DHEA & Gynecomastia
- 11-25-2005, 10:15 AM
DHEA & Gynecomastia
I used 100mg DHEA for about 2 months. When I stoped taking it I noticed a very strong loss in libido that recovered after about three weeks. It has now been 2 months and it look like im starting to get gynecomastia. I have never used steroids, just cretine and DHEA. Can this be caused by DHEA?
- 11-25-2005, 01:31 PM
Yes. In men, DHEA has a fairly strong tendency to convert to estrogen. Run a few weeks of Reboundxt or other AI and it should clear up..particularly since you caught it early.
While you're waiting for your anti-e to arrive, try vitamins B6 and C as well as green tea extract. All are known to lower estrogen levels to some degreee.
- 11-25-2005, 03:03 PM
My Gosh! To think I bought the bottle at Wal-Mart. They should be required to put possible side affects on the bottle. I guess I need to be more careful what I put in my body supplement or otherwise.
Thanks for the reply
11-25-2005, 03:11 PM
Unix..any hard lumps or is it just puffy nipples?
In all likelyhood it's not true gyno, rather it's puffy nipples as a result of a small estrogen build up. Many people run DHEA for atheletic and health purposes, it's just that at higher doses you will have to be aware that estrogen may get elevated and it's wise to have anti estrogen on hand to combat this.
11-25-2005, 09:37 PM
no lumps just sensitive puffy nipples. I have big sausage nipples so stuff like that is very noticeable. I do have a bottle of Rebound XT from a SD cycle I chickened out on. I started using it tonight. Thanks for the help.
12-03-2005, 02:58 AM
hmm.... i think thats what happened to me too bro. I have big nips too but on cycle with the d they didnt change, but now that im on my pct, which had 200 mg of dhea for 2 weeks then 100 for 2 weeks, my nips are PUFFY, and its really annoying. So i just ordered some raloxifine hopefully that should do the trick. However, i thought it was just fat but i really dont blieve it is hearing what u just said, so anyways... hope it all works out. Rxt didnt do **** for me gyno wise.
12-09-2005, 02:43 PM
12-09-2005, 03:07 PM
Why not? I'm using DHEA/7oxo/6oxo transderm with Nolva for PCT. I'm about 2 weeks into PCT and things are going great, I've maintained weight and appear to have dropped a tiny bit of BF. Please fill me in, so I can adjust my PCT if necessary. Thanks.Originally Posted by x_muscle
12-09-2005, 03:12 PM
12-09-2005, 03:30 PM
Endocrine, neuroendocrine and behavioral effects of oral dehydroepiandrosterone sulfate supplementation in postmenopausal women.
Stomati M, Rubino S, Spinetti A, Parrini D, Luisi S, Casarosa E, Petraglia F, Genazzani AR.
Department of Reproductive Medicine and Child Development, University of Pisa, Italy.
Aging in women and men is characterized by a progressive decline of circulating dehydroepiandrosterone (DHEA) levels and its sulfate ester (DHEAS). The improvement of wellbeing described in postmenopausal women treated with DHEA suggests that this steroid may exert specific actions on the central nervous system (CNS). The postmenopausal period is associated with several neuroendocrine modifications. The decrease of circulating levels of beta-endorphin is considered a hormonal marker of those changes. The aim of the present study was to investigate neuroendocrine and behavioral effects of three months of DHEAS supplementation in postmenopausal women. Postmenopausal women (n = 22) were divided in three groups: the first group was treated with oral DHEAS (n = 8) (50 mg/day), the second treated with the same dose of oral DHEAS + transdermal estradiol (n = 8) (DHEAS) 50 mg/day, estradiol 50 micrograms/patch) and the third with transdermal estradiol alone (n = 6) (50 micrograms/day). Before and after 1, 2 and 3 months of therapy, the following circulating steroid and protein hormone levels were evaluated: DHEA, DHEAS, androstenedione, testosterone, estrone, estradiol, 17-hydroxyprogesterone, sex hormone-binding globulin (SHBG), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta-endorphin, growth hormone (GH) and cortisol, and a Kupperman score was performed. Before and after treatments, plasma beta-endorphin levels were evaluated in response to three neuroendocrine tests: (a) clonidine, an alpha 2-presynaptic adrenergic agonist (1.25 mg i.v.) (b) naloxone, an opioid receptor antagonist (4 mg i.v.) and (c) fluoxetine, a serotonin selective reuptake inhibitor (30 mg p.o.). In both groups of women treated with DHEAS, mean basal serum DHEA, DHEAS, androstenedione, and testosterone levels significantly increased after treatment, while no changes were shown in the group receiving estradiol alone. Serum estradiol, estrone, GH and plasma beta-endorphin levels significantly increased progressively for the three months of treatment, with higher levels for estrone and estradiol in subjects receiving estradiol alone or plus DHEAS. Serum SHBG, cortisol, and 17-hydroxyprogesterone did not show significant variations under any treatment. Serum LH and FSH levels showed a significant decrease in groups treated with estradiol alone or plus DHEAS at the second and third months. The Kupperman score showed that all treatments were associated with similar and progressive improvement. Before therapy clonidine, naloxone and fluoxetine stimuli failed to modify circulating beta-endorphin levels. After each of the treatments, the beta-endorphin response was completely restored and was similar, independent of the kind of therapy. Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the neuroendocrine control of pituitary beta-endorphin secretion, which may support the therapeutic efficacy of the DHEAS on behavioral symptoms.
Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men.
Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS.
Exercise Biochemistry Laboratory, Department of Health and Human Performance, Iowa State University, Ames, Iowa 50011, USA.
This study examined the effects of acute dehydroepiandrosterone (DHEA) ingestion on serum steroid hormones and the effect of chronic DHEA intake on the adaptations to resistance training. In 10 young men (23 +/- 4 yr old), ingestion of 50 mg of DHEA increased serum androstenedione concentrations 150% within 60 min (P < 0.05) but did not affect serum testosterone and estrogen concentrations. An additional 19 men (23 +/- 1 yr old) participated in an 8-wk whole body resistance-training program and ingested DHEA (150 mg/day, n = 9) or placebo (n = 10) during weeks 1, 2, 4, 5, 7, and 8. Serum androstenedione concentrations were significantly (P < 0.05) increased in the DHEA-treated group after 2 and 5 wk. Serum concentrations of free and total testosterone, estrone, estradiol, estriol, lipids, and liver transaminases were unaffected by supplementation and training, while strength and lean body mass increased significantly and similarly (P < 0.05) in the men treated with placebo and DHEA. These results suggest that DHEA ingestion does not enhance serum testosterone concentrations or adaptations associated with resistance training in young men.
The effect of dehydroepiandrosterone supplementation to symptomatic perimenopausal women on serum endocrine profiles, lipid parameters, and health-related quality of life.
Barnhart KT, Freeman E, Grisso JA, Rader DJ, Sammel M, Kapoor S, Nestler JE.
Department of Obstetrics and Gynecology, University of Pennsylvania Medical Center, Philadelphia 19104, USA.
Dehydroepiandrosterone (DHEA), an androgenic steroid hormone, exhibits an age-related decline. Perimenopausal women have only approximately 50% of peak DHEA levels. Despite limited scientific data, DHEA has gained recognition as a dietary supplement to reduce the symptoms of aging and improve well-being. This randomized, double-blind placebo-controlled trial examined the effects of 50 mg/day of oral DHEA supplementation, for 3 months, on 60 perimenopausal women with complaints of altered mood and well-being. Changes in the serum endocrine profile of women in the DHEA group were significantly greater than the placebo group, including a 242% [95% confidence interval (CI) +60.1, +423.9] increase in DHEAS, a 94.8% (95% CI +34.2, +155.4) increase in testosterone, and a 13.2% (95% CI -27.88, +0.5) decline in cortisol compared to baseline. Women receiving DHEA had a 10.1% (95% CI -15.0, -5.1) decline in high-density lipoprotein and an 18.1% (95% CI -32.2, -3.9) decline in Lp(a) from baseline, but these declines did not significantly differ from women who received placebo. Women receiving DHEA did not have any improvements significantly greater than placebo in the severity of perimenopausal symptoms, mood, dysphoria, libido, cognition, memory, or well-being. DHEA supplementation significantly effects the endocrine profile, may affect the lipid profile, but does not improve perimenopausal symptoms or well-being compared to placebo.
Biotransformation of oral dehydroepiandrosterone in elderly men: significant increase in circulating estrogens.
Arlt W, Haas J, Callies F, Reincke M, Hubler D, Oettel M, Ernst M, Schulte HM, Allolio B.
Department of Endocrinology, Medical University Hospital Wuerzburg, Germany.
The most abundant human steroids, dehydroepiandrosterone (DHEA) and its sulfate ester DHEAS, may have a multitude of beneficial effects, but decline with age. DHEA possibly prevents immunosenescence, and as a neuroactive steroid it may influence processes of cognition and memory. Epidemiological studies revealed an inverse correlation between DHEAS levels and the incidence of cardiovascular disease in men, but not in women. To define a suitable dose for DHEA substitution in elderly men we studied pharmacokinetics and biotransformation of orally administered DHEA in 14 healthy male volunteers (mean age, 58.8 +/- 5.1 yr; mean body mass index, 25.5 +/- 1.5 kg/m2) with serum DHEAS concentrations below 4.1 micromol/L (1500 ng/mL). Diurnal blood sampling was performed on 3 occasions in a single dose, randomized, cross-over design (oral administration of placebo, 50 mg DHEA, or 100 mg DHEA). The intake of 50 mg DHEA led to an increase in serum DHEAS to mean levels of young adult men, whereas 100 mg DHEA induced supraphysiological concentrations [placebo vs. 50 mg DHEA vs. 100 mg DHEA; area under the curve (AUC) 0-12 h (mean +/- SD) for DHEA, 108 +/- 22 vs. 252 +/- 45 vs. 349 +/- 72 nmol/L x h; AUC 0-12 h for DHEAS, 33 +/- 9 vs. 114 +/- 19 vs. 164 +/- 36 micromol/L x h]. Serum testosterone and dihydrotestosterone remained unchanged after DHEA administration. In contrast, 17beta-estradiol and estrone significantly increased in a dose-dependent manner to concentrations still within the upper normal range for men [placebo vs. 50 mg DHEA vs. 100 mg DHEA; AUC 0-12 h for 17beta-estradiol, 510 +/- 198 vs. 635 +/- 156 vs. 700 +/- 209 pmol/L x h (P < 0.0001); AUC 0-12 h for estrone, 1443 +/- 269 vs. 2537 +/- 434 vs. 3254 +/- 671 pmol/L x h (P < 0.0001)]. In conclusion, 50 mg DHEA seems to be a suitable substitution dose in elderly men, as it leads to serum DHEAS concentrations usually measured in young healthy adults. The DHEA-induced increase in circulating estrogens may contribute to beneficial effects of DHEA in men.
12-09-2005, 03:34 PM
another thing, if you come off long cycle, and if you specially using orals, then DHEA is not good for your liver:
Dehydroepiandrosterone causes hyperplasia and impairs regeneration in rat liver.
Kopplow K, Wayss K, Enzmann H, Mayer D.
Hormones and Signal Transduction, Deutsches Krebsforschungszentrum, D-69120 Heidelberg, Germany.
DHEA, a steroid of the adrenal gland, is a non-genotoxic hepatocarcinogen of the peroxisome proliferator type in rodents. However, DHEA also exerts anti-carcinogenic effects by reducing the number and proliferation of preneoplastic and neoplastic lesions induced by N-nitrosomorpholine. The mechanism underlying this growth-modulating effect is unclear, and no data are available on DHEA effects on normal liver. Here, we show that DHEA is a liver mitogen, increasing proliferation in rat liver after 3 days of treatment (100 mg/kg body weight per day) as indicated by significantly enhanced expression of cyclin E, PCNA and Ki-67 and an elevated number of mitotic figures. Histological observation of the liver and biochemical evaluation of serum transaminases and bilirubin did not reveal any evidence for cell death, demonstrating that increased proliferation was not due to liver damage. After 2 weeks of DHEA-treatment, proliferation parameters returned to control values and, after 4 weeks, cyclin E and Ki-67 were even lower than in controls. To study the DHEA effect on regenerating liver, we performed partial hepatectomy (PHx) on rats pretreated for 4 weeks with DHEA and analyzed the kinetics of the cell cycle. DHEA-treatment delayed the entry of hepatocytes into G1 phase by about 6 h indicated by a later rise in Ki-67 and cyclin E expression. Reduced STAT-3 activation before G1-phase entry indicates an impaired recruitment of hepatocytes to regenerative proliferation in DHEA-treated livers. The rise in proliferation observed after PHx in DHEA-treated livers was more flat and, in contrast to controls, did not show a peak value within the first 35h as indicated by Ki-67, PCNA, cyclin E and BrdU-incorporation levels in hepatocytes. In conclusion, the results show that DHEA acts as a mitogen in rat liver but reduces the regenerative capacity of the liver.
12-09-2005, 04:23 PM
The study on young healthy men may not have shown any hormonal changes, however we've got people out there using massive 2 g doses and reporting good results. Not something I would do but hey, have fun.
The liver study on rats..100mg/kg of bodyweight seems to be a rather high dose. Anyone care to take a stab at what an equivalent dose for humans would be? I'd guess rats can weigh upwards of 1/4 to 1/2 of a kilo so 25 to 50 mg DHEA would be pretty substantial..but I could be wrong.
DHEA has always been a little mysterious to me and we're only just begining to see a snapshot of what it does and what it can do. I will vouch for it's use during PCT at least anecdotally, it seems to offset the worst of the PCT sides..improves mood and gets the testes up to size faster than without. I would nt stay on it long term unless bloodwork revealed a significant deficiency.
12-09-2005, 05:24 PM
i used and loved it leaned me out a lil bit too after my forst ergo cycle. Def get the boys swinging again, and i also liked the way it made me feel. But hey diffrent strokes for different folks...
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