Estrogen Related to Loss of Fat Free Mass with Aging

Also See:
Fat Tissue and Aging – Increased Estrogen
Estrogen Levels Increase with Age
Resistance Training Limits Age-Related Muscle & Strength Loss

A recent study (Toth, et al., 2000) shows that, at least in women, estrogen is closely associated with the general loss of fat-free tissue with aging. This shows a close association between the generalized atrophy of aging and the amount of estrogen in the tissues. -Ray Peat, PhD

“Muscle physiologists and endocrine physiologists know that fatigue, stress and excess estrogen can cause the tissues to swell hugely, increasing their weight and water content without increasing their protein content.

As soon as cheap synthetic estrogens, such as DES, became available in the 1940s, their use in animals was promoted because it was clear that they caused massive water retention. Women who suffer from hyperestrogenism always have a problem with water retention, but they have never been known to suffer from over-developed skeletal muscles. In fact, in humans of both sexes, an excess of estrogen has been commonly associated with sarcopenia, muscular dystrophy, and atrophy of the skeletal muscles. Similar observations have been made in a variety of animals. Meat scientists are the only people I know of who have ever referred to estrogen as an anabolic steroid, in the sense of “building muscle.” -Ray Peat, PhD

J Clin Endocrinol Metab. 2000 Apr;85(4):1382-7.
Regulation of protein metabolism in middle-aged, premenopausal women: roles of adiposity and estradiol.
Toth MJ, Tchernof A, Rosen CJ, Matthews DE, Poehlman ET.
The age-related loss of fat-free mass (FFM) is accelerated in women during the middle-age years and continues at an increased rate throughout the postmenopausal period. Because protein is the primary structural component of fat-free tissue, changes in FFM are largely due to alterations in protein metabolism. Knowledge of the hormonal and physiological correlates of protein metabolism in middle-aged women, therefore, has important implications for understanding the mechanisms underlying changes in FFM. We measured leucine kinetics (expressed relative to FFM: micromol/kg FFM/h) in 46 middle-aged, premenopausal women (mean +/- SD, 47 +/- 3 yr) after an overnight fast (i.e. basal) and during euglycemic hyperinsulinemia (40 mU/m2/min) using a 5.5-h infusion of [1-13C]leucine. Additionally, we measured insulin-stimulated glucose disposal by euglycemic hyperinsulinemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution by computed tomography, and hormone levels by RIA as possible correlates of protein metabolism. Under basal conditions, stepwise regression analysis showed that leucine appearance (i.e. protein breakdown) was related to percent body fat and serum estradiol (r2 = 40%; P < 0.01), and leucine oxidation was related to serum estradiol and percent body fat (r2 = 26%; P < 0.05). Under euglycemic hyperinsulinemic conditions, no variables correlated with the percent change in leucine appearance. The percent change in leucine oxidation was related to intraabdominal adipose tissue area and glucose disposal rate (r2 = 48%; P < 0.01). Correlates and r2 values for nonoxidative leucine disposal (i.e. protein synthesis) under basal and euglycemic hyperinsulinemic conditions were similar to those observed for leucine appearance. From these results, we conclude that adiposity and/or serum estradiol may contribute to the regulation of protein metabolism and FFM in middle-aged, premenopausal women.

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