From Dr. Scally: MESO-Rx - View Single Post - nolva vs clomid
Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary allowing gonadotropin production to resume. Administration produces an elevation of LH and secondarily gonadal sex hormones. The administration leads to an appropriate rise in the levels of LH, suggesting that the negative feedback control on the hypothalamus is intact and that the storage and release of gonadotropins by the pituitary is normal. If there was a successful stimulation of testicular T levels by hCG but an inadequate or no response in LH production than the patient has hypogonadotropic, secondary, hypogonadism.
As I responded to clomiphene in the past and Dr. Scally's entire PCT protocol, attained levels of 560 TT and FT in the mid-range then I am not secondary. In short the feedback control on the hpyothalmus is intact and pituitary is acting normal.
From my response here to my own post: https://thinksteroids.com/community/posts/731384 it is clear I have metabolic syndrome which lowers SHBG and Total T. Upon stopping the PCT therapy my number was a steady 390 after about 2 months. I then began to eat like a horse and then wham - low T early this year. Why did the PCT fail? All evidence points to MSX leading to low SHBG. LH and FSH, as far as I can tell, don't respond to total T, they respond to bio-T (how can they respond to T that is bound strongly to another molecule?). So if SHBG is low due to MSX (insulin resistance) then it stands to reason that Free-T will be normal to high-normal, and possibly high. LH and FSH won't be screaming high in this case, but rather be in the normal range or low-normal range. Remember, high Free-T will dump into estrogen and every other pathway it can find to normalize and excess estrogen in the hypothalmus will modulate LH down. If I control the estrogen by controlling the SHBG via controlling insulin resistance by losing weight then the issue is resolved.
This makes sense to me now. My idiopathic hypogonadism is - strictly speaking - probably due to insulin resistance. Yes MSX can lead to higher LH spikes, but I believe low SHBG dominates in the end and unless one is measuring LH all day long they will see the SHBG dominating effect of low-normal to normal LH.
The answer is easy - the path is not. Increase BMI and lose weight, sometimes a lot of it. I would not rule out TRT in this case - just take a cautious approach - because higher bio-T levels can help with energy and weight loss (as is happening to me very well) but may not help (yet) with ED and libido (also my situation) until SHBG is normalized and T doses can be increased. Yes, one can make a case that one of the side effects of all this is hypothalamic sensitivity to estrogen-mediated negative feedback and therefore I am idiopathic secondary but I would disagree. This is a side effect of insulin resistance and the idiopathic solution to my hypogonadism will - I strongly trust - be traced to my low levels of SHBG due to insulin resistance which, in the end, points to insulin resistance as the originating culprit with subjective hypogonadism complaints as a symptom, not a cause. It may sound like semantics, but arguing otherwise would be like stating the bullet killed the person and should be sent to prison without following back the chain of events that lead to the person who pulled the trigger.
Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary allowing gonadotropin production to resume. Administration produces an elevation of LH and secondarily gonadal sex hormones. The administration leads to an appropriate rise in the levels of LH, suggesting that the negative feedback control on the hypothalamus is intact and that the storage and release of gonadotropins by the pituitary is normal. If there was a successful stimulation of testicular T levels by hCG but an inadequate or no response in LH production than the patient has hypogonadotropic, secondary, hypogonadism.
As I responded to clomiphene in the past and Dr. Scally's entire PCT protocol, attained levels of 560 TT and FT in the mid-range then I am not secondary. In short the feedback control on the hpyothalmus is intact and pituitary is acting normal.
From my response here to my own post: https://thinksteroids.com/community/posts/731384 it is clear I have metabolic syndrome which lowers SHBG and Total T. Upon stopping the PCT therapy my number was a steady 390 after about 2 months. I then began to eat like a horse and then wham - low T early this year. Why did the PCT fail? All evidence points to MSX leading to low SHBG. LH and FSH, as far as I can tell, don't respond to total T, they respond to bio-T (how can they respond to T that is bound strongly to another molecule?). So if SHBG is low due to MSX (insulin resistance) then it stands to reason that Free-T will be normal to high-normal, and possibly high. LH and FSH won't be screaming high in this case, but rather be in the normal range or low-normal range. Remember, high Free-T will dump into estrogen and every other pathway it can find to normalize and excess estrogen in the hypothalmus will modulate LH down. If I control the estrogen by controlling the SHBG via controlling insulin resistance by losing weight then the issue is resolved.
This makes sense to me now. My idiopathic hypogonadism is - strictly speaking - probably due to insulin resistance. Yes MSX can lead to higher LH spikes, but I believe low SHBG dominates in the end and unless one is measuring LH all day long they will see the SHBG dominating effect of low-normal to normal LH.
The answer is easy - the path is not. Increase BMI and lose weight, sometimes a lot of it. I would not rule out TRT in this case - just take a cautious approach - because higher bio-T levels can help with energy and weight loss (as is happening to me very well) but may not help (yet) with ED and libido (also my situation) until SHBG is normalized and T doses can be increased. Yes, one can make a case that one of the side effects of all this is hypothalamic sensitivity to estrogen-mediated negative feedback and therefore I am idiopathic secondary but I would disagree. This is a side effect of insulin resistance and the idiopathic solution to my hypogonadism will - I strongly trust - be traced to my low levels of SHBG due to insulin resistance which, in the end, points to insulin resistance as the originating culprit with subjective hypogonadism complaints as a symptom, not a cause. It may sound like semantics, but arguing otherwise would be like stating the bullet killed the person and should be sent to prison without following back the chain of events that lead to the person who pulled the trigger.
