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Prostate cancer from test. ALL MUST READ!

"""""""""""Are any of these substances actually mutagenic? It takes some form of mutation (missense, frameshift, nonsense) in a few different areas to make a cell line carcinogenic, so where does the mutation come in to play?
As for the patient disscused in the begining, hes far from dead. I fuckin hate dumbass oncologists who say "terminal". You dont beat cancer without trying and no cancer is 100% "terminal". Try everytning in (and out of) the book to beat it. Cisplatin, Gimcidabine, various statin drugs, COX2 inhibitors, gamaglobulin, and interlukins,.......add em up, takem, see what happens, you have nothing to loose.""""""""""


Repeatin my post to see if any bros know of any mutagenic nature involved. If there is none, then you could look at hormones and cancer proliferation the same way as you could look at COX-2 and cancer growth.
We have cancer almost everyday of our lives bros, but we kill most of the cells with our immune system. It takes several mutations to trigger growth of a malignant tumor. Do hormones cause these mutations, or just feed malignant cells that we already have?
 
Realgains do you have research articles, to back up your statement that men without 5-alpha reductase never get prostate cancer? These same men also never would get an erection their entire lives. " Elevated estrogen" is also a culprit in prostate cancer? I have no doubt that DHT plays a major role in the development of prostate problems including cancer, however the majority of men that I have known who developed prostate cancer never used steroids. A few of them were quite young. It seems to me at least that some of the doctors you quoted are either jumping to conclusions and or may be on a typical anti anabolic crusade. I'm not totally disagreeing with you by no means. in fact I think that you brought up many valid ideas. I just see your post as somewhat slanted against steroid use. Please correct me if I'm wrong. One more question do you use gear?
 
My point in asking you about estrogen and prostate cancer, was that it seems that you or none of the doctors you quoted, were saying anything about estrogens role until Macro pointed it out.:D
 
Realgains sounds like a scared little puppy. LOL!! I would expect more from an educated professional than unfounded ramblings of his doctor friends, but then again we don't know if he actually has a degree or if he's just an idiot.

I don't think you can state any 'facts' here, realgains. Those are not facts, those are presumptions. I don't know if we understand all the factors involved but I certianly don't think we can make assumptions basted on unfounded and unsupported facts of 'realgains' that testosterone causes cancer unconditionally. And that DHT will make your nuts mutate. I think there are many factors, I think DHT will cause BPH which coincidentally usually arises due to low test and high estrogen later in age of a man in the abcense of high testosterone. Has anyone ever taken a huge dose of Primobolan, primo is mostly a synthetically derived DHT. Well, it causes BPH, and it will go down after a week or two.

No test, no estrogen, no cancer, just BPH due to the stimulation of the Androgen receptors of which DHT has the greatest affinity for which is there for a reason, and the stimulation causes the swelling in the fibrous sheath of the prostate itself. The receptors are there for a reason and it is DHT that stimulates the prostate to develop in early years and become larger and more fibrous. When DHT is unopposed by testosterone, progesterone and even low estrogen then the uppossition of the hormone with the greater affinity causes a overstimulation and it swells due to this stimulation. Since the prostate in the fetal developmental stage can also become a uterus in a female also has estrogen receptors at the core, which when overly stimulated by high estradiol at the utricle where the receptors are in the abscence of opposing and other balancing hormones that exist in abundance in youth, a different BPH occurs, one from within and can lead to bleeding and ultimately cancer. Estradiol is widely understood in endocrinology to be carcinogenic when unopposed at the receptor. Other estrogens like estriol and Progesterone never are. Estradiol is needed and has it's place, but in strong amounts when unopposed is where the problem occurs. THis is how it works folks.

Here's an article by an 'MD' since 'realgains' wont stop nagging about his surgeon and urology friends that gives a short basis for the mechanism of prostate cancer and risks. I'll also post some articles on estrogen and estrogen receptors and the prostate. AR receptors are on the prostate for a reason bros! So is estrogen receptors, but when in an unopposed environment there can be trouble. This is just heresay and a case without a complete history provided. And we are not there to see for ourselves to say what he did and did not do. Many patients can exagerate and leave things out of their history time and time again every day. I too, am a health care professional and I have heard the same things 'realgains' has heard and the same doctors also tell me that if I were to use deca then I would die of liver cancer. Which is pounded into their brain in med school. Remember there are many substances that will strongly suppress your HPTA, which will bring estradiol to level and lower test/dht. Like alcahol, many drugs, marijuana. With a poor recovery, his estrogen will be high for months until his test finally catches up. Then again he might just be the exception. If you take a bunch of proscar then you will increase your chances of gyno. And, it wont necessarily lower your risk of prostate cancer. Arimidex is probably the best choice, but remember to watch the dose because estrogen is needed also, and if you lower it too much then you will increase your cholestrol(bad LDLs...).



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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
 
Last edited:
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: 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
 
Why Billy Has Breasts, the Story of Estrogen

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.

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.
 
Here is one showing that actually giving older men pure DHT increased their strength and did not harm their prostates

: J Clin Endocrinol Metab 2001 Sep;86(9):4078-88

A double-blind, placebo-controlled, randomized clinical trial of transdermal dihydrotestosterone gel on muscular strength, mobility, and quality of life in older men with partial androgen deficiency.
Ly LP, Jimenez M, Zhuang TN, Celermajer DS, Conway AJ, Handelsman DJ.

Department of Andrology, Concord Hospital, Concord, New South Wales 2139, Australia.

The efficacy and safety of androgen supplementation in older men remains controversial. Despite biochemical evidence of partial androgen deficiency in older men, controlled studies using T demonstrate equivocal benefits. Furthermore, the importance of aromatization and 5alpha reduction in androgen actions among older men remains unclear. Dihydrotestosterone is the highest potency natural androgen with the additional features that it is neither aromatizable nor susceptible to potency amplification by 5alpha reduction. Therefore, the effects of dihydrotestosterone may differ from those of T in older men. This study evaluated the efficacy and safety of 3 months treatment with transdermal dihydrotestosterone gel on muscle strength, mobility, and quality of life in ambulant, community-dwelling men aged 60 yr or older. Eligible men (plasma T < or =15 nmol/liter) were randomized to undergo daily dermal application of 70 mg dihydrotestosterone gel (n = 18) or vehicle (n = 19) and were studied before, monthly during, and 1 month after treatment. Among 33 (17 dihydrotestosterone, 16 placebo) men completing the study with a high degree of compliance, dihydrotestosterone had significant effects on circulating hormones (increased dihydrotestosterone; decreased total and free testosterone, LH, and FSH; unchanged SHBG and estradiol), lipid profiles (decreased total and low-density lipoprotein cholesterols; unchanged high-density lipoprotein cholesterol and triglycerides), hematopoiesis (increased hemoglobin, hematocrit, and red cell counts), and body composition (decreased skinfold thickness and fat mass; unchanged lean mass and waist to hip ratio). Muscle strength measured by isokinetic peak torque was increased in flexion of the dominant knee but not in knee extension or shoulder contraction, nor was there any significant change in gait, balance, or mobility tests, in cognitive function, or in quality of life scales. Dihydrotestosterone treatment had no adverse effects on prostate (unchanged prostate volumes and prostate-specific antigen) and cardiovascular (no adverse change in vascular reactivity or lipids) safety markers. We conclude that 3 months treatment with transdermal dihydrotestosterone gel demonstrates expected androgenic effects, short-term safety, and limited improvement in lower limb muscle strength but no change in physical functioning or cognitive function.

Publication Types:
Clinical Trial
Evaluation Studies
Randomized Controlled Trial
 
On the other hand....

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 one with an increase of that ratio.

Are you confused yet? How can one of the most manly of anabolic steroids such as Deca Durabolin be considered a female hormone? How can female birth control pills be used as anabolic steroids? The simple answer to this question is that progesterone is best not considered as a female hormone, but as a hormone with properties somewhere in the middle between testosterone and estrogen. You can tweak the progesterone molecule slightly one way and have a hormone that is androgenic, or tweak it another way and be less androgenic or become more neutral in effect like the natural progesterone in the human body. Progesterone has its reputation as a female hormone due to its role in promoting pregnancy. But natural progesterone is still present in the male and also plays an important role in male physiology, but it has not yet been clearly elucidated. It should be noted that the "masculine" hormone nor-testosterone, that is the basis for the anabolic steroid Deca Durabolin, is actually found in highest concentrations in pregnant women (10).

So how can progesterone like molecules make me big or improve my athletic performance? Are large doses of Deca what you are referring to when you talk about "progesterone for men"? The answer is that nortestosterone drugs and prohormones have disadvantages over testosterone for use in hormone replacement therapy and in athletics / bodybuilding. The main reason nortestosterone is so popular is because of its lower androgenicity. It competes with testosterone for the 5-alpha reductase enzyme that converts testosterone to DHT and instead converts to dihydronortestosterone which is much less androgenic. Therefore you are less likely to experience side effects often associated with testosterone such as acne, hair loss, etc.

However, some people don’t know about nor understand the drawback of nortestosterone. For one thing, it can drastically lower libido. This is not surprising since other progestin based drugs are given to sex offenders to purposely lower their libidos. For male hormone replacement therapy, this can make nortestosterone a big no-no. Most men considering hormone replacement therapy are already suffering from a loss of libido, and nortestosterone can be almost like a castration agent for them. In addition, nortestosterone has a lower aromatization rate than testosterone. Since estrogen can raise HDL levels while androgens tend to lower HDL, this lack of estrogen from nortestosterone can cause HDL levels to drop further than when on testosterone. While temporarily low HDL levels may not be a big concern for a healthy young athlete, this is obviously a bigger concern for older men or those with heart disease risk factors.

Instead of using nortestosterone for hormone replacement therapy, I recommend a combination of natural testosterone and pulses of natural progesterone when testosterone is used. Progesterone, like nortestosterone, competes with testosterone for the 5-alpha reductase enzyme. A combination of testosterone/progesterone could allow for the benefits of increased testosterone while keeping DHT levels balanced. The concept is to help maintain a natural and youthful testosterone/estrogen/progesterone ratios throughout your lifetime. I believe a proper balance is the key to a healthy libido, prostate, and cardiovascular system.

While synthetic progesterone derivatives have been used to lower libido in men (1, 5), I believe that natural progesterone may in fact have the opposite effects in some men. I have heard patient anecdotes and from other medical doctors saying that application of a natural progesterone cream to the scrotum can increase libido and enhance orgasmic pleasure in some men.. I believe that just as high doses of synthetic progesterone derivatives can lower libido, so can low levels of natural progesterone. Natural progesterone can have a calming effect on the nervous system and may help those men who are "rapid ejaculators" or have other anxiety related sexual problems. Restoring or pulsing progesterone may enhance libido, and sexual function. While large doses of synthetic progestins may cause you to get fatter or lose muscle, the role of progesterone in increasing body temperature has been well studied in women (3) and may help bring back resting metabolic rate to a more youthful levels in men as well. Progesterone has the benefit of boosting metabolism but too much can lead to high insulin levels which would likely cancel out any benefits of increased metabolism.


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Conclusion: The Future of "Contrarian Endocrinology"

I believe that the effects of "female" hormones on men have been greatly over demonized and understudied and there are many benefits to be derived both for body compositioning and for anti-aging purposes. Just as testosterone use effects women more noticeably than men, other hormones found in smaller amounts in men such as estrogen and progesterone can effect men more profoundly than women. Too much estrogen and progesterone will of course lead to loss of muscle mass, gains in fat, and loss of libido. But proper levels and more importantly the ratios of these hormones could actually be beneficial for libido and body composition.

While much more research needs to be done, I believe the best protocol for hormone replacement therapy for men will be quite similar to the one I use for women. As you may recall from Part I of this series, my usual protocol for female hormone replacement therapy is to restore a balanced ratio of testosterone/estrogen/progesterone through use of natural testosterone and progesterone gels and small doses of natural estrogens if necessary. I believe a good protocol for men may soon be a similar protocol of maintaining a natural balance of testosterone/estrogen/progesterone. Once a proper baseline level of sex hormones is achieved through use of natural gels, both men and women may desire an additional spike in energy or libido from time to time. For this purpose, occasional use of the short acting forms of the prohormones such as androstenedione or 4-androstenediol can be extremely effective in causing temporary boosts of testosterone and estrogen without disrupting your hormonal balance.

As for body compositioning and athletics, young adult men (not teenagers) can probably benefit most from spiking estrogen levels occasionally since they may have the lowest estrogen levels to begin with. Young adult men may also wish to increase muscle mass through nortestosterone or nortestosterone prohormones, since these should have less androgenic side effects. Older men should probably avoid nortestosterone and should instead use natural testosterone with a small amount of natural progesterone pulsing to minimize androgenic side effects.

I am eagerly looking forward to the day when my ideas are no longer considered "contrarian". As advanced as medicine is in the United States, the American medical establishment and the media often act like emotional and irrational children when it comes to sex hormone research. Testosterone and other androgens have been highly politicized and demonized in the past to the point where no constructive research could be done. Only recently has the importance of estrogen and natural progesterone in men and testosterone in women is starting to be looked at seriously. As more and more research is done, I am highly confident that it will be shown that keeping all of these three main sex hormones balanced throughout your lifetime can both extend life as well as improve the quality of your life.

by Karlis Ullis and Josh Shackman
Authors of Age Right and Super T

References

1. Berlin FS. "Chemical castration" for sex offenders. N Engl J Med. 1997 Apr 3;336(14):1030

2. Crenshaw, Theresa L. ,With Goldberg, James P. "Sexual Pharmacology; Drugs That Affect Sexual Functioning", W. W. Norton & Company, March 1994

3. Cagnacci A, et al " Regulation of the 24-hour Rhythm of Body Temperature in Menstrual Cycles with Spontaneous and Gonadotropin-induced Ovulation" Fertil Steril. 1997 Sep;68(3):421-5.

4. Gladkova AI. "The Regulation of Male Sexual Behavior by the Sex Hormones"

Usp Fiziol Nauk. 1999 Jan-Mar;30(1):97-105

5. Kiersch TA. "Treatment of Sex Offenders with Depo-Provera." Bull Am Acad Psychiatry Law. 1990;18(2):179-87

6. King, DS, et al, "Effect of Oral Androstenedione on Serum Testosterone and Adaptations to Resistance Training in Young Men: a Randomized Controlled Trial". , JAMA. 1999 Jun 2;281(21):2020-8

7. Mauvais-Jarvis P, et al. "Inhibition of Testosterone Conversion to Dihydrotestosterone in Men Treated Percutaneously by Progesterone" J Clin Endocrinol Metab. 1974 Jan;38(1):142-7.

8. McEwen BS.," Clinical Review 108: The Molecular and Neuroanatomical Basis for Estrogen Effects in the Central Nervous System." J Clin Endocrinol Metab. 1999 Jun;84(6):1790-7

9. Personal communication to K. Ullis, M.D. from UCLA Sports Medicine researchers.

10. Reznik Y, et al. Rising plasma levels of 19-nortestosterone throughout pregnancy: determination by radioimmunoassay and validation by gas chromatography-mass spectrometry.

11. Thorneycroft IH. "Update on Androgenicity" Am J Obstet Gynecol. 1999 Feb;180(2 Pt 2):288-94
 
OH no it's GYNO!!

Here's an article from Tmag concerning the comprehensive concern of gyno and its sources, symptoms, causes, treatments, options ect. What's interesting, is they cite a study in which DHT at 125mg twice daily for 10 months had actually completely regressed gyno in 10 patients, and partial in others, study lasting 18 months. Along with some other interesting gyno details along with the link and the study copied..
Link...

http://www.testosterone.net/html/body_111gyno.html


Oh No! It's Gyno!
What can you do about it?
by Nelson Montana



Anthony should have known better. If fact, he did. As an amateur competitive bodybuilder, Anthony was knowledgeable in all matters of performance enhancement. He knew how to use steroids in order to make the best possible gains with the least risk of side effects. In the past, he'd used short cycles in conservative dosages. He was fond of saying, "Nobody can tell me that 500 mg a week aren't enough." His progress was, by all accounts, impressive.

On the average, he put on an additional 10 pounds (7 of which he kept — post cycle) each time he did a cycle, and that wasn't bad at all. That's a total of almost 30 pounds of lean muscle tissue in a year's time! And the best part of it was that he never experienced any of the negative effects associated with steroid use. No crash. No noticeable suppression. No gyno. He was too smart for that. Or so he thought.

Since he wasn't particularly sensitive to potential side effects, Anthony decided it was time to "up the ante." He knew of several other competitors who pushed the envelope much harder than he had and suffered no problems. He also kept abreast of the latest information on steroid use and was familiar with the works of several authorities in the field. "Straight Testosterone is what the big boys take," was the suggestion of a renowned expert in pharmacology. Another infamous guru advised: "Try some Anadrol — it's not as bad as they say." An acquaintance that just moved up the ranks into the pros insisted, "Unless you're doing 1500 mg a week, you're wasting your time."

In the past, Anthony had always stuck with the milder stacks: Primobolan along with a little D-bol; Deca and Winstrol; Equipoise and Anavar. This time, however, he wanted to get the biggest bang for his buck.

Anthony decided on 600 mg of Testosterone cypionate a week along with 50 mg of Anadrol a day — still below what the consensus considered "moderate." He loved what he saw. Fast gains and vein-bursting pumps were noticeable within just a few days. He shot up 12 pounds in one week. After 14 days, he looked like a different person — huge, vascular and powerful. There was only one problem. He started to feel tenderness under his right nipple. He noticed a lump. "Damn!" he thought to himself. "I've got it. I've got gyno."

Suddenly, all the expert advice was meaningless. The only recourse was to abort the cycle. Unfortunately, the sudden cessation of androgens was too abrupt. His natural Testosterone levels were down and his estrogen was up. The gyno got worse. It was in both nipples now. He had developed tiny breasts. In an effort to look as manly as possible, Anthony was turning into a woman! It was tragically ironic. It was also poetically profound. Apparently, you can only pull the wool over Mother Nature's eyes for so long before she strikes back. In Anthony's case, payback was a bitch. Bitch tits, that is.

Anthony isn't alone. Each year, thousands of men develop gynecomastia. The technical definition is: "a benign growth or enlargement of the male breast tissue." Although gyno is more prevalent than ever, there are historical writings and artifacts showing that it's been a problem since the time of ancient Greek civilization. The term "gyne" comes from the Greek word meaning "woman" and "mastos" meaning "breast." Statues of the Pharaoh Seti depict a man with enlarged breasts. Aristotle, too, had reported encountering the problem and there's even documentation in the writings of Paulus of Aegineta (635—690 AD) which describes a primitive surgical procedure for the removal of gynecomastia. That must've hurt.

One reason why gyno reaches the advanced stages is because the early symptoms are barely noticeable. It may start as a slight itch in the nipple area. This can be easily ignored or overlooked since the sensation is not unlike when the nipples become irritated from either cold weather or wearing certain materials. In some cases, the lump, which develops under the pectoral, is often mistaken for muscle growth! No such luck.

There are several causes of gyno, all stemming from hormonal fluctuation. It's fairly common among older men. Once Testosterone levels begin to drop, the Testosterone/estradiol ratio can cause increased fatty tissue to develop under the breast. Combine that with looser skin, increased weight, and decreased muscle mass and the results aren't pretty. Those of you familiar with "Seinfeld" may remember the episode when George was horrified to see that his father had grown breasts! (Which prompted Kramer to invent the "Mansiere.") George was convinced he had witnessed his own future. He was right, since the propensity to develop gynecomastia is, to a great degree, genetically determined.

Gyno is also prevalent among adolescents. There are probably a couple of causes, but all stem from some sort of estrogen/androgen imbalance. Often, adolescents suffer from low T levels and thus have higher E/T ratios (estrogen to Testosterone). Additionally, some adolescents (and adults) have increased aromatase (the enzyme which turns T into estrogen) in peripheral tissue, and this is probably determined by genetics.

Another reason for adolescent gyno might be a direct cause of the buckets of hormones he starts producing at puberty. The Testosterone increases probably trigger an increase in aromatase activity, and the resultant increase in estrogen leads to gyno.

This is exactly what happens when anabolic steroids are introduced into the system. The body reacts, not unlike someone going through puberty. What is also common is the inability of the liver to handle the increased surge of Testosterone. In an effort to maintain balance, some of the androgen "spills over" and is converted to estrogen. The higher the level, as well as the more paid the rise of exogenous Testosterone, the greater the chances of aromatization.

Progesterone can quite possibly be another protagonist toward gyno. For instance, when athletes use a steroid like Deca or Anadrol, these drugs sometimes exert progestagenic activity at the progesterone receptor, and progesterone, as seen in females, can contribute to enlarged breasts. Consequently, it's not too large a deductive leap to assume that this progestagenic influence can contribute to the same problem in males.

Although it appears to be the scourge of youths, seniors and steroid users, anyone can get gyno. And your chances now are better than ever. Environmental toxins, pollution, heavy metals, radiation and even ions from computers have shown to decrease Testosterone and increase estrogen levels. Lack of natural sunlight can contribute to lowered hormone production. Alcohol consumption and marijuana use have also been linked to decreased Testosterone.

Diet is also a factor. Excess weight can cause "droopy pecs" (not really gyno, of course, but cosmetically undesirable, nonetheless). A diet low in fat (as in the case of many vegetarians) will cause a drop in natural occurring Testosterone. Certain foods, notably soy products, contain estrogen-like compounds, which can knock hormonal levels into an unfavorable ratio.

Probably the biggest instigator of gyno in the last few years is the use of prohormones. In the case of androstenedione, it converts not only to Testosterone, but more so into estrone, which is a mild estrogen. Oral prohormones also produce a sharp "spike" in Testosterone levels, which in turn causes some aromatization since the elevation occurs too rapidly for the body to handle them. And, since the body greets the increase in T levels by sending the balls on vacation, the use is left with decreased T levels. Add it all up and you have a triple whammied prescription for bigger boobs!

If you decide to use prohormones, it would make more sense to keep the elevation constant and controlled for a very short time. Prohormone expert Bill Roberts recommends hitting them hard and heavy for two weeks and two weeks only, and then getting off them.

Despite the increased potential for developing gyno, there are ways of fighting back. Let's take a look at some of the options.


Herbs and Nutritional Weapons in General

Herbology is a field which still has a big question mark connected to it. The research on herbs is sketchy at best. That's not to say that they're inert compounds, it's just that it's difficult to accurately determine the efficacy of a particular substance due to a host of variables. Herbs can work like drugs but with a far greater margin for error. For example, echinacea may have antibiotic properties, but its effectiveness is inexact. Penicillin, on the other hand is very precise. X amount will cure you — case closed. Still, you may want to try some herbal therapy for preventative measures against gyno and see for yourself how well you respond to them. Among the better options are....

Tribulus terrestris. You probably figured we'd get around to this sooner or later since Tribulus is the active ingredient in Tribex-500 a popular Biotest product. Be that as it may, the evidence supporting its effectiveness is the most strongly substantiated of the various herbal therapies. Keep in mind, among all the brands currently on the market, only Tribex contains the high concentrations of saponin extracts necessary to stimulate Luteinizing hormone enough to render an increase in Testosterone.

Avena sativa. Shown to increase libido and erectile function, Avena sativa may also increase Testosterone levels, which can help stabilize HPTA output after a steroid cycle. Incidentally, it's also contained in Tribex 500.

Mauira puama. Arguably effective in freeing "bound" Testosterone.

As far as nutritional weapons, the following may allow for some protection or, in some cases, partial relief of the problem:

Zinc. Zinc is vital for proper hormonal function. Although zinc deficiency, to the point where disease may occur is very rare, zinc levels in men are far lower than they were just 20 years ago. Besides the environmental issue, people today are exposed to greater stress levels. The soil in which much of our food is grown is depleted of naturally occurring nutrients. Supplemental zinc acts as an easy, economical safeguard for optimum Testosterone levels (thus helping to offset the chance of a Testosterone/estrogen imbalance).

Flax seed oil. Besides the increased essential fatty acids, (notably Omega 3's) flaxseeds contain lignans, which have been shown to have anti-tumor properties. What does this have to do with gyno? Gyno is, in a way, a benign tumor. Flaxseed oil should be a part of every bodybuilder's supplement regime for health, strength and prevention of gyno. Flaxseeds in their original state are also a great choice. (Great on cereal!)


Drugs

Our panel of experts, including Brock Strasser, Bill Roberts and Brian Batcheldor all agree that an anti-aromatase is a vital adjunct to any steroid cycle. The overwhelming favorite is...

Clomid. Intended for use as an ovarian stimulant, Clomid works in men as both an anti-estrogen and a Testosterone stimulator.

Among some of the other anti-estrogen drugs are....

Cyclofenil. Milder than Clomid but similar in efficacy.

Nolvadex. An anti breast cancer drug, which is also thought to lower IGF.

Arimidex. The latest addition used in the treatment of breast tumors. It works so well it may actually lower estrogen levels too much, leading to suppressed HDL (good cholesterol)

Teslac. Supposedly superior to Nolvadex but very expensive and virtually unobtainable.

Proviron. This isn't an anti-estrogen but a weak oral Testosterone. Some people claim that it helps maintain Testosterone levels when coming off a steroid cycle. The only way I see it helping is if the gyno was a temporary condition.

DHT. In one study conducted for 18 months on 40 men, twice daily application of DHT resulted in complete disappearance of gynecomastia in 10 patients; partial regression in 19; and no change in 11 after 4 to 20 weeks (Kuhn et al, 1983). The dosage used was 125 mg of DHT applied twice daily.

(Interestingly enough, the DHT was almost a complete failure in patients who had developed gyno as adolescents. It seems that the longer the condition persists, the more fibrous and thus, more resistant, the gyno becomes.)

Incidentally, most of these products aren't legally available to men for the purpose of preventing or alleviating gynecomastia.

Unfortunately, once you get gyno, if it's bad enough, it tends to be a permanent condition. Once that becomes the case, the only alternative is...


Surgery

The surgical removal of breast lumps is quickly becoming standard practice among professional bodybuilders. We spoke about this recent phenomenon with the man who has performed more gynecomastia operations than anyone else in the world, Dr. Bruce Nadler.

"After the gyno gets past a certain stage, surgical removal is the only option," says Dr. Nadler. He goes on to explain: "No medication can shrink the inflamed area. The good news is, once the operation is performed, there's less of a chance of re-developing gyno since the majority of the target tissue is removed."

Dr. Nadler sees men like our aforementioned friend "Anthony" every day. According to the good doctor, the first question out of their mouths is usually something like; "Doc, I got bitch tits! Am I fucked or what?!" The answer is yes! — unless you decide to do something about it. The condition can be reversed, but it'll cost ya. The total cost of an operation is around $6,000. (Light training can resume after 3 weeks.) If you decide to get the procedure, I would strongly recommend contacting Dr. Nadler.

A botched operation can leave you looking worse than you did when you had the gyno. When it comes to something as important as this, it isn't the time to bargain shop. If you've already developed gyno, Bruce Nadler is the man to see. For more information go to DrNadler.com.

Maybe you're lucky and have managed to avoid the malady thus far. But if you're even thinking about dabbling with anabolics, take all the proper precautions in order to keep the dreaded bitch tits at bay.

As the old saying goes: "An ounce of prevention is worth a pound of cure." You can save yourself a ton of trouble if you avoid getting gyno in the first place. If you decide to use steroids, play it safe. Keep the hard androgens to the absolute minimum. After all, all the muscle in the world won't do you much good if you wind up sprouting tits! Think about it.
 
"So, even on high doses of aromatise inibitors, you still will get greater IGF-1 increase, and on high doses of Test + Finasteride/Saw Palmetto, you still will get better stimulation of CNS then from any other anabolics. "

panerai,

I'll agree to disagree with you on this one. I get much better CNS stimulation off tren, winstrol or anavar than from test/proscar, even when alot of test was used. There also was an abstract posted a while back about the unique CNS effects of Winstrol. When I did use suspension at relatively low doses WITHOUT proscar I did get greatly increased training drive though.
 
Evidence for autosomal dominant inheritance of prostate cancer.

Am J Hum Genet 1998 Jun;62(6):1425-38 (ISSN: 0002-9297)

Schaid DJ; McDonnell SK; Blute ML; Thibodeau SN [Find other articles with these Authors]
Department of Health Sciences Research, Mayo Clinic/Mayo Foundation, Rochester, MN 55905, USA. [email protected].

A family-history cancer survey was conducted on 5,486 men who underwent a radical prostatectomy, for clinically localized prostate cancer, in the Department of Urology at the Mayo Clinic during 1966-95; 4,288 men responded to the survey. Complex segregation analysis was performed to assess the genetic basis of age at diagnosis and the familial clustering of prostate cancer. For the total group, no single-gene model of inheritance clearly explained familial clustering of disease, which could be partly explained by lack of Hardy-Weinberg equilibrium, with an excess of homozygotes. After accounting for deviations from Hardy-Weinberg equilibrium, the best-fitting model that explained the familial aggregation and age at diagnosis was a rare autosomal dominant susceptibility gene, and this model fitted best when probands were diagnosed at <60 years of age. The model predicts that the frequency of the susceptibility gene in the population is .006 and that the risk of prostate cancer by age 85 years is 89% among carriers of the gene and 3% among noncarriers. A strength of our study is its large size, such that genetic models could be fitted within strata defined by the age of the proband. Although the autosomal dominant model was consistently the best model, the parameter estimates differed somewhat (P=.03) across the different age groups, suggesting genetic heterogeneity. Additional evidence that the hereditary basis of prostate cancer is likely to be genetically complex was provided by the following: (1) there was a significantly elevated age-adjusted risk of prostate cancer among brothers of probands, compared with their fathers (relative risk 1.5 [95% confidence interval 1.4-1.7]); (2) the autosomal dominant model predicted an excess of homozygotes, over that predicted by Hardy-Weinberg equilibrium; and (3) the model-predicted risk of prostate cancer among relatives was inadequate when probands were diagnosed at age >=70 years.

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Genetics
 
I don't have the clinical study on hand but there was a study done on the comparison of 'Saw Palmetto' and 'Proscar' and saw palmetto increased urine flow 4 times faster and more effective than proscar did. Saw Palmetto also has anti-estrogen effects. Did you know that? So, could it be that Saw Palmetto not only has a balancing effect with DHT but also works to minimize estrogen thus producing somewhat of a balanced hormonal environment? Also, if you take proscar, all too often DHT is minimized so aggressively that strength, sex drive, CNS, mood are all affected. But, Saw Palmetto seems to only minimize DHT to a 'point' and doens't go beyond that.

Speaking of CNS here is an article concerning androgens and CNS effects that you might find interesting. Psychological and Sexual Actions of Androgens and its Relationships with DHT




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
 
Mister X, comparing Saw Palmetto and Finasteride is like comparing finger and dick, lol :). At least, in a real life. I'm using both and when I took a pretty long break from Finasteride (about 6 month) I noticed the difference, and tell you the truth, I didn't expect it, I actually used to believe that Saw Palmetto can be used in place of Finasteride.
Personally, I think, it's due to many reasons, including the way supplement companies cut their cost, but also, considering huge difference in the way my prostate and hair reacted to cut off Finasteride, may be due to much less of effectiveness of Saw Palmetto, comparing to Finasteride.
 
What is the theory behind how ephedrine affects the prostate? And, from a comparative standpoint, how bad is ephedrine for the prostate? Are the negative effects related to cancer or enlargement?
 
gwl9dta4 said:
OK, there is very little validity here. First off the doctor saying "the anabolic steroid testosterone", statement. Well Testosterone is NOT an anabolic steroid. Second Prostate cancer is not something you contract. It's a genetic defect. BUT prostate enlargement is a different story. Currently there is a debate as to what couses it. In one camp the train of thought is that high levels of test are to blame, and on the other side doctors say it's the low test levels that are to blame. The reasoning being that low test levels in the blood stream cause the prostate to swell like a "sail" to catch more free test. Makes sence, espacially since most old men with swollen prostates can't exactly be said to have particularly high test levels. It's the prolonged low testosterone level that can actually cause these problems. Of course using steroids that have a very high rate of conversion to DHT is a bad thing as well. I remember how it was difficult to urinate when i did my first cycle of d-ball.

Be careful. It might be technically incorrect to refer to test as an 'anabolic' steroid, but that doesn't mean the tale lacks validity.

Secondly, regarding your comment on contracting cancer. You can contract any cancer given the right circumstances.. i.e. smoking causes cancer in many people. Genetics play a part (but the mechanics of cancers of all types is still largely unknown). Therefore, it is impossible to substantiate your claim that genetics causes cancer. Yes, some cancers seem to occur in family members, however, this is not always the case. And anyway, you don't know if you are susceptible to any given cancer until it happens. It is unwise to believe that you are free of the ability to get cancer. 1 in 2, 1 in 3 remember that. Half of you reading this will deal with cancer at some point in your lives.

1 in 2 men get cancer of some kind. 1 in 3 women. Prostate cancer and testicular cancer are the most common cancers seen in men.
 
Testoman said:
this story is a bunch of crap. testosterone is causing prostate growth? b u l l s h i t ! please tell me one thing: why do young men who produce lots of test do not get prostate problems while older men whose test production has dwindled down do get prostate problems?

Testoman

Because they may well produce less test, but have higher DHT conversion? Because the effects have cumulated over time and were never checked out....
 
Good points GW
EVERYONE gets cancer. Our bodies usually can detect cancerous cells and kill them, but sometimes a cell can multiply without being detected (i think they dont present an antigen). Everyone is suceptible to this, some more than others (for example, people with the FAP gene, famillial adenomous pollupus or some shit like that who seem to produce lots of precancerous pollups in the colon).

In any event, i dont believe that androgens CAUSE cancer, that is, they dont mutate cell lines, but rather feed existing tumor growth.
 
after reading that last 7 pages...
i am going to go get a PSA done,
and start taking Finasteride with my test.
but one question... somebody said something about Arimidex... that it would also be a great thing to take.. is this true?
what does it do??
 
I read this above. PSA stands for Prostate Specific Antigen. They are referring to a test done to measure levels of this antigen, if levels are elevated, this may be indicative of cancer.
 
Excellent thread. I'm subscribing to it.

Above it was mentioned that finasteride/proscar should not be used with deca since it will result in additonal hair loss. I have two important questions:

1) What other drugs, if any, should not be used with finasteride? (eq.?)

2) How much of a time cushion should you leave between use of deca (and/or any other drugs that should not be combined with finasteride) and finasteride?
 
Trevdog said:


1) What other drugs, if any, should not be used with finasteride? (eq.?)

2) How much of a time cushion should you leave between use of deca (and/or any other drugs that should not be combined with finasteride) and finasteride?

1) In my personal opinion, Deca only. Some said Trenbolone, but there's only one shady looking study from China, which found some 5-alpha metabolites of Trenbolone, but even they didn't say it for sure, they used word "probably", lol..
In the same time, there are plenty of other studies that list major metabolites of Trenbolone and 5-alpha are not among them. So, Trenbolone, IMO, doesn't get 5-alpha reduced.

2) Use of Finasteride is a long term commitement. You simply can't stop it for period of a few month and not expect loss of benefits. If you are prone to MPB, and using Finasteride, you have to forget about Deca, period. No loopholes there.
 
panerai said:


2) Use of Finasteride is a long term commitement. You simply can't stop it for period of a few month and not expect loss of benefits. If you are prone to MPB, and using Finasteride, you have to forget about Deca, period. No loopholes there.

Thanks bro. I should have been more specific. I do have a receding hairline, but it doesn't seem to be getting much worse. If I took finasteride, it wouldn't be for MPB, it would be to prevent prostate cancer. Thus, it would seem that I could take deca, wait a month, then take test with finasteride, winny, primo, tren, eq, etc. Is that true?
 
Hey, first of all, how long of a break do you take in between cycles? If it's only a month, especially after Deca, may be, it doesn't even make sense to go off, at all?
I think, it make sense to use Finasteride(for prostate) on high amount of Test cycles only. Also, use aromatise inhibitor, and take it easy on Ephedrine.
 
I take at least as much time off as I was on. Again I didn't think when I posted. I'm aware that deca takes about 3 weeks to clear your system.
 
So to sum this thread up, please correct me if I'm wrong:

1. We should take finasteride while on test

2. We should take saw palmetto year round, unless on deca

3. Deca is the greatest steriod ever made for sides vs results and wont hurt your prostate or cause you to loose your hair when used alone

4. We should use anti-e's and an anti aromatise such as liquidex while on AS that aromatise

5. everything else that I over simplified or left out

Am I correct in all of the above?

Questions:

1. Where does Eq fall in the prostate/finasteride/hairloss realm

2. Will someone elaborate why ephedrine is bad for the prostate. Does it cause prostate cancer?

3. Will someone elaborate on why proviron is bad for the prostate. And, if it caues prostate cancer?

Thanks in advance

;)
 
All I have to say is

READ THIS:


Is low serum free testosterone a marker for high grade prostate cancer?

Hoffman MA, DeWolf WC, Morgentaler A.

Division of Urology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

PURPOSE: The association of free and total testosterone with prostate cancer is incompletely understood. We investigated the relationship of serum free and total testosterone to the clinical and pathological characteristics of prostate cancer. MATERIALS AND METHODS: We retrospectively reviewed the clinical records of 117 consecutive patients treated by 1 physician and diagnosed with prostate cancer at our medical center between 1994 and 1997. Low free and total testosterone levels were defined as 1.5 or less and 300 ng./dl., respectively. RESULTS: After evaluating all 117 patients we noted no correlation of free and total testosterone with prostate specific antigen, patient age, prostatic volume, percent of positive biopsies, biopsy Gleason score or clinical stage. However, in patients with low versus normal free testosterone there were an increased mean percent of biopsies that showed cancer (43% versus 22%, p = 0.013) and an increased incidence of a biopsy Gleason score of 8 or greater (7 of 64 versus 0 of 48, p = 0.025). Of the 117 patients 57 underwent radical retropubic prostatectomy. In those with low versus normal free testosterone an increased mean percent of biopsies demonstrated cancer (47% versus 28%, p = 0.018). Pathological evaluation revealed stage pT2ab, pT2c, pT3 and pT4 disease, respectively, in 31%, 64%, 8% and 0% of patients with low and in 40%, 40.6%, 12.5% and 6.2% in those with normal free testosterone (p>0.05). CONCLUSIONS: In our study patients with prostate cancer and low free testosterone had more extensive disease. In addition, all men with a biopsy Gleason score of 8 or greater had low serum free testosterone. This finding suggests that low serum free testosterone may be a marker for more aggressive disease.

PMID: 10687985 [PubMed - indexed for MEDLINE]
Drugs Aging 1999 Aug;15(2):131-42 Related Articles, Books, LinkOut


LOW TEST LEVELS NOT HIGH
 
doctor or select online pharmacy, it is 1 mg proscar used for hair loss, 5mg proscar is used for prostate enlargement/problems.
 
Rosco said:


3. Will someone elaborate on why proviron is bad for the prostate. And, if it caues prostate cancer?

Thanks in advance

;)

Proviron is not bad for the Prostate unless you are taking more than 100mg a day which could significantly raise your DHT levels.
But remember DHT alone does not cause Prostate Cancer.
DHT, Estrogen, and Cortisol all play a role in causing Prostate cancer.

Proviron is NOT a bad drug. It is very safe and mild. Read my thread on why it's a very good drug that can be used year round.

http://boards.elitefitness.com/forum/showthread.php?s=&threadid=125539
 
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Where is the cheapest place for finasteride? Never looked into it personally but now I'm fucking paranoid so I think I will.
 
ok, i noticed that when i am on test that the area above my penis swells a little bit. is that my prostate or bladder? but after a while when i am off it goes down. i also noticed that i urinate a little bit more when i am off, which means a whole lot of urinating because i urinate a lot in the first place but i drink a lot of water too. so will proscar help me out or is it something else, just a swollen bladder which i don't think it is, because of drinking lots of H2O? i am leaning on taking it on my next round anyway, but some info would be nice.
 
fistfullofsteel,
Do you have a frequent urge to urinate and difficulty when urinating (pushing but nothing coming out really)? could be water retention in pubic fat. I dont think that a swollen prostate would be noticable by looking at your pubic region. Its not that big of an organ.
 
yeah sort of, and afterwards i urinate 2-5 minutes later. i also feel a little pain once a while when i am on when i ejaculate in that area, but i also got that when i was on andro. don't ask me why i used andro, i have no clue. fucking crap.
 
Realgains said:

All the urologists that I have talked to said men that take extra test are elevating DHT and estrogen levels and are playing with fire.......one said"who knows what will happen to them when they get a little older, say 50 or 60 or even 40!

This is just a process comment, but don't men in their 40's, 50's, and 60's get precribed hormone replacement therapy i.e. get put on test by their doctor. It seems weird that if such a clear correlation was there that physicians would be pushing their patients into the fire so to speak.
 
argent said:


This is just a process comment, but don't men in their 40's, 50's, and 60's get precribed hormone replacement therapy i.e. get put on test by their doctor. It seems weird that if such a clear correlation was there that physicians would be pushing their patients into the fire so to speak.

Same thing occurred to me.
 
First of all, the prostate gland is an area which has a very high number of andogenic receptors, therefore androgenic steroids (like testosterone) will bind heavily to this area.
Next you have to think about the aspect that your physiques do differ, this is the reason that some develope cancer while others don't, consequently some people have a higher number of receptors on their prostate gland and therfore has a higher risk of developing cancer.
 
sometimes when i take a shit when i am on i get like a cramp in that area, what's that all about. it happens like once or twice when i'm on!
 
Mr Anaboholic,

I dont think that the binding of the androgens to the AR will cause cancer, basically, androgens dont cause cancer. They facilitate a malignant tumors growth.
 
gwl9dta4 said:
OK, there is very little validity here. First off the doctor saying "the anabolic steroid testosterone", statement. Well Testosterone is NOT an anabolic steroid. Second Prostate cancer is not something you contract. It's a genetic defect. BUT prostate enlargement is a different story. Currently there is a debate as to what couses it. In one camp the train of thought is that high levels of test are to blame, and on the other side doctors say it's the low test levels that are to blame. The reasoning being that low test levels in the blood stream cause the prostate to swell like a "sail" to catch more free test. Makes sence, espacially since most old men with swollen prostates can't exactly be said to have particularly high test levels. It's the prolonged low testosterone level that can actually cause these problems. Of course using steroids that have a very high rate of conversion to DHT is a bad thing as well. I remember how it was difficult to urinate when i did my first cycle of d-ball.

First, testosterone IS an anabolic steroid by definition. How can you say it is not? :confused: Second, to think that you cannot develop prostate cancer by taking AAS makes you dangerously misinformed. :worried: Yes, genetic defects are IN PART responsible for development of the transformed phenotype, but under "normal" conditions in healthy individuals (unless you are one of the VERY unlucky few), carcinogenesis requires a stimulus. High levels of testosterone can serve as this stimulus. :( Testosterone is mitogenic in the prostate! Be careful, man! Get informed.

GG
 
scary shit!

i,m currently doing test 500mg/week for 10weeks,equipoise 400mg/week for 10 weeks,d-dol 30mg/day for six weeks, and running nolvadex 20mg/day if needed thru my cycle and doing 40mg/day on week 12 thru 15. now my question is should i run finasteride ? if so when and how much ? how about saw palmetto? an how much because this is scaring the shit out of me. thanks
 
Saw Palmetto will definitely reduce BPH by lowering DHT -- technically, by blocking the enzyme (5-alpha reductase) that converts it. This offers an interesting dilemma to older men in that DHT is necessary to achieve an erection. And the old guys need all the help they can get. In terms of using "natural" means toward prostate health, it looks as if Nettle and Pygeum are the smarter choices. (Nettle may also have the added benefit of lowering SHBG -- a plus for all bodybuilders) Lycopene has shown promise for possible prevention of prostate cancer. I'd also throw in some calcium D-Gluterate for estrogen removal.

And fuck a lot. And don't hold back too long -- it strains the prostate. (pisses off the wife though).
 
Anybody has info about clomid and nolvadex on the prostate? In some tissues, C and N work as an estrogen instead of an anti-estrogen.

BTW, I also am a strong believer that estrogens cause prostate problems. Ever heard of huge prostates by using dianabol? This stuff does not convert to a DHT derivative, but does to the very strong 17a-methyl-estradiol.

In France they now use DHT injections to treat prostate cancer.
 
Hmmm....

Anyone else see the irony? A doctor lecturing on what he "could have" taken to prevent undesired side effects.

Excuse me. Isn't it a bannable offense for a doctor to even consult a patient on anabolic steroid use? I don't know of a single doctor that will intelligently discuss the benefits/risks of steroid use for fear that if the AMA finds out, they'll yank his license.

Now, if we stopped keeping doctors out of the loop and allowed them to prescribe steroids for training purposes so long as the use was supervised, then perhaps his comments would be more well-deserved.
 
Realgains said:
I am an Operating Room nurse. Recently a 27year old body builder had protate surgery where I work. The cancer was beyond the prostate gland, and this means that we is a dead man. He may have up to five years to live if he either gets castrated OR takes medication that eliminates all test in his body.(prostate cancer feeds on test)

This poor fellow started using AAS at the age of 21. He told me that he has been doing two cycles per year, with the base as Test, at no more than 600mg/week and usually only 500.


This dude did twelve cycles?
 
Prostate cancer from test - anyone here experience or hear about this?

Can anyone validate or pitch in some info on the relationship between Test and prostrate cancer?

Not trying to undermine realgains post - just trying to get another angle going.
 
Ephedrine and prostate

For the person who asked about ephedrine and the prostate:

Ephedrine can make it more difficult to urinate by stimulating alpha-1 adrenergic receptors in the prostate. Hytrin is an alpha-1 blocker used to lower blood pressure and to help alleviate dysuria in patients with BPH, so that could help. Saw palmetto has recently been shown to block alpha-1 receptors in prostate, so it may help prevent this effect as well.

Also, any stimulus which increases rate of cell division over time will increase risk of carcinogenesis in the affected tissue. This is simply a matter of a greater chance for random genetic mutations per unit time during accelerated cell division. I'm not sure if androgens/estrogens cause prostatic hypertrophy or rather prostatic hyperplasia, but if hyperplasia is a factor, then there should be an increased risk of carcinogenesis over time due to stimulation by higher-than-normal levels of the offending steroid.
 
Gotta bump this thread, I think it is probably the most helpful thread I have ever read.

And to the person who asked, I really don't think that the risk of prostate cancer is really exaggerated. While genetics will play a MAJOR role in this, if you do the science out it just makes sense to take finastride with test. Although I have been told that finastride and other DHT inhibitors do increase aromatization (accourding to Big Cat), which is not a very good thing, especially if you are gyno prone like me.
 
I checked out the FAQ's on minoxidil.com and this is a cut and past for finasteride

Q. Does this mean that taking finasteride will help prevent prostate cancer?

A. No, that would be presumptuous. However, Merck is conducting a prospective seven year study of men taking 5 mg finasteride/day to determine whether or not they have a smaller incidence of prostate cancer as compared to a matching population.
 
bump for confirmation whether or not finastride will increase aromatization. I know that finastride users sometimes do experience small cases of gyno however after stopping finastride usage the gyno dissappear. At least in the abstract that I read.
 
"BTW, I also am a strong believer that estrogens cause prostate problems. Ever heard of huge prostates by using dianabol? This stuff does not convert to a DHT derivative, but does to the very strong 17a-methyl-estradiol.

In France they now use DHT injections to treat prostate cancer"

I am with Sigmund Roid on this one. I actually used quite a bit of straight DHT injectable when bruce was selling it as "masteron." i had absolutely no prostate discomfort. the only time i got that was when i ran test without armidex or did not use enough armidex...then i did have some friggin pre-ejac problems at "half-mast :( and needed to piss every 2 minuites.
 
I currently have some sort of prostate problem, Im pretty sure its an enlarged prostate. Ive been to a few different doctors and none of them did any thing that worked. Ive had Tubes stuck down my ureathra a few times and my prostate was inflamed so each time they had trouble getting it in.
I had my test levels checked and they came out as 580 and free test 2.0, does any one know what i can do about this, could it be my test levels that are affecting my prostate? I have some symtoms i can name if any one can help. thanks
 
the only way to tell is if your symptomatic (ie. trouble starting and maintaining a stream of uring, frequent urination, frequent bladder infections, post-renal azotemia) then go get checked out, but if you are using any steroid you should get annual prostate exams (the prostate is located below the bladder and the urethra goes thru it, the posterior portion can be examined by doing a rectal exam). I would also get a PSA for a baseline (PSA is a blood test that the actual number isnt as significant as a change in the baseline, if it goes up by .75ng/dL then it needs further evaluation).
Oh and as far as the finasteride goes, there doing a large scale study now on whether it will play a role in prostate Cancer prevention. a smaller study demonstrated no benefit in outcome of taking finasteride to prevent prostate CA, (reason being is too many factors that we do not know about act as initiators and promotors to prostate Ca--not just DHT) DHT does play a significant role in prostatic hypertrophy (enlargement) but that is very different then Cancer.
 
well the reason why i know i have an enlarged prostate is ive had like 2 tests where they stuck tubes down my shaft, they said i had an elarged prostate but never came to a conclusion why.
 
Realgains said:
Dudes doesn't all this make a strong case for DECA. Deca doesn't convert to estrogen or DHT!! Well a small convertion to estrogen does exist.

Deca is a progestin, I am NOT sure about what I'm going to state, so read it with skepticism: perhaps progetins just agonize estrogen at their receptor sites in the prostate.
 
macrophage69alpha said:
FINASTERIDE is an OK drug... and a reduction of DHT is helpful in many areas.. with the prostate it does help with BPH and may also help reduce risk of MPH(cancer) and MPB(hairloss).


however use of finasteride can ALSO increase risk of GYNO.. DHT has been shown to reduce ER stimulation in breast tissue... I will have to look for the study..

though even the insert warns that finasteride use can cause gyno.


its ok to use.. you just dont want too much..

and an aromatase inhibitor is ESSENTIAL for any aromatic cycle... men dont need more estrogen EVER...(there are a few caveats to this but not any that are relevant to 99+% of the population)

peace

Ironically, DHT supression might be putting you at a bigger risk for BPH and/or prostate cancer due to the strong antiestrogen properties of DHT. Did you know that, in fact, DHT administration has been used with success in order to treat people with BPH?
In fact, testosterone is likely to cause its prostate problems thru aromatization rather than thru 5-alfa-reduction.
I think that the best approach would be using a 5AR inhibitor and a estrogen blocker such as arimidex (Nolvadex, being a SERM could be benefitial, useless or harmful, we just don't know with how much potency it binds to the prostate ER). .
 
macrophage69alpha said:
FINASTERIDE is an OK drug... and a reduction of DHT is helpful in many areas.. with the prostate it does help with BPH and may also help reduce risk of MPH(cancer) and MPB(hairloss).


however use of finasteride can ALSO increase risk of GYNO.. DHT has been shown to reduce ER stimulation in breast tissue... I will have to look for the study..

though even the insert warns that finasteride use can cause gyno.


its ok to use.. you just dont want too much..

and an aromatase inhibitor is ESSENTIAL for any aromatic cycle... men dont need more estrogen EVER...(there are a few caveats to this but not any that are relevant to 99+% of the population)

peace

Ironically, DHT supression might be putting you at a bigger risk for BPH and/or prostate cancer due to the strong antiestrogen properties of DHT. Did you know that, in fact, DHT administration has been used with success in order to treat people with BPH?
In fact, testosterone is likely to cause its prostate problems thru aromatization rather than thru 5-alfa-reduction.
I think that the best approach would be using a 5AR inhibitor and a estrogen blocker such as arimidex (Nolvadex, being a SERM could be benefitial, useless or harmful, we just don't know with how much potency it binds to the prostate ER). .
 
macrophage69alpha said:
FINASTERIDE is an OK drug... and a reduction of DHT is helpful in many areas.. with the prostate it does help with BPH and may also help reduce risk of MPH(cancer) and MPB(hairloss).


however use of finasteride can ALSO increase risk of GYNO.. DHT has been shown to reduce ER stimulation in breast tissue... I will have to look for the study..

though even the insert warns that finasteride use can cause gyno.


its ok to use.. you just dont want too much..

and an aromatase inhibitor is ESSENTIAL for any aromatic cycle... men dont need more estrogen EVER...(there are a few caveats to this but not any that are relevant to 99+% of the population)

peace
 
panerai said:
Most likely, it's a synergism between DHT and oestradiol that most effectively promote growth of tumor cell in prostate.
DHT, by itself, will only make your penis grow...

Saw Palmetto suppose to be able to inhibit, to some degree 5AR type I, as well as other ways, but more studies are needed to be done, to state it as a fact.

Yes, we need more studies about Saw Palmetto that will possibly never exist :(
Saw palmetto is also supposed to avoid prostate problems both by strong anti-inflammatory properties and binding to the AR, whether this binding to the AR is prostate tissue specific or not remains unknown. If it binds to the AR in skeletal muscle it would totally defeat the purpose of exogenous steroid administration.
 
Re: Re: Prostate cancer from test. ALL MUST READ!

The_Eviscerator said:


I agree. No more test for me. After this last cycle of EQ/Deca/Winny and Tren, I realize that I do not test.

Tren is worse than testosterone. While testosterone has an anabolic/androgenic ratio of 1/1 tren has 2/3 . You do the math...
 
Testosterone injected is considered an anabolic steriod in the medical field.

whether it is endigenous or exogenous, testosterone is an anabolic androgenic steroid. Same as cortisol is a catabolic steroid in both cases.

Steroid refers to the chemical structure, this includes cholesterol derivatives. Ie" estradiol, progesterones, dhea, androstenedione, testsoterone, cortisol, aldosterone. etc etc



As was said earlier, the more androgenic an AAS, the more BPH it is likely to cause. Watch out for dbol,drol,tren,halo. Concurrently, DHT derivatives are also likely to cause probs IE masteron, winny, primo, OT, and proviron.

PG
 
This was posted by SWALE at cuttingedgemuscle.com in response to this thread:
"Neurotic--Perhaps someone would be willing to repost this over at EF. I would be happy to, except I am not allowed to post there.

I certainly appreciate your desire to be of service to all. However, there are a few "misconceptions" present in your heartfelt post.

First, this poor fellow developed prostatic CA because he had a profound genetic disposition for it. You did not provide any family history, but I would hazard a guess that his father, and his father before him, perished from same.

Next, you must separate prostate cancer from BPH (Benign Prostatic Hypertrophy), as there is no known association between the two (other than, IMPO, both are associated with the effects of elevated estogen levels). Prostate cancer rarely causes the urination issues you list here, which are symptoms of BPH.

Has anyone noticed that it is precisely the time in a man's life when a man's testosterone is the lowest (and also T/E ratio) when his prostate gets sick (with BOTH cancer and BPH)? The association is profound between prostate cancer and hypogonadism.

Also, the area when the nodules of BPH form also happens to be where there is the highest concentration of aromatase.

"There is no clinical evidence that the risk of either prostate cancer or BPH increases with TRT".

--Morley JE. Testosterone Replacement and the Physiologic Aspects of Aging in Men. Mayo Clin Proc. 2000 Jan;75 Suppl:S83-7.

Is DHT really the culprit? When it is employed as sole TRT, in fact (instead of using a standard testosterone preparation), there was no change in prostate weight or PSA. This was demonstarted in two different studies. If you know your metabolic pathways, you see that this strategy will actually lower E levels.

The Cenegenics Institute has treated over 5,000 men with TRT. Remember, these are men of appreciably advanced age compared to AAS athletes. They keep very careful records, and report that only a fraction of the men who would have been expected to develop prostate cancer actually did.

I would hasten to add that as HRT physicians we supplement only to the top of "normal" range, not the dosages employed for a steroid cycle.

For the above reasons, I STRONGLY advise those who have made the lifestyle decision to use steroids to control their estrogen levels.

Last, I am not in favor of using deca--for this, OR any other reason.

I'd suggest this Urologist learn a little about steroids before he makes such comments.

Also, I frequently hear from AAS athletes who complain of BPH symptoms. It usually end up being from the sympathetic nervous system stimulation the androgens induce.

Just some food--and facts--for thought."
 
pharmguy said:

Concurrently, DHT derivatives are also likely to cause probs IE masteron, winny, primo, OT, and proviron.

PG

1) Primo is not a DHT derivative, but a DHB (dihidroboldenone) derivative.
2) The fact that an anabolic steroid is a DHT derivative doesn't imply that it's going to be very androgenic. Add a methyl group or add something at the 17-alpha-position and you might change COMPLETELY the modus operandi of a substance. Your statement is a misconception started by the wrong teachings of Dan Duchaine.
3) It's nonsense to state that winstrol and primo are going to be androgenically problematic when, in fact, they were introduced in the market due to their very high anabolic/androgenic ratio. If anything, winstrol produces hairloss, maybe thru non-AR-mediated pathways and/or selective AR binding at scalp receptors.
 
I am currently on Androgel - not considered a strong form of Test. Should my nutritionist put me on Saw Palmetto when I told him about this. As you all know, I have quite a compromised immune system. Thanks!
 
i get up 5 times in the night to take a piss. never able to get it all out either . no blood though. test/androgenic thing enlarge your prostate definately. this is one of the prices you will pay. 23 now hopefully by the time there is a problem they will have figured out how to fix without cutting my dick off. i think japan has a high occurance of pros cancer from getting nuked. pollution/chemicals estrogen/hormones fuck you up. id say you dont want old semen just laying on your prostate like that. so find a gf who likes to fuck or jerk off a couple times a day. finasteride? no way. dht is one of the good guys. i wouldnt take that shit even if i had one hair left on my head. everybody looks back and has regrets- thats life. personally id rather pay the price later instead of gettin sand kicked in my face now. look, if your scared say your scared. dont juice
 
All this thread made me think twice...scary shit
Is Finasteride to hard on lipid profile, like cholesterol levels?
 
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