I'm looking to gain more insight about the role that DHEA plays in the endocrine system, as relates to strength athletes. Could someone direct me to a chart, that shows how DHEA breaks down in the body.
All the studies that I have come across that show a beneficial effect with DHEA seem to be dealing with the older crowd. How could a younger person (with normal levels of DHEA) stack DHEA with an anti-estrogen, test-booster, to get max results? Do you think it is worth it?
Full Version: DHEA conversion to test
QUOTE(Dr. Lats @ Mar 25 2008, 06:32 PM) [snapback]468044[/snapback]
How could a younger person (with normal levels of DHEA) stack DHEA with an anti-estrogen, test-booster, to get max results? Do you think it is worth it?
On paper this looks like a good idea but in practice it doesn't work. Anything above 25mg/day will generally result in increased estrogen in men.
I wonder what kind of man-boobies came out of this study, then...
QUOTE
A 1988 study reported that the oral administration of DHEA at a dose of 1600 mg/day to 22- to 25-year-old men for 28 days resulted in lowering of cholesterol and LDL cholesterol without changes in other lipid parameters and glucose disposal (8). Body fat significantly decreased, especially in the more obese individuals. And importantly, the DHEA supplementation caused an increase in muscle mass. This study, like the other high-dose study, demonstrates the apparent safety of DHEA use up to 1,600 mg per dayĐat least for a one-month period of supplementation.
which metabolites don't convert? (besides 7-keto)
Int J Obes. 1990 May;14(5):457-63.Links
Lack of effect of dehydroepiandrosterone in obese men.Usiskin KS, Butterworth S, Clore JN, Arad Y, Ginsberg HN, Blackard WG, Nestler JE.
Department of Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on weight and body fat mass in young obese men, six obese (body mass index, 31.5 +/- 2.9 (s.e.] men were studied at baseline, after 28 days of placebo administration, and again after 28 days of DHEA (1600 mg/day) administration. Body fat mass was assessed on each occasion by three separate methods: hydrostatic weighing, impedance plethysmography, and skinfold measurements at four body sites. Waist-to-hip ratios were recorded. In addition, tissue sensitivity to insulin was determined using the modified minimal model technique, and serum lipids were assayed. Serum DHEA-sulfate levels rose from 7.4 +/- 1.7 mumol/l at baseline to 39.8 +/- 11.9 mumol/l after DHEA administration (P less than 0.05). Although body fat mass was reduced in two of the six men following DHEA administration, for the group as a whole neither total body weight, body fat mass, or waist-to-hip ratio changed significantly during the study. No change in either tissue insulin sensitivity or serum lipids was observed. These observations suggest that, at a daily dose of 13.4-19.7 mg/kg, short-term DHEA administration does not affect the total weight, body fat mass, fat distribution, insulin sensitivity, or lipid status of obese young men.
J Clin Endocrinol Metab. 1988 Jan;66(1):57-61.Links
Dehydroepiandrosterone reduces serum low density lipoprotein levels and body fat but does not alter insulin sensitivity in normal men.Nestler JE, Barlascini CO, Clore JN, Blackard WG.
Division of Endocrinology and Metabolism, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on body fat mass, serum lipid levels, and tissue sensitivity to insulin, five normal men were given placebo and five normal men were given oral DHEA [1600 mg/day (554.7 mmol/day)] for 28 days in a randomized, double blind study. In the DHEA group serum DHEA-S levels rose 2.5- to 3.5-fold, and mean (+/- SEM) serum androstenedione rose from 4.3 +/- 0.6 to 8.6 +/- 1.2 nmol/L (P less than 0.004, by paired t test), but serum total testosterone, free testosterone, sex hormone-binding globulin, estradiol, and estrone levels did not change. In the DHEA group the mean percent body fat decreased by 31%, with no change in weight. This suggests that the reduction in fat mass was coupled with an increase in muscle mass. DHEA administration also resulted in a fall in mean serum total cholesterol concentration (4.82 +/- 0.21 vs. 4.48 +/- 0.29 nmol/L; P less than 0.05), which was due almost entirely to a fall of 7.5% in mean serum low density lipoprotein cholesterol (3.21 +/- 0.11 vs. 2.97 +/- 0.14 nmol/L; P less than 0.01). No changes in anthropometric parameters or serum lipid levels occurred in the placebo group. Tissue sensitivity to insulin, assessed by the hyperinsulinemic-euglycemic clamp technique, did not change in either the placebo or DHEA groups. These results suggest that in normal men DHEA administration reduces body fat, increases muscle mass, and reduces serum low density lipoprotein cholesterol levels. Tissue sensitivity to insulin was unaffected by short term DHEA administration.
Lack of effect of dehydroepiandrosterone in obese men.Usiskin KS, Butterworth S, Clore JN, Arad Y, Ginsberg HN, Blackard WG, Nestler JE.
Department of Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on weight and body fat mass in young obese men, six obese (body mass index, 31.5 +/- 2.9 (s.e.] men were studied at baseline, after 28 days of placebo administration, and again after 28 days of DHEA (1600 mg/day) administration. Body fat mass was assessed on each occasion by three separate methods: hydrostatic weighing, impedance plethysmography, and skinfold measurements at four body sites. Waist-to-hip ratios were recorded. In addition, tissue sensitivity to insulin was determined using the modified minimal model technique, and serum lipids were assayed. Serum DHEA-sulfate levels rose from 7.4 +/- 1.7 mumol/l at baseline to 39.8 +/- 11.9 mumol/l after DHEA administration (P less than 0.05). Although body fat mass was reduced in two of the six men following DHEA administration, for the group as a whole neither total body weight, body fat mass, or waist-to-hip ratio changed significantly during the study. No change in either tissue insulin sensitivity or serum lipids was observed. These observations suggest that, at a daily dose of 13.4-19.7 mg/kg, short-term DHEA administration does not affect the total weight, body fat mass, fat distribution, insulin sensitivity, or lipid status of obese young men.
J Clin Endocrinol Metab. 1988 Jan;66(1):57-61.Links
Dehydroepiandrosterone reduces serum low density lipoprotein levels and body fat but does not alter insulin sensitivity in normal men.Nestler JE, Barlascini CO, Clore JN, Blackard WG.
Division of Endocrinology and Metabolism, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on body fat mass, serum lipid levels, and tissue sensitivity to insulin, five normal men were given placebo and five normal men were given oral DHEA [1600 mg/day (554.7 mmol/day)] for 28 days in a randomized, double blind study. In the DHEA group serum DHEA-S levels rose 2.5- to 3.5-fold, and mean (+/- SEM) serum androstenedione rose from 4.3 +/- 0.6 to 8.6 +/- 1.2 nmol/L (P less than 0.004, by paired t test), but serum total testosterone, free testosterone, sex hormone-binding globulin, estradiol, and estrone levels did not change. In the DHEA group the mean percent body fat decreased by 31%, with no change in weight. This suggests that the reduction in fat mass was coupled with an increase in muscle mass. DHEA administration also resulted in a fall in mean serum total cholesterol concentration (4.82 +/- 0.21 vs. 4.48 +/- 0.29 nmol/L; P less than 0.05), which was due almost entirely to a fall of 7.5% in mean serum low density lipoprotein cholesterol (3.21 +/- 0.11 vs. 2.97 +/- 0.14 nmol/L; P less than 0.01). No changes in anthropometric parameters or serum lipid levels occurred in the placebo group. Tissue sensitivity to insulin, assessed by the hyperinsulinemic-euglycemic clamp technique, did not change in either the placebo or DHEA groups. These results suggest that in normal men DHEA administration reduces body fat, increases muscle mass, and reduces serum low density lipoprotein cholesterol levels. Tissue sensitivity to insulin was unaffected by short term DHEA administration.
So, DHEA is giving more raw material, for testosterone production. The extra testosterone production that comes from supplemental DHEA, is obviously going to convert into more estrogen in the body, through aromatise. This could be blocked, from a supplmental standpoint, by 6-oxo or ATD.
It looks like DHEA converts to three different products, androstendiol, androstendione, and 16-hydroxyDHEA. Is there a way,supplementally, to shuttle it in the direction of only androstenediol? Is this even safe? Does the body need androstenedione or 16-hydroxyDHEA?
Also, would too much DHEA cause suppression of one of the pregnenolone derivatives? From the chart, it looks like suppression of pregnenolone could actually reduce cortisol levels...
That is an awesome chart.
It looks like DHEA converts to three different products, androstendiol, androstendione, and 16-hydroxyDHEA. Is there a way,supplementally, to shuttle it in the direction of only androstenediol? Is this even safe? Does the body need androstenedione or 16-hydroxyDHEA?
Also, would too much DHEA cause suppression of one of the pregnenolone derivatives? From the chart, it looks like suppression of pregnenolone could actually reduce cortisol levels...
That is an awesome chart.
DHEA has its uses. and i can't find quite the study i remember seeing. but it seems that to build muscle from resistance exercise, the body needs to produce a DHEA increase. so if you're old, or maybe one of those weightlifting non-responders, DHEA might help.
in general, it tends to aromatize into estrogen and can decrease test. but most of you can make your own DHEA by just going and lifting some heavy shit.
i took it once and about the only result i saw was becoming a moody emotional bitch.
in general, it tends to aromatize into estrogen and can decrease test. but most of you can make your own DHEA by just going and lifting some heavy shit.
i took it once and about the only result i saw was becoming a moody emotional bitch.
QUOTE
Am J Physiol Endocrinol Metab. 2006 Nov;291(5):E1003-8. Epub 2006 Jun 20.Click here to read Links
DHEA enhances effects of weight training on muscle mass and strength in elderly women and men.
Villareal DT, Holloszy JO.
Division of Geriatrics and Nutritional Science, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
The plasma levels of dehydroepiandrosterone (DHEA) and its sulfated form (DHEAS) decline approximately 80% between the ages of 25 and 75 yr. Muscle mass and strength also decrease with aging. Published data on the effects of DHEA replacement on muscle mass and strength are conflicting. The goals of this study were to determine whether DHEA replacement increases muscle mass and strength and/or enhances the effects of heavy resistance exercise in elderly women and men. We conducted a randomized, double-blind, placebo-controlled study of the effects of 10 mo of DHEA replacement therapy with the addition of weightlifting exercise training during the last 4 mo of the study (DHEA + exercise group, n = 29; placebo + exercise group, n = 27). DHEA alone for 6 mo did not significantly increase strength or thigh muscle volume. However, DHEA therapy potentiated the effect of 4 mo of weightlifting training on muscle strength, evaluated by means of one-repetition maximum measurement and Cybex dynamometry, and on thigh muscle volume, measured by magnetic resonance imaging. Serum insulin-like growth factor concentration increased in response to DHEA replacement. This study provides evidence that DHEA replacement has the beneficial effect of enhancing the increases in muscle mass and strength induced by heavy resistance exercise in elderly individuals.
PMID: 16787962 [PubMed - indexed for MEDLINE]
DHEA enhances effects of weight training on muscle mass and strength in elderly women and men.
Villareal DT, Holloszy JO.
Division of Geriatrics and Nutritional Science, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
The plasma levels of dehydroepiandrosterone (DHEA) and its sulfated form (DHEAS) decline approximately 80% between the ages of 25 and 75 yr. Muscle mass and strength also decrease with aging. Published data on the effects of DHEA replacement on muscle mass and strength are conflicting. The goals of this study were to determine whether DHEA replacement increases muscle mass and strength and/or enhances the effects of heavy resistance exercise in elderly women and men. We conducted a randomized, double-blind, placebo-controlled study of the effects of 10 mo of DHEA replacement therapy with the addition of weightlifting exercise training during the last 4 mo of the study (DHEA + exercise group, n = 29; placebo + exercise group, n = 27). DHEA alone for 6 mo did not significantly increase strength or thigh muscle volume. However, DHEA therapy potentiated the effect of 4 mo of weightlifting training on muscle strength, evaluated by means of one-repetition maximum measurement and Cybex dynamometry, and on thigh muscle volume, measured by magnetic resonance imaging. Serum insulin-like growth factor concentration increased in response to DHEA replacement. This study provides evidence that DHEA replacement has the beneficial effect of enhancing the increases in muscle mass and strength induced by heavy resistance exercise in elderly individuals.
PMID: 16787962 [PubMed - indexed for MEDLINE]
QUOTE
J Appl Physiol. 2004 Feb;96(2):531-9. Epub 2003 Sep 26.Click here to read Links
Effect of training status and exercise mode on endogenous steroid hormones in men.
Tremblay MS, Copeland JL, Van Helder W.
College of Kinesiology, University of Saskatchewan, Saskatoon, Canada. mark.tremblay@statcan.ca
The purpose of this study was to determine the acute anabolic and catabolic hormone response to endurance and resistance exercise bouts of equal volume in subjects with differing training status. Twenty-two healthy men were recruited who were either resistance trained (n = 7), endurance trained (n = 8), or sedentary (n = 7). Three sessions were completed: a resting session, a 40-min run at 50-55% maximal oxygen consumption, and a resistance exercise session. Expired gases were monitored continuously during exercise, and the endurance and resistance exercise sessions were individually matched for caloric expenditure. Blood samples were drawn before exercise and 1, 2, 3, and 4 h after the start of the exercise. Plasma was analyzed for luteinizing hormone, dehydroepiandrosterone sulfate, cortisol, and free and total testosterone. Androgens increased in response to exercise, particularly resistance exercise, whereas cortisol only increased after resistance exercise. Dehydroepiandrosterone sulfate levels increased during the resistance exercise session and remained elevated during recovery in the resistance-trained subjects. Endurance-trained subjects displayed less pronounced changes in hormone concentrations in response to exercise than resistance-trained subjects. After an initial postexercise increase, there was a significant decline in free and total testosterone during recovery from resistance exercise (P < 0.05), particularly in resistance-trained subjects. On the basis of the results of this study, it appears that the endogenous hormone profile of men is more dependent on exercise mode or intensity than exercise volume as measured by caloric expenditure. The relatively catabolic environment observed during the resistance session may indicate an intensity-rather than a mode-dependent response.
PMID: 14514704 [PubMed - indexed for MEDLINE]
Effect of training status and exercise mode on endogenous steroid hormones in men.
Tremblay MS, Copeland JL, Van Helder W.
College of Kinesiology, University of Saskatchewan, Saskatoon, Canada. mark.tremblay@statcan.ca
The purpose of this study was to determine the acute anabolic and catabolic hormone response to endurance and resistance exercise bouts of equal volume in subjects with differing training status. Twenty-two healthy men were recruited who were either resistance trained (n = 7), endurance trained (n = 8), or sedentary (n = 7). Three sessions were completed: a resting session, a 40-min run at 50-55% maximal oxygen consumption, and a resistance exercise session. Expired gases were monitored continuously during exercise, and the endurance and resistance exercise sessions were individually matched for caloric expenditure. Blood samples were drawn before exercise and 1, 2, 3, and 4 h after the start of the exercise. Plasma was analyzed for luteinizing hormone, dehydroepiandrosterone sulfate, cortisol, and free and total testosterone. Androgens increased in response to exercise, particularly resistance exercise, whereas cortisol only increased after resistance exercise. Dehydroepiandrosterone sulfate levels increased during the resistance exercise session and remained elevated during recovery in the resistance-trained subjects. Endurance-trained subjects displayed less pronounced changes in hormone concentrations in response to exercise than resistance-trained subjects. After an initial postexercise increase, there was a significant decline in free and total testosterone during recovery from resistance exercise (P < 0.05), particularly in resistance-trained subjects. On the basis of the results of this study, it appears that the endogenous hormone profile of men is more dependent on exercise mode or intensity than exercise volume as measured by caloric expenditure. The relatively catabolic environment observed during the resistance session may indicate an intensity-rather than a mode-dependent response.
PMID: 14514704 [PubMed - indexed for MEDLINE]
It's also a sigma receptor agonist like cocaine.
Testosterone to estrodiol, androstenedione to estrone, and 16-hydroxyandrostenedione to 16-hydroxyestrone all involve aromatase enzyme. We all know that the suicide inhibitor, 6-oxo, is for real. Why not jack up your DHEA levels and prevent conversion to estrogen with 6-oxo?
I wonder how high someone could get their natural testosterone up to with this stack?
I wonder how high someone could get their natural testosterone up to with this stack?
QUOTE(Dr. Lats @ Mar 26 2008, 11:57 AM) [snapback]468181[/snapback]
Why not jack up your DHEA levels and prevent conversion to estrogen with 6-oxo?
Because you'd send your cortisol levels through the floor. Enter tendon pain, joint pain, and lethargy.
http://www.mindandmuscle.net/forum/index.p...DHEA+experiment
Here's an old thread about the same thing. I don't think anyone had any appreciable results. They did the same thing over at BB.com
Here's an old thread about the same thing. I don't think anyone had any appreciable results. They did the same thing over at BB.com
blunted lipolysis as well.
Some have hypothesized that dosing DHEA for anxiolytic effects in the evening could be beneficial, but in the morning high cortisol is actually adventageous.
Some have hypothesized that dosing DHEA for anxiolytic effects in the evening could be beneficial, but in the morning high cortisol is actually adventageous.
QUOTE(Dr. Lats @ Mar 26 2008, 11:57 AM) [snapback]468181[/snapback]
We all know that the suicide inhibitor, 6-oxo, is for real. Why not jack up your DHEA levels and prevent conversion to estrogen with 6-oxo?
Because it doesn't work...it seems like it should but for some reason or another, it doesn't.
Odium,
Higher DHEA levels lower cortisol, through some sort of negative feedback? Or a high DHEA, low estrogen ratio lowers cortisol?
Higher DHEA levels lower cortisol, through some sort of negative feedback? Or a high DHEA, low estrogen ratio lowers cortisol?
It seems like the negative sides you listed are caused by estrogen levels falling through the floor, not cortisol...
i have no idea whether it's doable or even safe, but from the steroid tree, it looks like you'd want to downregulate 16-alpha-hydroxylase when dosing DHEA, not aromitase.
QUOTE(Dr. Lats @ Mar 26 2008, 12:48 PM) [snapback]468204[/snapback]
It seems like the negative sides you listed are caused by estrogen levels falling through the floor, not cortisol...
The sides of both particularly joint pain are similar. Cortisol needs to be somewhat balanced to reduce inflammation in joints/ tendons. (think of a cortisone shot) Cortisol is also important for immune function, if you step back and look at the numerous people who crush there cortisol post cycle then complain about catching the flu or a bad cold this becomes evident. There's a ton of info scattered around on the subject already. I don't think high dose DHEA is good for much of anything. "high dose" is a relative term of course.
QUOTE(Proton Soup @ Mar 26 2008, 10:05 AM) [snapback]468210[/snapback]
i have no idea whether it's doable or even safe, but from the steroid tree, it looks like you'd want to downregulate 16-alpha-hydroxylase when dosing DHEA, not aromitase.
actually, i'm not so sure that'd work, either. especially as i think estradiol is worse than estriol. maybe upregulation ? or maybe it can't be done and that's why no one's done it? hmm.
QUOTE(Dr. Lats @ Mar 26 2008, 01:48 PM) [snapback]468204[/snapback]
It seems like the negative sides you listed are caused by estrogen levels falling through the floor, not cortisol...
Nah man, I have it right.
High DHEA -> Low cortisol -> Over-active immune reponse (i.e. inflammation in the joints and tendons and getting sick)
QUOTE(Benson @ Mar 26 2008, 11:56 AM) [snapback]468193[/snapback]
Because it doesn't work...it seems like it should but for some reason or another, it doesn't.
Can we put this to rest once and for all? DHEA has an estrogenic metabolite (5-AD) whose formation is not dependant on aromatase AND this:
Endocrinology. 2005 Nov;146(11):4568-76. Epub 2005 Jun 30. Links
Comment in:
Endocrinology. 2005 Nov;146(11):4565-7.
Direct agonist/antagonist functions of dehydroepiandrosterone.Chen F, Knecht K, Birzin E, Fisher J, Wilkinson H, Mojena M, Moreno CT, Schmidt A, Harada S, Freedman LP, Reszka AA.
Department of Molecular Endocrinology, Merck Research Laboratories, WP26A-1000, Sumneytown Pike, West Point, Pennsylvania 19486, USA. fang_chen@merck.com
Dehydroepiandrosterone (DHEA) exhibits peak adrenal secretion in the fetus at term and around age 30 yr in the adult. Levels then progressively decline, which is associated with decreased levels of testosterone, dihydrotestosterone, and estrogen in peripheral tissues. DHEA supplementation in postmenopausal women increases bone formation and density, an effect mainly attributed to peripheral conversion to sex hormones. In this study, we tested DHEA for direct effects on the androgen (AR) and estrogen (ER) receptors. DHEA bound to AR with a Ki of 1 microM, which was associated with AR transcriptional antagonism on both the mouse mammary tumor virus and prostate-specific antigen promoters, much like the effects of bicalutamide. Unlike bicalutamide, DHEA stimulated, rather than inhibited, LNCaP cell growth, suggesting possible interaction with other hormone receptors. Indeed DHEA bound to ERalpha and ERbeta, with Ki values of 1.1 and 0.5 microM, respectively. Despite the similar binding affinities, DHEA showed preferential agonism of ERbeta with an EC50 of approximately 200 nm and maximal activation at 1 microM. With ERalpha we found 30-70% agonism at 5 microM, depending on the assay. Physiological levels of DHEA are approximately 30 nM and up to 90 nM in the prostate. DHEA at 30 nM is actually sufficient to activate ERbeta transcription to the same degree as estrogen at its circulating concentration, and additive effects are seen when the two were combined. Taken together, DHEA has the potential for physiologically relevant direct activation of ERbeta. With peak levels at term and age 30 yr, there is also a potential for antagonist effects on AR and partial agonism of ERalpha.
Seriously though, I wonder what the sides were for the men who took 1600 mgs of it for a month straight. There had to be red flags going off all over the place. Right?
One would think so.
QUOTE(eclypz @ Mar 26 2008, 03:38 PM) [snapback]468240[/snapback]
Seriously though, I wonder what the sides were for the men who took 1600 mgs of it for a month straight. There had to be red flags going off all over the place. Right?
Anyone up for logging it?
QUOTE(SteveSliwa @ Mar 26 2008, 05:24 PM) [snapback]468244[/snapback]
Anyone up for logging it?
Done it and logged it someplace here. Turned me into an emotional sap. The only cool thing I noticed was a dramatic increase in color perception...watching television was an amazing experience.
QUOTE(Benson @ Mar 26 2008, 06:44 PM) [snapback]468267[/snapback]
Done it and logged it someplace here. Turned me into an emotional sap. The only cool thing I noticed was a dramatic increase in color perception...watching television was an amazing experience.
Logging it at 1,600 mg while testing your blood levels of hormones.
I'm pretty sure there's an old log over an AM of a guy running 2 grams.
Count me out.
Count me out.
QUOTE(SteveSliwa @ Mar 26 2008, 07:50 PM) [snapback]468270[/snapback]
Logging it at 1,600 mg while testing your blood levels of hormones.
I didn't need a blood test to tell me that my estrogen levels were through the roof but if someone else wants to give it a go, more power to them.
QUOTE(Benson @ Mar 26 2008, 07:04 PM) [snapback]468276[/snapback]
I didn't need a blood test to tell me that my estrogen levels were through the roof but if someone else wants to give it a go, more power to them.
Your levels of DHEA may have been high prior to taking it. I would be interested in seeing what happens when a regular BB takes it with a full hormone workup before and after taking it.
Benson,
How much 6-oxo did you take, while running the DHEA?
Also, in regards to this thread, it seems like everyone is thinking in the terms of a real high dose of DHEA...
What about just a low to moderate dose, coupled with 6-oxo?
How much 6-oxo did you take, while running the DHEA?
Also, in regards to this thread, it seems like everyone is thinking in the terms of a real high dose of DHEA...
What about just a low to moderate dose, coupled with 6-oxo?
QUOTE (SteveSliwa @ Mar 26 2008, 04:18 PM) 
Your levels of DHEA may have been high prior to taking it. I would be interested in seeing what happens when a regular BB takes it with a full hormone workup before and after taking it.
i would be interested in seeing what happens when a guy smashes his nads with a sledge. please post some vids and pics.
QUOTE (Proton Soup @ Mar 27 2008, 12:20 AM)
i would be interested in seeing what happens when a guy smashes his nads with a sledge. please post some vids and pics.
Sure come over tomorrow I'll be glad to smash your balls.
So far I don't see a problem to see if the study and be repeated and this time we can see if estrogen levels will go up or not. No side effects were noted.
J Clin Endocrinol Metab. 1988 Jan;66(1):57-61.Links
Dehydroepiandrosterone reduces serum low density lipoprotein levels and body fat but does not alter insulin sensitivity in normal men.Nestler JE, Barlascini CO, Clore JN, Blackard WG.
Division of Endocrinology and Metabolism, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on body fat mass, serum lipid levels, and tissue sensitivity to insulin, five normal men were given placebo and five normal men were given oral DHEA [1600 mg/day (554.7 mmol/day)] for 28 days in a randomized, double blind study. In the DHEA group serum DHEA-S levels rose 2.5- to 3.5-fold, and mean (+/- SEM) serum androstenedione rose from 4.3 +/- 0.6 to 8.6 +/- 1.2 nmol/L (P less than 0.004, by paired t test), but serum total testosterone, free testosterone, sex hormone-binding globulin, estradiol, and estrone levels did not change. In the DHEA group the mean percent body fat decreased by 31%, with no change in weight. This suggests that the reduction in fat mass was coupled with an increase in muscle mass. DHEA administration also resulted in a fall in mean serum total cholesterol concentration (4.82 +/- 0.21 vs. 4.48 +/- 0.29 nmol/L; P less than 0.05), which was due almost entirely to a fall of 7.5% in mean serum low density lipoprotein cholesterol (3.21 +/- 0.11 vs. 2.97 +/- 0.14 nmol/L; P less than 0.01). No changes in anthropometric parameters or serum lipid levels occurred in the placebo group. Tissue sensitivity to insulin, assessed by the hyperinsulinemic-euglycemic clamp technique, did not change in either the placebo or DHEA groups. These results suggest that in normal men DHEA administration reduces body fat, increases muscle mass, and reduces serum low density lipoprotein cholesterol levels.
QUOTE (Dr. Lats @ Mar 26 2008, 11:56 PM)
Benson,
How much 6-oxo did you take, while running the DHEA?
Also, in regards to this thread, it seems like everyone is thinking in the terms of a real high dose of DHEA...
What about just a low to moderate dose, coupled with 6-oxo?
How much 6-oxo did you take, while running the DHEA?
Also, in regards to this thread, it seems like everyone is thinking in the terms of a real high dose of DHEA...
What about just a low to moderate dose, coupled with 6-oxo?
I was using 100mg of TD formestane IIRC...
QUOTE (SteveSliwa @ Mar 26 2008, 10:20 PM)
Sure come over tomorrow I'll be glad to smash your balls.
So far I don't see a problem to see if the study and be repeated and this time we can see if estrogen levels will go up or not. No side effects were noted.
So far I don't see a problem to see if the study and be repeated and this time we can see if estrogen levels will go up or not. No side effects were noted.
are you deaf? he just told you what the side effects were. and you're like "but i'm curious". and he's like "no, it hurts".
perhaps you missed the point, but you could always do this type of thing on yourself.
I'm just saying, and I don't really have much invested in this at all, but if a group of men were given 1600mgs a day for a month there should have been reports of boobies all over the place. There's not one mentioning of anyone quitting because of estrogenic sides.
QUOTE (eclypz @ Mar 27 2008, 09:07 AM)
I'm just saying, and I don't really have much invested in this at all, but if a group of men were given 1600mgs a day for a month there should have been reports of boobies all over the place. There's not one mentioning of anyone quitting because of estrogenic sides.
Bump. This is definitely more complex than it looks superficially.
I doubt any of us are postmenopausal women but there is some interesting stuff in here:
QUOTE
J Steroid Biochem Mol Biol. 2007 Oct;107(1-2):57-69. Epub 2007 Jun 8.Click here to read Links
Bioavailability and metabolism of oral and percutaneous dehydroepiandrosterone in postmenopausal women.
Labrie F, Bélanger A, Labrie C, Candas B, Cusan L, Gomez JL.
Molecular Endocrinology and Oncology Research Center, Laval University Hospital (CHUL) and Laval University, Quebec City, Quebec G1V 4G2, Canada.
To study the bioavailability of dehydroepiandrosterone (DHEA) administered by the oral and percutaneous routes, three groups of 12 postmenopausal women aged 60-70 years received two capsules of 50mg of DHEA orally before breakfast daily for 14 days or applied 4 g of a 10% DHEA cream or gel at the same time of the day on a 30 cm x 30 cm surface area on the thighs. Detailed serial blood sampling over 24h was performed following 1st and 14th DHEA administration for measurement of DHEA and nine of its metabolites by liquid chromatography tandem mass spectrometry (LC-MS/MS) or gas chromatography mass spectrometry (GC-MS). Serum levels of estrone (E1) and estradiol (E2) did not change following DHEA administration by any of the three formulations, while serum androstenedione (4-dione), testosterone, DHEA sulfate (DHEA-S), E(1)-S, androsterone glucuronide (ADT-G) and 3alpha-androstanediol-G (3alpha-diol-G), increased in all cases, the effect on these parameters being more important after oral than percutaneous administration due to the metabolism of DHEA into these metabolites in the gastrointestinal tract and liver. No qualitative differences in DHEA metabolism are observed between the oral and percutaneous routes of DHEA administration while the levels of all steroids remain on a plateau during the 24h period during chronic percutaneous DHEA administration. The present data show that DHEA is transformed into active androgens and estrogens in peripheral intracrine tissues with no or minimal release of the active steroids E(1), E(2) or testosterone in the circulation. Moreover, DHEA is preferentially transformed into androgens rather than into estrogens. Most importantly, the present data show that changes in serum DHEA following oral or percutaneous DHEA administration are not a valid parameter of DHEA action since the increase in serum DHEA is at least 100% greater than the increase in the formation of active androgens and estrogens and thus much higher than the potential physiological effects.
PMID: 17627814 [PubMed - indexed for MEDLINE]
Bioavailability and metabolism of oral and percutaneous dehydroepiandrosterone in postmenopausal women.
Labrie F, Bélanger A, Labrie C, Candas B, Cusan L, Gomez JL.
Molecular Endocrinology and Oncology Research Center, Laval University Hospital (CHUL) and Laval University, Quebec City, Quebec G1V 4G2, Canada.
To study the bioavailability of dehydroepiandrosterone (DHEA) administered by the oral and percutaneous routes, three groups of 12 postmenopausal women aged 60-70 years received two capsules of 50mg of DHEA orally before breakfast daily for 14 days or applied 4 g of a 10% DHEA cream or gel at the same time of the day on a 30 cm x 30 cm surface area on the thighs. Detailed serial blood sampling over 24h was performed following 1st and 14th DHEA administration for measurement of DHEA and nine of its metabolites by liquid chromatography tandem mass spectrometry (LC-MS/MS) or gas chromatography mass spectrometry (GC-MS). Serum levels of estrone (E1) and estradiol (E2) did not change following DHEA administration by any of the three formulations, while serum androstenedione (4-dione), testosterone, DHEA sulfate (DHEA-S), E(1)-S, androsterone glucuronide (ADT-G) and 3alpha-androstanediol-G (3alpha-diol-G), increased in all cases, the effect on these parameters being more important after oral than percutaneous administration due to the metabolism of DHEA into these metabolites in the gastrointestinal tract and liver. No qualitative differences in DHEA metabolism are observed between the oral and percutaneous routes of DHEA administration while the levels of all steroids remain on a plateau during the 24h period during chronic percutaneous DHEA administration. The present data show that DHEA is transformed into active androgens and estrogens in peripheral intracrine tissues with no or minimal release of the active steroids E(1), E(2) or testosterone in the circulation. Moreover, DHEA is preferentially transformed into androgens rather than into estrogens. Most importantly, the present data show that changes in serum DHEA following oral or percutaneous DHEA administration are not a valid parameter of DHEA action since the increase in serum DHEA is at least 100% greater than the increase in the formation of active androgens and estrogens and thus much higher than the potential physiological effects.
PMID: 17627814 [PubMed - indexed for MEDLINE]
Just to let you all know today, I talked to a scientist today who got his natural testosterone levels up over 3,000 ng, while stacking DIM, 6-oxo, and DHEA. I forgot to ask him exactly how much DHEA he was taking though.
He did say that after stopping cold turkey, his testosterone levels went lower than his baseline for a while.
He did say that after stopping cold turkey, his testosterone levels went lower than his baseline for a while.
He was also supplementing with L-carnitine.
The highest he got up to on his blood test was either 3200 or 3600. No bull shit.
The highest he got up to on his blood test was either 3200 or 3600. No bull shit.
QUOTE (Dr. Lats @ Mar 27 2008, 11:49 AM)
He was also supplementing with L-carnitine.
The highest he got up to on his blood test was either 3200 or 3600. No bull shit.
The highest he got up to on his blood test was either 3200 or 3600. No bull shit.
ask him about his libido. and did he get hyooooge.
I'll try to next time. He is huge and strong though.
QUOTE (Proton Soup @ Mar 27 2008, 11:39 AM)
are you deaf? he just told you what the side effects were. and you're like "but i'm curious". and he's like "no, it hurts".
perhaps you missed the point, but you could always do this type of thing on yourself.
perhaps you missed the point, but you could always do this type of thing on yourself.
Personal experience without blood tests to back it up is nearly worthless. The study I posted did not list any side effects.
My DHEA levels are normally low thus I can't be included in a study.
QUOTE (eclypz @ Mar 27 2008, 12:07 PM)
I'm just saying, and I don't really have much invested in this at all, but if a group of men were given 1600mgs a day for a month there should have been reports of boobies all over the place. There's not one mentioning of anyone quitting because of estrogenic sides.
Exactly. Anyone interested I'll cover your blood tests before and during but you'll have to get your own DHEA.
I am going to run this cycle, after a little bit more research, getting my diet in line, and losing about 10 pounds of fat.
I need to figure out the correct DHEA dose. I already know that 6 caps of 6-oxo will work, for starters. I don't know about DIM dosage though. I need to get a blood test done, to see how I fair in the hormone department first.
I need to figure out the correct DHEA dose. I already know that 6 caps of 6-oxo will work, for starters. I don't know about DIM dosage though. I need to get a blood test done, to see how I fair in the hormone department first.
FWIW, I have in the past, and am now supplementing with 25mg of dhea transdermally. I ran it for about two months the last time with nothing in the way of estrogenic sides to report. I did however note an increased sense of energy and overall virility. More like a neurological thing. It was pretty sweet. It definitely enhances stimulants.
Great thread, not much to add from myself however I thought (dont quote me on this) Patrick Arnold was doing some sort of study on high dose DHEA. I know he was looking for participants about 6 months ago....
No idea how that turned out.
No idea how that turned out.
Int J Obes. 1990 May;14(5):457-63
J Clin Endocrinol Metab. 1988 Jan;66(1):57-61
Anyone have access to these in full-text?
J Clin Endocrinol Metab. 1988 Jan;66(1):57-61
Anyone have access to these in full-text?
QUOTE (eclypz @ Mar 27 2008, 02:34 PM)
FWIW, I have in the past, and am now supplementing with 25mg of dhea transdermally. I ran it for about two months the last time with nothing in the way of estrogenic sides to report. I did however note an increased sense of energy and overall virility. More like a neurological thing. It was pretty sweet. It definitely enhances stimulants.
Does it still get sulfated if you take it transdermally?
I'm sure some of it has to pass through the liver at some point.
QUOTE (eclypz @ Mar 27 2008, 11:07 AM)
I'm just saying, and I don't really have much invested in this at all, but if a group of men were given 1600mgs a day for a month there should have been reports of boobies all over the place. There's not one mentioning of anyone quitting because of estrogenic sides.
Don't forget that ER activation is ligand specific, and I no, don't know shit about "AP1 sites." An activated ER can INHIBIT mRNA transcription as well as initiate it.
Differential ligand activation of estrogen receptors ERalpha and ERbeta at AP1 sites.
Paech K, Webb P, Kuiper GG, Nilsson S, Gustafsson J, Kushner PJ, Scanlan TS.
Department of Pharmaceutical Chemistry, University of California, San Francisco, CA 94143-0446, USA.
The transactivation properties of the two estrogen receptors, ERalpha and ERbeta, were examined with different ligands in the context of an estrogen response element and an AP1 element. ERalpha and ERbeta were shown to signal in opposite ways when complexed with the natural hormone estradiol from an AP1 site: with ERalpha, 17beta-estradiol activated transcription, whereas with ERbeta, 17beta-estradiol inhibited transcription. Moreover, the antiestrogens tamoxifen, raloxifene, and Imperial Chemical Industries 164384 were potent transcriptional activators with ERbeta at an AP1 site. Thus, the two ERs signal in different ways depending on ligand and response element. This suggests that ERalpha and ERbeta may play different roles in gene regulation.
PMID: 9278514 [PubMed - indexed for MEDLINE]
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