Well this thread was posted over 3 months ago, but any how, I've never heard of melatonin being used for pct.
It doesn't have a role in PCT I don't think. The complimentary effect it has with tamoxifen is related to breast cancer. See:
NOTE
More importantly you can continue to take melatonin during PCT without it negatively effecting recovery.
"Taken together, these data suggest that long-term melatonin administration does not alter the secretory patterns of reproductive hormones in normal men." i.e. LH, FSH, testosterone - Long-term melatonin administration does not alter pituitary-gonadal hormone secretion in normal men, Rafael Luboshitzky et al, Human Reproduction, Vol. 15, No. 1, 60-65, January 2000
"Melatonin treatment did not cause any significant change in basal or post-stimulation LH and FSH levels either in men or in post-menopausal women." - Effect of melatonin on the basal and stimulated gonadotropin levels in normal men and postmenopausal women, H Fideleff, Journal of Clinical Endocrinology & Metabolism, Vol 42, 1014-1017
I wouldn't worry about melatonin increasing prolactin.
"The results suggest that melatonin has no acute modulatory effect on the secretion of these two sleep-related hormones." i.e Growth Hormone & Prolactin - A model for the study of the acute effects of melatonin in man, RJ Strassman, Journal of Clinical Endocrinology & Metabolism, Vol 65, 847-852
NOTE:
Source: Melatonin augments the sensitivity of MCF-7 human breast cancer cells to tamoxifen in vitro,
ST Wilson,
J. Clin. Endocrinol. Metab., Aug 1992; 75: 669 - 670.
ABBREVIATIONS:
Melatonin (MLT)
Tamoxifen (TAM)
Estradiol (E2)
Estrogen (E)
DISCUSSION:
The rationale for this experiment was based on previous studies demonstrating that MLT: 1) inhibits estrogen-stimulated MCF-7 cell growth, 2) alters ER levels in MCF-7 cells blocks the E2 rescue of TAM inhibited MCF-7 cells. Therefore, because of MLT’s modulatory effect on the estrogen-response pathway in this cell line, we tested the hypothesis that short-term MLT pretreatment increases the sensitivity of MCF-7 cells to the subsequent long-term inhibitory effects of either TAM or MLT itself.
As expected, TAM inhibited cell growth in the vehicle pretreated cells in a dose-response manner. However, the TAM dose-response curve was shifted to the left when cells were pre-exposed to MLT. Comparison of IC50 values for vehicle and MLT pretreated cells indicate that TAM is approximately 100-fold more potent when MCF-7 cells are preexposed to MLT rather than the vehicle for 24 hrs.
These results suggest that MLT somehow “sensitizes” the cells such that TAM is a more effective inhibitor of cell proliferation not only at its therapeutic dose (371 ug/mL) but at much lower doses which were ineffective.
Pretreatment of MCF-7 cells with MLT has a modest effect on augmenting their sensitivity to the inhibitory effects of a subsequent re-exposure to MLT. Comparison of the IC50 values for vehicle and MLT pretreated cells indicates that MLT is only about 8-fold more potent following pre-exposure of the cells to itself.
In the control experiment, a 24 hr pulse of MLT, in the absence of further MLT or TAM treatment had no effect on cell proliferation. These data indicate that the increased effectiveness of TAM in MLT pre-exposed cells is not due to an additive effect of growth inhibition during the MLT pre-exposure period.
Tamoxifen, because of its low toxicity and relative effectiveness in the treatment of metastatic ER-positive breast cancer now represents the endocrine treatment of choice in postmenopausal patients. However, in spite of its many advantages, some patients with ER-positive cancer respond for only a short time or not at all. The findings presented here may form the basis for a novel and effective approach to treating some TAM-failed patients by sensitizing their breast cancer cells to TAM with MLT.