Estrogen, all good or all bad?

[madmitch]

This is one I have been thinking about a long time. Problem is, as far as I know there are no experiments, tests or scientific data to prove it.

Posted my thoughts on estrogen on the Anabolic board, to much nashing of teeth from some of the mods and guy's on there.

Well anyway it was and still is my belief that the reason women gain better on Steroids is because of their higher Natural levels of Estrogen.

Popular belief holds that estrogen turns off the effects of Testosterone. However from recent studies in Prostate Cancer and Hair loss it seems that estrogen actually increases the receptiveness of cells to the effects of Androgens.

As far as I know no studies have been done on muscle cells.

Men tend not to gain well on things like Primo, Winstrol or Anavar, Why? Well Duchaine always maintained that a certain level of estrogen was required to gain maximum effect from a steroid cycle. This is why he told men that Winstrol etc where crap steroids, because they did not convert to estrogen.

This would also explain why women CAN get good gains from the non-aromatising steroids like Primo, Winstrol and Anavar as they already have naturally higher levels of estrogen. i.e. a small increase in Androgens coupled with a womans natural estrogen levels, magnifies the effects of the androgens.

Well why then does Estrogen get such a bad rap?

Well it seems that everything is ok until Estrogen levels are in excess, this is when Estrogens effects turn nasty. i.e. Instead of being benefical they become detrimental. Not just for Men but for Women also: see below.

With regard to too much estrogen and not enough progesterone she points out that:

 Hormone Replacement Therapy, i.e., estrogen and synthetic progestins, have a combined 120 possible risks and side-effects which, among other things, are initiating and promoting breast, ovarian and uterine cancer, causing blood clots, strokes and high blood pressure.

 Nature did not make a design fault in women's bodies causing their health to deteriorate when they arrive at menopause.

 The World Health Organization has found that an overweight post menopausal woman has more estrogen circulating in her body than a skinny pre-menopausal woman

 As a result of saliva testing, we now know that perimenopause is not a time of declining estrogen levels at all.

 Unfortunately what the medical experts believed were symptoms of estrogen deficiency are really estrogen excess symptoms.

If you want to read more go here:

http://thyroid.about.com/library/weekly/aa111600a.htm


So what am I trying to say?

Well women can make good gains on Non aromatising steroids alone, due to their higher natural estrogen levels than men. However when they cross the line into the aromatising steroids like Testosterone, Dianabol etc. this is when things start to go wrong and their health suffers.

Men need to use aromatizing steroids to gain much muscle, as they increase estrogen levels. However if they are not careful and estrogen is allowed to spiral out of control, they too end up with problems. This is why men need to use anti-aromatase agents like Armidex or Cytadren.

 

[MS]

Well it's a nice theory, but it doesn't hold up in the real world. There are (rare) men who have a complete deficiency of aromatase activity. Their skeletal muscle growth is not inhibited, but their bone growth plates never fuse and they become very tall.

I disagree with "Nature did not make a design fault in women's bodies causing their health to deteriorate when they arrive at menopause." Nature did not (could not) select for health and well being past childbearing years. Women never used to live that long, and even if they did it had no effect on the genes they had already past down to the next generation.

The statement that "Osteoporosis is NOT caused by an estrogen deficiency " is also absolutely false. Again, in the same aromatase deficient men, and in well studied mouse models, osteoporosis is one of the most noteable features (along with continuous bone growth).

I wholeheartedly agree that progesterone supplementation (NOT synthetic progestins) is a better option for peri/post menopausal women than estrogen. I also wholeheartedly agree with "To regain hormonal balance and support thyroid function, one really needs to a commit to a healthy diet filled with adequate protein, essential fatty acids and good quality carbohydrates (mostly from fruits and vegetables) and to embrace a healthy life style filled with physical exercise, stress reduction, and a loving and supportive community of friends. "

All in all, that link is a mixed bag of good advice and incorrect assertions.

I think what's most interesting of all, is that aromatase deficient males are much more prone to obesity than normal males. So you can't blame female obesity purely on the presence of estrogen, though excess estrogen is clearly something to be avoided.

 

[madmitch]

Found the question below at muscle monthly, it may back up some of what I am saying.

Will lowering my estrogen levels, while keeping my androgen levels constant, hurt or hinder my muscle gains?

Good question. The use of agents to lower estrogen levels (aromatase inhibitors), or to block estrogen action at the receptor (estrogen receptor antagonists), has become quite en vogue lately. Personally, I think they are overused and could hinder muscle mass gains.

I have discussed before the potential suppressant effects of anti-estrogen compounds on GH and IGF-1 production. But beyond that, there may be direct beneficial effects of estrogen on androgen activity in muscle that may be blocked by anti-estrogens.

One important mechanism involved in muscle growth is the formation of NADPH, which is used as the prime source of energy (reducing power) in anabolic processes. Androgens are well known to stimulate one of the key enzymes involved in the formation of NADPH, called glucose 6-phosphate dehydrogenase. Furthermore, glucose 6-phosphate dehydrogenase is also involved in the production of raw materials for nucleic acid synthesis. Nucleic acids biosynthesis is required at high rates in regenerating tissues.

One of the most widely documented effects of androgens is stimulation of glucose 6-phosphate dehydrogenase, and this is thought to be key to their anabolic activity. A recent study found however that without estrogens, androgens are not able to fully exert their stimulatory activity on this enzyme. The authors conclude that androgens and estrogens may exert synergistic effects on skeletal muscle. (Max SR ,"Androgen-estrogen synergy in rat levator ani muscle: glucose-6-phosphate dehydrogenase", Mol Cell Endocrinol 1984 Dec;38(2-3):103-7)

The same author also found another mechanism by which estrogens may increase the activity of androgens in skeletal muscle. He used rats that had their testes removed and then administered androgens to them, with and without estrogens. What he found was that estrogens caused a very substantial increase in the binding of androgens to their receptors. He hypothesized that this is due either to a greater synthesis, or a decreased degradation of, androgen receptors. (Rance NE, Max SR, "Modulation of the cytosolic androgen receptor in striated muscle by sex steroids", Endocrinology 1984 Sep;115(3):862-6)


Now although I believe what is said above, I also believe that excessive levels of estrogen are detrimental to muscle growth. There must be a delicate balance between just enough estrogen and too much.

 

[MS]

Isolated biochemistry is all well and fine when we have no in vivo models to draw on. But those old rat studies, by the authors own admission in later studies, suffered methodological problems as outlined below in some selected abstracts (I've got plenty more if you're really interested):

Max SR, Rance NE. 1985

………..There was no effect of sex hormone status on any of these parameters. Finally, 30 days of functional overload did not influence cytosolic androgen receptor binding. These results are not consistent with the idea that sex steroids and functional overload act synergistically.

J Neurochem 1986 Jun;46(6):1942-6

Neural control of muscle androgen receptors.

Bernard PA, Max SR.

The number of cytosolic androgen receptors in rat skeletal muscle increases following denervation and disuse. This increase was postulated to represent altered intracellular distribution and consequent diminished sensitivity of skeletal muscle to androgens. To test this hypothesis, we measured total (homogenate) androgen receptor levels after denervation. Total (homogenate) androgen receptor binding did not change in response to denervation of leg muscles from adult male rats. An increase in cytosolic receptor number with no increase in total (homogenate) receptor levels supports the hypothesis of altered intracellular distribution of androgen receptors in denervated muscle. Cytosolic androgen receptor binding in muscle from male rats increased by 40% after denervation, whereas in females the increase was 17%. These increases could not be altered by endocrine manipulations of males or females.

Androgen receptor in rat skeletal muscle: characterization and physiological variations.

Androgen binding has been studied in the quadriceps femoris of recently castrated adult and intact immature male and female rats using a variety of techniques for separating and measuring hormone-receptor complexes. ………………. METABOLITE FORMATION CAN JEOPARDIZE THE BINDING DATA, SPECIFICALLY ALTERING THE SIGNIFICANCE OF COMPETITION EXPERIMENTS WITH RELATIVELY HIGH CONCENTRATIONS OF STEROIDS APPROACHING THE km OF METABOLIZING ENZYMES. Therefore, most quantitative studies were performed in enzyme-free, receptor-containing cytosol preparations (THIS IS NOT IN VIVO WORK). …………….

And later work on mouse models of muscular dystrophy showed even more clearly that CYTOSOLIC androgen receptors are virtually irrelevant to any anabolic response to androgens…

Again, studies in aromatase deficient HUMAN males (in other words these men produce NO ESTROGEN) shows that estrogen is not important for functional skeletal muscle growth.

Most recently Marcell TJ et al 2001, (Comparison of GH, IGF-I, and testosterone with mRNA of receptors and myostatin in skeletal muscle in older men.) “hypothesized that circulating hormones would be related to the transcriptional levels of their respective receptors and that this expression would be negatively related to expression of the myostatin gene. We therefore determined content of mRNA transcripts for GH receptor (GHR), IGF-I, androgen receptor (AR), and myostatin in skeletal muscle biopsy samples from 27 healthy men >65 yr of age. There were NO SIGNIFICANT RELATIONSHIPS between age, lean body mass, or percent body fat and transcript levels of GHR, IGF-I, AR, or myostatin.” So again, we see that absolute levels of androgen receptors are not necessarily a good indicator of anabolic potential. Keep in mind that older men have a relatively higher ratio of estrogen floating around than their younger, more muscular counterparts.

Even if you’re not convinced that estrogen in not very important for muscle growth in men, you should take heart that even the best aromatase inhibitors (such as Arimidex) only inhibit estrogen synthesis in normal males by no more than 50%. This is likely to be even less for guys on high dose aromatizable androgens. For women with intact functional ovaries, drugs like arimidex are ineffective. No matter how you look at it, most of us are not suffering lack of muscle growth from not enough estrogen.

More likely, women get a better anabolic response to low dose androgens because their bodies are relatively naïve. It’s a bit like the first time you take an ECA stack-you’ve got all these beta adrenergic receptors out there flapping in the breeze, available to bind to any beta agonist that comes along. After prolonged exposure to beta agonists, the receptors undergo all sorts of changes in conformation, internalization, second messenger signalling, down regulation etc…..and your body adjusts to taking the ECA. This would explain why “pro” females need to take higher and higher doses of androgens, just like males, but “beginners” such as most of the women on this board, get a good response to low doses of androgens. Plenty of food for thought.

 

[madmitch]

Some how I don't think we will ever really know.

MS you can quote as many scientific studies as you want that say Estrogen has no postive effect on muscle growth when combined with Androgens. There will always be others that say the exact opposite.

For example one that is a very sore thumb with European Beef Farmers.

Estrogenic implants increase the circulating levels of somatotropin (ST) and insulin-like growth factor-1 (IGF-1). Both of these substances are produced by the animal and have a marked effect on how nutrients are used by the animal to produce muscle, bone, and fat. The approved androgenic agent, trenbolone acetate (TBA), does not seem to stimulate the production of ST, but does significantly increase the circulating levels of IGF-1 and decreases the normal loss of muscle tissue in sedentary animals.

In feeder cattle, estrogenic growth promoting implants improve feed efficiency and gain 5-15 percent. Implants which include TBA can provide an additional 3-5 percent improvement in feed efficiency and daily gain

Using growth promoting implants is one of the most cost effective methods of enhancing cattle gain and efficiency of gain. Implants enhance protein deposition while diminishing fat accretion.

 

[MS]

Nope, I cannot say 100% that estrogen doesn't make a difference. The genetic defects in men that I refer to is very rare, and to my knowledge none of then have ever taken up bodybuilding and had their LBM gains monitored! However, I will point out (as I always do ) that cattle and humans are not the same. Clenbuterol is also hugely anabolic in cattle. Cattle can convert nothing more than grass into one HUGE mofo prize bull that would put Coleman to shame. All I'm saying is that there is no evidnece, in humans, that estrogen makes a big difference to LBM gains. But as I also pointed out, men toally lacking in estrogen tend to have more fat/obesity, so you could say that some estrogen will help keep the fat off, but too much is bad. I don't honestly believe an ordinary young male will suffer problems due to lack of estrogen.

 

[madmitch]

It would be interesting to find out if these men who lack the aromatase enzyme also have low GH levels.

Studies have linked Estrogen with the regulation of Growth Hormone. In particular: Estrogen enhances growth hormone receptor expression and growth hormone action in rat osteoscarcoma cells and human osteoblast-like cells: Journal of Endocrinology (1997).

Yep and you are right MS, there never has been a study of the effects of estrogen on muscle growth in humans, combined with androgens i might add.

Some other things to think about:

Increased Estrogen levels, increases SHBG levels. High SHBG = low Free Testosterone + Lower Free Estrogen Levels.

Androgens lower SHBG levels = more free Testosterone + more free estrogen.

 

[MS]

hehehe, as most heterosexual men will testify, estrogen biology is very complex!

Although estrogen enhances GH receptor signalling in bone tissues, we also know there are different functional "forms" of GH. And in spite of this increase in GH sigalling, estrogen is required to STOP bone growth in maturing humans, as well as to increase bone deposition/inhibit bone loss in older men and women. Sounds a lot like a women's moods LOL. Women take extra hGH to enhance fat loss, but their own high levels of hGH/IGF-1 don't make them leaner than their male counterparts??? All in all, it's a balance thing, like you indicated with the SBHG and free hormones. And that's where science lets us down big time. We don't know the entire, intimate detail of the pathways, feedback, and exquisite balance/interplay of hormones in humans, so any time we manipulate our hormones (intentionally or otherwise) we take risks. One thing is certain. Normal, healthy men AND women respond anabolically to superphysiological doses of androgens! The only thing most bodybuilders need to worry about is MINIMIZING estrogen's direct, short term effects.