Transdermal versus oral DHEA

[1cc]

1: J Appl Physiol. 1999 Dec;87(6):2274-83.

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.

 

[Sunkist]

Sunkist,

Is there any reason that you do both oral and transdermal DHEA. Since it seems that transdermal DHEA does not impact estrogens very much, wouldn't it be better to do only transdermal DHEA.

1cc

There was a study I can't find real quick that basically said that oral DHEA after first pass degredation influences the production of hGH through metabolites. I have found nothing as to a repeated study, but I am experimenting anyway. I do 50 oral at bedtime with 2K glutamine, 1-2 K argenine, melatonin and folic acid. I can't attribute the results to anything with all the confounders, because I do deprenyl low dose as well... and TRT of course. All influence dopamine. BUT>>> I have half the gray in my hair after a year of this... only anecdotal, but something has changed.

Might just work for me and no body else. I do know everyone is different.

 

[frankwhardy]

Am I understanding this correctly? Would 10ml per day of 20% DHEA cream equate to 2000mg DHEA per day, or, did they apply 2000/14=142mg per day?

They did write that poorly, didn't they? They can't possibly mean 2000mg per day. Perhaps the author mean't to say 1mL (= 200mg) per day. Another possibility is that they provided the subjects with a 10mL volume container of 20% DHEA and the subjects were then instructed to apply a certain amount of that (e.g., 0.5mL) per day . . .

So transdermal DHEA had very little effect on Estrogen? It seems that transdermal would be the way to go for DHEA.
1. What would be the correct transdermal dose to use to equate to 50mg oral dose?
2. Is there any benefit to taking DHEA orally instead of transdermally?
3. Could one get similar results to transdermal if one took DHEA sublingually?

The benefit to oral DHEA versus transdermal, I believe, is that there is a greater conversion to the sulfate form, i.e., DHEA-S (due to first pass liver conversion), and that is the form your body apparently stores the DHEA in and draws upon as necessary. And having a higher DHEA-S level is what is apparently more directly linked to the oft cited health benefits of having a higher DHEA(-S) level (DHEA-S having a much longer half-life than DHEA and therefore providing a more accurate representation of one's DHEA capabilities). The other possible advantage is that the Growth Hormone (GH) potentiating ability of DHEA has so far only been demonstrated with oral administration - and maybe the increased levels of DHEA-S and/or metabolites thereof are what is doing that . . . (need another study to show that transdermal also increases GH).
Frank

 

[stat1951]

There was a study I can't find real quick that basically said that oral DHEA after first pass degredation influences the production of hGH through metabolites.

I recall reading somethng on that also - but didn't (apparently) bookmark the study.

Also have read specifically what Frank refered to with the convesion to DHEA-S...

The benefit to oral DHEA versus transdermal, I believe, is that there is a greater conversion to the sulfate form, i.e., DHEA-S (due to first pass liver conversion), and that is the form your body apparently stores the DHEA in and draws upon as necessary. And having a higher DHEA-S level is what is apparently more directly linked to the oft cited health benefits of having a higher DHEA(-S) level (DHEA-S having a much longer half-life than DHEA and therefore providing a more accurate representation of one's DHEA capabilities).

As to the study:

Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men.... 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

I wonder if that may have had to do with the fact that the researchers were using "healthy young men" (who presumably had optimal levels of DHEA to start with???).

As when one compares it with studies involving "older healthy males" (average age 58), there are noted differences:

Biotransformation of Oral Dehydroepiandrosterone in Elderly Men: Significant Increase in Circulating Estrogens ... Wiebke Arlt, Joachim Haas, Frank Callies, Martin Reincke, Doris Hübler, Michael Oettel, Michael Ernst, Heinrich Maria Schulte and Bruno Allolio ... Department of Endocrinology, Medical University Hospital Wuerzburg (W.A., J. H., F.C., M.R., B.A.), 97080 Wuerzburg; Jenapharm GmbH & Co. KG (D.H., M.O., M.E.), Jena; and Institute for Hormone and Fertility Research (H.M.S.), Hamburg, Germany ...

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 µmol/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... Serum testosterone and dihydrotestosterone remained unchanged after DHEA administration. In contrast, 17ß-estradiol and estrone significantly increased in a dose-dependent manner... The aim of our study was, therefore, to define a DHEA dose suitable for restoration of low DHEAS levels in elderly men to concentrations usually found in young healthy adult men. To this end, we studied the pharmacokinetics and biotransformation of orally administered DHEA in healthy men between 50–70 yr of age with endogenous serum DHEAS concentrations below 4.1 µmol/L (1500 ng/mL), which is equivalent to the lower limit of the normal range for serum DHEAS in 15- to 39-yr-old men... Main inclusion criteria for participation in the study were a serum DHEAS concentration below 4.1 µmol/L (<1500 ng/mL), an age between 50–70 yr, a body mass index (BMI) between 20–30 kg/m2, and a state of general good health... serum cortisol concentrations exhibited the typical diurnal variation which was not altered by DHEA administration... After oral administration of DHEA, serum DHEA concentrations significantly increased in a dose-dependent manner, with maximum concentrations (cmax) measured between 60–480 min (tmax, 2.6 ± 2.0 h and 2.5 ± 1.2 h for 50 and 100 mg DHEA, respectively; Fig. 1B). Also, serum DHEAS increased rapidly, peaking between 120–480 min (tmax, 4.2 ± 2.1 and 3.8 ± 1.5 h for 50 and 100 mg DHEA, respectively. After reaching cmax, both DHEA and DHEAS decreased only slowly to levels still above baseline at 12 h, with serum DHEA more rapidly declining... Comparing the AUC 0–12 h, the administration of 50 mg DHEA led to an increase of 234% of baseline serum DHEA and 343% of baseline serum DHEAS, whereas 100 mg induced increases of 323% and 494%, respectively. While 50 mg DHEA induced increases in serum DHEA and DHEAS to levels found in young adult men, 100 mg DHEA clearly induced supraphysiological concentrations.... Neither the administration of 50 nor 100 mg DHEA led to an increase in total serum T (Fig. 2A) or DHT concentrations (Fig. 2B), whereas a slight, but significant, increase in free T concentrations to 113% (50 mg DHEA; tmax, 1.9 ± 1.4 h) and 115% (100 mg DHEA; tmax, 2.9 ± 2.2 h) was observed... After DHEA administration, serum E1 (Fig. 3A) as well as serum E2 (Fig. 3B) increased significantly in a dose-dependent manner. Peak concentrations for E1 were measured 30–720 min after DHEA administration (tmax, 3.3 ± 2.7 h for 50 mg DHEA and 3.6 ± 2.7 h for 100 mg DHEA). Serum E2 concentrations also peaked between 60–600 min after DHEA ingestion (tmax, 4.4 ± 2.5 h for 50 mg DHEA and 4.7 ± 2.3 h for 100 mg DHEA). The AUC 0–12 h after 50 mg DHEA was equivalent to 176% (E1) and 124% (E2) of baseline values, whereas 100 mg DHEA induced increase to 226% (E1) and 137% (E2) of baseline values...The major finding of our study is that in elderly men a dose of 50 mg DHEA, which restores serum DHEA and DHEAS to youthful levels in healthy men, induces significant increases in serum E1 and E2 concentrations, whereas total T and DHT, the main circulating androgens in men, remain unaffected. This contrasts with the results of our previous study on the pharmacokinetics and bioconversion of DHEA in women showing a significant increase in serum androgens but only a slight increase in serum E1 and no change in serum E2 after oral DHEA administration. Thus, oral administration of DHEA influences the androgen/estrogen ratio in both genders in opposite directions...

Similar tests - somewhat significantly different results. Only thing that I can think of is the use of healthy young male test subjects versus use of healthy older male test subjects???

Larry

 

[Sunkist]

Exactly... So many studies are skewed. When I have the time I download the study and not the abstract... often tells a different tale.

The fist Andro study at I think it was ISU... where they give it orally and we all know what happens to Andro orally.. then say it does not work.

 

[1cc]

Oral vs Sublingual DHEA

This issue was examined clinically in the longest (1 year) controlled
study of DHEA ever conducted in humans. See Yen SSC, Morales AJ, and
Khorram O. "Replacement of DHEA in aging men and women. Potential
remedial effects." _Annals of the New York Academy of Sciences_ Dec. 19,
1995; 774: 128-142 (see pp. 129-31). Yen et al. write:

The time course and circulating levels of DHEA and DHEAS after oral
versus sublingual routes of adminstration of 50 mg DHEA in gelatin
capsules were determined in eight men and eight women....[W]ith the
exception of serum DHEA levels, the increments over time of
circulating DHEAS...were rapid and were similar between oral and
sublingual routes of adminstration. DHEA levels, in contrast, showed a
rapid (within 30 minutes) and marked elevation lasting for 2 hours
after sublingual than after oral administration. Thereafter, all
steroid levels, including those of DHEA, were similar with a slight
decline towards the end of the experiment at the 8th hour. Thus we
chose the oral route of adminstration for subsequent studies because
of its ease and reliability of administration in the aging population.
(Pp. 129-31).

 

[1cc]

Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age [published erratum appears in J Clin Endocrinol Metab 1995 Sep;80(9):2799]
AJ Morales, JJ Nolan, JC Nelson and SS Yen
Department of Reproductive Medicine, University of California School of Medicine, La Jolla 92093-0802.

Aging in humans is accompanied by a progressive decline in the secretion of the adrenal androgens dehydroepiandrosterone (DHEA) and DHEA sulfate (DS), paralleling that of the GH-insulin-like growth factor-I (GH-IGF-I) axis. Although the functional relationship of the decline of the GH-IGF-I system and catabolism is recognized, the biological role of DHEA in human aging remains undefined. To test the hypothesis that the decline in DHEA may contribute to the shift from anabolism to catabolism associated with aging, we studied the effect of a replacement dose of DHEA in 13 men and 17 women, 40-70 yr of age. A randomized placebo-controlled cross-over trial of nightly oral DHEA administration (50 mg) of 6-month duration was conducted. During each treatment period, concentrations of androgens, lipids, apolipoproteins, IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, insulin sensitivity, percent body fat, libido, and sense of well-being were measured. A subgroup of men (n = 8) and women (n = 5) underwent 24-h sampling at 20- min intervals for GH determinations. DHEA and DS serum levels were restored to those found in young adults within 2 weeks of DHEA replacement and were sustained throughout the 3 months of the study. A 2-fold increase in serum levels of androgens (androstenedione, testosterone, and dihydrotestosterone) was observed in women, with only a small rise in androstenedione in men. There was no change in circulating levels of sex hormone-binding globulin, estrone, or estradiol in either gender. High density lipoprotein levels declined slightly in women, with no other lipid changes noted for either gender. Insulin sensitivity and percent body fat were unaltered. Although mean 24-h GH and IGFBP-3 levels were unchanged, serum IGF-I levels increased significantly, and IGFBP-1 decreased significantly for both genders, suggesting an increased bioavailability of IGF-I to target tissues. This was associated with a remarkable increase in perceived physical and psychological well-being for both men (67%) and women (84%) and no change in libido. In conclusion, restoring DHEA and DS to young adult levels in men and women of advancing age induced an increase in the bioavailability of IGF-I, as reflected by an increase in IGF-I and a decrease in IGFBP-1 levels. These observations together with improvement of physical and psychological well-being in both genders and the absence of side-effects constitute the first demonstration of novel effects of DHEA replacement in age-advanced men and women.

 

[1cc]

Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age [published erratum appears in J Clin Endocrinol Metab 1995 Sep;80(9):2799]
AJ Morales, JJ Nolan, JC Nelson and SS Yen
Department of Reproductive Medicine, University of California School of Medicine, La Jolla 92093-0802.

Aging in humans is accompanied by a progressive decline in the secretion of the adrenal androgens dehydroepiandrosterone (DHEA) and DHEA sulfate (DS), paralleling that of the GH-insulin-like growth factor-I (GH-IGF-I) axis. Although the functional relationship of the decline of the GH-IGF-I system and catabolism is recognized, the biological role of DHEA in human aging remains undefined. To test the hypothesis that the decline in DHEA may contribute to the shift from anabolism to catabolism associated with aging, we studied the effect of a replacement dose of DHEA in 13 men and 17 women, 40-70 yr of age. A randomized placebo-controlled cross-over trial of nightly oral DHEA administration (50 mg) of 6-month duration was conducted. During each treatment period, concentrations of androgens, lipids, apolipoproteins, IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, insulin sensitivity, percent body fat, libido, and sense of well-being were measured. A subgroup of men (n = 8) and women (n = 5) underwent 24-h sampling at 20- min intervals for GH determinations. DHEA and DS serum levels were restored to those found in young adults within 2 weeks of DHEA replacement and were sustained throughout the 3 months of the study. A 2-fold increase in serum levels of androgens (androstenedione, testosterone, and dihydrotestosterone) was observed in women, with only a small rise in androstenedione in men. There was no change in circulating levels of sex hormone-binding globulin, estrone, or estradiol in either gender. High density lipoprotein levels declined slightly in women, with no other lipid changes noted for either gender. Insulin sensitivity and percent body fat were unaltered. Although mean 24-h GH and IGFBP-3 levels were unchanged, serum IGF-I levels increased significantly, and IGFBP-1 decreased significantly for both genders, suggesting an increased bioavailability of IGF-I to target tissues. This was associated with a remarkable increase in perceived physical and psychological well-being for both men (67%) and women (84%) and no change in libido. In conclusion, restoring DHEA and DS to young adult levels in men and women of advancing age induced an increase in the bioavailability of IGF-I, as reflected by an increase in IGF-I and a decrease in IGFBP-1 levels. These observations together with improvement of physical and psychological well-being in both genders and the absence of side-effects constitute the first demonstration of novel effects of DHEA replacement in age-advanced men and women.

I found this in the full text:

Each subject received 3 months of DHEA and 3 months of placebo
at bedtime in random order.

Blood was drawn at each visit between 0800-0900 h after an overnight
fast for determination of serum steroid hormones and sex hormonebindine
elobulin (SHBG) levels as well as liver function, renal function, V .

Since the tests were at least 8 hours later, it is possible that the Estrogen normalized after this amount of time as mentioned in:

Biotransformation of Oral Dehydroepiandrosterone in Elderly Men: Significant Increase in Circulating Estrogens

Compared to placebo, Young et al. (18) found significant increases in serum E1 and E2 after 50 mg DHEA, but there was no longer a significant difference 8 h after administration.

 

[1cc]

What transdermal dose of DHEA would provide the same result as 50mg oral dose?

 

[1cc]

Am I understanding this correctly? Would 10ml per day of 20% DHEA cream equate to 2000mg DHEA per day, or, did they apply 2000/14=142mg per day?

So transdermal DHEA had very little effect on Estrogen? It seems that transdermal would be the way to go for DHEA.
1. What would be the correct transdermal dose to use to equate to 50mg oral dose?
2. Is there any benefit to taking DHEA orally instead of transdermally?
3. Could one get similar results to transdermal if one took DHEA sublingually?

From what I have seen at some links, 15mg DHEA Transdermal = 50mg DHEA oral. Since this is the case, I'm not sure why the studies mentioned above are using what amounts to 142mg per day transdermal which = about 473mg oral DHEA.

Sunkist,

What strength is your DHEA transdermal?

 

[1cc]

Micronized DHEA vs regular DHEA

Micronized DHEA vs regular DHEA

Which is better and why?

Here is a study I found, but I don't understand what they are concluding (the part in bold and underlined).

Am J Obstet Gynecol. 1996 Feb;174(2):649-53. Related Articles, Links


Delivery of dehydroepiandrosterone to premenopausal women: effects of micronization and nonoral administration.

Casson PR, Straughn AB, Umstot ES, Abraham GE, Carson SA, Buster JE.

Division of Reproductive Endocrinology and Infertility, The University of Tennessee, Memphis, USA.

OBJECTIVES: This single-dose study compares three dehydroepiandrosterone delivery methods (oral crystalline steroid, micronized steroid, and vaginal administration) to ascertain whether physiologic levels of circulating dehydroepiandrosterone and dehydroepiandrosterone sulfate can be obtained while increases in testosterone are minimized. STUDY DESIGN: Two randomized, double-blind, placebo-controlled single-dose comparisons were made. For oral micronized versus crystalline dehydroepiandrosterone 300 mg doses of micronized or crystalline dehydroepiandrosterone were administered, followed by 6 hours of blood sampling (n=7). Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and testosterone levels were measured; areas under the curve and mean peak values were analyzed by Student-Newman-Keuls tests. For oral versus vaginal micronized dehydroepiandrosterone 150 mg oral or vaginal doses of micronized dehydroepiandrosterone were administered, followed by blood sampling over 12 hours (n=5). Data analysis was as described. RESULTS: Oral micronized and unmicronized dehydroepiandrosterone resulted in increases in serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and testosterone. Micronization increased the area-under-the-curve ratios for dehydroepiandrosterone sulfate/dehydroepiandrosterone and dehydroepiandrosterone sulfate/testosterone. Vaginal administration provided equivalent serum dehydroepiandrosterone; however, it failed to increase dehydroepiandrosterone sulfate or testosterone over placebo. CONCLUSION: Micronization of oral dehydroepiandrosterone diminishes bioconversion to testosterone. Vaginal dehydroepiandrosterone delivers equivalent dehydroepiandrosterone but substantially diminishes dehydroepiandrosterone bioconversion.

 

[1cc]

Micronized DHEA vs Regular DHEA

Am J Obstet Gynecol. 1992 Apr;166(4):1163-8; discussion 1168-70. Related Articles, Links


Postmenopausal steroid replacement with micronized dehydroepiandrosterone: preliminary oral bioavailability and dose proportionality studies.

Buster JE, Casson PR, Straughn AB, Dale D, Umstot ES, Chiamori N, Abraham GE.

Department of Obstetrics and Gynecology, University of Tennessee, Memphis.

OBJECTIVES: Because dehydroepiandrosterone may protect against neoplasia, osteoporosis, and cardiac disease, we investigated the bioavailability of oral micronized dehydroepiandrosterone, anticipating its adjunctive use in postmenopausal steroid replacement. STUDY DESIGN: Eight postmenopausal women randomly received either a placebo or 150 or 300 mg of oral micronized dehydroepiandrosterone in a lipid matrix. Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, and estradiol were measured periodically over the 12 hours after each dose. All treatments, all doses, and mean serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and testosterone were compared with analysis of variance for repeated measures and Newman-Keuls a posteriori test of statistical significance. RESULTS: Mean peak steroid concentrations after 150 mg (300 mg) doses were dehydroepiandrosterone 1617 (2639) ng/dl, 7 (11.5)-fold above placebo; dehydroepiandrosterone S 1185 (1688) micrograms/dl, 14 (20)-fold above placebo; and testosterone 183 (311) ng/dl, 4 (7)-fold above placebo. Estradiol concentrations remained less than 20 pg/ml, but androgen concentrations rose by 1 hour and remained elevated through the twelfth hour. Peak androgen concentrations and areas under the curves exhibited proportionality with both doses. A testosterone radioimmunoassay with celite chromatography revealed a 300% overestimation for testosterone in the direct-assay method used in this study. Thus after appropriate readjustment maximum testosterone concentrations were observed consistently within physiologic premenopausal ranges after the 150 mg dose. CONCLUSIONS: Micronized dehydroepiandrosterone may provide a steroidal postmenopausal replacement that is adjunctive to estrogens and worthy of further investigation.

 

[1cc]

Another nice diagram of the sex hormone cascade.

 

[Sunkist]

From what I have seen at some links, 15mg DHEA Transdermal = 50mg DHEA oral. Since this is the case, I'm not sure why the studies mentioned above are using what amounts to 142mg per day transdermal which = about 473mg oral DHEA.

Sunkist,

What strength is your DHEA transdermal?

I go the same route as I do with T, cept I am compounding my own. If one places 100mg of T on the skin surface they expected level is the normal body daily secretion of about 10mg. I place 10x the mg of DHEA on the epithelium that I want in my blood. This would be relative to what one wants and needs independently. Since I take some oral DHEA at bedtime alternately, I myself mix the 'potion' to put 50 mg on in the appropriate vehicle. I do this every other day right now pending my next panel. I am also doing a compounded andro mix one/ol. This is Rx. I simply don't want all my T to come from the TRT. I want some natural and some quasi natural.

Right now except for the lipid profile I am on target. I hope the fish oil et al. will help there. My E was a little up last time so I am increasing chysin and 6 oxo.

 

[The_Skeptic]

All these studies, all these opinions. Is there anyone who can simplify this thread for a guy with ADD who has never taken DHEA?

1. If I'm currently on 100 mg of TRT a week, should I or should I not consider DHEA as well?
   
2. If the answer is yes, should I take oral or transdermal DHEA?
   
3. Will DHEA help with virilization if I am a 37-year-old with secondary hypogonadism with incomplete virilization?
   
4. Will DHEA improve my libido?

 

[pmgamer18]

We are all different I did DHEA in my cream when I was on it and it did not bring my levels up as high as the pills I am taking now.
http://www.myvitanet.com/dhea260capph.html
I take one pill at lunch time before eating. My levels came up from low normal to the middle of the range. Do I feel any different no I can't tell but I have been feeling my best for over a yr. now. I say get some and try it to see if it helps you need to be on it for over 90 days to tell.

 

[1cc]

Micronized DHEA vs regular DHEA

Which is better and why?

Here is a study I found, but I don't understand what they are concluding (the part in bold and underlined).

Am J Obstet Gynecol. 1996 Feb;174(2):649-53. Related Articles, Links


Delivery of dehydroepiandrosterone to premenopausal women: effects of micronization and nonoral administration.

Casson PR, Straughn AB, Umstot ES, Abraham GE, Carson SA, Buster JE.

Division of Reproductive Endocrinology and Infertility, The University of Tennessee, Memphis, USA.

OBJECTIVES: This single-dose study compares three dehydroepiandrosterone delivery methods (oral crystalline steroid, micronized steroid, and vaginal administration) to ascertain whether physiologic levels of circulating dehydroepiandrosterone and dehydroepiandrosterone sulfate can be obtained while increases in testosterone are minimized. STUDY DESIGN: Two randomized, double-blind, placebo-controlled single-dose comparisons were made. For oral micronized versus crystalline dehydroepiandrosterone 300 mg doses of micronized or crystalline dehydroepiandrosterone were administered, followed by 6 hours of blood sampling (n=7). Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and testosterone levels were measured; areas under the curve and mean peak values were analyzed by Student-Newman-Keuls tests. For oral versus vaginal micronized dehydroepiandrosterone 150 mg oral or vaginal doses of micronized dehydroepiandrosterone were administered, followed by blood sampling over 12 hours (n=5). Data analysis was as described. RESULTS: Oral micronized and unmicronized dehydroepiandrosterone resulted in increases in serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, and testosterone. Micronization increased the area-under-the-curve ratios for dehydroepiandrosterone sulfate/dehydroepiandrosterone and dehydroepiandrosterone sulfate/testosterone. Vaginal administration provided equivalent serum dehydroepiandrosterone; however, it failed to increase dehydroepiandrosterone sulfate or testosterone over placebo. CONCLUSION: Micronization of oral dehydroepiandrosterone diminishes bioconversion to testosterone. Vaginal dehydroepiandrosterone delivers equivalent dehydroepiandrosterone but substantially diminishes dehydroepiandrosterone bioconversion.

I have been trying to make sense of some of these studies myself. I hope someone will jump in and provide some input.

So far, from what I have understood, I have come to the following conclusions.

1. Transdermal DHEA does not convert to DHEA-S. In order to measure blood levels of DHEA, one tests for DHEA-S, and so there is no way of knowing if you're getting too much or too little.
2. Taking regular DHEA orally may or may not raise E2 and/or Total Estrogens. I am very weary of the possibility of raising Estrogen, and so am looking for another option.
3. Then I decided to read up on Micronized DHEA. I was surprised to find that Micronized DHEA has better absorption and bypasses liver first pass DHEA metabolism (so less stress on the liver I believe). This though can also be accomplished I believe by mixing regular DHEA with oil before taking it. Then the highlighted portions of the above study also seem to suggest that there is less conversion to testosterone with micronized DHEA. I am hoping that this also applies to Estrogen. Blood levels can be measured by testing DHEA-S.

If anyone can get the full text of the above study and post it, that would be great.

 

[jboldman]

the simple answer is 50-100 mg of dhea in tablet form will not raise your estrogen to above normal levels! Period!

jb

 

[1cc]

the simple answer is 50-100 mg of dhea in tablet form will not raise your estrogen to above normal levels! Period!

jb

JB,

It's not that I don't agree with your statement. It is just that I am trying to determine a better way of taking it. That's all.

Do you have any knowledge about Micronized DHEA?

Thanks

 

[hackskii]

Stinging Nettle can reduce the amount of free (active) testosterone circulating in the blood and help to inhibit aromatase, one of the enzymes responsible for testosterone synthesis.

I think you made a typo there mate, it can increase the free test and this is a good thing.

A study in Germany, showed that stinging nettle extract may inhibit the enzyme aromatase.
Other studies have shown that stinging nettle extract binds to the protein SHBG allowing less testosterone to be bound to SHBG allowing for more free testosterone bioavailability.
So if stinging nettle hinders aromatization (actually keeping more testosterone around), and less estradiol floating around (which can reduce LH bad for test production), and bind to SHBG which allows more free testosterone to circulate around in the body.
This would be a good thing, especially for us older guys.