STEW, here is your study, I am sure you will try to find some flaw with it, but with just a little search I found this for you.

Environ Qual Saf Suppl 1976;(5):79-88

"The anabolic effect of estrogens on nitrogen metabolism of growing and finishing cattle and sheep."

Trenkle A

Estrogenic compounds are effective in stimulating live weight gains and improving feed efficiency of growing and finishing ruminants. With the proper use of diethylstilbestrol or estradiol, weight gain and feed efficiency are improved approximately 15 and 12 percent, respectively. The administration of estrogenic substances to finishing cattle or sheep results in heavier carcasses containing more protein and moisture and less fat. Estrogens do not appreciably affect rumen fermentation or digestibility of the diet but improve the utilization of the absorbed nutrients. Evidence to support the concept that the increased weight gained with estrogen treatment is the result of anabolic reactions includes a decrease in plasma urea, decrease in plasma levels of most of the essential amino-acids, decreased excretion of urea and total nitrogen in the urine and increased retention of nitrogen, phosphorus and calcium. There is no change in body water space or tubular reabsorption of urea in sheep treated with diethylstilbestrol to account for some of these observations. More direct evidence that estrogens exert their major influence on nitrogen metabolism in the body and more specifically on protein synthesis comes from an experiment where cattle fed diethylstilbestrol deposited 33 percent more protein and 18 percent less fat in body weight gain as compared with control animals. The use of the hormone resulted in a significant improvement in the efficiency of utilizing dietary protein for body gain and a slight decrease in the efficiency of converting dietary energy to body gain. Enlargement of the pituitary, thyroid and adrenal glands and higher plasma levels of growth hormone, insulin and glucose have been found in experiments designed to study the effect of estrogens on the endocrine system of ruminants. These studies, along with the observation that an intact pituitary gland is necessary for estrogens to increase nitrogen retention in sheep, support the theory that estrogens are anabolic in ruminants because of increased secretion of growth hormone by the anterior pituitary. If follows that the increased secretion of growth hormone results in increased blood glucose which then stimulates secretion of insulin. Both growth hormone and insulin would be stimulatory to protein synthesis. This theory of the mode of action is further supported by the findings that injections of growth hormone closely resemble the effects of diethylstilbestrol on nitrogen retention and blood metabolites in sheep.

lump

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quote:

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Originally posted by macrophage69alpha:
Animals, as one might guess, vary considerably in their responses to various hormones. In RUMINANTS- estrogen has an anabolic effect because of its stimulation of the anterior pitiutary, increasing release of GH and other growth peptides. In HUMANS estrogen makes you FAT- on this point both anecdotal and scientific evidence seem to agree(ie. estrogens activity with a2 adrenoreceptor). If you perchance have found a study that implicates estrogen's anabolic effects in humans by all means post it. One anecdotal notae, the addition of arimidex to test cycles, with the few test cases I have observed, greatly INCREASED anabolism while decreasing fat gain.

peace

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MACRO, I am not able to find the study, online, referenced in the edition of The Pharmacological Basis of Therapeutics, 3rd Edition, but it is stated that studies have shown (undoubtedly older studies, given the age of this book) that estrogen has a near equal anabolic response as an equal amount of test. propionate. Also, if you look at the studies on estrogen suppression in men and women, whether by aromatase inhibition or receptor blocking, there is an alteration in GH and IGF levels. In the often cited study concerning estrogen suppression in men, using anastrazole, there was an 18% reduction in IGF-1 levels.

You make the claim that ruminents are affected by hormones differently than humans, but I was not able to find any studies showing this. The reason for the disproportionate number of animal studies is simple: money. As of yet no company is looking into how to grow a bigger person for food, so until then, the number of studies directly addressing this issue will remain small, and we will have to extrapolate from indirect studies. But the estrogen blocking and suppression studies in humans do give good evidence for estrogen's effects on anabolic hormones.

Estrogen CAN cause fat accrual, and I never ever stated that estrogen was a great drug for bodybuilders, my statement was that there was studies showing an anabolic effect of estrogens. But lets look at estrogen's fat accrual propensity: it does increase lipoprotein lipase activity in the lower body area, BUT it decreases it in the abdominal area. This is the reason for the hour-glass figure of women, and the reason for the difficulty for women to lose this fat. Testosterone INCREASES lipoprotein lipase activity in the abdominal region, thus the beer-belly fat. What the studies show is that the sex hormones DISTRIBUTE fat.

Somehow I thought that more people would have made the extrapolation that estrogen does influence anabolism simply from the studies showing testosterone increasing GH levels and non-aromatizing steroids, like oxandrolone, lacking this ability.

FONZ,
though I find you demeanor quite infantile and your criticism misdirected- as I did address the theory presented...

concurrent administration of tamoxifin, which because of its mixed ER activity, might be responsible for reduction in IGF and GH production based on the findings in the animal studies. This would of course depend on its activity in the anterior pituitary.

one other thing- test has been shown to increase interperitoneal fat, the sub Q abdominal fat is a result of ER activity. Which is why women find it so difficult to get a six pack.

well two,
I want to make it clear that I agree that estrogen may have some anabolic regulatory activity, but that what is the importance of such activity in the face of exogenous androgen administration and its concurrent effects on anterior pituitary stimulation.

quote:

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Originally posted by macrophage69alpha:

one other thing- test has been shown to increase interperitoneal fat, the sub Q abdominal fat is a result of ER activity.

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Macro I understand from reading your previous posts you mentioned testosterone raised metabolic rate, now providing you prevent the estrogen related side effects it would be perfect for leaning up. If you have time would you be able to go in a little depth about this increase in mr.

Peace & Thanks

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Q:
I'm confused about the whole testosterone - estrogen - aromatization issue. I know from experience that the more an androgenic hormone aromatizes the more effective at building muscle it is. Any time I try to stop this aromatization then the hormone's muscle building effects go way down. Can you explain why this happens and why companies sell anti-estrogen supplements?



A:
First off, I have yet to see any supplement company/magazine exhibit a true understanding of the key hormonal involvements in muscle growth with respect to testosterone and its unmitigated reliance on estrogen.

The layman "researchers" that are writing articles in many of the fitness magazines and the individuals that are developing (developing is probably the wrong choice of words) products for supplement companies are apparently oblivious to the fact that estrogen is actually an integral and necessary piece to the hormone puzzle as it relates to testosterone's effect on building muscle. In fact, without estrogen testosterone's (the primary muscle building hormone) effects on muscle growth is greatly diminished.

What you mostly read about estrogen from the "experts" (I use this term very lightly) is that it's a bodybuilder's worst enemy. Nothing could be further from the truth. Estrogen is not a bodybuilder's worst enemy. It is a key hormone necessary for the full anabolic effects of testosterone.

To understand this you have to realize the close relationship shared between estrogen and testosterone. Estrogen acts a receptor trigger for testosterone. In fact, estrogen is responsible for signaling the androgen receptor to accept testosterone. Reducing the amount of estrogen available for receptor (a receptor is a protein molecule on the surface of a cell that binds or accepts hormone molecule) signaling can reduce circulating androgens from binding to the receptor sites by 30 fold. In essence, reducing circulating estrogen makes the circulating androgens 30 times less effective.

Men and women produce both testosterone and estrogen. Men of course produce more testosterone than women and women produce more estrogen than men. But men also produce estrogen. What most "experts" don't realize is that there is a reason men produce estrogen and that reason is to assist the function of testosterone.

Men produce estrogen in two ways. One is through natural hormone production in the testes and another way is through the aromatization of testosterone into estrogen. This is where the mass confusion and complete misunderstanding of estrogen in men comes in. Aromatization is not a nasty out of control side effect of excess testosterone. It's is more of a precisely controlled hormonal equilibrium modulator that specifically assists the utilization of testosterone.

In other words, aromatization is a necessary function in the hormone pathway to produce the very hormone, estrogen, necessary to trigger or signal the androgen receptors. Without aromatization, testosterone would only mildly exert its effects. Aromatization has been completely misunderstood and misinterpreted by all but a few immensely perceptive researchers. And because of this the athletic population has been led down the wrong path of hormonal understanding.

The reason you have a corresponding increase in estrogen when you increase your levels of testosterone is to provide the key, if you will, to unlock the door so that testosterone can exert it's anabolic effects (protein synthesis, muscle growth, strength increase) within the muscle.

Because estrogen is a female hormone it is associated with female characteristics. This association has carried over to effects in men as well, but at the expense of a true understanding of why men need estrogen. Because of this the "experts" have mistakenly coined estrogen as an unwanted hormone in men. Not only is it wanted, but for maximum anabolic effects it is needed.

Following the "experts" advice and taking drugs (Nolvadex) or supplements (Chrysin and IC3) designed to blunt or reduce aromatization will actually diminish, not only supplemental testosterone, but your natural testosterone as well. In other words, taking supplements like Chrysin will diminish the anabolic effects of your naturally occurring testosterone.

It's not just about increasing your testosterone that helps increase muscle mass and strength, it's about enhancing the total hormonal supply to allow for full androgen receptor participation. Any time you increase testosterone you have to have a corresponding increase in estrogen to utilize this testosterone increase. You can jack your testosterone levels to the the moon, but if corresponding estrogen is blocked or eliminated the increased testosterone will have very little effect on muscle growth.

The only time estrogen presents a problem is when you have too much. Then you may see estrogenic side effects. However, the way to go about minimizing this is not by blunting or eliminating estrogen (remember, this will diminish testosterone's muscle building properties). What you need to do is supply a more accurate increase in testosterone with natural correlating estrogen assistance. In other words, find out the maximum increase in testosterone your body will use and maintain this level without going over.

So what you need to do is boost your testosterone levels to the point where you realize the muscle building effects of this increase and not past this level to where you experience residual estrogen effects due to unused testosterone. In other words, if the level of testosterone increase causes a noticeable estrogenic effect then the increase is too much and your body will not utilize or benefit from the excess. You do not combat this excess with anti-estrogen compounds. You simply lower the level of the testosterone increase.

This is where everyone drops the ball. Wouldn't it be nice if we could capture all the positive effects of testosterone and eliminate all the negative effects from estrogen? Well wake up. It doesn't work like that, it can't work like that, and it won't work like that. Your body is a much more complicated machine than these "yo-yo" supplement shysters would have you to believe. Let make something else clear here. It's not always that these supplement companies are out to scam you. In fact, that probably happens less than I elude to. The main problem is they simply are not educated enough to truly understand the complexities of ergogenic performance enhancement. Through their ignorance they market flawed and worthless supplements that they actually think are good. And since they do no research their supplements hit the market and are backed entirely on hype and disinformation.

Supplement companies that are selling "anti-estrogen" supplements are doing you a grave injustice because of their own ignorance of testosterone's physiological effects. Honestly, when I read the ads and promotional material these companies are using to promote their products it looks like they've gleaned their knowledge from a newspaper article. Most likely the comic section. It's more than obvious few companies employ individuals that possess the skills to interpret and disseminate the real research. A casual look at the ads in the magazines solidifies this.

I'm not saying this just to slam other supplement companies. I'm just trying to show you how truly amateurish and far from the real research these companies really are. And ultimately it slaps the consumer right in the face. You see, when it's all said and done these supplement companies still rake in the cash while the consumers that fall for their product are left with nothing but a smaller bank account, empty supplement bottles, and no results to show for it.

This is nothing new, Duchaine worked this one out years ago.

quote:

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Originally posted by madmitch:

What you mostly read about estrogen from the "experts" (I use this term very lightly) is that it's a bodybuilder's worst enemy. Nothing could be further from the truth. Estrogen is not a bodybuilder's worst enemy. It is a key hormone necessary for the full anabolic effects of testosterone. THIS CHARACTER OBVIOUSLY THINKS HE IS AN EXPERT

Estrogen acts a receptor trigger for testosterone. In fact, estrogen is responsible for signaling the androgen receptor to accept testosterone. Reducing the amount of estrogen available for receptor (a receptor is a protein molecule on the surface of a cell that binds or accepts hormone molecule) signaling can reduce circulating androgens from binding to the receptor sites by 30 fold. In essence, reducing circulating estrogen makes the circulating androgens 30 times less effective. ABSOLUTE NONSENSE--

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THE ABOVE ARTICLE, WITH THE EXCEPTION OF ITS CRITICISM OF THE SUPPLEMENT INDUSTRY, IS COMPLETE NONSENSE.

PEACE

Having said that, I have noticed that anytime I add Nolvadex to my stack, I do not gain as much mass and strength. BTW, it has nothing to do with water weight gain either. I can tell the difference between water weight and muscle weight, and Nolvadex does, in fact, hinder my gains. I've never tried Arimidex, but I'm sure it would have an even more profound effect on a cycle. I tend to believe that Arimidex is only good for cutting cycles. JMHO though.

perhaps you should read ms. ullis's article-

NOWHERE does it state that estrogen is anabolic.

Now Nolvadex might hinder gains if estrogen binds in a similar manner to the anterior pituitary- because it might cause the inactivation of these sites- as opposed to just less activity.