Could A Shotgun Approach Be More Effective Than A Stepwise Approach?

[Sliceofbread]

I realize the scenarios are quite different, but consider how both pathogens and and cancer respond to our current therapies. With tuberculosis if we use simple mono therapy then we select for bacteria that are resistant and it ends up harder to treat, so we use RIPE therapy that is much more effective. Same principle with HAART therapy and HIV.

With Acute lymphocytic leukemia giving prednisone mono therapy prior to our modern day chemo regimens (built around prednisone) then we actually worsen overall prognosis and response to treatment.

I feel I see a similar phenomenon with hairloss... most try one therapy at a time and add on if there is no success. What if someone failed with fina and instead of moving to just duta they added on duta+seti. Or maybe even duta+seti+ru, maybe even something crazy like cpa or estrogen... would it be easier or harder for our hair follicles to reach a hairloss homeostasis?

 

[Sliceofbread]

Or perhaps the exact opposite is true, that if we change the endocrine homeostasis in an extremely step wise gradual fashion then we get less counter regulation...

What I am positive is the worst thing you can do is fina eod. I think the constant hormonal seesaw will quite quickly predispose you to upregulation

 

[alekgn]

I realize the scenarios are quite different, but consider how both pathogens and and cancer respond to our current therapies. With tuberculosis if we use simple mono therapy then we select for bacteria that are resistant and it ends up harder to treat, so we use RIPE therapy that is much more effective. Same principle with HAART therapy and HIV.

With Acute lymphocytic leukemia giving prednisone mono therapy prior to our modern day chemo regimens (built around prednisone) then we actually worsen overall prognosis and response to treatment.

I feel I see a similar phenomenon with hairloss... most try one therapy at a time and add on if there is no success. What if someone failed with fina and instead of moving to just duta they added on duta+seti. Or maybe even duta+seti+ru, maybe even something crazy like cpa or estrogen... would it be easier or harder for our hair follicles to reach a hairloss homeostasis?

I think the reason most take a stepwise rather than shotgun or kitchen sink approach is minimizing the amount of stuff needed. Suppose you had some temporal recession. If you could get the same result with min and nizoral compared to finasteride,min, and nizoral, why have finasteride in the first place? Hair loss treatments aren't exactly like advil pills, where you can just take as many as you want with little consequence. dutasteride, finasteride, Estrogen, Seti, CPA, RU, etc all seriously mess with your body chemistry in different ways. As a result, I think it's a good idea to just try new treatments one at a time to prevent nuking your body unnecessarily. Could it be more effective? Possibly, but why take the risk of a possibly more jacked up body chemistry?