation. Furthermore, it suggests that MPB region follicles are not individually programmed for hair loss. A redirection of genetic research towards the identification of those genes responsible for skull shape and development would be appropriate, and may reveal the genetic connection to AGA including its paternal link.

Introduction

There is still much debate about the true cause of androgenetic alopecia (AGA), a condition that can affect up to 80% of men [1] and 50% of women [2] at some stage in their lives. For men, AGA will always develop within what appears to be a predetermined area of the scalp. Within this male pattern baldness (MPB) region, near identical horseshoe shaped patterns of hair loss will develop in most advanced cases of AGA. For women, AGA will typically involve diffuse thinning (evenly spread hair loss) throughout the same region as in men. AGA has no serious implications to health, but is, nevertheless, an area of great concern for a vast number of people. Several factors have been linked to it including genetics, male sex hormones (androgens), sebum overproduction, nutrition, etc., and a number of theories exist which attempt to explain the exact mechanism taking place.

Section snippets

Current understanding

It is generally accepted that androgens are the primary cause of AGA, and it has long been known that a derivative of testosterone called dihydrotestosterone (DHT) is directly related to this condition [2]. However, the actual mechanism that explains how DHT causes AGA is subject to speculation.

Most research suggests that this mechanism involves DHT accumulation within scalp follicles. The enzyme 5-alpha-reductase (5α-R) will convert testosterone into DHT which then attaches to androgen

Development of new hypothesis

The skull expansion hypothesis places focus on an area beyond the localised arena of the hair follicle. A study of the bones underlying the MPB region and analysis of the bone resorption and remodelling processes has yielded an alternative model for the primary mechanism of AGA.

It is generally thought that, upon reaching puberty, the human skull stops growing in size. However, research has shown that the bones of the human skull can continue to grow as people age [6]. For those who develop AGA

Evidence in support of the skull expansion hypothesis

Using basic human physiology, analysis of cranial bone structure, and characteristics of AGA development, supportive evidence for the skull expansion hypothesis can be presented. Such research has revealed features of AGA that cannot be accounted for using the current model.

Hypothesis implications

Validation of the skull expansion hypothesis would expose inaccuracies within key areas of the current model for AGA. Specifically, the following points would be highlighted:

  • 1.

    DHT is primarily involved with AGA through its stimulation of the skull expansion process rather than interaction with individual follicles. A secondary effect also takes place in which DHT does interact directly with follicles to produce an excess of sebum. Increased androgen receptor gene expression and 5α-R activity

Conclusion

The skull expansion hypothesis can give a definitive underlying mechanism for AGA. Further study, testing and confirmation of the skull expansion process may yield alternative forms of treatment for this type of hair loss. This may involve identification of the gene(s) responsible for inherited skull shape.

References (23)

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