Obesity is known to increase the risk for cancer of the reproductive tract in women. The mechanism underlying this association can be explained by increased estrogenic stimulus to estrogen-target tissues as the result of three factors. First, increased adrenal secretory activity makes more androgen precursors available for conversion to estrogen in peripheral tissues. Second, the efficiency of conversion of androstenedione (A) to estrone (E1), is elevated in obese subjects because adipose tissue is the major tissue site of conversion. Third, plasma levels of SHBG, which binds estradiol (E2), are depressed in obese subjects and greater than normal amounts of serum estradiol are therefore available to target tissues from the circulation. Recent studies have shown that the levels of estrogens and other steroid hormones in breast fluids are much higher than in serum, which may be the result of local synthesis or increased uptake from the circulation. No differences in estrogen levels of breast fluid have been found between normal women and those with breast disease. A possible explanation may be differences in the levels of estrogen antagonists, such as progesterone.
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