GH and the pill

[wilson6]

Oral estrogen antagonizes the metabolic actions of growth hormone in growth hormone-deficient women

Troels Wolthers1, David M. Hoffman1, Ailish G. Nugent1, Mark W Duncan2, Margot Umpleby2, and Ken K. Y. Ho1

1 The Garvan Institute of Medical Research, St. Vincent's Hospital and Biomedical Mass Spectrometry Unit, University of New South Wales, Sydney, New South Wales 2010, Australia; and 2 Endocrine and Diabetic Unit, St. Thomas's Hospital, London SE1 7EH, United Kingdom

We have determined whether oral estrogen reduces the biological effects of growth hormone (GH) in GH-deficient (GHD) women compared with transdermal estrogen treatment. In two separate studies, eight GHD women randomly received either oral or transdermal estrogen for 8 wk before crossing over to the alternate route of administration. The first study assessed the effects of incremental doses of GH (0.5, 1.0, 2.0 IU/day for 1 wk each) on insulin-like growth factor I (IGF-I) levels during each estrogen treatment phase. The second study assessed the effects of GH (2 IU/day) on lipid oxidation and on protein metabolism using the whole body leucine turnover technique. Mean IGF-I level was significantly lower during oral estrogen treatment (P < 0.05) and rose dose dependently during GH administration by a lesser magnitude (P < 0.05) compared with transdermal treatment. Postprandial lipid oxidation was significantly lower with oral estrogen treatment, both before (P < 0.05) and during (P < 0.05) GH administration, compared with transdermal treatment. Protein synthesis was lower during oral estrogen both before and during GH administration (P < 0.05). Oral estrogen antagonizes several of the metabolic actions of GH. It may aggravate body composition abnormalities already present in GHD women and attenuate the beneficial effects of GH therapy. Estrogen replacement in GHD women should be administered by a nonoral route.

W6

 

[MS]

Makes ya wonder what oral estrogen does to women with normal GH. Mind you, there is a big black ? over HRT anyway.

I'm guessing (since it wasn't explicitly stated) that these women were on unopposed estrogen therapy, which should be a NO NO NO option IMHO.

 

[wilson6]

MS

They administered 10 mg/d of medroxyprogesterone acetate the last 12 d of each 4 week cycle.

There is also evidence that the supression of lipid oxidation, protein synthesis and reduced circulating IGF-I occurs in normal post-menopausal women with oral E therapy.

From these studies and animal lit., it seems like evidence is mounting that estrogen inhibits muscle growth and increases fat deposition.

W6

 

[new@gettinbig]

The overwhelming benefits of being a woman!! PMS...Childbirth...Estrogen....dealing w/ men...and so on..Makes one so thankful!

 

[ann]

Only thing that came to my mind when reading this was : midget women= Growth hormone-deficienct women.

Sorry hee hee

 

[Benz1]

W6:
Let me make sure I understand this correctly, If you have 2 women exactly the same (A and B) and A is on the bc pill (or some other estrogen replacement therapy) and B is not, that with the exact same training style and diet that A will increase muscle growth/decrease fat at a faster rate than B??

 

[wilson6]

That would make an interesting study. Don't think it's been done.

W6

 

[wilson6]

Checked some body comp studies relating to the pill. Not much change, but in those that gained weight, it was all fat.

BUT..........

I'd like to see a weight-training study with one group on the pill and one group on something that maintains their E levels in the low normal range (perhaps Lupron or some other GnRH agonist) for a 12 - 16 week period. Control everything else and see what happens. I just have this feeling that estrogen inhibits muscle growth and increases fat deposition or repartitions food toward fat. At least it does in rats. In fact, I'll bet that E turns on the myostatin gene and androgens turn it off.



W6

 

[Sheena]

Hey Wilson

Before I comment on this Wilson, may I just say that I thoroughly concur with most of things you contribute to and i find all your information highly informative.

Ok.

So without sounding naive, or dismissing of the entire sceintific points you have conveyed, I'm just gonna say this, I have been out of training for ages, I'm just going back, now after 18 months, I have been on the BC Pill since I was 17 years and just about to approach 30 very shortly.

I blieve the pill makes me crave, sugar and carbs like a bitch and I believe the sudden increase of bodyfat I have had over the past two years or so is down to the pill.

So I coming off as an experiment in literally a few days time (i have two left on the strip) I will see if it makes me leaner (obviously eating a good clean diet) and if I increase in muscularity.

I will let y'all know.

Your'e right it would be interesting....

Let me be the guinea pig! lol

Just kidding.

I'm trying it anyway, I'm quite excitied about it actually.

My partner isn't though! lol Too bad.

Sheena

 

[MS]

I have no doubt that EXCESS estrogen inhibits muscle growth and increases fat gain in women. I would also like to see studies done like W6 outlined. Maybe even comparing 'normal' to excess and very low E levels. Another thing that would be good to look at in this type of study is the effect of changing E levels on other major hormonal factors such as T levels, P levels, cortisol, insulin resisitance, and of course GH and IGF-1 levels, all done in bodybuilders on a decent diet of course. What is known for certain is that there is a significant loss of LBM and redistribution of fat mass in post menopausal women. The fat tends to move from the thighs to the abs, but doesn't decrease overall. HRT prevents or slows this redistribution of fat mass. Addition of Test reduces the amount of fat gain but not the redistribution of fat.

Obesity and estrogen levels are so tightly entertwined. Increases in adipose mass leads to increases in estrogen levels, and increased estrogen levels lead to increased adipose deposition. Talk about a nasty catch 22.

Personally I'm betting on AAS inhibiting calpastatin for their main anticatabolic/anabolic effect (or at least altering the ratio of calpastatin to calpains in favour of the statin). It is even likely in my mind that the anabolic activity of AAS is due to inhibition of myostatin while the anticatabolic activity works by inhibiting calpains.