Atlaz
New member
As someone who is currently taking a Serm I am not feeling the full effects of the treatment. Does the bellow theory hold some truth?
" This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don***8217;t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?
There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.
SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.
Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected).
However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound."
I find this information useful to have laying around the forum for future reference.
" This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don***8217;t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?
There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.
SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.
Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected).
However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound."
I find this information useful to have laying around the forum for future reference.
Unfortunately I don't have any recent data on it to see if it climbed again.
