Within the culture of the chemically enhanced lies the so-called middle-aged athlete in search of a wiser adolescence…or at least the physique of an enhanced youth with the absence of ignorance and mistakes. They are notably the individuals most concerned with the potential negative side-effects of chemical muscle enhancement, yet should be recognized as cause for interest by all who seek such goals of excellence. This is a rarely addressed area yet in truth there are likely more (legal and otherwise) AAS (anabolic/androgenic steroids) users of the middle-aged nature than those of the 20-something variety. From their concerns we each can learn how to progress with efficiency and greater health. Thanks to several pioneering physicians, HRT (Hormone replacement therapy) is finally moving out of the Ice Age and into the New Millennium. Like the hard-core athletes of younger years many have realized certain problems associated with the use of AAS and are choosing their progress based upon specific intent.
With the employment of HRT in middle-aged males came concerns for health issues such as BPH (Benign Prostate Hyperplasia) and libido to name a few. We will discuss chemical muscle enhancement in a moment, but first we have a some things to understand and consider too aid our goals…
A Healthy Prostate Is A Lagging Body Part
*A male’s prostate (females do not have one) is quite small at birth. However it does undergo two growth phases as we progress through life. The initial growth phase occurs during puberty when hormone levels rise. The second occurs around the time that we are 25 at which time the gland starts slowly growing again. A note of interest is that research has as of yet been unable to validate as to why this second growth phase happens. This second growth phase will continue during most of a man’s life. But the growth during this phase is not uniform and is commonly expressed as nodules of excess tissue development that are somewhat tumor-like. This enlargement of the prostate is called BPH or benign prostatic hyperplasia. The term “benign” refers to the neither fact that the condition is not cancerous, nor does it in itself lead to cancer.
**BPH occurs in almost every man who lives long enough and whose “Boys” remain functional. The misuse of AAS can possibly lead to early BPH. Though symptoms often occur in many males in their 40’s, better than 50% of men in their 60s have BPH. The incidence rate goes up to 90% or more among men older than age 80.
The prostate gland itself is about the size of a walnut normally. It is made up of two regions, or lobes, enclosed within an outer layer of tissue.
*As you can see by the diagram the prostate is located in front of the rectum and just below the bladder (where urine is stored). The prostate also surrounds the canal that urine passes through to exit the body, which is, of course, called the urethra.
*Researchers are not sure of all prostate functions. One of its main roles however is to squeeze fluid into the urethra as sperm move through during sexual climax, this fluid helps make up semen, energizes the sperm and makes the normally acidic vaginal canal less so. A note of interest for those readers who have had children (at least their female partners have) this is a common factor deciding the baby’s sexual gender.
*As stated prior the prostate continues to grow during most of a man’s life. But the enlargement does not usually cause reason for concern until later in life. As a rule, BPH rarely causes symptoms before the age of 40, but more than half of men in their 60’s and as much as 90% in their 70’s and 80’s have some degree of notable symptoms of BPH. This is reason enough to at least discuss this in some depth I believe.
As the prostate enlarges, the layer of tissue surrounding it stops it from expanding. This in turn forces the gland to place pressure against the urethra like a clamp on a water hose. As a result the bladder wall becomes irritated and thicker. An obvious sign of this is when the bladder begins to contract even when it contains relatively minute amounts of urine. This of course causes frequent dry runs to the bathroom and long moments of staring into white porcelain with your appendage in hand and longing eyes. As time passes the bladder weakens and loses the ability to void itself properly and urine stays in the bladder. The narrowing of the urethra and partial emptying of the bladder is one primary cause of most of the problems associated with BPH. A case of the dribbles on occasion is not a reason to panic and run to the nearest physician for a rectal prostate exam however. (Ouch!)
It should be noted that all males suffer “occasional” symptoms but there are those to be aware of when they remain consistent. So what are the most common symptoms of BPH?
* Weak and interrupted urinary stream.
* Dribbling or leaking of urine.
* An increase in the number of trips to the toilet to urinate without an increase in total urine excreted.
The Cause of BPH?
For a few hundred years now medical research has been aware of the fact that BPH occurs predominantly in older men and that it doesn’t develop in men whose testes were removed before puberty (no joke, there are statistics for this). For this reason some of the more narrow sighted researchers believe that factors related to aging and the testes only may induce the development of BPH.
*During their entire lives, men produce the so-called male hormone testosterone and interesting female hormone estrogen. (I say, “interesting” simply because it is the hormone that makes women the fun and interesting creatures that they are) As men age they realize decreasing circulatory testosterone levels resulting in a higher proportion of estrogen. Estrogen, and many of its chemical cousins, promotes IGF-1 formation in cells that it contacts. As most are aware, IGF-1 refers to Insulin-like Growth factor-1 meaning that it has a specific growth effect upon tissues of a type one variety. In this case the effect is predominantly that of hyperplasia and inclusion. (Huh?)
*Our body’s are constantly in need of repair and/or replacement of cells due to many metabolic factors. Most protein-based tissues (like, uh, muscle) have a sort of “cell nursery” where new cells are formed. These new cells are called satellite cells (or stem cells in some areas of the body). Since these satellite cells are metabolically active, but are as of yet undisclosed as to type or action (what kind of cell they want to become when they grow up…they got no job in short), they pretty much just eat and lay around like a teenager. Like a teenager, these cells require a powerful stimulus to induce decision and action. In the case of satellite cells the stimulus is cellular receptor-site mergence with IGF-1, which initiates growth and inclusion. The growth can be by hyperplasia as well as hypertrophy. Hyperplasia simply means that a cell splits and becomes two cells therefore larger by number. Hypertrophy means that the cell itself grows in size and volume. Of course inclusion means that the satellite cells join other working cells in a host area and now have a job. In the case of muscle fibers this is great, but in the case of prostate tissue this is bad as a prostate gland the size of a grapefruit can be a real pain in the…well, you get the point.
The most commonly blamed hormone for BHP is dihydrotestosterone (DHT). DHT is the chemical result of testosterone being reduced by the 5-alpha reductase enzyme. Though there is some circulatory 5-alpha, the predominance of it is found in sex specific tissues such as the prostate gland and hair follicles. Interesting fact is that even though a man’s testosterone production declines with age, the ability and accumulation of DHT does not. Some researchers hold to another theory in relation to DHT’s role in BHP in that there appears to be some evidence of DHT induced mediation of growth. So the elimination of DHT from the system may be an action that promotes BPH in certain hormonal environments.Prostate Cancer
Since BPH relates to the growth of prostate cells we should also briefly discuss prostate cancer. I think that this is paramount since the occurrence of prostate related illness has reached an epidemic level in the West. Every year between 40 and 50 thousand die due to prostate related illness. In fact prostate cancer is the second leading cause of death among men in the US.
Though the debate continues over the primary hormone of growth in relation to prostate BPH and cancer alike continues, more recent research has shown a commonality of dependency for all camps of thought. Please bear with me while I give you some needed facts to consider as we progress.
Prostate cancer is a multi-staged carcinogenesis. What this means is that prostate cancer has 3 distinct phases of development:
1. Initiation 2. Promotion 3. Progression
Now For Some Scarier Facts
Most are not aware of the fact that most males have early expressions of prostate cancer when they are in their 20’s. This is referred to as the initiation stage, but it is what occurs next that is the deciding factor as to whether or not the disease is going to progress in a life-threatening manner. Basically males do not die simply because they have prostate cancer. It is a fact that mortality is a function of the proliferation and growth of the cancer cells into other organ systems. So the question of threat is actually…are all of the necessary ingredients for tumor promotion available to allow the cancer to grow and spread? Cancer cells are like any other organism in that they require a specific nutrient profile to grow and flourish. Without the specific nutrients and the proper means of obtaining them the cancer cells die.
5-LO and Behold…Some Answers
*As any athlete will tell you the human body produces an amazing number of chemicals from the raw materials we feed it through whatever means. Though it seems likely that estrogen and its ability to increase IGF-1 in prostate tissue has a profound effect upon BPH and prostate cancer cells alike, the cells must still be fed to survive. An enzyme called 5-Lipooxygenase (5-LO) is utilized by the body to metabolize arachidonic acid into another chemical called 5-HETE. Arachidonic acid is an omega-6 fatty acid found in red meats and other animal protein sources. And 5-HETE is prostate cancer cell food. In fact it is the only food it eats. So, if the 5-LO enzyme is inhibited then the 5-HETE/cancer-cell food is not produced and the cells cannot grow or proliferate. Several studies, including a 1999 study published in the distinguished Proceedings of the National Academy of Sciences from the University of Virginia Cancer Center, have continued to prove that prostate cancer cell apoptosis (cellular suicide) occurs “massively and rapidly” no more than 1 to 2 hours after the production of 5-HETE (by inhibition of the 5-LO enzyme) has been inhibited.Inhibitors of 5-LO
*I have little doubt that most male athletes were aware of research being done into chemo-preventive via fruits, herbs and vegetables. (Chemoprevention basically means chemical prevention) Research has found that there are some common food items rich in nutrients that specifically inhibit the activity of the 5-LO enzyme. They include; ginger, green tea, saw palmetto, olive oil, and many others. Ginger is the top of the list in the government’s USDA database of 5-LO inhibitors. This is due to the fact that ginger has been shown to contain at least 22 different chemicals that act as effective 5-LO inhibitors.
In my opinion an athlete cannot consume enough organic ginger. It also seems intelligent to reduce ingestion of large amounts of Omega-6 arachidonic acid. Arachidonic acid is found in high levels in the red meats and certain cooking oils like corn and peanut oils. Additional protection can be achieved through consumption of more of the “good” Omega 3 fatty acids (in particular DHA) as the balance or ratio of Omega 3- to – 6 fatty acids is another way to inhibit the inappropriate formation of arachidonic acid by-products.AAS and The Prostate
*There seems to be a major conspiracy in the world, that in and of it places all things male in a dimming yet foreboding light of evil. Such is the case for testosterone and other natural manly hormones alike as well. With terms like “roid rage” being inherently a factor of man, and PMS being a mere trait of the “softer sex,” it seems that, as per usual, we as males must bear the brunt of responsibility for the world as it exists. (Cool with me!)
We have already discussed the possible effects that DHT and estrogens can have upon the prostate gland. Naturally the issue of hair loss due to the same factors is obvious though there is an existing notable correlation of course. But now we should consider some “how and why” info as well.
Naturally occurring testosterone and many man-made Anabolic/Androgenic Steroids (AAS) are susceptible to chemical conversion once they enter the circulatory system. Testosterone can be reduced to dihydrotestosterone (DHT) by the 5-Alpha-Reductase enzyme or aromatized to estrogens by the aromatase enzyme. However the reader must realize that even though most AAS are chemical variations of testosterone some are resistant to chemical alteration in the circulatory system. This suggests the potential to medically (or otherwise) introduce an improved hormone profile in regards to prostate health.
Many know of the AAS nandrolone as nortestosterone. Due to slight alterations in the ring structure nandrolone has been given unique high anabolic/low androgenic properties and an interesting aromatization/reduction profile.
Since nandrolone is a nortestosterone it should not come as a surprise that it aromatizes to estrogens like any other testosterone. Interesting thing here is that the estrogen product is a nor-estrogen called norestradiol that has less activity than the estradiol produced from aromatization of testosterone itself. This means that it is a weaker estrogen and as such actually has minor anti-estrogen value in that it has the ability to block receptor-sites from being pillaged by more powerful estrogens. For those of you who stayed awake through the earlier science stuff this also means less site-specific IGF-1 formation in prostatic tissues. Additionally nandrolone aromatizes at about 1/5th the rate of testosterone. Some physicians have noted the decrease in PSA values when nandrolone alone is utilized instead of solely testosterone as HRT (Hormone Replacement Therapy) in hypogonadal males. Since PSA test values are indicative of BPH it appears that the estrogen/IGF-1 theory has some value to consider.
**PSA (Prostate Specific Antigens) Test is a means of evaluating BPH
Like testosterone nandrolone is susceptible to the 5-Alpha-Reductase enzyme and reduction to DHT. However the nor structure again positively influences or mediates the potential negative. The reduction product of nandrolone is the weaker androgen nor-DHT (dihydronandrolone or DHN). As such the resulting weaker nor-DHT has a blocking effect upon the more powerful DHT at the receptor-sites in prostate tissues thus resulting in a mitigating value.
Unfortunately nandrolone has progestin-like qualities and therefore can negatively effect libido and certainly interact with progesterone receptors in a manner that is similar in action to estrogens. This explains the puffy appearance many realize during administration since, like its estrogen cousins, progestins can induce an alteration in the water table toward retention (especially subcutaneously). When nandrolone is administered alone the result is a profound increase in muscle protein synthesis with potential BPH inhibitory value. But what of the lack of wood that occurs from long-term or high dose therapy?
The reader must realize that testosterone, estrogens and DHT each play a crucial role in pro-sexual responses in males and females alike. An increase in circulatory androgens will result in an increase in libido and oddly enough the total absence of estrogens from either gender will result in an absolute libido crash. So the issue of ratios comes to the foreground in the question of prostate health vs. libido.
An average healthy male possesses about 50mg of endogenous testosterone weekly. In truth, the male produces a great deal more, but due to various metabolic factors the remaining circulatory total for actual testosterone is about 50mg weekly. Those who have used AAS for HRT or other purposes are aware of the fact that the average accepted replacement equivalent for this 50mg of endogenously produced testosterone is 200mg of either testosterone enanthate or testosterone cypionate weekly. Though about 33% of either of these exogenous testosterones is ester weight, this still means that the administration dosage delivers about 3 times the amount of testosterone (about 140mg) weekly when compared to natural production. Simply stated, approximately 2/3rd of the administered dosage is metabolized. A great deal is converted to the prosteroids 4-androstene 3, 17-diols as a sort of functionary reserve androgen and some is aromatized to estrogens or reduced to DHT. The point being is that the body creates a specific hormone profile to facilitate physiological needs like sex and survival. But how much actual testosterone is necessary to keep the fires burning while preventing the possibility of adding to the potential of BPH and prostate cancer?
As we have discussed prior nandrolone has an aromatization rate of about 1/5th that of testosterone and a comparable 1/5th reduction profile to the weaker nor-DHT. This suggests that a weekly dosage in the 1000mg range would likely have less of a negative potential effect upon the prostate gland than the recognized 200mg weekly administration of testosterone cypionate. Since this would result in a reduction in libido the simplest answer has become to administer either 50mg of testosterone cypionate with up to 1000mg of nandrolone decanoate weekly, or 100mg of testosterone cypionate with 500mg of nandrolone decanoate. Of course there are many other options as well.
*There are many different AAS and as such a wider diversity of possibilities than some may realize in this particular case, an example is the oral drug oxandrolone. Though it is an androstane, it has low affinity for sex specific tissue such as the prostate. It does not aromatize nor is it susceptible to DHT conversion. Interesting enough is its potential to act as a weak DHT antagonist at the receptor yet still allowing for an acceptable degree of DHT activity for the so-called hardening effect. This means that the drug interacts well with both D-1 and D-2 brain receptors for sportin’ wood and orgasms respectively. The 17c–alkylated structure would be a concern in long term administration but as of yet has shown little reason for liver concerns even in dosages of well over 50mg plus daily in AIDS patients.
Though not approved for medical HRT use, there are many who have employed the effectual properties of the AAS boldenone (Equipoise). Boldenone aromatizes at a rate 50% less than testosterone and results in little DHT formation. This is quite interesting in theory since boldenone is more anabolic yet less androgenic than testosterone as well.
Legal Androgens And Playing Nice With The Prostate
Oddly enough some of the most BPH friendly androgens are OTC products until 2005. The really silly part is that they are being removed from the market by the FDA and reclassified as Controlled Substances.
Due to the addition of a hydroxy group in the testosterone chemical structure a new compound called 4-Hydroxytestosterone (AKA Testosterone-OH) has been created. It does not reduce to DHT nor is it susceptible to aromatization to estrogens. The androgen is highly anabolic yet less androgenic than testosterone itself. Hmmm, that is pretty prostate friendly already.
Another interesting aspect of Testosterone-OH is that it does convert in the body, to some extent, to another very useful androgen called Androstenoldione (AKA Formestane).
Formestane is a powerful suicide aromatase inhibitor. This means that it decreases estrogen production by preventing the aromatase enzyme from doing its thing with androgens such as testosterone. It also decreases the receptor counts for both estrogen and progesterone. (Yup, an effective way to control progestin activity even from AAS like Trenbolone and Nandrolone…no more “Deca Dick”)
Formestane is somewhat unique in that it increases IGF-1 production by about 26% though it decreases total circulatory estrogen…and it has been shown to decrease BPH.
*Tamoxifen citrate (Nolvadex) is a weak, yet “somewhat” effective progesterone receptor-site antagonist. This means that, though it is actually a weak estrogen, it can also affect progesterone receptors thus having the ability to act as a weak progesterone receptor-site blocker. Some have realized a return to normal sexual function by adding as little as 10mg 2 times daily to protocols employing the administration of higher dosages of nandrolone.
The only truly effective antiprogestin are the abortion drug RU-486 (mifepristone) and onapristone. Like tamoxifen they are receptor antagonists. The exception here is that they are very effective. In fact, in the field of breast cancer treatment researchers and women’s health advocates alike are seeking approval for the use of RU-486 as a breast cancer treatment for progesterone dependant tumors. Anything effective enough to get the AMA off of their butts is very effective indeed!Breast Feeding = No Erections?
*Now that we have discussed how athletes of all ages who utilize AAS can improve the safety and sexual profile for bigger muscles and a “harder” appendage appearance, the reader will (I hope) recall there is a hormone ratio factor to be concerned with. All is well in the world of the chemically enhanced…right? Like all other alterations we attempt to make in the body’s sense of homeostasis, there is a reaction to our intended action to consider.
When a woman’s body prepares to give birth it begins to produce a hormone called prolactin. Its job is to trigger an increase in breast and glandular tissue to produce milk for the coming baby’s sustenance. Men produce prolactin as well!
*When a man’s prolactin levels elevate there is a marked decrease in libido, GH and leptin. The result is a fat guy with little muscle and the sex-dive of a eunuch cadaver. (Pretty vivid huh!!!)
*Prolactin is a single-chain protein hormone that is closely related to growth hormone (GH). It is secreted by so-called lactotrophs in the anterior pituitary gland. It should be noted however that is also synthesized and secreted by a broad range of other cells in the body, most prominently various immune cells, the brain and the decidua of the pregnant uterus.Prolactin Control
*In opposition to what we normally see with all of the other pituitary hormones, the hypothalamus predominantly suppresses prolactin release from the pituitary gland. In other words, there is usually a hypothalamic “Stop that” order set against the lactotroph, and prolactin is released only when the order is released or ended. A note of interest is that if the pituitary stalk is severed, prolactin release increases, while secretion of all the other pituitary hormones decreases dramatically due to loss of hypothalamic releasing hormones. But this is an unlikely scenario for most athletes and should obviously be avoided nonetheless.
The neurotransmitter Dopamine appears to act as the top dog prolactin-inhibiting factor. Dopamine is secreted into portal blood by the hypothalamic neurons. Next it binds to receptors on lactotrophs, and inhibits both the synthesis and release of prolactin. So chemicals and drugs that interfere with dopamine release or receptor binding also increase the release of prolactin. These are called antagonists. Drugs and chemicals that either increase, act as, or potentate dopamine are agonists.
Of course there are other chemicals in the body’s Action/Reaction Factor closet that positively regulate prolactin. The major ones are GnRH, TRH (thyroid Releasing Hormone) and VIP (Vasoactive Intestinal Polypeptide). By the way, hyper-stimulation of the nipples may have a stimulatory effect upon prolactin release as well. But that is one we will leave alone.
So, Why Do Non-Cross Dressing Men Produce Prolactin?
*As a man ages his body begins to decrease the amount of androgens that it synthesizes. In fact many studies have shown that an average 40-year-old male produces about half of the testosterone that he did when he was 18. So, he possesses a lower rate of muscle anabolism yet a higher rate of fat anabolism. Many researches have claimed that this is due to normal physiological changes that occur as we progress through the years. In truth this is bullshit and supposition based upon average sedimentary individuals. I monitor the physiological indicators of athletes for a living. I can say conclusively that almost any otherwise healthy male that remains in peak condition and eats a proper diet will retain a superior androgen production profile. So this is more so a matter of choice than pre-programmed physiological events. With that said let’s get on with the “why” of prolactin.
Estrogen is a primary promoter of prolactin release. Of course there are other factors to consider (which we will discuss in a moment) that may trigger excessive prolactin secretion, but the normal trend toward increased prolactin release is due to increased estrogen synthesis.
The clinical term for excessive release of prolactin is hyperprolactinemia. It is actually a relatively common disorder in humans, especially those who utilize AAS. There are many causes that initiate the condition including prolactin-secreting tumors and therapy with certain drugs.
Males that experience hyperprolactinemia commonly develop hypogonadism (the shut down of the HPTA) with decreased sperm production, decreased sex-drive and impotence. Those affected normally show breast enlargement (gynecomastia), but very rarely actually lactate. The gyno can initially manifest itself as an increase in fatty tissue under the lower pectorals and a puffy appearance to the areola and nipple prior to formation of the painful benign (usually) tumors.
A simple blood test for serum prolactin levels is commonly employed to evaluate the degree of potential feminization a male can or is experiencing. The lab results are quite simple to read, though a trained professional should interpret the results.
1. Adult: 2. Newborn: 100 to 300 (falls below 20 after 6 weeks)
a. First Trimester: b. Second trimester: c. Third Trimester:
*References Bakerman (1984) ABCs of Lab Data, p. 342
An older drug called Parlodel (bromocriptine) is enjoying new popularity for multiple uses. Though commonly prescribed for the treatment of pituitary tumors resulting in heavy prolactin secretion the drug has found itself in a newer position as a sexual stimulant. This is simply explained since the drug is a dopamine agonist with profound stimulatory effects upon the brains D-2 receptors. The sexual side of this drugs effects coupled with the antiprolactin value is reason enough to include it in this article. Additional consideration for all athletes has been the drug’s pro-GH and pro-Leptin values due to a respectable up-regulation in production of both seen in patients who have been treated with bromocriptine. The result is leaner more muscular individuals that are obviously hornier as well. Some who have used bromocriptine suffered from nasal and sinus congestion as well as nausea and a decrease in blood pressure. Due to the 12 hour half-life for bromocriptine 2.5mg in the morning is highly effective though some have had need to progress to 2.5mg 2-3 times daily after the first two weeks of administration.
*The drug Dostinex (cabergoline) is another dopamine agonist drug employed for treatment of medical conditions that occur from an over production of prolactin and some menstrual problems. (The correct term for an anti-prolactin is antihyperprolactinemic by the way) Over all, the sexual and anti-prolactin effects of cabergoline are similar to bromocriptine. Many who have suffered from the nausea, sinus and nasal congestion side effects of bromocriptine, report none with administration of this drug. Cabergoline has a rather long half-life and as such as little as 0.25mg once weekly has been notably effective. Some have had to increase their dosage up to 0.50mg twice weekly to maintain the result value.There Are Always Options To Consider…
There have been notable results obtained by many who have employed some of this discussion in a sort of Tide-Cycle. The idea behind a Tide-Cycle is to create a hormonal environment that ebbs and flows within the body’s Action/Reaction Factor time frames. As such the exposure to negative side effects and diminishing returns is reduced significantly. If constructed correctly the result in better net gains per protocol is improved as well.
Tide-Cycle Example 3 (daily)
1. Testosterone Cypionate 600mg/Oxandrolone 25mg
2. Oxandrolone 25mg
3. Oxandrolone 25mg
4. Oxandrolone 25mg
5. Oxandrolone 25mg
6. Oxandrolone 25mg
7. Oxandrolone 25mg
8. Nandrolone Decanoate 800mg/Oxandrolone 25mg
9. Oxandrolone 25mg
10. Oxandrolone 25mg
11. Oxandrolone 25mg
12. Oxandrolone 25mg
13. Oxandrolone 25mg
14. Oxandrolone 25mg
15. Testosterone Cypionate 600mg/Oxandrolone 25mg/Bromocriptine 2.5mg
16. Oxandrolone 25mg/Bromocriptine 2.5mg
17. Oxandrolone 25mg/Bromocriptine 2.5mg
18. Oxandrolone 25mg/Bromocriptine 2.5mg
19. Oxandrolone 25mg/Bromocriptine 2.5mg
20. Oxandrolone 25mg/Bromocriptine 2.5mg
21. Oxandrolone 25mg/Bromocriptine 2.5mg
22. Nandrolone Decanoate 800mg/Oxandrolone 25mg/Bromocriptine 2.5mg
23. Oxandrolone 25mg/Bromocriptine 2.5mg
24. Oxandrolone 25mg/Bromocriptine 2.5mg
25. Oxandrolone 25mg/Bromocriptine 2.5mg
26. Oxandrolone 25mg/Bromocriptine 2.5mg
27. Oxandrolone 25mg/Bromocriptine 2.5mg
28. Oxandrolone 25mg/Bromocriptine 2.5mg
* Tamoxifen 10mg 2xd
* Optional: Aromasin 25mg EOD Day 1-15
*The use of testosterone cypionate and nandrolone decanoate as chosen esters in administration opposition allows for washout periods for each potential negative effect. As an example, by using the correct 14-16 day active-life for each of the drugs, you can see that the actual circulating dosage dwindles for one drug and is replaced by the other in a constant plasma level protocol. Remembering the fact that it is usually prolonged exposure to a given substance that triggers a negative reaction. Consider the fact that this potentially voids most problems with prolonged exposure to estrogens, DHT and progestin-like androgens. By employing bromocriptine during the second two weeks the prolactin build-up is no longer an issue as well. Real simple: Action/Reaction. Plan ahead.
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About the Author:
Author L. Rea has lived his entire life by this motto, and he knew in 2001 that the time had to come to apply the knowledge he had learned from a lifetime spent in bodybuilding and research to a new purpose. ALR Industries was born to provide those who refuse to accept mediocrity the tools to reach their full potential. Author L. Rea is not only a bodybuilder himself, but also one of the scientists behind the development of all the ALR Industries products. His combined experience of more than three decades in the worlds of bodybuilding, and biological research and development, has lead to some of the most inventive and effective supplements for bodybuilding, health, and fitness ever created. As the author of three books and 100’s of article on human performance and health, Author L. Rea has shared his passion for never accepting mediocrity with the world. Chemical Muscle Enhancement
1.) The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, THE , 87(4):1467-1472 2002
2.) Effects of long-term administration of androgens and estrogen on rhesus monkey prostate: Possible induction of benign prostatic hyperplasia. JOURNAL OF ANDROLOGY , 21(6):833-841 2000
3.) Endocrine treatment in prostate cancer. SEMINARS IN SURGICAL ONCOLOGY , 18(1):52-74 2000
4.) Gonadal Steroids in the Treatment of Mood Disorders. PSYCHOSOMATIC MEDICINE , 61(5):676-697 1999
5.) Hormonal contraception for human males: prospects. ASIAN JOURNAL OF ANDROLOGY , 2(1):46-50 2001
6.) Hormones, genes, and behavior. PNAS: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA , 94(26):14213-14216. 1997
7.) Prolactin and antipsychotic medications: mechanism of action. SCHIZOPHRENIA RESEARCH , 35(2):S67-S74 1999
8.) Treatment of macroprolactinoma with cabergoline: A study of 85 patients. CLINICAL ENDOCRINOLOGY , 46(4):409-413 1997
9.) LACK OF EVIDENCE FOR AROMATASE IN HUMAN PROSTATIC TISSUES EFFECTS OF 4 HYDROXYANDROSTENEDIONE AND OTHER INHIBITORS ON ANDROGEN METABOLISM, [CANCER RESEARCH , 49(23):6551-6555 1989
10.) The effect of aromatase inhibitor 4-hydroxyandrostenedione on steroid receptors in hormone-dependent tissues of the rat JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY , 52(1):71 1995
11.) Regulation of insulin-like growth factor I receptor expression by the pure antiestrogen ICI Lady Davis Research Institute, and Department of Medicine, McGill University, 3755 Cote St. Catherine Road, Montreal, Quebec H3T 1E2, Canada. Clin Cancer Res 1996 Dec;2(12):2037-42