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Events/Trips Vital Force Institute Wellness Center Articles |
Hormone Replacement Therapy Revisited
2009 Nothing in woman's health care has been more controversial than hormone replacement therapy (HRT). At one point HRT was seen as a panacea in the treatment of post-menopausal women; it would eliminate (vasomotor symptoms), hot flashes, night sweats, prevent heart disease, and would prevent osteoporosis. Then came the famous Women's Health Initiative (WHI) study in early 2000 which debunked all the reputed benefits of synthetic HRT; instead, the study found that HRT actually increased the risk of breast cancer and cardiovascular disease. It is evident for practitioners who deal with women's issues, in a routine basis, that women vary in their degree of menopausal symptoms as well as their complications from HRT, including breast cancer. This variability happens regardless of whether one compares synthetic vs bio identical hormones, ethnic groups, or family histories. Some women go through menopause with only minor hot flashes, while others have it way into their 70's. Some women took HRT all their lives and never developed breast cancer while others develop it without ever taking any hormones. There have been several studies looking into the way women metabolize estrogen and their findings might help you to understand these differences. Estrogen is metabolized by two main pathways. The 2hydroxy-estrone ("the good pathway") and the 16 alpha-hydroxy-estrone ("the bad pathway"). The 2hydroxy-estrone metabolites have no estrogenic activities therefore stimulation for cell proliferation, like breast tissue, is nil. On the other hand, the 16 alpha-hydroxy estrone metabolites have a very stron estrogenic effect which lasts longer than the effect of estrogen itself. It is this stronger cell stimulation by 16 alphahydroxy-estrone that may be the mechanism for breast cancer induction. It has been found that as long as one metabolizes estrogen twice as much through the "good way" pathway than the "bad way" pathway (2:1 ratio), the risk of breast cancer is minimized. These values can be measured through a special urinary test. Fortunately, there are several simple dietary and exposure modifications that can be done to help maintain the optimal 2 hydroxy-estrone / 16 alphya hydroxy-estrone ratio ( 2/16 > 2.0). Limiting exposure to environmental estrogen (xenoestrogents) such as nonylphenol and bisphenol, the latter is leached from polycarbonate plastics when they are heated. Other xenoestrogen include DDT, aromatic hydrocarbon, and the weed killer Atrazine. It appears that some xenoestrogens are mainly metabolized by the 16 alpha hydroxy-estrone pathway. Cruciferous vegetables (cabbage, cauliflower, broccoli, and brussel sprouts ), are rich in a compound called indole-3-carbinol (1-3-C) which in the stomach, by the action of gastric juice, converts into diindolylmethane (DIM). Both 1-3-C and DIM work by steering estrogen to be metabolized by the "good pathway", therefore, improving the 2/16 ration towards the optimum ratio of . 2.0. I recommend to supplement with 1-3-C and DIM combined, to my patients in addition to eating a generous supply of vegetables, since an optimal amount is seldom reached by eating the vegetables alone. Omega-3 fatty acids increases the 2-hydroxylation of estradiol; however, Omega-6 increases the 16 alpha hydroxylation. Omega-3 fatty acids may suppress the growth of estrogen sensitive tumors. DHA inhibits the growth of human papillomavirus (HPV) infected cervical cells but not normal cervical cells. Flax seed are a rich source of lignans (a form of phytoestrogen); they are metabolized by intestinal bacteria into compounds that closely resemble estradiol. Lignans appear to help estroben metabolism in two ways; a preferential elimination of estrogen by the "good pathway", and also by retention of estrogen in the gut for elimination in the feces. Soy consumption has been shown to alter the 2-hydroxy-estrone/16 alpha hydroxy-estrone ration as well as decreasing estradiol levels in women. Isoflavones, a class of phytoestrogen present in soy, can bind to estrogen receptors and modulate it's function. Both of these functions may explain the link between soy consumption and reduce risk of breast cancer, although , studies on this regard have been equivocal.
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