Androgens And Breast Cancer

Although menopause is a normal physiological process, the symptoms that are so commonly associated with this hormonal transition, such as hot flashes, night sweats, and many other symptoms, are only clinical indicators of a deeper problem, merely clues reflecting an underlying state of hormonal imbalance. Current research studies are clearly demonstrating that other hormones besides estrogen potentially contribute to health problems and are, themselves, clear independent risk factors that must be measured and controlled directly and intentionally. Postmenopausal women, for instance, can have increased risks for developing breast cancer, not only from having elevated estrogen but also from high levels of testosterone being converted to estrogen, low levels of sex hormone binding globulin (SHBG), and the consequential higher levels of free steroid sex hormones.2 Numerous other risk factors are also linked to this enhanced risk, including elevated adrenal secretions and chronic hyperinsulinemia.

A woman with elevated androgen levels is at a higher risk for developing breast cancer and other hormone-dependent diseases. Specific correlations with deleterious androgenic effects have been associated with increased levels of dehydroepiandrosterone (DHEA), DHEA sulfate,3 androstenedione,4 and testosterone concentrations. However, the correlation of DHEA and breast cancer has not been substantiated in other research, and it appears that testosterone has an indirect effect on breast cancer risk, via its influence on the amount of bioavailable estrogen.5 Hyperandrogenism is associated with decreased SHBG, polycystic ovary syndrome, and insulin resistance.6 (See Chapter 29 on polycystic ovary syndrome.)

There is a significantly lower prevalence of cancer risk in Asian populations whose diets are high in soy products.

Testing actively for levels of each of these specific hormones and metabolites provides the opportunity to correlate clinical presentations better and perform more focused interventions to modify hormonal dysregulation. Elevated androstenedione can arise from either ovarian or adrenal sources or from peripheral conversion of DHEA. However, increased testosterone levels are more likely to be a result of increased ovarian secretion of androstenedione and=or DHEA or peripheral conversion. Once again, seeking the source and addressing the global impact of such hormonal fluctuations is of paramount clinical significance. When hydroxyand-rostenedione (11b OHA) is elevated and the androstenedione:11b OHA ratio is depressed, the adrenal glands are the primary source of the elevated androstenedione. If the androstenedione: 11b OHA ratio is elevated, the primary source of the problem is ovarian in nature. These ratios, again, illustrate that a comprehensive examination of hormonal balance and prevalence is crucial. Research findings reveal that women who experience a hyperandrogenic effect frequently have mixed adrenal and ovarian androgen production that has been correlated with adrenal cortical hyperplasia and ovarian stroma hyperplasia as determined by autopsies conducted on patients with breast cancer.7-9

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