A hypothetical pathogenesis model for androgenic alopecia: clarifying the dihydrotestosterone paradox and rate-limiting recovery factors
February 2018
in “Medical Hypotheses”
TLDR The model suggests that scalp tension could lead to hair loss, with factors like blood vessel hardening, enlarged oil glands, and poor microcirculation also playing a role. It also hints at a possible link between skull shape and baldness pattern.
The 2018 document proposed a hypothetical model for the development of androgenic alopecia (AGA), a condition affecting a significant portion of men and women. The model suggested that chronic scalp tension could induce an inflammatory response, leading to an increase in dihydrotestosterone (DHT) levels in AGA-prone tissues. However, DHT was not directly linked to hair follicle miniaturization, but rather to tissue remodeling conditions that restrict follicle growth. The document also suggested a link between AGA progression and factors such as capillary network calcification, sebaceous gland enlargement, and microvascular deficiency. It highlighted a potential relationship between skull shape and baldness patterning and suggested that scalp tension could contribute to AGA hair thinning. The document also discussed the role of androgens in arterial calcification and fibrosis, and the potential role of transforming growth factor beta-1 (TGF-ß1) in AGA. Further research was needed to confirm these hypotheses.
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