Juice Junkie
New member
I am trying to get an idea on the different opinions regarding clomid therapy to treat testicular atrophy and bring HPTA back on-line after a cycle. Here's couple of threads from Doc Mark regarding his opinions on clomid and post cycle proceedures.
Regarding Atrophy:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=51.topic
Regarding cycling and post cycle clomid:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=44.topic
Regarding Nootropics to stimulate HPTA:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=11.topic
----------------------------------------------
Weinstein RL, Reitz RE.
Clinical Investigation Center, Naval Hospital, Oakland, USA.
An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (H.C.G.) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with H.C.G. resulted in the return of plasma testosterone to low, pretreatment levels. That H.C.G. therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after H.C.G., confirm pituitary and Leydig cell responsiveness in these subjects.
Basically what this says is that neither H.C.G. or Clomid did anything to bring natural test production back on-line after treatment had stopped.
Regarding Atrophy:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=51.topic
Regarding cycling and post cycle clomid:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=44.topic
Regarding Nootropics to stimulate HPTA:
http://pub65.ezboard.com/ferogenicmedicationsandchronicillnessfrm1.showMessage?topicID=11.topic
----------------------------------------------
Weinstein RL, Reitz RE.
Clinical Investigation Center, Naval Hospital, Oakland, USA.
An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (H.C.G.) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with H.C.G. resulted in the return of plasma testosterone to low, pretreatment levels. That H.C.G. therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after H.C.G., confirm pituitary and Leydig cell responsiveness in these subjects.
Basically what this says is that neither H.C.G. or Clomid did anything to bring natural test production back on-line after treatment had stopped.

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