kemo
New Member
Swale,
Here is the info on the research I was talking about. As you read this, please keep a couple of things in mind. First, I was typing at about 75wpm just to get it done, hence spelling and grammar may have been compromised. Second, although I am sure you already know a lot of the things here, I have explained them in a little more detail for the interest of the casual reader on here, I certainly dont mean any of it to sound talking down.
O.K. First to the disease: Alopecia Universalis, an auto-immune disease which affects the hair follicle. Although perhaps thought to be cosmetic, problems can be associated with the loss of nasal hair follicles, eyelashes, etc. Beyond that, the normal patients are often as young as 10, which can have a tremendous psychological impact on their childhood.
Many theories as the exact mechanism have been researched, with the primary finding that the bodies own immune system attacks the hair follicle, causing release of the shaft.
The disease is most commonly treated with prednisone or other glucocortisones.
Subject A (Male) took 60mg/day of prednisone which resulted in complete hair regrowth after 6 months. This dose was maintained from age 21 through age 26. After cessation of therapy, the hair rapidly fell back out.
At age 31, subject starting self administering anabolic steroids. The drugs administered were Testosterone (different esthers) at 300mg/week, Nandrolone Decanoate at 300mg/week, and Tamoxifen Citrate at 10mg/day. These drugs were cycled 10 weeks on / 8 weeks off. After the second cycle, subject had hair growth over 90% of scapal area, and 25% of remaining body.
With that background, here is a little of my theory:
Cortisol is our main anti-inflammatory hormone, so if the hair molecules were getting choked off by inflammation (as most theories suggest) the cortisone should help. This would tend to be reflected in the way prednisone can regrow hair. However, why would AAS also cause a regrowth?
Perhaps it is not the stopping of inflammation that causes cortisone to regrow hair. Perhaps there is some mechanism whereby endogenous cortisone is actually causing the condition?
Prednisone is a cortisone drug, meaning that although it increases the levels of cortisone in the bloodstream, it decrease the endogenous levels of cortisone. When the subject was taking AAS, it should also decrease the natural levels of cortisone, or at least compete at the receptor site. Therefore, in both instances of hair regrowth, it would seem the endogenous levels of Cortisol had been reduced.
I am not sure if there is any other link possible? I have tried to research all the other pathways of steroids and prednisone, and cannot find out anywhere they overlap other than the suppression of natural cortisone levels.
Here is a bit further breakdown of my theory. Perhaps AU rests in some sort of amino acid breakdown. Although cortisone is anti-inflammatory, it's primary job is tell the cells to start breaking down amino acids. This may also point to where the two drugs overlap. Deca is a well known blocker of cortisol receptors. If you block the receptor, or somehow flood it with "fake" cortisol, is it possible that this breakdown occurs at a different pace or in a different method? Since Amino Acids are a key ingredient to hair, it may be possible
Another somewhat limited possibility is that the HPTA is permanently depressed in individuals with AU. By taking AAS perhaps the HPTA would be tricked into producing more cortisol? Now, assuming that normally the HPTA was actually causing too little cortisone to be produced, I would think you would see other factors in individuals with AU. For instance, Subject A has all the classic symptoms of cushings syndrome even after 6 years of glucocortisoid cessation. Perhaps this is due to years of predisone use, but it would still seem to indicate that his cortisone levels were high enough, or some of the symptoms would have reversed? I am not sure about this...but just my thought?
Further, if the levels of cortisol were low in patients with AU, wouldn't it mean the system would be in a continual anabolic state? That would tend to indicate that if the body was trying to return to a neutral state that males would have lower testosterone levels. Three subjects tested with AU all had T levels in the normal range.
Finally, in the three subjects, all had free cortisol levels near high normal.
So, what about cortisol receptor damage?
However, I see two problems: First, the amount of cortisone receptors are limited, so flooding the body with cortisone should only be effective up to a point. If there were some sort of receptor damage, more free blood levels of cortisone shouldn't really help. Finally, a drug like Deca which blocks cortisol receptors should then have absolutely no effect..unless perhaps it caused some sort of receptor upregulation in addition?
Again, I am totally not sure about this, perhaps I am overthinking the whole cortisol factor, but it must have some sort of play in this, or the AAS and prednisone would have had no effect.
What other methods do you think would have caused the steroids to regrow the hair? I haven't been able to find any other possible mechanisms other than the suppression of endogenous cortisol, the action of cortisol in the amino acid chain, and the blocking of receptor sites.
So, what should be the next step in the research. In Subject A, the internal factors for cushings syndrome has been ruled out. The only possible reason is extended tissue exposure to exogenous cortisol. Therefore, the next step is to administer 250mg of aminoglutethimide three times daily for four weeks. This should be sufficient to suppress the cortisol levels and see where things stand. Testing by 24 hour urine analysis will be conducted to prevent a total drop in cortisol levels. I also want to make sure we arent getting the escape effect from increase ACTH, so the cycle will be vital to make certain we avoid escape, but yet give the follicle time to respond.
O.K. So there you have the 10 minute version of about 6 months of research. Please feel free to blast as many holes in it as possible, it makes me think a little more.
Kemo
Here is the info on the research I was talking about. As you read this, please keep a couple of things in mind. First, I was typing at about 75wpm just to get it done, hence spelling and grammar may have been compromised. Second, although I am sure you already know a lot of the things here, I have explained them in a little more detail for the interest of the casual reader on here, I certainly dont mean any of it to sound talking down.
O.K. First to the disease: Alopecia Universalis, an auto-immune disease which affects the hair follicle. Although perhaps thought to be cosmetic, problems can be associated with the loss of nasal hair follicles, eyelashes, etc. Beyond that, the normal patients are often as young as 10, which can have a tremendous psychological impact on their childhood.
Many theories as the exact mechanism have been researched, with the primary finding that the bodies own immune system attacks the hair follicle, causing release of the shaft.
The disease is most commonly treated with prednisone or other glucocortisones.
Subject A (Male) took 60mg/day of prednisone which resulted in complete hair regrowth after 6 months. This dose was maintained from age 21 through age 26. After cessation of therapy, the hair rapidly fell back out.
At age 31, subject starting self administering anabolic steroids. The drugs administered were Testosterone (different esthers) at 300mg/week, Nandrolone Decanoate at 300mg/week, and Tamoxifen Citrate at 10mg/day. These drugs were cycled 10 weeks on / 8 weeks off. After the second cycle, subject had hair growth over 90% of scapal area, and 25% of remaining body.
With that background, here is a little of my theory:
Cortisol is our main anti-inflammatory hormone, so if the hair molecules were getting choked off by inflammation (as most theories suggest) the cortisone should help. This would tend to be reflected in the way prednisone can regrow hair. However, why would AAS also cause a regrowth?
Perhaps it is not the stopping of inflammation that causes cortisone to regrow hair. Perhaps there is some mechanism whereby endogenous cortisone is actually causing the condition?
Prednisone is a cortisone drug, meaning that although it increases the levels of cortisone in the bloodstream, it decrease the endogenous levels of cortisone. When the subject was taking AAS, it should also decrease the natural levels of cortisone, or at least compete at the receptor site. Therefore, in both instances of hair regrowth, it would seem the endogenous levels of Cortisol had been reduced.
I am not sure if there is any other link possible? I have tried to research all the other pathways of steroids and prednisone, and cannot find out anywhere they overlap other than the suppression of natural cortisone levels.
Here is a bit further breakdown of my theory. Perhaps AU rests in some sort of amino acid breakdown. Although cortisone is anti-inflammatory, it's primary job is tell the cells to start breaking down amino acids. This may also point to where the two drugs overlap. Deca is a well known blocker of cortisol receptors. If you block the receptor, or somehow flood it with "fake" cortisol, is it possible that this breakdown occurs at a different pace or in a different method? Since Amino Acids are a key ingredient to hair, it may be possible
Another somewhat limited possibility is that the HPTA is permanently depressed in individuals with AU. By taking AAS perhaps the HPTA would be tricked into producing more cortisol? Now, assuming that normally the HPTA was actually causing too little cortisone to be produced, I would think you would see other factors in individuals with AU. For instance, Subject A has all the classic symptoms of cushings syndrome even after 6 years of glucocortisoid cessation. Perhaps this is due to years of predisone use, but it would still seem to indicate that his cortisone levels were high enough, or some of the symptoms would have reversed? I am not sure about this...but just my thought?
Further, if the levels of cortisol were low in patients with AU, wouldn't it mean the system would be in a continual anabolic state? That would tend to indicate that if the body was trying to return to a neutral state that males would have lower testosterone levels. Three subjects tested with AU all had T levels in the normal range.
Finally, in the three subjects, all had free cortisol levels near high normal.
So, what about cortisol receptor damage?
However, I see two problems: First, the amount of cortisone receptors are limited, so flooding the body with cortisone should only be effective up to a point. If there were some sort of receptor damage, more free blood levels of cortisone shouldn't really help. Finally, a drug like Deca which blocks cortisol receptors should then have absolutely no effect..unless perhaps it caused some sort of receptor upregulation in addition?
Again, I am totally not sure about this, perhaps I am overthinking the whole cortisol factor, but it must have some sort of play in this, or the AAS and prednisone would have had no effect.
What other methods do you think would have caused the steroids to regrow the hair? I haven't been able to find any other possible mechanisms other than the suppression of endogenous cortisol, the action of cortisol in the amino acid chain, and the blocking of receptor sites.
So, what should be the next step in the research. In Subject A, the internal factors for cushings syndrome has been ruled out. The only possible reason is extended tissue exposure to exogenous cortisol. Therefore, the next step is to administer 250mg of aminoglutethimide three times daily for four weeks. This should be sufficient to suppress the cortisol levels and see where things stand. Testing by 24 hour urine analysis will be conducted to prevent a total drop in cortisol levels. I also want to make sure we arent getting the escape effect from increase ACTH, so the cycle will be vital to make certain we avoid escape, but yet give the follicle time to respond.
O.K. So there you have the 10 minute version of about 6 months of research. Please feel free to blast as many holes in it as possible, it makes me think a little more.
Kemo
