DHT our friend??

[MisterX]

DHT as all hormones have their proper place and purpose. But in excess of anything, bad things can happen. But, with certain hormones, these bad things sometimes can be over inflated or over exposed to produced ledgendary horrors that just aren't real. DHT is excess can produce negative side effects that we all might want to avoid. BUt is blocking or preventing DHT from bieng produced the answer? Don't throw out that Proscar yet, but you may just want to keep it out of your next cycle and weigh your benefits. DHT does have it's place, and after reading this article you, as did I just may gain alittle more respect for this hormone with the bad rap. DHT's function is widely misunderstood all too often, and maybe this might clear the air. I know you might not appreciate 'all' that is presented. I hope you can appreciate the information presented.

Article by Pat Arnold,

A considerable chunk of my work day is always spent answering people’s questions about prohormones and steroids. Of course, one of the biggest concerns people have is about estrogen and estrogen related side effects. Right behind that however are questions about DHT. It seems that people have the misconception that DHT is some evil androgen by product that serves no purpose in the body but to make our prostates blow up and our hair fall out.

The real situation is of course much more complex. DHT is one of those good guy / bad guy hormones that is sorely misunderstood. For many people, it is NOT something that you want to reduce or eliminate in the body. For some others though, keeping DHT levels under control is probably a prudent course of action. Knowing the facts about DHT will help you decide just which group you belong to.

Testosterone is a prohormone?

The main androgen secreted by the testes is of course testosterone. However, in most of the body, the androgenic signal is not carried through by testosterone. In these tissues, which include the brain (CNS), skin, genitals – practically everything but muscle – the active androgen is actually DHT. Testosterone in this case simply acts as a prohormone that is converted to the active androgen DHT by the action of the enzyme 5alpha reductase (5-AR).

5-AR is concentrated heavily in practically every androgen dependent area of the body except for skeletal muscle. This results in very little testosterone actually getting through to these parts of the body to bind to androgen receptors. Instead, it is quickly transformed into DHT, which then interacts with receptors.

This transformation serves a very important biological function in these tissues. You see, DHT is a much stronger androgen than testosterone – it binds about 3-5 times more strongly to the androgen receptor. If you took away 5-AR from these tissues and blocked the formation of DHT, then you would see some dramatic changes in physiology.

A good case in point is demonstrated in male pseudohermaphroditism due to congenital 5-AR deficiency. This is a relatively rare disorder, however it is actually quite common in the Dominican Republic. In this disorder, males are born with little or no 5-AR enzyme. They have ambiguous genitalia and are often raised as girls. When puberty occurs, their testosterone levels elevate normally although their DHT levels remain very low. Their musculature develops normally like that of other adults, however, they end up with little or no pubic / body hair and underdeveloped prostate and penis. Their libido and sexual function is often disrupted also.

Testosterone is the active androgen in muscle

Skeletal muscle is unique from other androgen dependent tissues in the body. It actually contains little or no 5-AR, so little or no DHT is actually formed in the muscle. In addition to this, any DHT that is formed, or that is already present in the blood and travels to the muscle, is quickly deactivated by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD).

So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.

It is important to understand that even though testosterone is the active androgen in muscle, and DHT exhibits relatively little direct anabolic effects on muscle in men, DHT is still very important for the full performance enhancement effects from testosterone. What I specifically mean here are the effects of DHT on the central nervous system, which lead to increased neurological efficiency (strength), and increased resistance to psychological and physical stress - not to mention optimal sexual function and libido.

I have heard several anecdotal reports of individuals who have stacked testosterone with proscar (a 5-AR inhibitor) and have noticed significantly reduced performance enhancement effects. What’s going on here? We know it couldn’t be due to the inhibition of the direct anabolic activity of testosterone on muscle anabolism. Most likely it is due to the reduction of androgenic effects in other parts of the body that contribute to the ergogenic effects, specifically the CNS, which is stimulated by androgens to increase neural output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors (such as IGF-1), since DHT is an important androgen in the liver.

Anti – Estrogen effects of DHT

One important function of DHT in the body that does not get much discussion is its antagonism of estrogen. Some men that take proscar learn this the hard way – by developing a case of gynecomastia. By reducing DHT’s protection against estrogen in the body, these men have fallen victim to its most dreaded ramification – bitch tits!

How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

Lastly, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production – testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section.

DHT, estrogen, and the prostate

When it comes to sex hormones, few things are as misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly simplistic attitude that DHT is responsible for prostate hypertrophy, and even prostate cancer predominates amongst most people.

The real situation is, of course, much more complex. One must understand that there are marked differences between healthy prostate growth (developmental growth), prostate growth due to BPH, and cancerous prostate growth.

The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate from its prepubertal dormancy to the normal sized, healthy, and functional prostate gland of an adult. During the early and mid adult years the prostate stays at this stage, despite the constant high levels of androgens in the body. However, if androgens are blocked in the body then the adult prostate will shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active androgen in the prostate).

Later in life, there is often a second stage of growth. This growth is deemed benign prostate hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen / androgen ratio – a condition common in older men – is highly correlated to the development of BPH.

Experimental studies have shown the inability of androgens with saturated A rings (DHT related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. Aromatizable androgens on the other hand, such as testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but these effects are reversed by the addition of an aromatase inhibitor.

So apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.

None of this may come as news to many of you, but I bet that very few of you know that DHT can actually be used to treat BPH!! How can it do that? It basically does this by replacing the testosterone in the body, which then has the effect of reducing the amount of estrogen in the body. As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH.

The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."

This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?

Conclusion

People have a natural tendency to classify things as either good or bad, with no gray areas. DHT (like estrogen) has recently been on everyone’s bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give DHT a break. I now pronounce June "DHT Appreciation Month". Thank you.

-Pat Arnold

_____________________________________

I know DHT can cause nasty sides, and in excess can cause many problems but I hope we can all appreciate that 'not enough' DHT(due to Proscar ect) can be a problem as well as too much DHT.

-X


__________________________________________________

Credat Judaeus Apella, non ego. -

Horace's Satires, book 1, satire 5, lines 100-101

[archive_Mr. Nobody]

very nice, I always knew it was important for sex drive, hence the limpy problems on finasteride.
Now if it wasn't so hard on the hair

Disclaimer:
Mr. Nobody is presenting fictitious opinions and does in no way, shape or form encourage nor condone the use of any illegal substances or the use of legal substances in an illegal manner.
The information discussed is strictly for entertainment purposes only.

Good post. May have to reread it once or twice.

[E2]

Good post!

He speaks about a later prostate growth due to a high androgen/estrogen ratio, then speaks of dht being used to treat BPH yet attributes it to it's estrogen blocking capabilities. Wouldnt' one naturally think that the dht's ability to treat BPH would be due to a reversal in the high estrogen/androgen ratio to a more normal ratio by increasing the amount of dht present?

I wonder why that's not stated.

[MisterX]

This goes along with that post that Corelone stated he was experiencing problems with 'hard wood' lately, and it was complicating sexual activity. I'm not sure about the BPH, but I do have a book that goes into that further. Let me find the article and try to post it, it may elaborate further on that. I've also found that sexual drive isn't just based on DHT, but also relies on estrogen levels as well as 5a reductase levels to balence androgen metabolites to tissues involved in sexual activity. So on the related topic, let me just throw in this article as well. This might also further elaborate on the importance of not only DHT levels, but also the presence of substantial estrogen levels for a healthy sex drive, libido and function. Without ALL THREE, one may experience problems in not only sex drive, but also in other areas as well that are different in everyone but also consistant in all. I'm not saying Arimidex doesn't have it's place, or Proscar doesn't serve a purpose, all I'm proposing is that these hormones have their place and perhaps drugs that inhibit or eliminate their function and or presence can be counter productive if used in excessive amounts in a cycle. Here is another Article for your review on the subject. You be the judge, since it is 'your body' that we are all trying to improve.

Article.....

Androgenic hormones such as testosterone and anabolic steroids (as well as prohormones) have long been used by athletes for their effects on increasing muscle mass and strength. The anabolic effect on muscle is certainly not the only physiological effect that these hormones possess however, and for many people not particularly interested in bigger muscles androgens might offer other special benefits that justify their usage. Specifically, these involve improvement in the overall psychological state, and optimization of the libido and sexual function.

BACKGROUND BIOCHEMISTRY

Testosterone is the primary androgenic hormone. It instills its effects on the body both directly, and through its conversion to metabolites (DHT, estradiol, etc). Androgens and other steroid hormones primarily exert their direct activities through binding to specific receptors present in the cytosol of cells. Upon binding to the receptor, the hormone forms a complex that then travels to the nucleus of cells where it interacts with DNA to promote the formation of specific proteins that then direct the actual biological changes.

Within the central nervous system (CNS), androgen receptors are heavily located in specific places. Androgens and other steroid hormones are able to penetrate the blood brain barrier and interact with their appropriate CNS cytosolic receptors. The hypothalamus and anterior pituitary gland are particularly dense in androgen receptors, and here they help regulate the secretion of androgens as well as other hormones that control a wide variety of biological functions. Androgen receptors are also located in parts of the cerebral cortex, medulla, and amygdala. Here their specific functions are not as well characterized.

The processes of androgen action that involve receptor binding and DNA translation are known as receptor mediated, or "genomic", hormone actions. However, there are also lesser known actions of steroid hormones that are non-genomic in mechanism. Non-genomic activities are particularly key in the central nervous system where they combine with genomic activities to produce specific effects.

Non-genomic actions of steroid hormones differ in a very important way from genomic actions. Genomic effects are manifested over a relatively long period of time (days) because they require a complex cascade of events (binding, translation, transcription, accumulation of active enzyme products) before the actual physiology of the target organ is altered. On the other hand, genomic actions are extremely rapid (<1 minute). They are rapid because their effects involve an immediate modulation of the membranes of cells (particularly neural cells). These modulations may include changes to the permeability of the membrane, as well as effects on the opening of vital ligand-gated ion channels. The end result is a quick and significant influence upon the activities of key areas of the brain, and the relevance of this to the medicinal use of androgenic hormones or prohormones should not be overlooked.

PARACRINE METABOLISM

So far I have briefly covered the basic mechanics of androgen activity in the central nervous system. However, one very important aspect of this has yet to be covered, and this concerns the "activation" of androgens at the CNS targets by enzymatic metabolism, specifically speaking, the conversion of testosterone to its two most powerful metabolites; dihydrotestosterone (DHT) and estradiol.

One thing most people do not realize is that although testosterone is an active hormone, its primary function in some of the most vital areas of the body and the brain is as a prohormone. There are locations all over the CNS that are rich in 5 alpha-reductase, or aromatase, or both; in particular areas of the CNS that involve libido. It is in these areas that testosterone must first be converted to fully carry on its message.

5 alpha-reductase is found in high concentrations in various parts of the brain, particularly in the white matter. It is localized specifically in the myelin (outer fatty sheath of neurons). 5 alpha reductase (5-AR) converts testosterone into DHT, which is a much more potent androgen than testosterone. As a result, the androgenic signal of testosterone is "amplified" in 5-AR rich tissues. The significance of 5 alpha-reduction to the psychosexual actions of testosterone is made depressingly evident to many individuals that take finasteride (Proscar, Propecia) for prostate hypertrophy or male pattern baldness. In a considerable portion of these individuals, a loss of libido and sexual function is experienced as a side effect, this despite a slight increase in circulating testosterone.

Aromatase is the enzyme that catalyzes the conversion of androgens (androstenedione, testosterone) to estrogens. It also is found in certain areas of the brain in high concentration (often in conjunction with 5-alpha reductase), specifically in areas that are essential for the neuroendocrine control of gonadotropin secretion and sexual behavior. Androgens are well known to be essential to sexuality, but without the concomitant presence of estrogens, they are essentially without effect. Studies have demonstrated that the abolition of estrogen formation through the use of aromatase inhibitors, or resulting from a congenital aromatase defect, greatly reduces sexual desire and function despite the presence of normal or high androgen levels.

EAST GERMAN RESEARCH

A group of East German scientists performed what is probably the most elaborate "practical" research on the psychological benefits of androgens. Their research did not center much on the prosexual effects of androgens, but rather on what they termed the "psychophysical" properties.

The psychophysiological capacity, as the researchers describe it, is the ability of an individual to handle stress (physical, mental, and emotional). This capacity is determined by one’s ability to activate appropriate centers in the central nervous system. Psychophysiological capacity can be evaluated by applying stressful stimuli and measuring shifts in the alpha-frequency of an encephalogram. Specifically, the researchers found that physical or psychic stresses lead to increases of approximately 4 to 6 Hertz compared to the starting value in individuals possessing the psychophysiological capacity to handle the particular stress. If the stress becomes excessive for an individual, the alpha frequency decreases after passing through the 4-6 Hertz optimum, and can then sink to levels below the original baseline.

At the time that this research was carried out, there was a substantial government sponsored research effort in the field of athletic performance enhancement, and as you may have guessed, the aforementioned research was carried out on sportsmen. The alpha wave increase in athletes is associated not just with the physical stress of training or competition, but with the mental effort associated with preparation and the events themselves. The psychophysical capacity of the athletes, as measured by encephalogram, is adversely affected by circumstances such as false preparation, fear, overstressing, and disturbing personal problems. As a result, performance often suffers substantially. The East Germans believed that not only was it vital to avoid such pre-contest stressors, but they also believed they had to find ways to increase one’s psychophysiological capacity so as to increase the ability to handle these pre-contest stressors (not to mention the stress at contest time itself).

Now keep in mind that the matter of this research is not just applicable to athletes, but also to anyone with decreased psychophysiological capacity (i.e. elderly), or who have to handle large amounts of stress (i.e. college exam studiers).

The East German’s discovered that appropriate administration of androgenic hormones had a marked effect on the psychophysiological capacity. Substances that they are known to have studied and used for this purpose include mestanolone (methyl DHT), Oral-Turinabol (dehydrochloromethyltestosterone), testosterone, and androstenedione. Of particular significance are the compounds mestanolone and androstenedione. These two substances are known to have minimal anabolic properties on muscle mass, yet their ability to activate the stress handling capabilities of the CNS are equal to or greater than that of testosterone or other androgenic/anabolic steroids.

One example in the literature describes the oral administration daily of 10mg mestanolone to 54 individuals who had been undergoing long term stress. An alpha wave increase of up to 4 Hertz was observed, and this was associated with a great increase in performance on tasks requiring high physical output, mental concentration, and physical coordination.

Although effective, oral administration of androgens was not the preferred technique of the East Germans. Instead they preferred the intra-nasal route.

Due to the proximity of the nasal passages to the base of the brain, the East Germans believed that absorption here maximized the passage of steroids through the blood-brain barrier and into the cerebrospinal fluid where they are available to stimulate genomic and non-genomic CNS androgenic activity.

The intranasal route was also fast acting, which made it ideal for pre-contest usage. According to the East German data, after intra-nasal administration, levels of steroids in the blood maximize at 15 minutes and decline to baseline by 90 minutes. Levels in the CNS are probably elevated even sooner (seconds to minutes). Furthermore, with the usage of intranasal testosterone and androstenedione, the East Germans discovered that the ratio of urinary testosterone/epitestosterone was normalized within 24 hours, allowing them to pass post-competition drug testing.


REFERENCES:

1) Carani C, et.al., "Role of Oestrogen in Male Sexual Behavior: Insights from the Natural Model of Aromatase Deficiency", Clin Endocrinol 1999, 51(4): 517-24

2) Celotti F et.al., "The 5 alpha-reductase in the Brain: Molecular Aspects and Relation to Brain Function", Front Neuroendocrinol 1992, 13(2): 163-215

3) Choate JV, et.al., "Immunocytochemical Localization of Androgen Receptors in Brains of Developing and Adult Male Rhesus Monkeys", Endocrine 1998, 8(1): 51-60

4) Mattern C, Hacker R, "Method for Nasally Administering Aerosols of Therapeutic Agents to Enhance Penetration of the Blood Brain Barrier", German Patent Application DE9300442A1

5) Mattern C, Hacker R, "Medicament for Influencing the Degree of Activation of the Central Nervous System", German Patent Application DE9300473A1

6) McClellan KJ, et.al., "Finasteride: A Review of its Use in Male Pattern Hair Loss". Drugs 1999, 57(1): 111-26

7) Mooradian AD, et.al. "Biological Actions of Androgens", Endocr Rev 1987, 8(1): 1-28

8) Poisson M, et.al., "Steroid Receptors in the Central Nervous System. Implications in Neurology", Rev Neurol 1984, 140(4): 233-248

9) Roselli CE, et.al., "The Distribution and Regulation of Aromatase Activity in the Central Nervous System", Steroids 1987, 50(4-6): 495-508

10) Zumpe D, et.al., "Effects of the Non-Steroidal Aromatase Inhibitor, Fadrozole, on the Sexual Behavior of Male Cynomolgus Monkeys (Macaca Fascicuiaris)", Horm Behav 1993, 27(2): 200-15


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Credat Judaeus Apella, non ego. -

Horace's Satires, book 1, satire 5, lines 100-101

[archive_robbb]

Thanks for the digging that up Mister X. I was wondering what you guys thought about using a little Saw Palmetto as a kind of weak replacement for people who are NOT susceptable to MPB, but still are concerned about losing a little hair. I usually use 160mg standardized which is 2 caps with the brand I use just to try to keep the prostate and hair healthy without going overboard on trying to reduce DHT. I don't lose hair and probably wouldn't even without the Saw Palmetto either. Just a precaution. This article was a real eye opener though so thanks again. Any thoughts on using the Saw Palmetto? Thought Dr. Scruggs was a real fan of it.

Saw palmetto is also an anti-estrogen. maybe its prostatic protective properties have been innappropriately attributed to its anti-DHT effect. But I took ALOT of Saw palmetto with my last cycle and still my DHT was unbelievably high. As was my sex drive.

I read it again MisterX. It is a really good read. I have a similar article on estrogen that says when Eve ate of the forbidden fruit estrogen was formed in her body which is the entire cause of the fall of man....okay, just kidding. Estrogen is not the cause of evil. Lets see if I can cut and paste it here:
==========================================
Dr. Lee's Letter for Treatment of Prostate Cancer

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Peter Eckhart, M.D.

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Dr. John Lee, a Norwegian practicing in California, has written the following for treatment of Prostate Cancer.

Prostate Cancer and Testosterone

In 1941, Dr. Huggins showed that castration slowed the progression of prostate cancer. The cancer benefit was assumed to be due to testosterone reduction. Since that time, physicians have relied on suppression of testosterone production in their treatment of the disease. However, the benefit does not last and eventually prostate cancer progresses, presumably a result of an androgen-insensitive state of the cancer cells. Despite this fact, metastatic prostate cancer patients continue to be treated with androgen blockade. Castration and/or synthetic analogs of gonadotropin releasing hormone (e.g. Lupron) eliminate testicular testosterone but do not diminish androgens of adrenal origin. Total androgen blockade can be achieved by a combination of castration or gonadotropin-releasing hormone with an anti-androgen that blocks cell nucleus uptake of all androgens. One such anti-androgen drug is flutamide. A recent (8 Oct 1998 NEJM) study reported that, in patients with metastatic prostate cancer, the combination of orchiectomy plus flutamide conferred nosurvival advantage over orchiectomy alone. In fact, the only observed effect of flutamide was a reduction in quality of life, particularly more diarrhea and worse emotional functioning. Brain cells, as we know need some testosterone.


This finding raises several interesting points. One is that medicine has made no real progress in treating prostate cancer by androgen reduction since 1941. Second, flutamide has been under study since at least 1989, and recommended for prostate cancer treatment for over five years. Conventional medicine claims superiority over alternative practice by reason of being "evidence based." Why did it take five years for conventional medicine to discover that it had embraced a worthless drug? Perhaps this recent study will stimulate a re-examination of the conventional hypothesis concerning the role of testicular hormones.


Orchiectomy removes not only testicular testosterone production but also its production of estradiol. Why chose testosterone as the cause of prostate cancer? Is it not clear that the time of life when testosterone is at its highest level (around age 18) is the same time of life when prostate cancer is least likely? Why does prostate cancer occur so often in aging men? Testosterone supplementation prevents survival of prostate cancer cells transplanted to test mammals. Testosterone given to test mammals after transplantation of prostate cancer tissue will slow tumor growth. In prostate cancer cell culture, testosterone kills the cancer cells. It is time for a new hypothesis.


Consider three changes in testicular hormone production as men age. Progesterone production falls and since progesterone is a potent inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), this decline of progesterone causes increased testosterone conversion to DHT. Since testosterone is a direct antagonist of estradiol (and DHT isn't), relative estradiol effect increases. Could this be the cause of prostate cancer?


Embryology teaches us that the prostate is the male equivalent of the female uterus. They differentiate from the same embryonic cells and they share many of the same genes such as the oncogene, Bcl-2, and the cancer protector gene, p53. It is, therefore, no surprise that the hormonal relationships in endometrial cancer will be the SAME in prostate cancer. Researchers TS Wiley and Prof. Bent Formby, using prostate cancer cell cultures, have clarified much of the relationships between hormones, gene effects, and prostate cancer cell growth. Their in vitro test show the following:


Estradiol increases Bcl-2 product that leads to cell proliferation and delay in apoptosis, both of which increase cancer risk. Progesterone suppresses Bcl-2 action and increases p53 product that slows cell proliferation and restores proper apoptosis, both of which decrease cancer risk. Testosterone (but not the DHT) stops cancer cell growth. Insulin increases cancer cell growth.

It should be recalled that adult male's estradiol levels are equivalent to or greater than that of post menopausal females. Estradiol's effects, however, are suppressed (antagonized) by the male's greater production of testosterone. As noted above, progesterone is a potent inhibitor of 5 alpha-reductase and, as males age, the decline of progesterone increases the conversion rate of testosterone to DHT. Thus, in aging males, testosterone levels fall not only because of less production of but also by its increased conversion to DHT. In this situation, estradiol effect rises. Just as estradiol is a known endometrial carcinogen, so also is estradiol a likely prostate cancer carcinogen in aging males.


Lastly, it is recognized that chronic inflammation may also be carcinogenic. It is wise therefore, to maintain one's intake of anti-oxidants such as vitamin C, selenium, and the fat soluble anti-oxidant vitamins, A, E, D, and K.


It is time to revamp the prostate cancer hypothesis. Orchiectomy provided a prostate cancer benefit not because it removed testicular testosterone but it lowered estradiol levels. The course of prostate cancer growth is not a linear progression of cancer cells multiplying from one rogue cell; it is due to continued change of normal prostate cells to cancer cells because of the continued presence of an underlying metabolic imbalance. The most likely underlying metabolic imbalance in all hormone dependent cancers is estrogen dominance (too much estrogen). Prevent the estrogen dominance and you will prevent the cancer. If the cancer is already underway, correcting the estrogen dominance will slow the cancer growth and prolong life.


In the case of prostate cancer, the new treatment plan would include the following:


1. Diet should avoid sugar, refined starches, and other glycemic (insulin-raising) foods as well as high estrogen foods such as feedlot meat and milk.


2. Maintain a good intake of anti-oxidants.


3. Monitor saliva hormone levels of progesterone and testosterone in males over 50.


4. Supplement progesterone and testosterone by transdermal cream to maintain saliva levels consistent with that of healthy mature males. When supplemented in this manner, the doses required are quite small: I suspect that appropriate doses will be in the range of 8-10 mg/day of progesterone and 2-3 mg/day of testosterone.


From my clinical experience, it would not surprise that exercise and an active sex life are also protective factors against prostate cancer.


Male castration's prostate cancer benefit stemmed from estradiol reduction, not testosterone reduction. Given the choice, I would choose testosterone and progesterone supplementation over castration.


John Lee, M.D.


January 1999

Three other books of note to buy are:


What Your Doctor May Not Tell You About Menopause by John Lee, M.D.

Our Stolen Future by Theo Colborn

Healthy Living in a Toxic World by Cynthia Fincher, Ph.D.


-Eckhart, M.D.

Although the articles you post and mine seem to disagree a bit about whether testo or DHT has more of a protective effect against estrogen, they are in agreement in the potential role of estrogen in causing cancer. My article is a bit more of an informercial for his book and treatment, so that tends to make me see it a bit more skeptically then yours in terms of accuracy and objectivity, MisterX.

[Unity66]

some great info.......my folder pertaining to training under 'my documents' is getting yet another additon.....

what implicatios does this have for using proviron for its anti-aromataze properties and its ability to restore libido? will 25mg am/pm shut one's hpta down?

also, have you came accross any research to lay to rest the debate as to if proviron and/or any synthetic DHT derivitive hinders gains by occupying androgen receptors or is their evidence to to contrary that DHT binds more readily to SHGB(or SGHB-lol), allowing exogenous test to exist in 'free, unbound state'--hence increasing 'free testosterone'?

great post brother.........

Unity66

Unity66, I will try to find out. I too am curious about that.

Hey look at this article showing estrogen causes prostate enlargement:
==============================
: Prostate 2000 Jun 15;44(1):8-18

Estradiol causes a dose-dependent stimulation of prostate growth in castrated beagle dogs.

Rhodes L, Ding VD, Kemp RK, Khan MS, Nakhla AM, Pikounis B, Rosner W, Saunders HM, Feeney WP.

Department of Clinical Development, Merial Ltd., Iselin, New Jersey, USA.

BACKGROUND: Previous studies have shown that chronic treatment of castrate dogs with androgen and estrogen results in significant prostate growth. Estrogen treatment of castrate dogs in the absence of androgen has resulted in conflicting data as reported by several authors. The purpose of this experiment was to evaluate the effect of a physiological dose of estradiol on prostate growth in dogs, using ultrasound to study size changes over time. METHODS: Dogs (n = 25) were randomly divided into groups (n = 5) and treated as follows: castration alone (CC), castration plus low dose estradiol (E(2) low), castration plus high estradiol (E(2) high), castration plus estradiol and androstanediol (E(2)A), or no treatment (normal controls, NC). Silastic implants containing 5alpha-androstan-3alpha-17beta-diol (3alphadiol), and/or 17beta-estradiol were used for continous delivery of steroids. Prostate volume was measured by transrectal ultrasonography, and blood was drawn for hormone and sex hormone binding globulin (SHBG) determinations. RESULTS: Results show that serum estradiol and SHBG levels were fairly constant over 12 weeks in all groups. Estradiol-treated groups had mean serum estradiol values of approximately 40 and 60 pg/ml, respectively. Initially, all groups had similar prostate volumes. Over 12 weeks the castrate dogs had a decline in prostate volume, whereas the intact dogs and those treated with E(2) and 3alpha-diol maintained a constant prostate volume. Estradiol treatment caused a large, late onset (week 7), dose-dependent increase in prostate volume relative to the intact group (P < 0.01). At 12 weeks, animals were euthanized and prostates weighed. The mean prostate weights in each group were: NC 14.8 +/- 2. 9, CC 2.4 +/- 0.5, E(2)A 9.7 +/- 2.0, E(2) low 21.7 +/- 4.3, and E(2) high 63.6 +/- 12.6 g (geometric mean +/- SEM). Histologically, prostates of estrogen-treated dogs showed metaplastic squamous epithelium.

CONCLUSIONS: These results demonstrate that estradiol causes marked dose-dependent stimulation of prostate growth in the castrate dog. Copyright 2000 Wiley-Liss, Inc.

PMID: 10861752 [PubMed - indexed for MEDLINE

[MisterX]

ON the topic of Estrogen and it's ugly side..

Here is an interesting article concerning estrogen, it's nasty sides due to the result little or no anti-estrogens present during cycling with Anabolics by Grendel over at AE.

Article...

Why Billy has Breasts: The Story of Estrogen
A Biochemical Over-View of Estrogen
By Grendel

Meet poor Billy. Billy stands over 6 feet tall and weighs around 270 pounds. Billy was born a healthy normal man, but now Billy has an exciting career as an exotic dancer thanks to his use of steroids without anti-estrogens. To understand what happened to poor Billy lets examine estrogen and its relationship to male use of anabolic steroids.

Estrogens regulate the growth, differentiation, and functioning of diverse target tissues, both within and outside of the reproductive system. Most of the actions of estrogens appear to be exerted via the estrogen receptor (ER) of target cells, an intracellular receptor that is a member of a large super family of proteins that function as ligand-activated transcription factors, regulating the synthesis of specific RNAs and proteins. This process is almost identical to the action by which anabolic steroids effect protein synthesis.

Estrogen is also a steroid hormone, although not used for athletic enhancement. However, estrogen plays a key role in the use of AAS. Certain steroids, at high enough dosages, can convert via the enzyme aromatase into other hormones; in the case of testosterone-based steroids this other hormone is usually estrogen. Steroids with a dihydrotestosterone (DHT) base are not subject to aromatization; as a metabolite of testosterone its structure is not affected by the aromatase. Steroids with 17-alkylated structures generally convert into weaker estrogens. Some steroids, such as nandrolone (deca-durabolin) or trenbolone (parabolan, or in most people's cases Finaplex) convert into progesterone.

High dosages of steroids for prolonged periods also shut down the body's natural production of certain hormones (particularly testosterone) when steroid therapy is stopped the body attempts to establish homeostasis by adjusting hormonal levels. The average ratio of testosterone to estrogen in a healthy male is 100:1. When drugs increase the testosterone in the body, the body will respond by increasing the estrogen in the body. Additionally, estrogen circulates in the body bound to the protein SHBG (sex hormone binding globulin) as does the testosterone. SHBG is produced in the liver and use of steroids increases the production of this protein; which has a very high receptor affinity for testosterone. With more SHBG in the body, more testosterone is bound, becoming inactive as only free testosterone can activate an androgen receptor. SHBG, however, has poorer receptor affinity for estrogen and more active free estrogen circulates in the body, further altering the hormonal balance. These effects of steroids (i.e. the potential for conversion into estrogen, as well as the disruption of the hormonal balance in the body) can cause serious side effects in male users Thus, steroid users seek ways to block this estrogen from affecting them.

That is all a very nice and formal way of saying that you need to be taking anti-estrogens when you are using steroids. See, without the anti-estrogens you get all sorts of pleasant side effects, not limited to a nice pair of breasts (with oh -so tender nipples) and extra body fat! Without anti-estrogens you will end up like poor Bobby, shaking his titties in the face of wealthy Japanese businessmen. No, seriously, this article will explore how to effectively use anti-estrogens to prevent many of the side effects that accompany anabolic steroid usage.

The Drugs Are Your Friends
Oral clomiphene citrate (Clomid) is an ovulation stimulant used to treat ovulatory failure in women. Oral tamoxifen citrate (Nolvadex) belongs to a class of antineoplastics called antiestrogens. It is used to treat breast cancer. Body builders use both of these drugs. Why on earth would they do that? The answer is that both of these drugs are anti-estrogens. The term anti-estrogen is a little inaccurate. This class of pharmaceutical does not engage in some sort of matter/anti-matter reaction, annihilating estrogen in a blinding burst of anabolic goodness. Rather, let us think of the classical anti-estrogen drugs (such as nolvadex and clomid) as estrogen receptor antagonists (ERA). These ERAs are chemicals that are close enough in structure to estrogen to fit into the estrogen receptor site; however these chemicals do not have the same chemical effect as estrogen. The result is that any estrogen produced by the body or exogenous estrogen cannot find an open receptor site to attach to. The free-floating estrogen then presents far less problems to homeostasis.

There is a lot of conflict over using nolvadex, clomid and other ERAs. The regulation of estrogen-induced cellular effects is a multi-step molecular process. The diversity of estrogen and anti-estrogen effects on cellular functions is also modulated by tissue and gene specificity. This diversity of reaction may be explained by different levels of molecular regulation, including the presence of two distinct estrogen receptor isoforms (ER alpha and ER beta), their binding to activator or co-repressor transcriptional proteins, and their affinity to different DNA binding domains of target genes (estrogen responsive element or API). These mechanisms may account for the specific responses to estrogens or anti-estrogens according to tissue, cell or gene level. Therefore, in English, a drug like nolvadex, which targets breast tissues, is going to do a better job of preventing gynocomastia than is clomid. However clomid has the benefit of boosting the levels of follicle stimulating hormone, which helps restore the bodies natural testosterone levels and protects against testicular atrophy. It also increases ejaculatory capacity; by the way, so it's best to be considerate to those you care about (or those you employ, I suppose). That was my public service message for the month, by the way. I imagine that this is has something to do with LSH and FSH production in the body triggering the production of more semen, but I am not sure. Ask Bill Roberts over at the mighty TOSSED-OFF-TERONE.NET, or better yet, contact Greg Zulak c/o MuscleMag.

Many people stop using their ERA drugs when they end the cycle. That is a terrible idea. Clomid, as we have already discussed, helps immensely with your recovery processes. But remember, there is almost always an estrogen backlash to having been using testosterone drugs for so long. Therefore, many symptoms of high estrogen levels appear after the cycle. I would continue to use both Clomid and Nolvadex for up to 3 weeks after the last of the drugs have left your body. Remember, if on Friday you take 500 mg of a longer acting drug like Sustanon, then don't consider the following few weeks are truly off time. That is why it is important to know how long the drugs are effective in your body and yet another reason to switch to faster acting drugs in the last few weeks of a cycle.

Effective dosages of these two drugs are debated. I would recommend that the two drugs be used together, Nolvadex at 20 mg per day, and clomid at 50 mg per day. If Nolvadex is used by itself, 20-40 mg are sufficient. 50-100 mg of clomid can be used if clomid is the only ERA drug. Clomid should be used for two weeks after the last steroid injection to help return your body to its natural hormonal state. Nolvadex and Clomid are mildly expensive, but very available because they are not scheduled drugs and can be legally imported. Check the Anabolic Extreme Forum for the email address of one Mr. SBC who can help obtain these vital drugs.

There is a second class of drug used to combat estrogen side effects from what is grandly called steroid therapy; there are aromatase inhibitors. As mentioned previously in this article, the body can convert testosterone into estrogen using the enzyme aromatase. This second group of drugs, which I will call the inhibitors, prevents this process from occurring at all. This class of medication is generally only prescribed for severe conditions and is generally more expensive then any of the ERA.

Teslac, (testolactone), has fallen out of favor for several reasons. First of all, almost one gram daily is needed to achieve sufficient estrogen synthesis inhibition. This makes this a very expensive drug to use. Also, it is currently a scheduled drug because it is a testosterone derivate. Cytadren (aminoglutethimide) is a better choice, requiring dosages of between 250-500 mg per day to suppress estrogen synthesis. 250mg cytadren doesn't cause significant desmolase inhibition, so there would still be cortisol and other steroids, while estrogen is minimized! Cytadren is used therapeutically to combat Cushing's syndrome because it also interferes with the body's ability to synthesis cortisol. Sounds like fun, huh…no cortisol, no estrogen. What a fantastic environment. Tell that to Andreas Munzer! Cytadren can cause cysts as well as effect things like blood clotting. It is reported that Munzer used 1-2g(!) of cytadren/day! Therefore cytadren use should be done with precision. Arimidex (anastrozole) is a drug designed to combat second stage breast cancer. It is an extremely potent drug; one pill per day is sufficient to almost entirely inhibit estrogen in the body. However, the draw back is that this one pill per day can cost you around ten dollars.

The final conclusion about inhibitors is that these are far more powerful drugs then the ERA. All the drugs listed above effect a much wider hormonal spread then the anti-estrogens and they are also going to cost you a lot more. Of all the drugs mentioned, I think that arimidex is the most useful drug for the body builder. Duchaine helped promote cytadren, particularly because of its anti-catabolic ability to suppress cortisol. But, even he acknowledged the double-edged sword that this drug was. Too little cortisol is painful to the joints and in the end, extremely dangerous. I would not recommend the use of cytadren, but I have provided the moderate dosage schemes. The bottom line: These are not drugs to pop like M&Ms.

The Argument Against Our Little Friends:
But these drugs decrease your gains right? Damn it. I hate hearing that phrase clutched to…you guessed it…peoples' breast like a mantra. First of all, there is no way of telling what your gains would have been like without nolvadex or clomid. The scientific evidence that gave rise to this whole dispute (which I believe Duchaine had a hand in too) is that in addition to its anti-estrogenic action requiring estrogen receptors (ER) and leading to growth arrest of breast cancers, studies have previously shown that the anti-hormone tamoxifen (nolvadex) is able to block EGF, insulin and IGF-I mitogenic activities in total absence of estrogens. Thus the excessive use of anti-estrogens will actually result in a loss of some of the most anabolic of hormones (insulin and insulin-like growth factor 1). Steroid antagonists can inhibit not only the action of agonist ligands of the receptors they are binding to, but can also modulate the action of growth factors by decreasing their receptor concentrations or altering their functionality.

Translation: Yes, you are probably compromising your anabolic state by using ERA. But does that mean they shouldn't be used? No. I have heard statements so ridiculous as "Don't use anti-estrogens, they cut into your gains and cost too much. Just get surgery". Lovely, just fucking brilliant. Sure, like surgery isn't going to cut into your workouts or your gains. If you are swayed by the logic of just getting the surgery, I have a recommendation. Go get a pair of kitchen scissors. Ok, now, pull down your pants exposing your atrophied testicles suspended in your pimpled scrotum. Place the base of the scrotum in-between the scissor blades and apply extreme force. Thank you, you have helped the human race by ensuring you cannot procreate and pass on your inferior genetics…if you already have children please place them in a sack and toss them into a lake to drown.

I hope this article has proved helpful to you. If only poor Billy had spent those extra dollars on some Nolvadex, then perhaps he would not be the top billing at the local titty bar. This article may have gotten a little heavy at times with the technical jargon, and I apologize for that. Certainly, its not as much fun as discussing getting huge or getting ripped so you can get laid. But this an important topic if you are going to responsibly use steroids. I do not think that anyone should take their first shot or pill before they have secured enough ERA and/or inhibitors. All you have to do is look at almost any message board to see a desperate plea for Nolvadex or clomid from someone who is mid-cycle and has started to feel the begins of a lump under his nipple. The telltale tumor, you got to love it, huh Ronnie Coleman. There are always those people who claim to never get any problems no matter how much they take, that's great. There are also people who get gyno from androstenediol. I wouldn't want to find out I was a member of the second group and not have the appropriate drugs on hand. How do you know if you are going to be effected? You really can't know until you have some experience with heavy androgens. If you were over-weight as a child (many men experience some degree of gyno in puberty) you have a higher risk. But the bottom line is that no one should begin a cycle without having these drugs nearby. Surgery is not a viable alternative to anti-estrogens.


__________________________________________________

Credat Judaeus Apella, non ego. -

Horace's Satires, book 1, satire 5, lines 100-101

[Big Dave]

Great posts, thanks guys. I'll send my father the prostate cancer article Got Wood?, I know he'll ignore it, but thanks anyway.

[MisterX]

Estrogen and progesterone induced sides can be nasty, extremely annoying and troublesome to put it lightly. But, Karlis Ullis and Josh Shackman
make their point that estrogen and progesterone have their place and without them you can experience many metabolic problems including but not limited to libido dysfunctions. Can it be true? WithOUT estrogen, sex drives can be effected drastically. This all sounds good in theory, but practically most of us don't have any trouble with estrogen levels getting too low, unless we are using excessive amounts of Arimidex coupled with DHT derivative anabolics, and possibly anti-estrogens. I've never heard of anyone 'lacking' in estrogen, but it can be a problem if once again estrogen levels were to be too low with Anti-e's Aromatase inhibitors ect. So, they make their point, and make it well that estrogen and progesterone which can be nasty and cause problems in excess, have their place. But, elevate those estrogens, like estradiol without opposing hormones like DHT, Testosterone, even possibly progesterone or estriol and you can exerience what has been link to several disorders leading to cancer. Take it for what it's worth. I especially don't agree with them on androstendione, I think powdered dirt has more worth, personally. Estrogen does play a role and have it's place as we all know, just a very small place, unless you want to be a woman.

Here's the article by ..
Karlis Ullis and Josh Shackman


Estrogen and Progesterone for Men


When you saw the title of this article, your first reaction might have been "has Dr. Ullis lost his mind?" or "Why the hell would I want to put these hormones into my body that will make me fat and grow breasts?" But before you have me committed, remember from Part I of this series on Contrarian Endocrinology that there is no such thing as a "good" or "bad" hormone, nor is there such thing as a strictly "male" or "female" hormone. Just as testosterone plays an important role in the female body and has many positive health benefits for woman, estrogen and progesterone also have numerous health benefits for men if used properly. However, remember that the arena of sex hormone research is highly politically laden and is still in somewhat of a state of infancy regarding long term research. Just as there is precious little research on testosterone for women, there is also very little research on progesterone or estrogen for men. But given both the research data currently available as well as my own clinical experience, I am very excited about the potential of these two traditional "female" hormones for their use and role in men.


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Estrogen for Men

Yeah, yeah, I know – most male readers of Meso-Rx are far more concerned with keeping their estrogen levels down than raising them. No, I am not crazy in case you are wondering, and this is not an article aimed at transsexuals. To be sure, if my male patients have estrogen levels that are too high I may prescribe anti-estrogen therapies which may include such drugs as Arimidex (an aromatase inhibitor most commonly used in women with breast cancers and have estrogen sensitive tumors), Tamoxifen (an estrogen tissue receptor blocker) and natural methods of blocking the potent estrogen effects on tissues with phytoestrogens (soy, flax seeds and many other plants that contain the weak estrogen like compounds), or decreasing the negative effects of some of the "bad estrogen metabolites" (16 alpha hydoxyestrone, and 4 hydroxyestrone) with the use of the cruciferous vegetables or their extracts (i.e. indole -3 -carbinole or its related more potent cousin diindoylmethane) as part of an overall hormone replacement/anti-aging treatment program. Most men as they get older will have an increase in estrogen levels and decrease in testosterone as they get older. Overall, the ratio of testostesterone to estrogen declines with age and I believe the increased load of different estrogens and some of their toxic metabolites contributes to some of diseases associated with aging in men (prostate, cardiovascular, and immunological diseases, and even age associated gynecomastia).

With this above disclaimer, I would also like to add that estrogen also has many benefits and is far from being a "bad" hormone. Just as women are more sensitive to the effects of testosterone to women, some men are very sensitive to the effects of estrogen. Giving brief spikes of estrogen to a man may induce surges in energy and libido similar to what you would expect to see in a woman given a testosterone injection. A recent review article in the Journal of Clinical Endocrinology and Metabolism (June, 1999) by one of the world’s authorities on brain biochemistry and function, B.S. McEwen describes the many potent effects estrogen can have on the brain and the central nervous system and the two estrogen receptors. For example, estrogen has been shown to have wide ranging effects on the noradrenergic, dopaminergic, and cholinergic systems, all of which are profoundly important for mood and energy (8). The stimulatory effects of estrogen on our neurotransmitter systems and other aspects of the central nervous system may be a major reason why some men get a big boost of energy and libido when their estrogen levels rise.

So should I go steal some of my wife’s or mother's Premarin tablets and pop a few before my workouts? The answer is of course not! Just as I don’t recommend estrogen replacement therapy for all women and without a concurrent testosterone replacement program, I most certainly don’t recommend giving estrogen directly to men. Instead, I have chosen alternative treatments that give a produce a physiologic rise in both testosterone and estrogen for maximum libido and energy.

One drug that is extremely effective for enhancing libido is Human Chorionic Gonadotrophin (***, a form of lutenizing hormone or LH), which when injected even subcutaneously gives both a simultaneous boost in both testosterone and estrogen levels. From clinical experience, I have found it much more effective than plain testosterone for enhancing libido. However, I do not think it is the best drug for bodybuilders or athletes. *** is popular drug for bodybuilders who use it to boost their natural testosterone production during or after an anabolic steroid cycle. However, some bodybuilders complain develop gynecomastia from *** use, due to the surge in estrogen. In addition, *** only stimulates natural testicular output briefly (a few days) but is counter-productive to use in the long run. Chronic use of *** may shut down natural testosterone production by negative feedback signalling and thereby blocking the brain-pituitary gland production of LH.

A much simpler choice for athletes or bodybuilders seeking a natural concurrent boost of estrogen and testosterone is a much cheaper supplement that you have all heard of before – androstenedione! In spite of the "shocking" revelation that androstenedione causes increases in estrogen in the recent EAS sponsored study (6) in JAMA, my response to this study was "No @#$^ Sherlock!" Androstenedione is well established and well known to be a precursor to both testosterone and estrogen. I have found that many people notice more of an energizing effect from androstenedione than from any of the other testosterone prohormones. I believe this is largely due to the increase in estrogen levels.

It should be noted that finding the "optimal" or "normal" level of estrogen for men is extremely problematic. Estrogen levels can be difficult to measure accurately, as medical doctors in some countries even resort to using sex hormone binding globulin as a rough measure of estrogen levels. Since most men experience an increase instead of a decrease in estrogen as they get older, little attention is paid to the importance of estrogen deficiency in men. It has recently been shown that too little estrogen is linked to male osteoporosis. Studies of men who genetically lack the enzyme for the conversion of testosterone to estrogen, (aromatase deficiency), can be very osteoporotic. However, testosterone replacement therapy, if sufficient, is usually enough to restore both testosterone and estrogen levels high enough to prevent osteoporosis.


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Progesterone for Men

Once again, I am not crazy. I know that most of you think of progesterone as an "evil" catabolic and fattening hormone. What many of you may not remember is that the extremely popular anabolic steroid nandrolone decanoate (aka Deca Durabolin or nortestosterone) is in fact classified as a progestin (hormone with progesterone-like activity)! In addition, many progestins given to women in birth control pills and other drugs such as norgestrel and norethidrone are classified as 19-nor-testosterone or 19 nor- progesterone derivatives. Eastern German female Olympic athletes were known to have taken large quantities of these nor-testosterone derivatives to build muscle with the notorious masculinizing side effects that was obvious to all Olympic observers. Modern Olympic testing can now distinguish the difference between nor-progesterone and nor-testosterone derivatives. Since birth control pills aren’t yet on the list of drugs banned from competition, these "women" were able to pass all drug testing without any worries. Of course, I don’t suggest you raid your girlfriends birth control pill case in order to make yourself "feel like Deca". Recent studies at UCLA (9) have shown that different types of birth control pills have different androgenic capacity and can change the Olympic doping standard of testosterone to epitestosterone ratio of six to