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Both Finasteride and Resveratrol stop apoptosis; programmed cell death, in Androgenetic Alopecia

      Apoptosis is a distinct mechanism of programmed cell death, which occurs when the body regulates cell numbers and eliminates unhealthy cells. Abnormalities in apoptosis can result in a host of disorders, including cancer (not enough apoptosis) and neuro-degeneration, (excessive apoptosis).

      Apoptosis has been conclusively identified in many studies as a central feature in the inflammation and progressive hair follicle miniaturization in Androgenetic Alopecia. Apoptosis is mediated by an intracellular proteolytic cascade composed primarily of the caspase family of proteases (Caspases). Caspases have been conclusively implicated with Androgenetic Alopecia.

      Caspase-1 level is higher in the scalp in androgenetic alopecia

      AGA affected hair follicles show a significantly higher level of caspase activity compared to normal hair follicles. One study showed that after 6 months of finasteride treatment, expression of caspases were similar to levels exhibited by normal follicles.

      Effects of finasteride on apoptosis and regulation of the human hair cycle.

      Multiple studies have shown Resveratrol to be a potent Caspase de-activator, which can at least partially explain its pronounced hair growth effects when combined with Curcumin.

      
      
Protective Action of Resveratrol in Human Skin: Possible Involvement of Specific Receptor Binding Sites

      These results suggest that alterations in the levels of caspases and inhibitors of apoptosis play a role in the development of AGA, with increased apoptosis seen in androgenetic tissues as compared to normals, and as one of the finasteride-caspase study concluded, provide a basis for development of novel treatments for inflammatory skin and hair diseases.

      It is well documented, Finasteride (Propecia) is wrought with an ever increasing negative side effect profile. The combination of Resveratrol and Curcumin can more directly address the mechanisms underlying the inflammatory follicular miniaturization by de-activating caspase activity, and promoting hair growth.



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