Using Metabolomics to Explore the Role of Postmenopausal Adiposity in Breast Cancer Risk

Excess adiposity after menopause is a well-established, and potentially modifiable, breast cancer risk factor (1). Breast cancer has a clear hormonal origin, and adiposity is likely to influence breast cancer risk through estrogens given that aromatization of androgens in adipose tissue is the primary estrogen source after menopause. In fact, overweight and obese postmenopausal women have 50% higher circulating estrogen levels compared with lean women (2). Underpinning the prominent hormonal hypothesis, excess adiposity is more strongly associated with estrogen receptor–positive (ER+) breast cancers (1). In addition to estrogen (3), other mechanisms that may contribute to the body mass index (BMI)–breast cancer association include inflammation and insulin resistance. Perturbations in metabolic systems are hallmarks of obesity, and a logical place to investigate additional mechanisms.

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