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Clinical research has demonstrated that increased or decreased estradiol 2-hydroxylation can easily be achieved with a number of experimental approaches. In contrast, estradiol 16 alpha-hydroxylation, which may have potentially deleterious effects in estrogen-dependent tissues, cannot be readily altered. Predictable hormonal consequences have thus far been found in response to the modification of 2-hydroxylation. This approach offers promise as a method for specifically altering the risk for diseases associated with either too little estrogen (osteoporosis) or too much estrogen (breast and uterine cancer).
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Michnovicz et al. (1990) studied this question.
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