We have located links that may give you full text access.
Big head? Bald head! Skull expansion: alternative model for the primary mechanism of AGA.
Medical Hypotheses 2009 January
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 (5alpha-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, 5alpha-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.
Full text links
Related Resources
Trending Papers
Heart failure with preserved ejection fraction: diagnosis, risk assessment, and treatment.Clinical Research in Cardiology : Official Journal of the German Cardiac Society 2024 April 12
Proximal versus distal diuretics in congestive heart failure.Nephrology, Dialysis, Transplantation 2024 Februrary 30
World Health Organization and International Consensus Classification of eosinophilic disorders: 2024 update on diagnosis, risk stratification, and management.American Journal of Hematology 2024 March 30
Efficacy and safety of pharmacotherapy in chronic insomnia: A review of clinical guidelines and case reports.Mental Health Clinician 2023 October
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app