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The PCT to end all!!???

KillerStack said:
Just shoot it subcutaneously like hGH. You don't have to shoot it IM.

Really, so you can shoot it in your gut as well?
Learning new things everyday.
 
The Wolf said:
Really, so you can shoot it in your gut as well?
Learning new things everyday.

Uh yes, I would actually probably call this common knowledge on most of the boards bro....you need to research a little bit more I think.
 
DHEA is probably not a good idea, especially at a higher dosage. You don't want to ingest any suppressive compounds when you already have trouble recovering.

Why take DHEA?

One study conducted said that it is possible that anabolic steroids inhibit the immunomodulatory and antiviral activities of androgens like DHEA (acts on adrenal glands to induce the production of corticosteroids and dehydroepiandrosterone) (Hughes, Rady, Smith; 1998). Also, this study further indicated that anabolic steroids significantly inhibited the production of corticotrophin in blood lymphocytes immediately following a viral infection. Simply stated, they can cause the prevention of antibodies when you get sick and lead to altered immune reactions.

Also here is an insert from a 7-Keto DHEA product that explains alot of bennefits. I was referring to 7-Keto DHEA use also not regular DHEA. I should have been more clear. I have had great results using it.

Most anyone around for the past 10 years is aware of the naturally occurring steroid DHEA (Dehydroepiandrosterone). When adequate amounts are present I the body its positive effects are changes in the immune system, inflammation, lipid and carbohydrate metabolism, anticarcinogenic effects, neuroprotection, and antioxidant effects. Obviously good for recovery and general lean body mass, huh? So just take lots of DHEA, right? Nope! Most of the positive biological actions of DHEA likely are not due to DHEA itself, but its metabolites. This is due to some rather interesting facts: Specific metabolites of DHEA share its properties but are significantly stronger. The direct mechanism of action of DHEA has not been identified in the endless research available. This shows us that the metabolites are the goodies responsible for its effects. It is well proven that large doses are generally required for DHEA to have an effect in animal studies, indicating that it may function as a precursor to more active steroids such as the metabolites we are working with.
Well-structured research studies have recently identified a number of DHEA metabolites which do not convert to androgens or estrogens or interact with sex steroid receptors. However they do posses the best of the in vivo properties of DHEA, such as increased thermogenesis, increaded immune response, neuroprotection and memory improvement, and improved overall cardiovascular health. Without doubt the most important of these are 7alpha-hydroxy-DHEA 7-oxo-DHEA (also known as the patented product 7-keto-DHEA), and 7beta-hydroxy-DHEA. Among the DHEA derivatives, the patented 7-oxo-DHEA is most readily available as a supplement. However 7-oxo-DHEA is converted into both 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA in humans, and in human liver microsomes, this occurs at an approximately 1:2 ratio. Both of these steroids can also be converted back into 7-oxo-DHEA thus supporting better efficiency and synergy from the 7alpha-hydroxy-DHEA and 7beta-hydroxy-DHEA metabolites than from the 7-oxo-DHEA metabolite itself. Credit and patent rights for these two superior DHEA metabolite finds goes to a rather bright lad at Designer Supplements. So why did we replace 7-oxo-DHEA with 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA? Simple: Does it make good sense to use a supplement you "hope" will turn into something in your body, or is it obviously more effective to just use the actual synergistic active compounds? Please do not get me wrong: 7-oxo-DHEA is a wonderful and effective supplement. But why take it to help the body make more 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA.
So What's The Take Home Facts Here?
7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA are wonderful compounds that serve two roles in the Impact Ultra matrix. I already discussed the ugly effects that cortisol can have for us iron addicts, and the role that PS plays in blunting some of it's release. However, 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEAare also happy to provide some cortisol controlling contributions!
* More Cotisol Control
* Both 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA are more potent than DHEA in enhancing immune response and counteracting glucocorticoid-induced immunosuppression meaning that cortisol just loses out to better chemistry.
There is an interesting method of action here, in that there is an enzyme in the liver called 11 beta-hydroxysteroid dehydrogenase (11betaHSD1), whose role it is to convert inactive glucocorticoids to their active form, such as the conversion of cortisone to cortisol. Well, it seems that 7alpha-Hydroxy-DHEA, 7beta-Hydroxy-DHEA and 7-oxo-DHEA interchanging metabolites compete with the inactive glucocorticoids for the 11betaHSD1 enzyme, thus blocking some of the body's ability to make cortisol. While not as strong as a cortisol blocker as PS, 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA certainly provide a nice jab before PS throws the knockout punch!
Improved Fat Loss Synergy
The second role that new 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA are so generous to provide is potent lipolytic capabilities. Yup, this stuff also burns fat! This helps prevent the normal and post cycle accumulation of adipose tissue, allowing you to keep that lean, hard look we all work are asses off to get! There are several possible mechanisms of action here that I will just briefly touch on, cause I know that by now you must be chomping at the bit to get your own supply of Impact Ultra. The first lies in the potentiation of thyroid hormone activity and an increase in levels of triiodothyronine, also known as the fat burning thyroid hormone T-3. And you all know what a powerful fat burning agent T3 is! Another study examined the association between natural 7beta-Hydroxy-DHEA levels and T3 levels in 152 men and women, and found them to be significantly correlated, indicating a possible link between the two factors meaning that superior levels of 7beta-Hydroxy-DHEA optimize natural thyroid function for a better lean mass environment. 7alpha-Hydroxy-DHEA also administration resulted in significant decreases in body weight in rats and a better ratio of lean mass. This is an effect that was greater than that of DHEA itself. However, in a study in monkeys, 7-oxo-DHEA failed to have an effect on body weight over the course of a month.
Next, 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA have been shown to up-regulate thermogenic enzymes in the liver, effectively enhancing calorie burning and use of fat for fuel. The third mechanism by which these two advanced substrates seem to work their fat-melting magic is induction of PPAR receptors. This can have multiple effects leading to fat loss, including increased mitochondrial uncoupling, regulation of genes that play a role in lipid metabolism, and an increase of L-carnitine levels in various body tissues. No doubt about it, 7alpha-Hydroxy-DHEA and 7beta-Hydroxy-DHEA bitch'n cortisol blocking, fat incinerating compounds!

Why are adrenal glands taxed hard during a cycle?
The hypothalamic-pituitary-adrenal/gonadal axis (HPA) and the peripheral nervous system are all connected and influenced with steroid use.


The hypothalamus is an area of the brain that produces the "controlling" hormones. These hormones regulate body processes such as metabolism, and control the release of hormones from glands like the thyroid, the adrenals and the gonads (testes or ovaries).

Adrenal glands, which are also called suprarenal glands, are small, triangular glands located on top of both kidneys. An adrenal gland is made of two parts: the outer region is called the adrenal cortex and the inner region is called the adrenal medulla.The adrenal glands work interactively with the hypothalamus and pituitary gland in the following process:
The hypothalamus produces corticotropin-releasing hormones, which stimulate the pituitary gland. The pituitary gland, in turn, produces corticotropin hormones, which stimulate the adrenal glands to produce corticosteroid hormones.
One of these hromones is (ACTH), which controls the secretion of steroid hormones by the adrenal cortex, which affects glucose, protein, and fat metabolism.

The reproductive axis is inhibited at all levels by various components of the HPA axis when using steroids.
 
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Try this link to see how the hypothalamic-pituitary-adrenal/gonadal axis (HPA) functions.

**broken link removed**
 
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HELLA SWOLE said:
Uh yes, I would actually probably call this common knowledge on most of the boards bro....you need to research a little bit more I think.

Yes bro I understand, but my wife whos a nurse told me its IM and she showed me the instructions written in Turkish of course and it said, once mixed must be used immediately and must be used IM. It kinda contradicts what you guys have been saying but I guess we use it differently to the medical people which they use it on women.:confused:
 
HELLA SWOLE said:
Uh yes, I would actually probably call this common knowledge on most of the boards bro....you need to research a little bit more I think.

Yes bro I understand, but my wife whos a nurse told me its IM and she showed me the instructions written in Turkish of course and it said, once mixed must be used immediately and must be used IM. It kinda contradicts what you guys have been saying but I guess we use it differently to the medical people which they use it on women.:confused: btw the make is Pregnyl.
 
The Wolf said:
Yes bro I understand, but my wife whos a nurse told me its IM and she showed me the instructions written in Turkish of course and it said, once mixed must be used immediately and must be used IM. It kinda contradicts what you guys have been saying but I guess we use it differently to the medical people which they use it on women.:confused: btw the make is Pregnyl.
I've always done mine IM with a slin pin in the forearm. Thin skin, right into the muscle. Easy. It should keep for a few weeks after being reconstituted but it will degrade of course. HCG (Pregnyl) is used for women AND men. It's a gonadatropin. It will stimulate the gonads in women and men...

Wolf, what are you doing in Turkey? Don't ever try to smuggle hashish across the border Billy! Oh, Bill-eeee!
 
OuchThatHurts said:
I've always done mine IM with a slin pin in the forearm. Thin skin, right into the muscle. Easy. It should keep for a few weeks after being reconstituted but it will degrade of course. HCG (Pregnyl) is used for women AND men. It's a gonadatropin. It will stimulate the gonads in women and men...

Wolf, what are you doing in Turkey? Don't ever try to smuggle hashish across the border Billy! Oh, Bill-eeee!

Been watching too much midnight express eh? Lol actually my father is of Turkish origin and he decided to move back to Turkey and Northern Cyprus after spending half a century in London. He invited me and made me an offer I couldnt refuse;) Still sometimes I wish I stayed in London.

Anyway slin pin in the forearm? Im learning something new all the time, I suppose you never stop learning in this bussiness.
 
The Wolf said:
Yes bro I understand, but my wife whos a nurse told me its IM and she showed me the instructions written in Turkish of course and it said, once mixed must be used immediately and must be used IM. It kinda contradicts what you guys have been saying but I guess we use it differently to the medical people which they use it on women.:confused: btw the make is Pregnyl.

Don't get me wrong, you CAN inject IM, but the norm is usually Sub-Q Although I do not believe it matters too much. The fact that you didn't know that you could inject HCG Sub-Q into the gut gave me reason to believe that you really hadn't researched a lot. I am not flaming you I am just trying to look out for you and make sure you know everything you need to in order to use these drugs safely.
 
HELLA SWOLE said:
Don't get me wrong, you CAN inject IM, but the norm is usually Sub-Q Although I do not believe it matters too much. The fact that you didn't know that you could inject HCG Sub-Q into the gut gave me reason to believe that you really hadn't researched a lot. I am not flaming you I am just trying to look out for you and make sure you know everything you need to in order to use these drugs safely.

Thanks bro, I know that you were looking out for me. Hcg I suppose was one drug that I thought was so simple that I didnt have to research on it. After I spoke with a few competetive bodybuilders at my gym today even they were suprised that you could inject it sub-q. From day one my mentor in London told me I should take it twice at the end of a cycle at 5000ius a shot and I never looked back since. Now of course thanks to you guys Im getting more clued up and also educating these eastern european bros as well, which after a bit of knowledge they might actually get somewhere in bodybuilding for a change instead of all that powerlifting crap that they do, lol!
 
Gotta say thanks to all of you who have provided valuable input into this topic as well as some thought into the future of PCT protocols. I think the common "PCT" is extremely understated and in my mind, is probably more important than any other aspect of the typical AAS cycle. Who wants to dish out $$$ on gear, food and a gym membership, bust ass day in and day out and tax their bodies to quite a significant degree, to finally reach a state of anabolism (growth) to only 'come off' and lose it ALL! Sound's dramatic BUT it happens! I don't have the correct PCT protocol and it seems that most of us are "shooting dice in the dark" so to speak. There seems to be some valid theories out there but that's all they are, theories! The most prominent seems to be low doses of HCG (250 - 1000 iu's) EOD, Clomid OR Nolvadex (but never both) and Proviron (Mesterolone). These seem to be the most favorable among the "athlete's" I've discussed this with, with some variation on time (how long you run the PCT). Most are in favor of using HCG longer as opposed to increasing the dose over 1000 units. Clomid/Nolvadex seems to be all about preference! Some BB's hate Clomid and some find it VERY effective and would never come off a cycle without Clomid on hand.

ALL of your responses are welcomed and appreciated as this topic STILL has a "large Grey" area surrounding it and we all would love to know that what we're doing PCT, is not only helping to retain our hard earned mass but more importantly, helping our bodies reach a level of hormonal homeostasis.
JD~
 
STEEDA69 said:
Gotta say thanks to all of you who have provided valuable input into this topic as well as some thought into the future of PCT protocols. I think the common "PCT" is extremely understated and in my mind, is probably more important than any other aspect of the typical AAS cycle. Who wants to dish out $$$ on gear, food and a gym membership, bust ass day in and day out and tax their bodies to quite a significant degree, to finally reach a state of anabolism (growth) to only 'come off' and lose it ALL! Sound's dramatic BUT it happens! I don't have the correct PCT protocol and it seems that most of us are "shooting dice in the dark" so to speak. There seems to be some valid theories out there but that's all they are, theories! The most prominent seems to be low doses of HCG (250 - 1000 iu's) EOD, Clomid OR Nolvadex (but never both) and Proviron (Mesterolone). These seem to be the most favorable among the "athlete's" I've discussed this with, with some variation on time (how long you run the PCT). Most are in favor of using HCG longer as opposed to increasing the dose over 1000 units. Clomid/Nolvadex seems to be all about preference! Some BB's hate Clomid and some find it VERY effective and would never come off a cycle without Clomid on hand.

ALL of your responses are welcomed and appreciated as this topic STILL has a "large Grey" area surrounding it and we all would love to know that what we're doing PCT, is not only helping to retain our hard earned mass but more importantly, helping our bodies reach a level of hormonal homeostasis.
JD~
I hope what is taken away from the thread at least is that these are all organic compounds that have a direct effect on your body chemistry. Since every single person's body chemistry is different, there is unlikely to be a therapy that is right for everyone. You could give 100 people a given amount of testosterone or clomid or rHGH and you'd have 100 different responses. There would probably be a Gaussian curve (bell shaped) that the majority of people would fall in to the center but you cannot predict where on that curve you would fall. You know what else will create a Gaussian curve? Repeatedly rolling a pair of dice. The curve for a pair of dice is bell shaped because more combinations can produce a 5,6, or 7 than say, a 2 or a 12.

Am I equating what we're dicussing to a roll of the dice? Possibly. I'm just saying that the effects (or results) would have the same curve. There's no reason that I've seen or read yet to assume that clomiphene and tamoxifen taken in conjunction with each other would have bad results. In fact, for some, the results might prove favorable. It's impossible to ever know for sure.

On another board we were discussing Ockhams Razor. Rather than rolling the dice with no knowledge, learn as much as you can so you can understand what will be an effective therapy for most people and then work from there. Trial and error? Definitely. Unscientific? Of course not.
 
The Wolf said:
Yes bro I understand, but my wife whos a nurse told me its IM and she showed me the instructions written in Turkish of course and it said, once mixed must be used immediately and must be used IM. It kinda contradicts what you guys have been saying but I guess we use it differently to the medical people which they use it on women.:confused: btw the make is Pregnyl.
Yes, it says IM. However, some HRT docs like John Crisler aka "SWALE" have their patients inject it subcutaneously. Also if you look at pubmed the drug has been used SC in studies.

Regarding the stability rxlist.com says:
Reconstituted solution is stable for 60 days when refrigerated.
http://www.rxlist.com/cgi/generic/chorionic_ids.htm

Whenever taking a new drug I would suggest reading the prescribing info. I see a lot of posts here about whether this or that side is due to some new drug they are taking. Why not read the prescribing info to see if it's a reported side first? Makes sense to me. :)
 
Good link KillerStack:)
 
PCT TO END ALL

:D OK, for the PCT to end all!

Well I am going to take an eclectic approach to my PCT from the various protocols out there. My PCT would look something like this.

HCG 250-500iu throughout cycle 2 consecutive days a week up to 2 weeks past last injection
Clomid 50mg twice a day (100mg total) for 30 days starting week after last injection.
Nolvadex 20mg for 45 days starting week after last injection.
7-Keto DHEA,25- 50 mg a day up to 60 days after last injection
Phosphatidylserine capsules, 600 mg a day up to 60 days after last injection
Piracetam if felt needed between 3-6gm a day for 30 days after last injection
Bromcriptine 1.5mg ed up to 4 weeks after last injection
Vitamin E I already take 1000mg ed anyhow



I feel if one is serious about PCT the only way to really tell what you need is to get blood work done.You can determine if your DHEA is low along with other hormones. Many people don’t recover from typical PCT because they have high prolactin levels. Blood test would determine this and then something like bromocriptine could be in cooperated into the PCT. I can bet a lot of users prolactin levels are high after a cycle and it is not being addressed.
 
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dragonfire101 said:
:D OK, for the PCT to end all!

Well I am going to take an eclectic approach to my PCT from the various protocols out there. My PCT would look something like this.

HCG 250-500iu throughout cycle 2 consecutive days a week up to 2 weeks past last injection
Clomid 50mg twice a day (100mg total) for 30 days starting week after last injection.
Nolvadex 20mg for 45 days starting week after last injection.
7-Keto DHEA, 50 mg a day up to 60 days after last injection
Phosphatidylserine capsules, 600 mg a day up to 60 days after last injection
Piracetam if felt needed between 3-6gm a day for 30 days after last injection
Bromcriptine 1.5mg ed up to 4 weeks after last injection
Vitamin E I already take 1000mg ed anyhow
Looks pretty good. Looks like you've done your research and are placing your money on what looks like a good course of therapy. The results will probably be positive for you, having done your homework. My own therapy is not much different from yours:

HCG 250iu EOD month on, month off. Last month of cycle on.
- This should keep your leydig cells from becoming dormant and ensure that they are ready to continue to produce test after you have stopped supplementing your natural levels.

Nolvadex 40mg/day for two weeks, 30, 20, 10mg, in the weeks immediatedly following your cycle.
- This should be enough to create a feedback loop for your hypothalamus and pituitary to begin to produce their own FSH and LH again as they will have most assuredly stopped.

Arimidex - 1mg ED, .5mg ED (two to three weeks each strating immediately after cycle)
- This should be sufficient to lower your estrogen levels to ensure that your test:estro ratio is closer to what a man's should be (I think it's 20-50:1)

Dostinex - 500mcg, twice per week
- Lower the increased levels of prolactin

Intense workouts - continue workouts as intense as possible with major movements. This will help you maintain your size while nudging your body to produce the chemicals that you are trying to regain.

You should have no need for HCG post cycle unless you finish this entire therapy and your testicles are still continuing to shrink. If they are, wait a month and repeat the entire protocol including HCG as if you were coming off again.

HCG is inhibitory so use only while you're HPTA is shut down. Everything else regarding your adrenal glands and DHEA is something I haven't studied enough. You adrenal glands produce only a small fraction of your total test and exogenous DHEA may be inhibitory itself. But now that it is brought up, I will look more into into it definitely. Earlier in this thread, I described what worked for me. I'm thinking Dostinex would have helped had I thought of it. In any case, it sure is good to be back to normal.
 
Last year when I was shut down and even firing blanks at one point, my prolactin was very high and they thought I might have a tumour and they mentioned bromocriptine to bring the tumour down, if it didnt need an op. However it was the good old juice and a few months after everything was back to normal but the endocrine didnt give me anything, he said leave it and let it fix it itself.
 
Everything else regarding your adrenal glands and DHEA is something I haven't studied enough. You adrenal glands produce only a small fraction of your total test and exogenous DHEA may be inhibitory itself.


One study conducted said that it is possible that anabolic steroids inhibit the immunomodulatory and antiviral activities of androgens like DHEA (acts on adrenal glands to induce the production of corticosteroids and dehydroepiandrosterone) (Hughes, Rady, Smith; 1998). Also, this study further indicated that anabolic steroids significantly inhibited the production of corticotrophin in blood lymphocytes immediately following a viral infection. Simply stated, they can cause the prevention of antibodies when you get sick and lead to altered immune reactions.



Well-structured research studies have recently identified a number of DHEA metabolites which do not convert to androgens or estrogens or interact with sex steroid receptors. However they do posses the best of the in vivo properties of DHEA, such as increased thermogenesis, increased immune response, neuro protection and memory improvement, and improved overall cardiovascular health. Without doubt the most important of these are 7alpha-hydroxy-DHEA 7-oxo-DHEA (also known as the patented product 7-keto-DHEA), and 7beta-hydroxy-DHEA. Among the DHEA derivatives

OTH though you might find this interesting article below. I coundn't pull up the abstarct though. Think you have to $ for it.

Dehydroepiandrosterone may also be an important protective hormone, mitigating the adverse effects of dysregulation of the HPA axis. (Australian and New Zealand Journal of PsychiatryVolume 40 Issue 9 Page 722 - September 2006
To cite this article: Richard Porter (2006) The hypothalamic-pituitary-adrenal axis: a target for intervention in early psychosis? Australian and New Zealand Journal of Psychiatry 40 (9), 722–724.)

Found this interesting read below on HPA and alcohol.

EFFECTS OF ACUTE ALCOHOL INTOXICATION ON PITUITARY–GONADAL AXIS HORMONES, PITUITARY–ADRENAL AXIS HORMONES, ß-ENDORPHIN AND PROLACTIN IN HUMAN ADULTS OF BOTH SEXES

J. Frias1, J. M. Torres, M. T. Miranda2, E. Ruiz and E. Ortega,*
Department of Biochemistry and Molecular Biology and Institute of Neurosciences, School of Medicine,
1 Trauma Emergency Department, Virgen de las Nieves University Hospital and
2 Department of Biostatistics, School of Medicine, University of Granada, Avda. de Madrid, s/n, 18012, Granada, Spain
Received 9 March 2001; in revised form 16 July 2001; accepted 20 August 2001
— The effects of acute alcohol intoxication (AAI) on the pituitary–gonadal axis hormones, and the possible contribution of pituitary–adrenal axis hormones, ß-endorphin and prolactin to alcohol-induced dysfunction of pituitary–gonadal axis hormones were studied in adult men and women. Blood samples were drawn from adults of both sexes who arrived at the emergency department with evident behavioural symptoms of drunkenness (AAI) or from adult volunteers with nil consumption of alcohol (controls). Our results demonstrated that AAI produces a high increase in plasma prolactin, corticotropin (adrenocorticotropic hormone, ACTH), and cortisol in adults of both sexes, a decrease in luteinizing hormone levels only in men, an increase in dehydroepiandrosterone-sulphate (DHEAS) and a contradictory behaviour of testosterone according to gender, with increased plasma testosterone in women and a decrease in men. ACTH and prolactin correlated positively with cortisol, DHEAS and testosterone in women, which suggests that prolactin and ACTH could contribute to stimulated adrenal androgen production. In contrast, the decrease in testosterone and increase in ß-endorphin in men suggests that AAI could have an inhibitory effect on testicular testosterone, perhaps mediated by ß-endorphin. Our results suggest that the effect of alcohol on pituitary–gonadal axis hormones in humans could depend on the gender and degree of sexual maturity of the individual.


Full text here

http://hera.ugr.es/doi/15003371.pdf
 
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Good DHEA read with referances sited.

DHEA, the next generation
by James South MA

Dehydroepiandrosterone (DHEA), in its sulphated form (DHEA-S), is the most plentiful adrenal steroid circulating in the human bloodstream. Along with the major human glucosticoid, cortisol, DHEA is produced in the adrenal cortex. DHEA circulates primarily as DHEA-S, which is generally metabolically inactive. As cells take DHEA-S from the blood, they reconvert it into DHEA, and possibly other metabolites. The pregnenolone metabolite, 17-hydroxypregnolone, is the common parent molecule for both DHEA and cortisol.(2) Humans, along with some other primates, are unique in having adrenals which secrete large amounts of DHEA/DHEA-S.(1) "Adrenal secretion of DHEA and DHEA-S increases in children at the age of 6 - 8 yr, and maximal values of circulating DHEA-S are reached between the ages of 20-30 yr. Thereafter, serum DHEA and DHEA-S levels decrease progressively. In fact, at 70 yr of age, serum DHEA-S levels have decreased to approximately 20% of their peak values, and they further decrease to only 5% [of their peak values] by the age of 85-90 yr. It is remarkable that up to 60% of the age-related decrease in serum DHEA and DHEA-S concentration, however, takes place before the age of 50-60 yr." (1)

There have been literally thousands of scientific articles published on the metabolic and health properties of DHEA during the last 50 years, yet only in the 1990's did a reasonably clear picture of DHEA's role in human health and physiology begin to emerge. Ironically, one of the chief perplexities facing researchers has been the amazingly wide diversity of DHEA's effects. DHEA has been reported to have anti-diabetic, anti-dementia, anti-obesity, anti-carcinogenic, anti-stress, immune-enhancing, anti-viral and anti-bacterial, anti-aging and anti-heart disease effects. (3,4,5) One paper alone lists eight different possible mechanisms of DHEA's "protean physiologic activity," aside from any possible standard steroid-genetic effects. (5) In order to better understand the wide-ranging protective power of DHEA, it will be helpful to survey some recent studies which highlight DHEA's role as "molecular Superman."

IMMUNE EFFECTS

It is in the field of immunology that DHEA has perhaps shown its most broad-spectrum positive action. A recent study found a strong inverse correlation between human serum DHEA-S levels and interleukin 6 (IL-6) levels. IL-6 is one of many cytokines, or immune cell "quasi-hormones," which collectively regulate immune activity. High IL-6 levels are implicated as a causal factor in many diseases, such as rheumatoid arthritis, osteoporosis, B-cell cancers, atherosclerosis and Parkinson's disease. (7) IL-6 levels tend to dramatically increase with aging, just as DHEA-S levels decrease with aging. (6) After studying 120 healthy human subjects, 15-75 years of age, R.H. Straub and colleagues concluded: "decreased DHEA serum concentrations during aging or inflammatory diseases will be paralleled by a significant increase in IL-6 production. Thus, we conclude that the decrease in DHEA levels is a deleterious process, in particular during chronic inflammatory diseases."(7)

In a recent study with eleven postmenopausal women, P.R. Casson and co-workers administered 50 mg DHEA daily in a double-blind crossover study. They reported that "The major finding in this study was the dramatic enhancement in natural killer cell activity. This natural killer cell enhancement was seen in each of the 11 subjects. In this study DHEA appeared to suppress the unexplained increase in stimulated IL-6 production seen in the placebo group" (8) Natural killer cells are a key part of the immune stystem. They are (ideally) in constant surveillance mode, looking especially for viruses and cancer cells to destroy.

R.A. Daynes and B.A. Araneo have published many articles on DHEA and immunity. In a 1992 brief review paper on natural immuno-regulation, they state: "Our studies support the concept that DHEA may function as important regulators of the mammalian immune system in vivo. The effects of DHEA on T cells are to enhance their ability to produce [immune-activating] IL-2, IL-3, and ¡-IFN [gamma interferon]. Such effects only occur if the cells are activated while under the influence of this hormone, and appear to be most prominent in lymphoid [immune] organs that contain the greatest ability to convert the circulating precursor DHEA sulfate to the active metabolite [DHEA]. Replacement therapy [i.e. giving DHEA] should therefore restore normal immuno-competence [that tends to be lost with aging]." (9)

O.Khorram, L.Vu and S.S.C. Yen, long-time DHEA researchers, published an important DHEA study in 1997. Nine healthy "age-advanced men" (mean age: 63) were given 50 mg DHEA daily for 20 weeks after 2 weeks' placebo treatment. They noted that "Our study demonstrates the stimulatory effects of DHEA on the immune function of age-advanced men. DHEA rejuvenated the immune system by increasing the secretion of IL-2, a potent T-cell growth factor, increasing the number of cells expressing the [IL-2 receptor], and enhancing T cell responsiveness to mitogen stimulation. All of which decline during physiologic aging. The significant increase in NK [natural killer] cell cytotoxicity in DHEA treated subjects was potentially related to the increased number of NK cells, both events being mediated by [DHEA-induced] IL-2 stimulation. There were no adverse effects noted with DHEA administration." (10)

H. Danenberg and colleagues reported the ability of DHEA to protect mice from endotoxin (LPS) shock. LPS-endotoxins are released from bacterial cell walls during gram-negative infections, and can cause a high incidence of death from "endotoxic shock." They reported that "Mortality of CD-1 mice exposed to a lethal dose of [LPS-endotoxin] was reduced from 95% to 24% by treatment with a single dose of DHEA, given 5 minutes before LPS." (11)

The preceding represents just the "tip of the iceberg" of a myriad of pro-immune DHEA studies done with humans and animals in recent years, but it should make the point: DHEA has great potential to restore age-degraded immune systems.

DHEA vs. INSULIN

In his recent book The Anti-Aging Zone, (12) B. Sears declared age-related increases in insulin levels/insulin resistance to be the chief "pillar of aging." Similarly, Dilman and Dean in their masterpiece The Neuroendocrine Theory of Aging and Degenerative Disease also consider age-related derangements of insulin /glucose metabolism to be a chief culprit of aging and degenerative disease. (13) A growing body of evidence indicates DHEA has a significant role to play in reducing age-related increases in insulin levels, insulin resistance, and blood glucose. In 1995 Jakubowicz, Beer and Rengifo reported their results from a 30 day double blind, placebo controlled study with 22 men (mean age:57), using 100 mg DHEA nightly. Serum insulin decreased from 35.3 to 25.8 mU/ml, while serum glucose declined from 93.4 to 88.9 mg/ml. Serum insulin and glucose did not change significantly in the placebo group. (14)

The P. Diamond group of Quebec, Canada performed a 12 month study with 15 60-70 year old women, using a 10% DHEA cream applied to the skin. "a 3.8% increase (P< 0.05) in femoral fat and a 3.5% increase (P < 0.05) in femoral muscular areas were observed at 12 months. These changes in body fat and muscular mass were associated with a 11% decrease (P < 0.05) in fasting plasma glucose and a 17% decrease (P < 0.05) in fasting insulin levels." (15)

In a 1993 case report study of a 15 year old woman with Type II diabetes, C. Buffington and co-workers reported that a 150 mg twice daily dose of DHEA led to "a marked improvement in insulin sensitivity, as determined by a more than 30 % reduction in fasting and oral glucose tolerance test insulin levels, a threefold stimulation of the rate of glucose disappearance with intravenous insulin, and a 30% increase in insulin binding. DHEA improved insulin sensitivity and ameliorated the diabetic state." (16)

G.W. Bates et al gave 15 postmenopausal women (mean age:62) 50 mg DHEA for 3 weeks. They concluded that DHEA supplementation in postmenopausal women may decrease age-related increases in insulin resistance. (17)
P. Casson and colleagues gave 50 mg DHEA to 11 postmenopausal women in a 3-week placebo/crossover double-blind study. They noted, "T-lymphocyte insulin binding and degradation increased with DHEA. Enhancement in T-lymphocyte insulin binding and degradation [is] a previously defined marker of insulin sensitivity." (18)

It should be obvious by now that supplementation of DHEA from early middle age on holds the prospect of decreased insulin levels/ resistance and decreased blood glucose - a key factor to promote healthy aging.

ENERGY AND WELL-BEING

A.J. Morales, S.S.C. Yen and co-workers published in 1994 the results of a 6 month placebo /double-blind crossover trial of 50 mg DHEA daily in 13 men and 17 women, age 40 - 70. One of their key findings was "a remarkable increase in perceived physical and psychological well-being for both men (67%) and women (84%) after 12 weeks of DHEA administration, whereas less than 10% reported any change after placebo. Specific statements of well-being ranged from improved quality of sleep, more relaxed, increased energy, to better ability to handle stress. Of note, there were five subjects who self-reported marked improvements of pre-existing joint pains and mobility during DHEA replacement." (19)

F. Labrie, P. Diamond et al published a further data in 1997 from the 12 month DHEA-skin cream study previously mentioned. While focusing on the anti-osteoporosis, bone-building benefits of DHEA, they also noted: "Well-being and an increase in energy were reported in 80% of all women. Our data also confirm the beneficial effects of DHEA on well-being and energy previously reported [in the 1994 Morales/Yen study]." (1)
In 1996 a group led by C. Berr and E.E. Baulieu (the pioneer of DHEA research) published their epidemiological results from a 4 year study of 622 subjects over 65 years of age living in a small community in France. Among the 356 women assessed, lack of limitation in activities of daily living, lack of confinement to bed or home, lack of dyspnea [shortness of breath], lack of depressive symptoms, self-perceived good health, general life satisfaction and low medication use were all statistically significantly correlated with high mean levels of DHEA-S. Among men (266) only self-perceived good health and low medication use were statistically correlated with high mean DHEA-S levels. Clearly, for the elderly women of this study, high (natural) levels of DHEA-S were strongly correlated with well-being and quality of life. (20)
In a 1999 study, M. Bloch et al used a double blind crossover trial of DHEA to treat 15 patients suffering from midlife dysthymia (minor depression of middle-age onset). There was a 60% improvement during the DHEA phase, while only 20% improvement during the placebo phase. "The symptoms that improved most were anhedonia [lack of joy in daily living] loss of energy, lack of motivation, emotional 'numbness', sadness, inability to cope, and worry". (2)
The authors note that due to lack of correlation between baseline DHEA-S levels and positive therapeutic response "one cannot infer that the mood disorder in any way reflects a defiency of DHEA." (21) Nonetheless, the study clearly showed the ability of DHEA to significantly enhance energy and well-being in people where that was seriously lacking.

DEMENTIA

Two of the most feared and debilitating impairments of old age are Alzheimer's dementia (AD), and multi-infarct dementia (MID), which is the result of numerous mini-strokes. A growing body of DHEA literature connects low DHEA levels with both AD and MID.

D.Rudman, K. Shetty and D. Mattson published a major study on DHEA and the elderly in 1990. They compared DHEA-S levels in 50 independently-living community men, age 55 - 94 with DHEA-S levels in 61 nursing home men, age 57 - 104. "DHEA was significantly lower in the nursing home men [who were generally more debilitated] than in the community men. Plasma DHEA-S was subnormal (less than 30 mcg/dL) in 40% [25] of the nursing home residents and in only 6% [3] of the community subjects. In the nursing home men plasma DHEA-S was inversely related to the presence of an organic brain syndrome [AD or MID] and to the degree of dependence in activities of daily living. Plasma DHEA-S was subnormal in 80% of the nursing home men who required total care. In total care patients with either [AD] or [MID] the prevalence of low DHEA-S was 68% and 100% respectively." (3)

B. N…sman and co-workers compared 45 AD and 41 MID patients to an elderly control group. They state: "Patients with Alzheimer's dementia and MID had significantly lower serum DHEA-S values than the control group the ratio of plasma cortisol to serum DHEA-S was higher in AD and MID patients than in healthy controls. DHEA has been suggested to act as an antiglucocortiticoid. A high cortisol/DHEA-S ratio in demented patients may thus damage hippocampal cells [these mid-brain "memory cells" die off in organic dementia] especially - as these neurons are preferentially sensitive to the toxic effects of [cortico]steroids." (22)

T. Yanase and colleagues also found low DHEA-S levels in AD and CVD (cerebrovascular dementia). "We also determined the serum concentrations of DHEA-S in 19 patients with AD, 21 patients with CVD and 45 age and gender matched elderly control individuals. The patients with Alzheimer's dementia and the patients with CVD were found to have lower concentrations of serum DHEA-S. Interestingly, one preliminary clinical trial based on an intravenous administration of 200 mg a day of DHEA-S for 8 weeks suggested slight and modest improvements in cognition and behavior in patients with Alzheimer's dementia and CVD, respectively." (2)
H.D Danenberg et al reported findings in 1996 that may help explain a key aspect of DHEA's anti-dementia neuroprotection. "Amyloid b protein (Ab) is the major component of senile plagues, a distinct lesion in brain tissue of Alzheimer's dementia patients." These toxic amyloid deposits which gradually kill AD brain cells are produced from amyloid precursor protein (APP) by a specific enzymatic pathway - the "amyloidogenic pathway." "DHEA treatment increases APP processing via the nonamyloidogenic pathway and may reserve the [gradual accumulation of toxic Ab proteins] observed in the elderly. The increase in APP production in DHEA-treated cells is accompanied by increased secretion of the nonamyloidogenic [non-toxic protein forms]. These [non-toxic] isoforms demonstrate neuroprotective properties, and participate in neurite outgrowth. Thus, not only is increased production of APP not ultimately [harmful], it may be beneficial when followed by [nonamyloidogenic processing]. It is possible that the age-associated decline in DHEA levels may contribute to the pathological APP processing and eventually to the development of AD." (24)
Thus, there is hope for protecting the structure and function of aging brains through long-term DHEA supplementation.

IGF-1

One of the most exciting results of 1990's DHEA research has been the discovery that it may enhance insulin-like growth factor -1 (IGF-1) release. IGF-1 (formerly called "Somatomedin C") is the "hidden anabolic power behind the throne" of growth hormone (GH). GH stimulates the liver to produce and release IGF-1. It is the IGF-1 that then circulates through the bloodstream and leads to the anabolic (tissue-building) actions GH gets credit for. (19)
The Morales/Yen study previously referred to under ENERGY & WELL-BEING also found significant increases in both men and women in IGF-1 status. "DHEA replacement induced an approximately 10% rise in serum IGF-1 levels and an approximately 19% decline in IGFBP-1 [IGF-1 binding protein] levels, resulting in an IGF-1/IGFBP-1 ratio by 50% in both men and women." (19) The authors also remark that the increased IGF-1/IGFBP-1 ratios suggest "an increased bioavailability of IGF-1 to target tissues." (19)
Yen, Morales and Khorram conducted a one year double-blind placebo-controlled crossover experiment with 100 mg DHEA with 16 men and women, age 50-65 years. A significant increase in IGF-1 levels occurred in both men and women after 6 months' DHEA treatment, while IGF-1 levels dropped below baseline levels during placebo. Men gained approximately 20% in IGF-1, while women gained about 30% in serum IGF-1. The relative increase in IGF-1 was greater in those with low DHEA-S levels at baseline. (31)

The Jakubowicz study previously mentioned under INSULIN also found a significant increase in IGF-1 from 100 mg DHEA nightly for 30 days. "Serum IGF-1 increased from 96.7 to 183ng/ml (p<0.001). Serum concentration of IGF-1 did not change in the placebo group." (14)

In the Khorram study previously mentioned under IMMUNE ASPECTS, 50 mg DHEA daily for 20 weeks also led to increased IGF-1. Khorram et al note that "DHEA administration resulted in a 20% increase (p < 0.01) in serum IGF-1m a decreasing trend in IGFBP-1, and a 32% increase in the ratio of IGF-1 /IGFBP-1 (p< 0.01)." (10) The authors also report a 4-fold increase in the DHEA-S/cortisol ratio. (10) As will become evident shortly, this major increase in DHEA-S/cortisol ratio may hold the key to many of DHEA's diverse benefits.

In 1995 E. Bernton and colleagues reported their results from testing U.S. Army Ranger School trainees during their gruelling training, which included a loss of 8-15% of bodyweight over 8 weeks from intentional caloric deprivation and continuous physical work, limitation of sleep to 4 hours per night, and long exposures to extreme environments.

They reported a decrease in mean salivary DHEA/cortisol ratio from 0.076 to 0.041 (p< 0.001), and a mean decrease of serum IGF-1 of 60% during Ranger training, while growth hormone increased 4-fold, "reflecting a dissociation of growth hormone from IGF-1 secretion, attributable in part to negative [food] energy balance and high cortisol levels. In vivo, IGF-1 levels are therefore increased by glucocorticoids [i.e. cortisol] and increased by DHEA. We hypothesize that tissue ratios of DHEA to cortisol may regulate IGF-1 secretion in stressed individuals such as ranger trainees." (25)

DHEA: NATURAL COUNTER-REGULTOR OF CORTISOL

The emphasis on the DHEA/cortisol ratio as a key health determinant is hardly unique to the Army Ranger and Khorram studies just described. Most of the papers I reviewed to prepare this article specifically mention DHEA's anti-glucocorticoid (i.e. anti-cortisol) action and/or the DHEA/cortisol ratio as key factors in DHEA's benefits. The following assessment by Regelson and Kalimi, veteran DHEA researchers, is somewhat typical of the DHEA literature: "Among the myriad of biological actions, the anti-glucocorticoid properties of DHEA are now clearly emerging. In fact the anti-glucocorticoid action of DHEA may explain many of the seemingly diverse biological activities of DHEA, such as its effects on stress, obesity, diabetes, immune response and protection against acute lethal viral infections."

In fact, even Regelson and Kalimi's enumeration of areas of biological effect of the antagonistic action of DHEA and cortisol does not go far enough. I listed 14 of the key properties of cortisol (excess) action - i.e. its "dark side." As can be seen from Table 1, DHEA has actions opposite to cortisol in all 14 areas listed. It thus becomes obvious that one of the key functions of DHEA is to serve as a counter-regulator to cortisol - to "put the brakes on the cortisol gas pedal," as it were - so that cortisol's catabolic (tissue-destroying) actions do not get out of control. And since cortisol tends to remain constant or increase with age (cortisol also increases dramatically with severe/prolonged stress), while DHEA drops dramatically with age/stress, it is obvious that there is a general life-long, progressively worsening failure of DHEA to oppose the catabolic excesses of cortisol.

B. Sears calls excess cortisol the "second pillar of aging", (12) while Dilman and Dean also focus on the general age-related failure of human physiology to control cortisol levels. (13)
Thus, it should be clear that maintaining a lifelong high DHEA /low cortisol ratio is a key anti-aging strategy. And the simplest way to maintain high blood levels of DHEA from the 30's onwards is through DHEA supplementation.

DHEA SUPPLEMENTION: POSSIBLE CONCERNS

The biggest concern over DHEA supplementation repeatedly raised in the DHEA scientific literature is the issue of androgen/estrogen production from DHEA. Various tissues can locally convert DHEA to either androgens (testosterone, dihydrotestosterone, androstenedione) or estrogens (estrone, estradiol). Many DHEA studies report significant androgen increases in women, even at the relatively low dose of 50 mg. (1, 8, 18, 19, 21) Increased androgen levels in women may relate not only to the mild effects of excess facial hair and acne, but to the more serious issues of abdominal obesity, hyper-glycemia and insulin resistance. (26) And one report found a decreased testosterone level in men, combined with an increase in estradiol, hardly ideal for a man's health. (21) Fortunately, a natural metabolite of DHEA, normally found in the human body, and which cannot be bio-transformed into androgens or estrogens, (28) is now available. And preliminary evidence indicates this "new" DHEA metabolite may be even more potent than DHEA.

7-KETO - DHEA TO THE RESCUE!

7-keto DHEA (also called "7-oxo DHEA,)" is almost identical in structure to DHEA. Human skin (and other tissues) contain enzymes that convert DHEA to 7- keto DHEA in a two-stage process. (27) (Interestingly, many animal experiments with DHEA get best results if the DHEA is given subcutaneously, hinting at skin DHEA bio-processing.) Research into 7- keto DHEA has been conducted primarily by Dr. Henry Lardy and associates at the University of Wisconsin. (28, 29, 30) Based on his research, Lardy has been granted various patents on the use of 7- keto DHEA, including immune enhancement/modulation, Alzheimer's treatment and weight loss.

"7-keto DHEA has been evaluated in both preclinical studies and human clinical trials for safety. These studies show no mutagenic activity and no adverse effects for 7-keto DHEA up to doses of 2000 mg /kg in rats and 500 mg /kg in primates. It should be noted that 500 mg /kg is 3.5 grams in a normal 70 kg human." (30) Zenk notes that a clinical trial conducted to measure the effects of 7- keto DHEA on several endocrine and safety parameters in healthy adult men found 7- keto DHEA to be safe and well-tolerated at doses up to 200 mg/day of a 28-day period. (30) Zenk also reports that laboratory safety tests also showed 7- keto DHEA does not affect haematology, serum chemistry, or urine chemistry differently than healthy subjects taking placebo. (30)

Lardy has found that 7- keto DHEA (7-oxo-DHEA) is a potent increaser of liver thermogenic enzymes. He reports that "The 7-oxo-derivatives of both DHEA [i.e. 7- keto DHEA] and androstenediol are the most active compounds tested. Over the range of 0.01 to 0.1% of the diet, 7-oxo-DHEA was 2.5 times as active as DHEA." (28) Research at the University of Wisconsin found 7- keto DHEA helpful in treating primates infected with Simian Immunodeficiency Virus (SIV). CD-4 (T helper) cell counts, CD-8 cell counts, and total white blood cells increased. The SIV-infected primates also showed improvements in their physical state, increased weight, and overall improvement in behavior and clinical condition. (30)

7- keto DHEA was also shown to increase IL-2 production better than DHEA, in human lymphocytes. IL-2 is the key cytokine regulator of T-helper cells, along with interferon-gamma, which activates the immune system to "go into battle" against invading pathogens. (30) Lardy and colleagues also found 7- keto DHEA to enhance memory in 2-year old mice. "The mice were trained to negotiate a water maze and then were given DHEA or 7-keto DHEA. They were retested after two weeks. The control mice took 34 seconds [to negotiate the maze]; those on DHEA took 22 seconds; and those on 7-keto DHEA took only 7.6 seconds.

Dr. Lardy found similar results in mice using scopolamine to abolish memory. When protected with 7-keto DHEA [and given anti-memory scopolamine] the mice were able to negotiate the water maze in 6.5 seconds, compared to 11.5 with DHEA treatment and 22 seconds with scopolamine treatment only." (30)

7-KETO DHEA: A PERSONAL COMMENT

I have been interested in DHEA since 1984. However, my personal experience with DHEA was disappointing. I found DHEA to induce a severe depression after only 1 - 3 doses. I retried DHEA about a dozen times between 1984 to 1996, always getting the same rapid-onset depression. I talked to a doctor colleague, who reported that she had the same response to DHEA, and that some 5-10% of her patients who tried DHEA also experienced a relatively rapid onset of depression (1 - 10 days). I began taking 7-keto DHEA in the fall of 1998, hoping for a different response. Much to my surprise, I found 7-keto DHEA experientially very different from DHEA. I have been taking 7-keto DHEA for about 18 months now, gradually reducing my dose from 25 mg/day to 10-15 mg/day. I have found 7-keto DHEA to be an energy enhancer, anti-cortisol stress reducer, and general revitalizing agent. I have gradually dropped 20 pounds of weight, have experienced a significant thinning of my face away from the classic cortisol "moon face" I was developing in recent years. I consider 7-keto DHEA one of my core anti-aging supplements. I have also used 7-keto DHEA to quickly revive 2 cats traumatized from combined surgical/anaesthesia/vaccine stress. My wife finds 7-keto DHEA to be the single most energizing supplement she's ever taken.

DHEA/ 7-KETO DHEA: DOSAGES

For those wishing to get the potential androgenic benefits of DHEA, extremely low doses are advised. 10-25 mg /day for women, 20-40 mg/day for men. Anyone suffering any serious disease or hormonal condition should only use DHEA under competent medical supervision. 7- keto DHEA may be effective at doses as low as 5-10 mg/day, with 25-50 mg/day being probably adequate for all but medical use in disease treatment under medical supervision.


REFERENCES

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2) Murphy, B. & Wolkowitz, O. (1993) "The pathophysiologic significance of hyperadrenocorticism: antiglucocorticoid strategies" Psychiatr Ann 23: 682-90.

3) Rudman, D. et al (1990) "Plasma dehydroepiandrosterone sulfate in nursing home men" J Ann Geriatr Soc 38: 421-27.

4) Kalimi, M. et al (1994) "Anti-glucocorticoid effects of dehydroepiandrosterone (DHEA)" Molec Cell Biochem 131: 99-104.

5) Regelson, W. & Kalimi, M. (1994) "Dehydroepiandrosterone (DHEA) - the multifunctional steroid" Ann NY Acad Sci 719: 564-75.

6) Zhang, Z. & Watson, R. "DHEA in Immune modulation and aging", in Health Promotion and Aging, R. Watson, ed. Harwood Acad. Pub. 1999, pp. 113-23.

7) Straub, R. et al (1998) "Serum DHEA and DHEA sulfate are negatively correlated with serum interleukin-6 (IL-6), and DHEA inhibits IL-6 secretion from mononuclear cells in man in vitro." J Clin Endocrino. Metab 83: 2012-17.

8) Casson, P. et al (1993) "Oral dehydroepiandrosterone in physiologic doses modulates immune function in postmenopausal women" Am J Obstet Gynecol 169: 1536-39.

9) Daynes, R. K. Araneo, B. (1992) "Natural regulators of T-cell lymphokine production in vivo" J Immunother 12: 174-79.

10) Khorram, O. et al (1997) "Activation of immune function by dehydroepiandrosterone (DHEA) in age-advanced men" J. Gerontol 52A: M1-M7

11) Danenberg, H. et al (1992) "Dehyroepiandrosterone protects mice from endotoxin toxicity and reduces tumor necrosis factor production" Antimicrob Agents Chemother 36: 2275-79.

12) Sears, B. The Anti-Aging Zone. NY: Regan Brooks. 1999.

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15) Diamond, P. et al (1996) "Metabolic effects of 12-month percutaneous dehydroepiandrosterone replacement therapy in postmenopausal women" J Endocrinol 150: S43-S5*

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29) Lardy, H. "Dehydroepiandrosterone and ergosteroids affect energy expenditure", in Health Promotion and Aging, R. Watson, ed. Harwood Acad. Pub. 1999. pp. 33-42.

30) Zenk, J. Living Longer in the Boomer Age. NY: Advanced Research Press, 1998.

31) Yen, S.S.C. et al (1995) "Replacement of DHEA in aging men and women" Ann NY Acad Sci 774: 128-42.

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33) May, M. et al (1990) "Protection from glucocorticoid induced thymic involution by dehydroepiandrosterone" Life Sci 46: 1627-31.

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dragonfire101 said:
]
Found this interesting read below on HPA and alcohol.

EFFECTS OF ACUTE ALCOHOL INTOXICATION ON PITUITARY–GONADAL AXIS HORMONES, PITUITARY–ADRENAL AXIS HORMONES, ß-ENDORPHIN AND PROLACTIN IN HUMAN ADULTS OF BOTH SEXES

J. Frias1, J. M. Torres, M. T. Miranda2, E. Ruiz and E. Ortega,*
Department of Biochemistry and Molecular Biology and Institute of Neurosciences, School of Medicine,
1 Trauma Emergency Department, Virgen de las Nieves University Hospital and
2 Department of Biostatistics, School of Medicine, University of Granada, Avda. de Madrid, s/n, 18012, Granada, Spain
Received 9 March 2001; in revised form 16 July 2001; accepted 20 August 2001
— The effects of acute alcohol intoxication (AAI) on the pituitary–gonadal axis hormones, and the possible contribution of pituitary–adrenal axis hormones, ß-endorphin and prolactin to alcohol-induced dysfunction of pituitary–gonadal axis hormones were studied in adult men and women. Blood samples were drawn from adults of both sexes who arrived at the emergency department with evident behavioural symptoms of drunkenness (AAI) or from adult volunteers with nil consumption of alcohol (controls). Our results demonstrated that AAI produces a high increase in plasma prolactin, corticotropin (adrenocorticotropic hormone, ACTH), and cortisol in adults of both sexes, a decrease in luteinizing hormone levels only in men, an increase in dehydroepiandrosterone-sulphate (DHEAS) and a contradictory behaviour of testosterone according to gender, with increased plasma testosterone in women and a decrease in men. ACTH and prolactin correlated positively with cortisol, DHEAS and testosterone in women, which suggests that prolactin and ACTH could contribute to stimulated adrenal androgen production. In contrast, the decrease in testosterone and increase in ß-endorphin in men suggests that AAI could have an inhibitory effect on testicular testosterone, perhaps mediated by ß-endorphin. Our results suggest that the effect of alcohol on pituitary–gonadal axis hormones in humans could depend on the gender and degree of sexual maturity of the individual.


Full text here

http://hera.ugr.es/doi/15003371.pdf


THis article could explina the reason for "whiskey dick" (not being able to get it up when too drunk) SO it makes sens to me! :)
 

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