hardasnails1973
New Member
After looking into this topic for a long time. I found a few places where it has been noted it does. I think that its really the carrier that is the main reason it has not been able to be properly measured in the blood. Since switching to a lipodermn base Dhea gel, I notice there is a greater increase in what appears to be some estrogenic like sides effects even at 25 mgs. Another thing I notice is that I do not get the sensations of fuller muscles when I apply it to the forearms vs shoulder. I know it should be applied to forearm due increased absorption, but i am just reporting my response. I was applying it on forearms for over 5 days but then immediately I swtich to the shoulder felt increased muscle fullness. It could have just been a fluke and was just the gel actually starting to build in my body..
Now my questions are
1. How fast does Dhea TD get absorbed in the system?
After speaking to a few compounding pharmacists they noted that TD Dhea should be able to me measured with in 10-14 days after application in urine..
2. If a person has been on cortef for many years comes off of it and has no issue, is there a possibility DHEA levels been suppressed with cortef may actually come back into normal range where supplementation would not be needed? Phil and I talked about this and it seems plausible. I like to get others imput on this topic.
3. Do I really need the TD dhea? I had my DHEA urine measured while on 20 mgs cortef. Was the cortef causing decreased DHEA in urine? My last urine readings on 25 mgs of TD DHEA were 1.4 (.4-7) dhea 24 hour.
If one should stop it what time frame should one test to get inaccurate readings?
The interesting thing about this study was the slight modification in the carrier improved the results dramatically.
Once a person is using a more absorbable gel could dhea-s be potential be measured in dhea-s serum ? These 2 study seems to support it.
Transdermal Delivery Of Dehydroepiandrosterone
EXAMPLE 16
Transdermal Administration of a Composition Containing Dehydroepiandrosterone and Phosphatidylcholine
BJR, a 46 year old postmenopausal woman had a long history of fatigue, anxiety, decreased libido, cellulite, and was mildly overweight and otherwise in apparent good health. She volunteered to test the effects of topical lecithin-DHEA. A
fasting blood sample was drawn on day 1 through day 21 for complete blood count, chemistry panel and dehydroepiandrosterone sulfate serum levels.
She was given the following instructions.
1) Apply 30 ml (one tablespoon) of the cream to each thigh and rub it in well every morning for three weeks.
2) Wait for at least two hours before washing off the unabsorbed material on the skin.
The cream provided to her had the following composition:
______________________________________ Phosphatidylcholine 250 ml Ethanol 75 ml Cetyl alcohol 10 ml Distilled water 60 ml Medium chain triglycerides 10 ml DHEA 1000 mg ______________________________________
BJR returned every third day for analysis.
Over three weeks she related a progressive sense of well being, increased energy and libido, and diminished anxiety. Objectively there was a three pound weight loss and somewhat less cellulite.
Baseline level of DHEA sulfate was 1.8 micrograms/ml. After 10 days and thereafter the serum DHEA sulfate level was over 4 micrograms/ml. There was no change in her complete blood count or liver function tests. There was also no staining or
discoloration of her skin or clothing at any time during or after administering the composition.
The results of this example provide positive evidence of successful transdermal administration of DHEA to a person in accordance with this invention
EXAMPLE 17
Transdermal Administration of a Composition Containing Dehydroepiandrosterone and Phosphatidylcholine and Attempted Transdermal Administration of Dehydroepiandrosterone Without Phosphatidylcholine
RRR, a 69 year old postmenopausal woman in apparent good health volunteered to try four different topical creams for two weeks at a time. Serum levels of DHEA were taken after seven and fourteen days.
1) Topical DHEA in cold cream (30 ml on two sites daily for two weeks) produced no change in serum DHEA levels.2)
Topical DHEA in aromatic carbocyclic permeation enhancer 10% concentration of DHEA in 30 ml on two sites daily for two weeks produced no change in serum DHEA levels.
3) Topical DHEA in aliphatic carbocyclic permeation enhancer with 10% concentration of DHEA in 30 ml on two sites daily for two weeks produced no change in serum DHEA levels.
4) Topical DHEA-phospholipid 10% concentration of DHEA in 30 ml on two sites daily produced a doubling of the baseline serum concentration by the 14th day.
The results of this example provide evidence of the unexpected advantage of phospholipid used together with DHEA to effect dramatically increased serum levels of DHEA.
Another one.
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.
I would be curious to see what transdermal carrier they used gel or cream for the last study..
Now my questions are
1. How fast does Dhea TD get absorbed in the system?
After speaking to a few compounding pharmacists they noted that TD Dhea should be able to me measured with in 10-14 days after application in urine..
2. If a person has been on cortef for many years comes off of it and has no issue, is there a possibility DHEA levels been suppressed with cortef may actually come back into normal range where supplementation would not be needed? Phil and I talked about this and it seems plausible. I like to get others imput on this topic.
3. Do I really need the TD dhea? I had my DHEA urine measured while on 20 mgs cortef. Was the cortef causing decreased DHEA in urine? My last urine readings on 25 mgs of TD DHEA were 1.4 (.4-7) dhea 24 hour.
If one should stop it what time frame should one test to get inaccurate readings?
The interesting thing about this study was the slight modification in the carrier improved the results dramatically.
Once a person is using a more absorbable gel could dhea-s be potential be measured in dhea-s serum ? These 2 study seems to support it.
Transdermal Delivery Of Dehydroepiandrosterone
EXAMPLE 16
Transdermal Administration of a Composition Containing Dehydroepiandrosterone and Phosphatidylcholine
BJR, a 46 year old postmenopausal woman had a long history of fatigue, anxiety, decreased libido, cellulite, and was mildly overweight and otherwise in apparent good health. She volunteered to test the effects of topical lecithin-DHEA. A
fasting blood sample was drawn on day 1 through day 21 for complete blood count, chemistry panel and dehydroepiandrosterone sulfate serum levels.
She was given the following instructions.
1) Apply 30 ml (one tablespoon) of the cream to each thigh and rub it in well every morning for three weeks.
2) Wait for at least two hours before washing off the unabsorbed material on the skin.
The cream provided to her had the following composition:
______________________________________ Phosphatidylcholine 250 ml Ethanol 75 ml Cetyl alcohol 10 ml Distilled water 60 ml Medium chain triglycerides 10 ml DHEA 1000 mg ______________________________________
BJR returned every third day for analysis.
Over three weeks she related a progressive sense of well being, increased energy and libido, and diminished anxiety. Objectively there was a three pound weight loss and somewhat less cellulite.
Baseline level of DHEA sulfate was 1.8 micrograms/ml. After 10 days and thereafter the serum DHEA sulfate level was over 4 micrograms/ml. There was no change in her complete blood count or liver function tests. There was also no staining or
discoloration of her skin or clothing at any time during or after administering the composition.
The results of this example provide positive evidence of successful transdermal administration of DHEA to a person in accordance with this invention
EXAMPLE 17
Transdermal Administration of a Composition Containing Dehydroepiandrosterone and Phosphatidylcholine and Attempted Transdermal Administration of Dehydroepiandrosterone Without Phosphatidylcholine
RRR, a 69 year old postmenopausal woman in apparent good health volunteered to try four different topical creams for two weeks at a time. Serum levels of DHEA were taken after seven and fourteen days.
1) Topical DHEA in cold cream (30 ml on two sites daily for two weeks) produced no change in serum DHEA levels.2)
Topical DHEA in aromatic carbocyclic permeation enhancer 10% concentration of DHEA in 30 ml on two sites daily for two weeks produced no change in serum DHEA levels.
3) Topical DHEA in aliphatic carbocyclic permeation enhancer with 10% concentration of DHEA in 30 ml on two sites daily for two weeks produced no change in serum DHEA levels.
4) Topical DHEA-phospholipid 10% concentration of DHEA in 30 ml on two sites daily produced a doubling of the baseline serum concentration by the 14th day.
The results of this example provide evidence of the unexpected advantage of phospholipid used together with DHEA to effect dramatically increased serum levels of DHEA.
Another one.
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.
I would be curious to see what transdermal carrier they used gel or cream for the last study..
