If you're not experiencing those dreaded side effects from finasteride, and it isn't doing a damn thing for your hairloss (for months I thought I was simply receiving bad pills), perhaps you are suffering from a condition so simple and obvious, it's explained in the basic FAQ on this website, yet there seems to be very little discussion elsewhere. I seriously urge everyone to think about the concept of reflex hyperandrogenicity. The FAQ explains it pretty damn quickly and well enough. If the concept of up and down-regulation of receptors makes perfect intuitive sense, which it does, then this concept makes as much sense as anything else posted on this site.
Let me know if these questions have previously been discussed, but is it possible that those who continue to lose hair on finasteride, and especially the ones who claim to get worse, (such as myself- been on 9 months, hair worsening exponentially over past 6) are experiencing a sub-clinical hyperandrogenicity? This concept could explain why side effects often disappear over time, as they did in my case. My sides-effects were terrible, but waned and mostly vanished after a month or two. I'm not saying you couldn't still have reflex hyperand. if you have side effects.
Could reflex hyperandrogenicity be quietly accounting for a significant percentage of the perceived “finasteride sheds� Are there any studies that prove such a "finasteride shed" even truly exists? If so, please post them, because virtually all hairloss sufferers seem to put great faith in this concept. (If it does, than perhaps it's a temporary reflex hyperandrogenicity that successful users are able to eventually counteract?) Obviously, there are countless satisfied finasteride. users out there, and many of them testify to the shed, so I'm not denying it works for them, perhaps most successful users. However, it seems like people could have easily started spinning ideas to convince one another that the drug would eventually start working and said if there’s a minoxidil. shed, and minoxidil. works, why not just assume that any long-term hairloss treatment could cause sheds? Surely Merck wouldn’t mind if users believed this, as people wouldn’t quit treatment right away. Interesting though that Merck doesn’t report this as a side effect, to my knowledge. That seems very fishy. Moreover, Dr. Rassman (He seems to be well respected from what I've seen) writes that he very rarely sees such finasteride. sheds in practice, despite all the hype on these hairloss forums. It’s extremely easy to see why this concept would get so much hype, why something could be so loathed and dreaded, yet such a welcome relief (because that’s a sign that it’s working!), depending on where one happens to find themselves flailing in their own hairgrowth/hairloss cycle.
Now, I’ve read some posts that seem to indicate a true clinical hyperand., but these cases seem very rare. The distinguishing feature there seems to be that the scalp becomes very inflamed and painful. Those people lose hair very quickly. But what about the rest of us who could possibly have subclinical cases, meaning no overt physical symptoms, except for hairloss. Couldn’t that be possible? For instance, I don’t seem to have any more acne or oily skin than usual. I do have increased libido, and increased facial hair. This brings me to my next point. Do not most people think of finasteride as decreasing libido? Yet there are wide ranging reports of increased libido. What causes this? True, there are certainly sexual side effects, but these evidently need not necessarily decrease libido.
Anyhow, just because I don’t have the acne/oily skin/other symptoms, why does that mean I cannot still have a mild case of hyperandrogenicity? Given the extreme sensitivity of hair follicles to the damaging effect of DHT in those with male pattern baldness such as myself, it seems like the hair might rather be the thing most easily affected by small hormonal fluctuations. The point many have made I think is that hairloss would only occur after obvious symptoms of hyperandr. occur in someone taking finasteride., because hair follicles would be much more resistant because of the DHT blocking effect of the drug. This point is very important, and must be examined. I wonder if this DHT blocking continues to remain successful even when the sensitivity and number of DHT receptors has greatly increased as with reflex hyperandr.? Again, my question is, how do we know that acne or oily skin would be evident before hairloss. I hope there’s a simple answer to this, but right now I’m really wondering if those who are trying to help their hairloss but not responding to finasteride. are not responding because of a reflex DHT receptor upregulation resulting in mild, relatively undetectable hyperandrogenicity, which always leads in the other direction to hairloss?
If so, how would you reverse it without quitting finasteride?
Let me know if these questions have previously been discussed, but is it possible that those who continue to lose hair on finasteride, and especially the ones who claim to get worse, (such as myself- been on 9 months, hair worsening exponentially over past 6) are experiencing a sub-clinical hyperandrogenicity? This concept could explain why side effects often disappear over time, as they did in my case. My sides-effects were terrible, but waned and mostly vanished after a month or two. I'm not saying you couldn't still have reflex hyperand. if you have side effects.
Could reflex hyperandrogenicity be quietly accounting for a significant percentage of the perceived “finasteride sheds� Are there any studies that prove such a "finasteride shed" even truly exists? If so, please post them, because virtually all hairloss sufferers seem to put great faith in this concept. (If it does, than perhaps it's a temporary reflex hyperandrogenicity that successful users are able to eventually counteract?) Obviously, there are countless satisfied finasteride. users out there, and many of them testify to the shed, so I'm not denying it works for them, perhaps most successful users. However, it seems like people could have easily started spinning ideas to convince one another that the drug would eventually start working and said if there’s a minoxidil. shed, and minoxidil. works, why not just assume that any long-term hairloss treatment could cause sheds? Surely Merck wouldn’t mind if users believed this, as people wouldn’t quit treatment right away. Interesting though that Merck doesn’t report this as a side effect, to my knowledge. That seems very fishy. Moreover, Dr. Rassman (He seems to be well respected from what I've seen) writes that he very rarely sees such finasteride. sheds in practice, despite all the hype on these hairloss forums. It’s extremely easy to see why this concept would get so much hype, why something could be so loathed and dreaded, yet such a welcome relief (because that’s a sign that it’s working!), depending on where one happens to find themselves flailing in their own hairgrowth/hairloss cycle.
Now, I’ve read some posts that seem to indicate a true clinical hyperand., but these cases seem very rare. The distinguishing feature there seems to be that the scalp becomes very inflamed and painful. Those people lose hair very quickly. But what about the rest of us who could possibly have subclinical cases, meaning no overt physical symptoms, except for hairloss. Couldn’t that be possible? For instance, I don’t seem to have any more acne or oily skin than usual. I do have increased libido, and increased facial hair. This brings me to my next point. Do not most people think of finasteride as decreasing libido? Yet there are wide ranging reports of increased libido. What causes this? True, there are certainly sexual side effects, but these evidently need not necessarily decrease libido.
Anyhow, just because I don’t have the acne/oily skin/other symptoms, why does that mean I cannot still have a mild case of hyperandrogenicity? Given the extreme sensitivity of hair follicles to the damaging effect of DHT in those with male pattern baldness such as myself, it seems like the hair might rather be the thing most easily affected by small hormonal fluctuations. The point many have made I think is that hairloss would only occur after obvious symptoms of hyperandr. occur in someone taking finasteride., because hair follicles would be much more resistant because of the DHT blocking effect of the drug. This point is very important, and must be examined. I wonder if this DHT blocking continues to remain successful even when the sensitivity and number of DHT receptors has greatly increased as with reflex hyperandr.? Again, my question is, how do we know that acne or oily skin would be evident before hairloss. I hope there’s a simple answer to this, but right now I’m really wondering if those who are trying to help their hairloss but not responding to finasteride. are not responding because of a reflex DHT receptor upregulation resulting in mild, relatively undetectable hyperandrogenicity, which always leads in the other direction to hairloss?
If so, how would you reverse it without quitting finasteride?