Transdermal versus oral DHEA

[frankwhardy]

Here is an interesting study on transdermal DHEA. From what I can tell, the dose used is something like 142 mg/day!

Physiological changes in dehydroepiandrosterone are not reflected by serum levels of active androgens and estrogens but of their metabolites: intracrinology.

Labrie F, Belanger A, Cusan L, Candas B.

Medical Research Council Group in Molecular Endocrinology, Centre Hospitalier de l'Universite Laval Research Center, Le Centre Hospitalier Universitaire de Quebec, Canada.

This study analyzes in detail the serum concentration of the active androgens and estrogens, as well as a series of free and conjugated forms of their precursors and metabolites, after daily application for 2 weeks of 10 mL 20% dehydroepiandrosterone (DHEA) solution on the skin to avoid first passage through the liver. In men, DHEA administration caused 175%, 90%, 200% and 120% increases in the circulating levels of DHEA and its sulfate (DHEA-S), DHEA-fatty acid esters, and androst-5-ene-3 beta,17 beta-diol, respectively, with a return to basal values 7 days after cessation of the 14-day treatment. Serum androstenedione increased by approximately 80%, whereas serum testosterone and dihydrotestosterone (DHT) remained unchanged. In parallel with the changes in serum DHEA, the concentrations of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, and androstane-3 beta,17 beta-diol-G increased by about 75%, 50%, and 75%, respectively, whereas androsterone-sulfate increased 115%. No consistent change was observed in serum estrone (E1) or estradiol (E2) in men receiving DHEA, whereas serum E1-sulfate and E2-sulfate were slightly and inconsistently increased by about 20%, and serum cortisol and aldosterone concentrations were unaffected by DHEA administration. Almost superimposable results were obtained in women for most steroids except testosterone, which was about 50% increased during DHEA treatment. This increase corresponded to about 0.8 nM testosterone, an effect undetectable in men because they already have much higher (approximately 15 nM) basal testosterone levels. In women, the serum levels of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, androstane-3 beta,17 beta-diol-G, and androsterone-sulfate were increased by 125%, 140%, 120% and 150%, respectively. The present study demonstrates that the serum concentrations of testosterone, DHT, E1, and E2 are poor indicators of total androgenic and estrogenic activity. However, the esterified metabolites of DHT appear as reliable markers of the total androgen pool, because they directly reflect the intracrine formation of androgens in the tissues possessing the steroidogenic enzymes required to transform the inactive precursors DHEA and DHEA-S into DHT. As well demonstrated in women, who synthesize almost all their androgens from DHEA and DHEA-S, supplementation with physiological amounts of exogeneous DHEA permits the biosynthesis of androgens limited to the appropriate target tissues without leakage of significant amounts of active androgens into the circulation. This local or intracrine biosynthesis and action of androgens eliminates the inappropriate exposure of other tissues to androgens and thus minimizes the risks of undesirable masculinizing or other androgen-related side effects of DHEA.

PMID: 9253308 [PubMed - indexed for MEDLINE]

Very interesting study. I had bookmarked it and meant to reply earlier, but had gotten sidetracked.

An interesting question comes to mind. Previous studies - one of which was previously posted on this site - has shown that oral doses of DHEA in higher amounts (the study used 50 mg and 100 mg doses) led to the elevation of estradiol levels in the male test subjects. I note that this test - which uses a transdermal form of DHEA - the test results indicated the following:

No consistent change was observed in serum estrone (E1) or estradiol (E2) in men receiving DHEA, whereas serum E1-sulfate and E2-sulfate were slightly and inconsistently increased

So the question is.... would a transdermal form of DHEA supplementation be more appropriate than the oral form for individuals known to be low in levels of DHEA/DHEA-S? Is it possible that it is the oral form of DHEA is more likely to convert to / otherwise elevate E2?

Larry

This is an interesting topic to me as well. I've been doing 25mg DHEA orally for a few days now (my DHEA-S baseline level was at the low end of normal) and I've been consistently getting a very good "feel good" effect (maybe the same one that HCG gives?). I know that oral does a better job than transdermal of raising DHEA-S, which is apparently the storage form of DHEA, because of the sulfation that occurs in the liver on first pass from oral. I don't have the worry in my own case about excessive estrogen conversion from oral DHEA, but am worried about ADG (a major metabolite of DHT). The following article/study is the best I've seen so far on oral DHEA:

J Clin Endocrinol Metab. 1999 Jun;84(6):2170-6. [PMID: 10372727]

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.

The author makes a series of statements in which he cites the 1997 Labrie study (above), saying:

"Labrie et al. (19) administered a 20% DHEA cream in a daily dose of 10 mL for 14 days to a total of eight elderly men and women and found no significant increase in serum estrogen levels in either gender. These results differ from the findings of our study and those of Young et al. (18), but may be explained by the route of DHEA administration. As previously reported for transvaginal (20) and sublingual (13) administration of DHEA, Labrie et al. (18) also described an increased DHEA/DHEAS ratio after percutaneous DHEA administration compared to oral ingestion. Although many tissues contain sulfotransferases (21, 22) and may contribute to the peripheral conversion of DHEA to DHEAS, the hepatic sulfotransferase activity seems to be of predominant importance and is bypassed by nonoral DHEA administration due to avoidance of the hepatic first pass effect. An increased DHEA/DHEAS ratio may lead to a reduced conversion of DHEA to androgens and/or estrogens inside peripheral target cells, as DHEAS has a much longer half-life than DHEA, and it can be continuously converted back to DHEA by widespread tissue sulfatase activity (23, 24, 25, 26) followed by further bioconversion. Furthermore, avoidance of the first pass effect by nonoral administration of DHEA also leads to avoidance of hepatic aromatase and 5-reductase activities. This may explain a lack of conversion to estrogens in men as well as the reduced conversion to androgens in women after percutaneous DHEA administration (19). This view is supported by the data of Casson et al. (20), who found an increase in DHEA, but not in DHEAS and T, after transvaginal DHEA administration. Serum estrogen levels were not reported in this study (20).

In agreement with our results, Labrie et al. (19) and Morales et al. (12) found no significant changes in serum T and DHT in their elderly male volunteers, whereas Young et al. (18) in their patients with hypopituitarism (including six men with unreplaced secondary hypogonadism) reported a slight, but significant, increase in serum androgens still below the normal range for men even after the administration of 200 mg DHEA. However, although total T and DHT remained unaffected in our male volunteers, a small, but significant, increase in serum free T was observed. This may be explained by transient interference of DHEA and DHEAS with binding proteins (e.g. competitive binding of DHEA and free T to SHBG or albumin) rather than by changes in binding protein concentrations. Both DHEA and T bind to SHBG and albumin (27, 28), and the rapid increase in DHEA as well as in DHEAS after oral ingestion of DHEA may be sufficient to displace a significant percentage of the protein-bound fraction of T. However, the increase in free T was short-lived and is most likely of minor importance.

Additionally, in our male volunteers a significant increase in serum ADG, a major metabolite of DHT and also of androstenedione, was observed. This may indicate an enhanced conversion of DHEA to androgens inside peripheral target cells that is not reflected by circulating androgen concentrations. A DHEA-induced increase in androgenic capacity in men may be supported by the findings of Yen et al. (13), who described increased muscular strength and decreased body fat mass in men after 6 months of treatment with a daily dose of 100 mg DHEA, but this may also be a consequence of the reported increase in insulin-like growth factor I (13).

In accordance with previous results both in men (12, 19) and women (12, 13, 17, 19, 29), DHEA administration to our male volunteers also led to a significant increase in serum androstenedione. Thus, DHEA induces a significant increase in serum androstenedione in both sexes, but the direction of further bioconversion may differ depending on the surrounding hormonal background, which may affect peripheral 17-hydroxysteroid dehydrogenase, 5-reductase, and aromatase activities."

Full text is available here: http://jcem.endojournals.org/cgi/content/full/84/6/2170
Frank

 

[rgkstl]

Saw palmetto stops testosterone from being converted into DHT and prevents existing DHT from attaching itself to receptors in your prostate.

This may be off base of what you are asking, if so my apoligies.

 

[frankwhardy]

Hi rgkstl,

That's what I'm worried about alright (potential prostate problems), and my experience with saw palmetto hasn't been good so far because of the side effects (headache, congestion, fatigue). The article/study below initially raised the potential ADG concern. (I haven't been able to get a hold of the fulltext.)
Frank

[Abstract:]
Fertil Steril. 2004 Mar;81(3):595-604.

Pharmacokinetics of dehydroepiandrosterone and its metabolites after long-term daily oral administration to healthy young men.

Acacio BD, Stanczyk FZ, Mullin P, Saadat P, Jafarian N, Sokol RZ.

Department of Obstetrics and Gynecology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.

OBJECTIVE: To determine the effects of dehydroepiandrosterone (DHEA) supplementation on the pharmacokinetics of DHEA and its metabolites and the reproductive axis of healthy young men. DESIGN: A prospective, randomized, double-blind, placebo-controlled pharmacokinetic study. SETTING: General Clinical Research Center and laboratories at the Keck School of Medicine of the University of Southern California, Los Angeles, California. PATIENT(S): Fourteen healthy men, ages 18-42 years. INTERVENTION(S): Daily oral administration of placebo (n = 5), 50 mg DHEA (n = 4), or 200 mg DHEA (n = 5) for 6 months. Blood samples were collected at frequent intervals on day 1 and at months 3 and 6 of treatment. MAIN OUTCOME MEASURE(S): Quantification of DHEA, DHEA sulfate (DHEAS), androstenedione, T, E(2), dihydrotestosterone (DHT), and 5alpha-androstane-3alpha-17beta-diol glucuronide (ADG). Physical examination, semen analysis, serum LH, FSH, prostate-specific antigen, and general chemistries were carried out. RESULT(S): Baseline DHEA, DHEAS, and ADG levels increased significantly from day 1 to months 3 and 6 in the DHEA treatment groups but not in the placebo group. No significant changes were observed in pharmacokinetic values. Clinical parameters were not affected. CONCLUSION(S): DHEA, DHEAS, and ADG increased significantly during 6 months of daily DHEA supplementation. Although the pharmacokinetics of DHEA and its metabolites are not altered, sustained baseline elevation of ADG, a distal DHT metabolite, raises concerns about the potential negative impact of DHEA supplementation on the prostate gland.

 

[rgkstl]

Zinc, Vit. E, Selenium, Lycopene and Stinging Nettle are ideal. Briefly here...

Later in life, testosterone can undergo unhealthy changes that can harm your prostate. Zinc may be able to decrease the amount of this 'bad' testosterone your prostate absorbs.

All natural vitamin E is a powerful ally for complete prostate health. And selenium works with vitamin E to protect your cells. Together, they're a powerful defense against cell damage.

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.

In my opinion, vit. E, Selenium and Lycopene not withstanding(as they should always be part of your regimine), Saw and Stinging Nettle are tops. Most good prostate formulas you find on the market will contain these. You can for sure do them as a stand alone though.

 

[pmgamer18]

Hi rgkstl,

That's what I'm worried about alright (potential prostate problems), and my experience with saw palmetto hasn't been good so far because of the side effects (headache, congestion, fatigue). The article/study below initially raised the potential ADG concern. (I haven't been able to get a hold of the fulltext.)
Frank

[Abstract:]
Fertil Steril. 2004 Mar;81(3):595-604.

Pharmacokinetics of dehydroepiandrosterone and its metabolites after long-term daily oral administration to healthy young men.

Acacio BD, Stanczyk FZ, Mullin P, Saadat P, Jafarian N, Sokol RZ.

Department of Obstetrics and Gynecology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.

OBJECTIVE: To determine the effects of dehydroepiandrosterone (DHEA) supplementation on the pharmacokinetics of DHEA and its metabolites and the reproductive axis of healthy young men. DESIGN: A prospective, randomized, double-blind, placebo-controlled pharmacokinetic study. SETTING: General Clinical Research Center and laboratories at the Keck School of Medicine of the University of Southern California, Los Angeles, California. PATIENT(S): Fourteen healthy men, ages 18-42 years. INTERVENTION(S): Daily oral administration of placebo (n = 5), 50 mg DHEA (n = 4), or 200 mg DHEA (n = 5) for 6 months. Blood samples were collected at frequent intervals on day 1 and at months 3 and 6 of treatment. MAIN OUTCOME MEASURE(S): Quantification of DHEA, DHEA sulfate (DHEAS), androstenedione, T, E(2), dihydrotestosterone (DHT), and 5alpha-androstane-3alpha-17beta-diol glucuronide (ADG). Physical examination, semen analysis, serum LH, FSH, prostate-specific antigen, and general chemistries were carried out. RESULT(S): Baseline DHEA, DHEAS, and ADG levels increased significantly from day 1 to months 3 and 6 in the DHEA treatment groups but not in the placebo group. No significant changes were observed in pharmacokinetic values. Clinical parameters were not affected. CONCLUSION(S): DHEA, DHEAS, and ADG increased significantly during 6 months of daily DHEA supplementation. Although the pharmacokinetics of DHEA and its metabolites are not altered, sustained baseline elevation of ADG, a distal DHT metabolite, raises concerns about the potential negative impact of DHEA supplementation on the prostate gland.

I take DHEA and just started back on Saw Palmetto because my DHT when up so high. I take it 2 times a day after a meal have no trouble like that. I did DHEA in a cream and now doing pills 25 mgs. I have not seen my levels go any higher on the cream then the pills but I take it before I eat. That is what my DR. told me to do.

 

[Sunkist]

Two points from my studies:

Oral DHEA is poorly bio available, like 3% so to get much you need major doses. Most studies report little increased levels of any androgen from oral while transdermal may be as high as 30%.

While you are doing the Pub Meds look at a recent study on the increase in HGH from Transdermal DHEA. Very interesting.

I do both a morning and an evening trans DHEA one in conjunction with my trans T. As long as I keep my E and my Cholesterol in check and don't get lazy with what I need to do, my PSA stays on the decimals. It has never been over 1. If I let the E elevate, it elevates with E. As per most studies I have seen of late, BPH has little to do with DHT levels but ratio to Estrogen. If I had BPH I would treat it with increased DHT and antiaromitazes.

 

[1cc]

I find this subject to be very interesting, especially with regard to the possibility that transdermal DHEA does not convert to Estrogen.

What about sublingual DHEA? I would imagine that it also does not convert to Estrogen.

 

[Sunkist]

One of the interesting reported DHEA effects is increase in HGH. I notice the mention of IGF-1 in the study as well. I see reported that oral DHEA, while poorly bio available as DHEA, is an inducer of IGF-1 by its metabloites. Now, is the same IGF-1 effect present in transdermal and if so, is it greater or less than oral doses. I do some oral at bedtime with melatonin, 2 grams of glutamine, 2 grams of argenine and 50 DHEA... strictly for HGH -> IGF-1. I do transdermals of T, Andro, and DHEA for optimal TT and free T, but not for growth factor. If transdermal gives the proper metabolites to induce IGF-1, can I drop the oral? Just thinking.

 

[SPE]

Interesting Side Effect

So I had 15mg/ml compounded into my T Cream and was using .8ml/day. After about a week I broke out(acne) REALLY BAD! I'm talking on my chest, stomach, shoulders, and back. I've been on T since June with hardly a zit. Wonder what could have caused this? Another interesting thing I've noticed is that when I started the transdermal DHEA, I also added synthroid to my armour. Went Hyper real quick. Thing is, I dropped the synthroid and went back to my original armour dosage and I keep going hyper. I'm thinking the increased DHEA had an effect on my thyroid.

 

[1cc]

I'm thinking the increased DHEA had an effect on my thyroid.

I'm sure that it must have had some effect on your thyroid. I know for sure that 7-Keto DHEA, which is a metabolite of DHEA, increases T3.

 

[frankwhardy]

I posted the following on the Yahoo! Hypogonadism2 forum and thought I'd post it here as well:

The 3% oral bioavailability figure for DHEA that is touted about on
different websites is apparently taken from a 1996 rat study (I've
copied the abstract below). There are at least a half-dozen other
actual human studies that show that a 25-50mg oral dose of DHEA gives
a very significant increase in DHEA and (more importantly) DHEA-S
levels, increasing levels from low normal (and even from well below
normal in Addison's patients) to at least mid-range. So obviously,
oral bioavailability is reasonable. In humans, oral bioavailability
is probably more on the order of 10 times 3%, or 30%. Transdermal is
apparently more efficient in elevating serum levels of DHEA, but it
also bypasses first-pass liver sulfation, which means you get less
formation of the storage form, i.e., DHEA-S. My thinking is that
it's nice to have good DHEA numbers, but what you probably really
want is good DHEA-S numbers for the "long haul."
Frank

J Endocrinol. 1996 Sep;150 Suppl:S107-18.

High bioavailability of dehydroepiandrosterone administered
percutaneously in the rat.

Labrie C, Flamand M, Belanger A, Labrie F.

Laboratory of Molecular Endocrinology CHUL Research Center, Quebec,
Canada.

Dehydroepiandrosterone (DHEA) administered percutaneously by twice
daily application for 7 days to the dorsal skin of the rat stimulates
an increase in ventral prostate weight with approximately one third
the potency of the compound given by subcutaneous injection. The
doses required to achieve a 50% reversal of the inhibitory effect of
orchiectomy are approximately 3 and 1 mg respectively. By the oral
route, on the other hand. DHEA has only 10-15% of the activity of the
compound given percutaneously. Taking the bioavailability obtained by
the subcutaneous route as 100%, it is estimated that the potencies of
DHEA by the percutaneous and oral routes are approximately 33 and 3%
respectively. Similar ratios of activity were obtained when dorsal
prostate and seminal vesicle weight were used as parameters of
androgenic activity. When examined on an estrogen-sensitive
parameter, namely uterine weight in ovariectomized rats, the
stimulatory effect of DHEA was much less potent than its androgenic
activity measured in the male animal, a 50% reversal of the
inhibitory effect of ovariectomy on uterine weight being observed at
the 3 and 30 mg doses of DHEA administered by the subcutaneous and
percutaneous routes respectively. When measured on uterine weight,
percutaneous DHEA thus shows a 10% potency compared with the
subcutaneous route. The sulfate of DHEA (DHEA-S), on the other hand,
was approximately 50% as potent as DHEA at increasing ventral
prostate weight after subcutaneous or percutaneous administration.
When the effect was measured on dorsal prostate and seminal vesicle
weight, percutaneous DHEA-S had 10-25% of the activity of DHEA. DHEA
decreased serum LH levels in ovariectomized animals, an effect which
was completely reversed by treatment with the antiandrogen flutamide.
On the other hand, flutamide had no significant effect on the
increase in uterine weight caused by DHEA, thus suggesting a
predominant estrogenic effect of DHEA at the level of the uterus and
an estrogenic effect on the feedback control of LH secretion. The
present data show a relatively high bioavailability of percutaneous
DHEA as measured by its androgenic and/or estrogenic biological
activity in well-characterized peripheral target intracrime tissues
in the rat.

PMID: 8943794 [PubMed - indexed for MEDLINE]

 

[Sunkist]

Good stuff Frank, I had read that study before. I don't have one on human oral DHEA that shows the 30%, just ones that show lower bioavailability. I will take your word for it. Any oral steroid has to get hit with first pass anyway as I understand the physiology, I do believe DHEA may fare better than T or andro. The one study I have that again is interesting is using DHEA to induce a post adolsecent puberty response at very high doses. I have no idea of the entry route. This could be a bogus study... it need to be repeated a few times.

DHEA is a very interesting steroid with documented antiaging properties. I think DHEA/HGH is as important as TRT in maintaining virility in middle aged men. I think this is the future personally, just elevating T is not enough. IGF-1 and Dopamine have to come up as well.

 

[Sunkist]

So I had 15mg/ml compounded into my T Cream and was using .8ml/day. After about a week I broke out(acne) REALLY BAD! I'm talking on my chest, stomach, shoulders, and back. I've been on T since June with hardly a zit. Wonder what could have caused this? Another interesting thing I've noticed is that when I started the transdermal DHEA, I also added synthroid to my armour. Went Hyper real quick. Thing is, I dropped the synthroid and went back to my original armour dosage and I keep going hyper. I'm thinking the increased DHEA had an effect on my thyroid.

Elevated DHT to supraphysiologic levels?

 

[SPE]

That did occur to me but forgot to mention I'm also on proscar 1/4 tab eod.

 

[smitty4]

Zinc, Vit. E, Selenium, Lycopene and Stinging Nettle are ideal. Briefly here...

Later in life, testosterone can undergo unhealthy changes that can harm your prostate. Zinc may be able to decrease the amount of this 'bad' testosterone your prostate absorbs.

All natural vitamin E is a powerful ally for complete prostate health. And selenium works with vitamin E to protect your cells. Together, they're a powerful defense against cell damage.

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.

In my opinion, vit. E, Selenium and Lycopene not withstanding(as they should always be part of your regimine), Saw and Stinging Nettle are tops. Most good prostate formulas you find on the market will contain these. You can for sure do them as a stand alone though.

What do you mean that, "Later in life, testosterone can undergo unhealthy changes," and just what exactly is "bad testosterone?" Bad forms of Estrogen metabolites can have a negative impact on your prostate, but I don't recall ever reading anything about "bad testosterone". If it does exist, please provide some research about it. Otherwise, I am afraid you may be giving some misleading information.

 

[stat1951]

Thanks, Smitty, was going to ask the same thing....

"Bad" testosterone?

Changes later in life?

Later in life, testosterone can undergo unhealthy changes

Also, in regard to:

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.

Yes, stinging nettles can help inhibit aromatase to some extent - and also (I believe) reduce DHT levels, but actual clinical trials have shown that stinging nettles supplementation will INCREASE the amount of free T in the blood (if interested, try doing a search as I am sure that I posted that study previously).

Sounds like "Quack Science" to me.

I would like to see the links to these types of claims and specifically what research and studies were shown to have proven this!

As to the oral DHEA versus transdermal cream DHEA question, I have also seen the studies that have disputed the oft-claimed 3% bioavailability levels of oral supplementation. As reported, that 3% level was noted in a study performed with rats whereas human studies have repeatedly shown significant increases in blood DHEA levels following oral consumption (even when doses were very moderate as in the 10 mg range). I also believe that when oral DHEA supplements are metabolized that they primarily metabolize to DHEA-S which has a much longer half life (and is, I believe, converted to DHEA then as the body needs it).

Not sure that those specific studies are outlined in here, but this is a good overall info source on DHEA:

http://home.caregroup.org/clinical/altmed/interactions/Nutrients/DHEA.htm

One of the specific studies of note was this one:

Morales AJ, Nolan JJ, Nelson JC et al. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab. 1994; 78:1360-7.

In a randomized, placebo-controlled, crossover trial, 30 patients ages 40-70 years were given 50 mg of DHEA orally daily. Within two weeks, this dose restored serum DHEA levels in both men and women to those found in young adults.

Obviously more than 3% of the oral dosage was "bioavailable" to get those kind of results in two weeks!

Meanwhile... Hmmm... "bad" testosterone....

Larry

 

[Sunkist]

I saw a postulation once that after first pass degredation the metabolites initiated the production of DHEA by the body... not the actual absorption of the original DHEA. I believe any oral steroid gets killed in the liver even if it is absorbed from the gut. The study I had on that pointed to the fact that the increase in DHEA is not immediate... and it remains high for a good while after oral doses are ended.

It actually makes little difference where it comes from. I do take 50 mg at bed orally with melatonin, folic and mega argenine and glutamine. I also do transdermal andro and DHEA after the morning shower. I don't want all my T to come from external sources.

I do know that a lot of work is being done on DHEA now... if we can keep it legal.

 

[1cc]

This study analyzes in detail the serum concentration of the active androgens and estrogens, as well as a series of free and conjugated forms of their precursors and metabolites, after daily application for 2 weeks of 10 mL 20% dehydroepiandrosterone (DHEA) solution on the skin to avoid first passage through the liver.

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?

No consistent change was observed in serum estrone (E1) or estradiol (E2) in men receiving DHEA, whereas serum E1-sulfate and E2-sulfate were slightly and inconsistently increased by about 20%, and serum cortisol and aldosterone concentrations were unaffected by DHEA administration.

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?

 

[1cc]

It actually makes little difference where it comes from. I do take 50 mg at bed orally with melatonin, folic and mega argenine and glutamine. I also do transdermal andro and DHEA after the morning shower. I don't want all my T to come from external sources.

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

 

[stat1951]

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?

Personally I would like to see some more extensive testing of the transdermal variants before committing to how well it did or did not effect estradiol / estrogen levels. The couple of tests that I know of involving oral DHEA lasted a number of months (as I recall).

I bring it up for this reason (quoting from the study of transdermal DHEA):

This study analyzes in detail the serum concentration of the active androgens and estrogens, as well as a series of free and conjugated forms of their precursors and metabolites, after daily application for 2 weeks of 10 mL 20% dehydroepiandrosterone (DHEA) solution

Two weeks?

When I first posted on this topic I had hoped that someone was aware of a more comprehensive (time-wise) test or that I could possibly find one lasting more time, but no success so far.

Very interesting topic.

Larry