Big head? Bald head! Skull expansion: alternative model for the primary mechanism of AGA
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.
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A hypothetical pathogenesis model for androgenic alopecia: Clarifying the dihydrotestosterone paradox and rate-limiting recovery factors
2018, Medical HypothesesCitation Excerpt :The first is pubertal and post-pubertal skull bone growth. One study postulated a relationship between skull shape and baldness patterning [68], proposing that androgen-mediated skull bone growth [69,70] puts stress on capillary networks connected to AGA-prone hair follicles – leading to reduced blood flow and hair follicle miniaturization. Given that sagittal and coronal cranial sutures influence skull shape, underlie the GA, and fuse during adulthood [71] – GA-transmitted mechanical stress from bone growth may even occur after puberty.
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