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https://www.medical-hypotheses.com/article/S0306-9877(17)31041-1/fulltext
Androgenetic Alopecia is the result of chronic GA-transmitted scalp tension mediated by pubertal and post-pubertal skull bone growth and/or the overdevelopment and chronic contraction of muscles connected to the GA. This tension induces a pro-inflammatory cascade (increased ROS, COX-2 signaling, IL-1, TNF-α, etc.) which induces TGF-β1 alongside increased androgen activity (5-αR2, DHT, and AR), which furthers TGF-β1 expression in already-inflamed Androgenetic Alopecia-prone tissues. The concomitant presence of DHT and TGF-β1 mediates perifollicular fibrosis, dermal sheath thickening, and calcification of the capillary networks supporting Androgenetic Alopecia-prone hair follicles. These chronic, progressive conditions are the rate-limiting factors in Androgenetic Alopecia recovery. They restrict follicle growth space and decrease oxygen and nutrient supply to Androgenetic Alopecia-prone tissues – leading to tissue degradation, hair follicle miniaturization, and eventually pattern baldness.
This model allows for genetic influence during any step-process, but refutes the belief that Androgenetic Alopecia-prone follicles are genetically programmed to become sensitive to DHT. Rather, the model implies that Androgenetic Alopecia-prone tissues are predisposed to respond to chronic tension-mediated inflammation by inducing DHT and androgen-mediated TGF-β1, which restructure tissue – of which a symptom is hair loss. The model also provides a rationale for unexplained phenomena in Androgenetic Alopecia pathology, such as:
Future Androgenetic Alopecia research should focus on utilizing mechanotransduction to potentially reverse Androgenetic Alopecia-related tissue remodeling. If the model holds true, then reversing Androgenetic Alopecia tissue remodeling – rather than attenuating it – may pave the pathway to full Androgenetic Alopecia recoveries.
Androgenetic Alopecia is the result of chronic GA-transmitted scalp tension mediated by pubertal and post-pubertal skull bone growth and/or the overdevelopment and chronic contraction of muscles connected to the GA. This tension induces a pro-inflammatory cascade (increased ROS, COX-2 signaling, IL-1, TNF-α, etc.) which induces TGF-β1 alongside increased androgen activity (5-αR2, DHT, and AR), which furthers TGF-β1 expression in already-inflamed Androgenetic Alopecia-prone tissues. The concomitant presence of DHT and TGF-β1 mediates perifollicular fibrosis, dermal sheath thickening, and calcification of the capillary networks supporting Androgenetic Alopecia-prone hair follicles. These chronic, progressive conditions are the rate-limiting factors in Androgenetic Alopecia recovery. They restrict follicle growth space and decrease oxygen and nutrient supply to Androgenetic Alopecia-prone tissues – leading to tissue degradation, hair follicle miniaturization, and eventually pattern baldness.
This model allows for genetic influence during any step-process, but refutes the belief that Androgenetic Alopecia-prone follicles are genetically programmed to become sensitive to DHT. Rather, the model implies that Androgenetic Alopecia-prone tissues are predisposed to respond to chronic tension-mediated inflammation by inducing DHT and androgen-mediated TGF-β1, which restructure tissue – of which a symptom is hair loss. The model also provides a rationale for unexplained phenomena in Androgenetic Alopecia pathology, such as:
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Why DHT increases in Androgenetic Alopecia-prone scalp tissues (i.e., DHT is a response to tension-mediated inflammation)
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The mechanisms by which DHT is involved in Androgenetic Alopecia progression (i.e., DHT is involved in the onset of fibrosis and calcification)
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The pattern of Androgenetic Alopecia (i.e., Androgenetic Alopecia progression matches that of where GA-transmitted scalp tension is highest, and progresses as peak tension points change during fibrosis onset)
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Why Androgenetic Alopecia is observed more often in elderly populations versus young adults (i.e., calcification and fibrosis have had more time to accumulate)
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Why DHT is associated with body and facial hair growth and also Androgenetic Alopecia-related hair loss (i.e., tension-mediated inflammation induces TGF-β1 and DHT, and remodels tissue in Androgenetic Alopecia sites – a phenomenon not observed in body and facial hair growth sites)
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Why androgen suppression stops Androgenetic Alopecia, but does not regrow all hair (i.e.; DHT inhibitors may reduce fibrosis progression in Androgenetic Alopecia, but do not reverse fibrosis already present)
Future Androgenetic Alopecia research should focus on utilizing mechanotransduction to potentially reverse Androgenetic Alopecia-related tissue remodeling. If the model holds true, then reversing Androgenetic Alopecia tissue remodeling – rather than attenuating it – may pave the pathway to full Androgenetic Alopecia recoveries.
