estrogen blockers "good or bad"?

[MrStamina]

I was just wondering what a effect would estrogen blockers have on girl? Do they work ?
Any side effects?

My friend is thinking about taking them, she just stopped taking b/c pills and wants to get a kick start with her trainning. She was told that estrogen was one of the causes for water wieght and and fat gain.
So will estrogen blockers help to lose fat?

 

[Debu]

I was wondering the EXACT same thing but OTC types.

 

[MrStamina]

Yep only over the counter,
EngroFarm makes a brand........

 

[NubianBeauty]

Yep only over the counter,
EngroFarm makes a brand........

What's in it? Chrysin is an option.

 

[wilson6]

Personally, unless you're nearing contest ready (5 - 7% bodyfat) and juiced, even real drugs that reduce/block estrogen are unlikely to have an effect on the physique.

Regarding OTCs, don't waste your money.

The 6-OXO from ergoPharm is supposed to bind aromatase. Where's the data that it does that and in what tissue, reduces total circulating E (long-term) in women, and that it actually positively affects the physique. It is supposed to upregulate LH as well which would be counterproductive in women.

I see a number of threads on this board about women who are not competitors and are a millennia from anything that would resemble contest shape. Instead of thinking drugs or OTC drug-like products, try a solid course of diet and exercise for at least a year, perhaps some ECA if things stall at that point and be patient.

Personally, after years of hard diet and exercise, the route likely to make the most difference is a low dose of OX, not T3, clen, DNP or estrogen blockers. If you’re going to use any drug to potentially alter the way you look, all which have risks some far worse than AAS, you might as well use something that will produce solid results. Just my opinion, certainly not a recommendation.

Chyrsin supposedly blocks a subunit of the CYP enzyme system to reduce the conversion of T to E. Been looked at in andro studies, does nothing.

I3C upregulates the CYP enzyme responsible for routing estrone to 2-hydroxyestrone vs 16-alpha hydroxyestrone. May reduce breast cancer risk, but not enhance the physique.

Be careful what CYP enzyme inhibitor/activators you ingest as herbals. Some of the same enzymes they alter also process many xenobiotics and can also change the Phase II detox system. That means that they may alter the effectiveness of many drugs including OCs and make some of the toxins in our environment MORE carcinogenic in our bodies.

 

[Debu]

Wow, W6, lots of good info. 6 -oxo was the one I was thinking of. I've been doing this for about 20 years now, and never satisfied so I considered the 6 oxo. I know the real ox would be the best thing for me and my goals but can't go that route. I guess I'm looking at a lifetime of dieting! : (

 

[THeMaCHinE]

A few guys on the anabolic board had their girlfriends on anastrozole (I think one might have had his gf on letrozole); they reported results, but I don't think there was any science behind it other then "hey try this ..." I'm also not sure how healthy supression of estrogen in women is and at what lengths of time.

Definitely nothing I'd feel comfortable recommending to my wife. At this point the subject intrigues me, but I'm waiting for more real world experiences. I'm most interested in the effects of anastrozole or letrozole in women, sides, interaction with bc and periods, etc.

 

[MS]

"I'm also not sure how healthy supression of estrogen in women is and at what lengths of time."

You are wise to be concerned, although stopping a women's ovaries from producing estrogen is no easy task, and even drugs like anastrozole will likely only effect peripherally produced estrogen rather than ovarian estrogens. I agree with Wilson6 that AAS are prolly the most effective drugs for shutting down the ovaries estrogen production.

 

[THeMaCHinE]

"I'm also not sure how healthy supression of estrogen in women is and at what lengths of time."

You are wise to be concerned, although stopping a women's ovaries from producing estrogen is no easy task, and even drugs like anastrozole will likely only effect peripherally produced estrogen rather than ovarian estrogens. I agree with Wilson6 that AAS are prolly the most effective drugs for shutting down the ovaries estrogen production.

Hmmm... by this statement it would seem that anastrozole/letrozole would be safer in terms of HPOA impact than AAS? Am I understanding correctly?

 

[MS]

Anastrozole is less likely to alter her hormones enough to affect fat loss measurably. This does not make it a safer drug IMHO, just less effective. Even in males, anastozole only reduces circulating estrogens by ~50%, and it appears to have little effect on ovarian estrogen production in women, which is by far the largest source of female estrogens. However, she may increase her T levels somewhat with aromatase inhibitors. I dunno. It depends on how fat she is to begin with and how much peripheral E she produces as a result.

 

[THeMaCHinE]

Anastrozole is less likely to alter her hormones enough to affect fat loss measurably. This does not make it a safer drug IMHO, just less effective. Even in males, anastozole only reduces circulating estrogens by ~50%, and it appears to have little effect on ovarian estrogen production in women, which is by far the largest source of female estrogens. However, she may increase her T levels somewhat with aromatase inhibitors. I dunno. It depends on how fat she is to begin with and how much peripheral E she produces as a result.

Interesting -- and I see your point about safeness/effectiveness.

So, blocking ovarian estrogen and blocking circulating estrogen are two different things? Blocking ovarian estrogen being the more desireable of the two? Ovarian estrogen doesn't circulate? Thanks for helping me understand these things.

Letrozole is significantly stronger, but may cause peripheral edema in some subjects. (interesting, just found that out: http://www.cc.nih.gov/phar/updates/98mayjun.html) Of course, the peripheral edema, if it did occure, would go away upon elimination of the drug from the system. I wonder if letrozole would yield any benefit?

I wonder how tamoxifen would fare?

 

[MS]

"So, blocking ovarian estrogen and blocking circulating estrogen are two different things? Blocking ovarian estrogen being the more desireable of the two? Ovarian estrogen doesn't circulate?"

Ovarian estrogens certainly circulate, but remember that these estrogen inhibitors act by blocking the conversion INTO estrogen and for reasons unknown to me, they seem to only block aromatase activity in the periphery, not in the ovaries. If you want to drastically reduce a woman's circulating estrogen levels, you have to shut down the ovarian production. I don't know if I would use the word 'desirable'. However the best (safest??) way to do this is prolly through inhibition of the HPOA, and drugs such as AAS will do this quite nicely. So will oral contraceptives, but that kinda defeats the purpose of the exercise!

As far as i know, tamoxifen does not block estrogen receptors in the butt and thigh area of women, and may even be mildly estrogenic in those tissues like it is in the uterus. I'm not sure, but it is clear that the vast majority of women who take tamoxifen for cancer treatment in fact GAIN fat rather than lose it. Tamoxifen may, in my opinion, have other applications for already very lean (low leptin) bodybuilders, but may be worse than useless if you're a female much above 12%bf.

 

[THeMaCHinE]

Good point about the inhibitors -- duh.

Tell me, on a sidenote, what hormones/drugs would negate the contraceptive effects of oral bc? I've wondered this off and on when the wife was contemplating cycles. Or does it not matter? Once the bc is active, it's active no matter what you introduce?


Very interesting read, thanks for helping me understand.

 

[MS]

The only drugs that would inhibit oral contraceptives would be drugs that block the absorption from the gut, or drugs that induce the enzymes that degrade the hormones (grapefruit juice and antibiotics are classic examples). As far as I know, AAS would not negate the effectiveness of contraceptives.

 

[THeMaCHinE]

Thanks MS.

 

[witkowsd]

My doctor game me "EstraTest" which is estrogen with testosterone - I have had no water retention. As a matter of fact before this I was on OrthoPrefest - and I always was bloated - as soon as I stopped - and started this other stuff my stomach is flat as a board.

 

[THeMaCHinE]

EstraTest eh? I'll have to check that out.

I looked over lunch, she has Yasmin 28, then the last row (period week) is drospirenone + ethylil estradiol.

 

[Debu]

What is estratest prescribed for?

 

[wilson6]

"As far as I know, AAS would not negate the effectiveness of contraceptives."

I have to look this up but, OX for example at least in female rats upregulates a CYP enzyme only upregulated in male rats due to T, might be 3A4 but I can't remember, anyhow it might affect synthetic estrogen/progesterone metabolism and could possibly alter clinicial effectiveness. Same applies to other agents such as Milk Thistle.

and.....estratest is not my choice. Never cared much for methyl-T at any dose, in either gender, for any reason.

W6

 

[witkowsd]

I started my menapause - so my gyno put me on estratest - estragen and testastorone (sp?). He also knows I work out and working on building muscle (huge muscles) so he said this will also help in that area.

 

[wilson6]

Orthoprefest is a combination of estradiol and progestin.

Estratest is a combination of conjugated estrogens (mostly sodium estrone sulfate) and methyltestosterone.

Methyl-T is useless for building muscle and causes mood problems in some. The amount in Estratest is 2.5 mg. Most is extensively metabolized by the liver leaving very little to act peripherally. Moreover, unlike T-gel, Methyl-T will lower HDL cholesterol even in low doses.

I would think (MS comment here) that if I were post-menopausal, I would be taking a small amount of estradiol in a natural form and also a small amount of progestin also natural form to oppose it, and testosterone gel not Methyl-T.

W6

 

[THeMaCHinE]

I have to look this up but, OX for example at least in female rats upregulates a CYP enzyme only upregulated in male rats due to T, might be 3A4 but I can't remember, anyhow it might affect synthetic estrogen/progesterone metabolism and could possibly alter clinicial effectiveness. Same applies to other agents such as Milk Thistle.

W6

So, when she's on cycle (if she cycles again), it's a good idea to use an alternate form of bc? (condoms, etc.)

 

[wilson6]

I'd certainly recommend it. As Remo said in Casino, "why take a chance".

W6

 

[wilson6]

This is what I was looking for.

Author
Waskiewicz, M J; Choudhuri, S; Vanderbeck, S M; Zhang, X J; Thomas, P E

Title
Induction of "male-specific" cytochrome P450 isozymes in female rats by oxandrolone.

Drug metabolism and disposition: the biological fate of chemicals. vol. 23, no. 11 (1995 Nov): 1291-6.

Abstract
Oxandrolone (OXA) (5 alpha-androstan-2-oxa-17 alpha-methyl-17 beta-ol-3-one) is a clinically useful, synthetic, anabolic androgen steroid hormone. OXA was administered to rats orally twice daily for 3 days at 75 mg/kg to study the effect on hepatic cytochrome P450 (P450) isozymes. Western blots were performed on the hepatic microsomal fraction and probed with isozyme-specific monoclonal antibodies. Microsomes were also tested for catalytic activity in a testosterone metabolism assay. Data from Western blots revealed that, in female rats, there were increased levels of two male-specific isozymes, P4502C11 and P4503A2, as well as P4503A1. In contrast, male rats showed little or no change in expression of these P450 isozymes after OXA treatment. The 6 beta-hydroxylation of testosterone, which is catalyzed predominantly by P4503A1 and P4503A2, increased approximately 10-fold in female rats after treatment with OXA (from 0.05 +/- 0.01 to 0.52 +/- 0.05 nmol/min/mg protein), but only relatively small changes were seen in the male rats (from 1.02 +/- 0.05 to 1.38 +/- 0.07 nmol/min/mg protein). To investigate if the changes seen in P4503A1 and P4503A2 protein and activity were caused, at least in part, by an increase in mRNA levels, Northern blot analysis was performed. P4503A2 mRNA was increased dramatically in the female rat liver after OXA treatment, but only small increases in P4503A1 mRNA were seen. This data indicate that OXA induces P450 isozymes in the female but not in the male rat liver, probably through transcriptional activation, and some of these induced isozymes are male-specific.

 

[THeMaCHinE]

Interesting stuff ... the information about testosterone hydroxylation is interesting too.

It's also interesting to note that grapefruit juice (which was discussed by MS as a no-no above) effects the P450 isozyme. (Although it's the CYP3A4 isomer vs. those discussed here.)

Thanks for digging that up. Looks like we can plan on wrapping that rascal if she decides to cycle again ... lol ...

 

[MS]

I would go with Tri-est plus topical progesterone and testosterone for post menopause.

The rat enzymes upregulated by ox do not show the same gender differences in humans. In other words, 2C11 and 3A2 cannot be considered 'male-specific' in humans, and I doubt their upregualtion would have a huge impact on oral contraceptive clearance anyway. But when it comes to cantraception, my motto is also "better safe than sorry" and I would double up 24/7/365 if it were me!

 

[THeMaCHinE]

I would double up 24/7/365 if it were me!

 

[wilson6]

CYP3A4 metabolizes a number of drugs including OCs. It is upregulated by St John's Wort as well.

W6

 

[MS]

Cyp 3A4 is inhibited by grapefruit juice but increased by St John's Wort. In the grapefruit case you would predict excessively high plasma levels of OCs if taken with juice (can you say excess hormones!!!), in the St John's wort sitch you would expect decreased levels of hormone which could reduce the OCs effectiveness (can you say baby on the way). But in reality, the dose of St John's wort taken by most folks for depression doesn't significantly inhibit Cyp 3A4 enough to cause problems, but it can interfere with other drugs, mainly through 3A4 to a small extent, and increased P-glycoprotein expression to a larger extent.

 

[THeMaCHinE]

Cyp 3A4 is inhibited by grapefruit juice but increased by St John's Wort. In the grapefruit case you would predict excessively high plasma levels of OCs if taken with juice (can you say excess hormones!!!), in the St John's wort sitch you would expect decreased levels of hormone which could reduce the OCs effectiveness (can you say baby on the way). But in reality, the dose of St John's wort taken by most folks for depression doesn't significantly inhibit Cyp 3A4 enough to cause problems, but it can interfere with other drugs, mainly through 3A4 to a small extent, and increased P-glycoprotein expression to a larger extent.

I remember that grapefruit juice also effected p-glycoproteins (can't remember which way though) in the intestinal track -- this is what caused the delay or blocking of absorption in some drugs/supps.

Interesting about St. John's -- I didn't know that. I can't remember what the active component of St. John's is, but I wonder if it's intrinsic to that compound as well (or only the plant as a whole)?

 

[wilson6]

We're just starting to learn about many herbals/vitamins, etc. and their effects on both Phase I and Phase II systems.

Look at Beta-Carotene for example. Increases CYP 1A1, 1A2, 3A, 2B1, and 2A, and phase II detox enzymes.

If you're a smoker, this is bad news as an increase in these CYPs increase the rate of procarcinogen to carcinogen metabolism. Furthermore, beta-C is a pro-oxidant in tissue possessing a high partial pressure of O2 (i.e., lungs)

Not surprising that the studies done in the early 90's giving smokers Beta-C increased cancer instead of decreasing it.

Some of the above CYPs are also involved in T metabolism.

Loading up on seemingly harmless OTCs may not be as harmless as we once thought. Problem is, their toxicity is secondary and will take time to surface. A few DNA hits here and there add up.

W6