I Both raloxifene and tamoxifen reduce prolactin. Prolactin is a direct stimulator of DHEA production; if one reduces prolactin, one reduces DHEA. Raloxifene and tamoxifen do not affect prolactin identically, so one would expect differences.
(James Michael Howard)Before someone says..dude, those are chicks man, I know."Tamoxifen was given orally to 60 puerperal women to inhibit lactation. Twenty control puerperal women were given placebo. Fifteen women receiving tamoxifen and 15 women receiving placebo were studied before, during and after the use of a breast pump under basal conditions and after five days of treatment. Tamoxifen was effective in inhibiting lactation; no rebound phenomena were observed. Its administration was free from side effects. This drug was capable of preventing the prolactin release induced by mechanical breast stimulation. Placebo failed to inhibit lactation and had no effect on prolactin release induced by the use of a breast pump"
(A. Masala11Cattedra di Semeiotica Medica 2a, University of Sassari, viale S. Pietro 12, 07100 Sassari, ItalyG. Delitala**Clinics Ostetrica e Ginecologica, University of Sassari, viale S. Pietro 12, 07100 Sassari, ItalyG. Lo Dico11Cattedra di Semeiotica Medica 2a, University of Sassari, viale S. Pietro 12, 07100 Sassari, ItalyI. Stoppelli**Clinics Ostetrica e Ginecologica, University of Sassari, viale S. Pietro 12, 07100 Sassari, ItalyS. Alagna11Cattedra di Semeiotica Medica 2a, University of Sassari, viale S. Pietro 12, 07100 Sassari, ItalyANDL. Devilla11Cattedra di Semeiotica Medica 2a, University of Sassari, viale S. Pietro 12, 07100 Sassari, Italy)
And check this out.
"The effect of administering the antioestrogenic drug, tamoxifen, on the growth of the pituitary tumour 7315a in the rat was studied. This tumour is induced by the administration of oestrogen. When administered early after the implantation of the tumour, tamoxifen prevented its growth completely but when treatment was delayed until a later stage of its development, 20 microgram tamoxifen/100 g body wt each day for 7-12 days stopped further tumour growth, while 200 microgram/100 g body wt each day reduced the size of the tumours. These effects of tamoxifen on tumour growth were accompanied by a decrease in the level of prolactin in the circulation, if the treatment was started at an early stage of tumour development and if the high dose of tamoxifen was administered. Bromocriptine either when given alone or together with tamoxifen was unable to inhibit growth and secretion of prolactin by these rat pituitary tumours. The high plasma concentrations of prolactin in the tumour-bearing rats are known to produce atrophy of the pituitary gland of the host and to decrease the synthesis and release of prolactin. Despite the inhibitory effect of tamoxifen on both tumour size and plasma levels of prolactin, the ability of the pituitary glands of these animals to synthesize prolactin remained suppressed. It was concluded that tamoxifen has a dual effect on this model of a transplantable pituitary tumour that secretes prolactin in the rat; it prevents and/or inhibits tumour growth and it has an inhibitory effect on the synthesis of prolactin by the pituitary gland."
(M de Quijada, HA Timmermans, and SW Lamberts)
Four-day cyclic rats fed 7, 12-dimethylbenz(a)anthracene (dmba) (20 mg) at 50 days of age had peak prolactin, oestradiol and uterine wet weights at pro-oestrus. Tamoxifen (50, 200 and 800 mug daily), administered to ovariectomized rats, produced significant (P less than 0 X 05) decreases in oestrogen-stimulated prolactin levels but was unable to reduce prolactin to control values. Tamoxifen (12 X 5, 50 and 200 mug daily) produced decreases in size in DMBA-induced rat mammary carcinomata in intact rats although some tumours did not respond to therapy. The ability of the pituitary to produce prolactin was not impaired. Decreases in uterine wet weights and peripheral oestradiol levels occurred during tamoxifen treatment.
(J Endocrinol. 1976 Feb;68(02):305-11)
This lasts one just interesting, not really reducing, but maybe prevention.
Recently we completed a study designed to investigate the effect of melatonin administration (10 mg) at 1300 on menstrual characteristics, prolactin, and premenstrual syndrome-like symptoms during a simulated eastward deployment. Bright lights were utilized to simulate eastward movement across six time zones. During analysis of biochemical results, we made the fortuitous discovery that melatonin appears to alleviate the stress associated with the in-house simulated deployment. The study was double blind and placebo controlled. Melatonin was given to healthy females for 5 consecutive days during the late follicular and early luteal phases of the menstrual cycle. Volunteers spent 24 hours in the hospital before entering the dose administration phase of the study and again on the last dose day. On those 2 days, hourly blood samples were collected from an in-dwelling catheter and were used for analysis of melatonin and prolactin. Volunteers also completed a profile of moods state questionnaire upon waking on each of 8 days which overlapped the in-house dose administration days. The placebo group showed a prolactin peak at 1300 on the last dose day/blood draw, while the melatonin group showed a prolactin peak at 1500. It is well known that melatonin stimulates the release of prolactin, and a 2-hour delay between melatonin administration and the prolactin peak is within the normal expected delay.
(ARMY AEROMEDICAL RESEARCH LAB FORT RUCKER AL)