25-DM-4-LYFE
Greenlighter
- Joined
- Aug 16, 2009
- Messages
- 27
Hello, i have been using various stimulants at medium/high therapeutic doses for the last decade or so - primarily methylphenidate and adderall. im in my early 20s and have started to notice significant hair loss in the distinctive male pattern (recession at the temples with an intact frontal hairline and crown) this would be relatively normal except nobody in my family is bald even in their 60s let alone their early 20s. im aware this still does not rule out genetics.
the mechanism of the two FDA approved treatments for androgenic alopecia are inhibition of the type II 5-alpha reductase enzyme in finasteride and (ostensibly) dilation of the hair follicle in minoxidil. there are numerous indirect mechanism by which dopaminergic stimulants could accelerate hair loss eg stress and malnutrition but i wonder if prescription stimulants could directly accelerate hair loss through any of the following mechanisms:
1.) constriction of the hair follicle, i understand this would not be significant construction - probably a small fraction of a millimeter in diameter but given the fact that these stimulants often behave as vasoconstrictors it seems possible.
2.) endocrine imbalance of some kind - specifically increased production of testosterone
3.) some effect on the 5-alpha reductase enzyme enhancing its ability to convert testosterone to dihydrotestosterone.
any long term stimulant users experienced the same thing? any thoughts on the above hypotheses?
the mechanism of the two FDA approved treatments for androgenic alopecia are inhibition of the type II 5-alpha reductase enzyme in finasteride and (ostensibly) dilation of the hair follicle in minoxidil. there are numerous indirect mechanism by which dopaminergic stimulants could accelerate hair loss eg stress and malnutrition but i wonder if prescription stimulants could directly accelerate hair loss through any of the following mechanisms:
1.) constriction of the hair follicle, i understand this would not be significant construction - probably a small fraction of a millimeter in diameter but given the fact that these stimulants often behave as vasoconstrictors it seems possible.
2.) endocrine imbalance of some kind - specifically increased production of testosterone
3.) some effect on the 5-alpha reductase enzyme enhancing its ability to convert testosterone to dihydrotestosterone.
any long term stimulant users experienced the same thing? any thoughts on the above hypotheses?
