A recently published study in this year’s edition of Proceedings in the National Academy of Sciences suggests that biochemical changes resulting from metabolic syndrome likely increase breast cancer risk, independent from the role estrogen plays.
The research findings, based on a mouse model using a modified diet to induce metabolic syndrome in combination with estrogen-blocking medication, demonstrated that increased breast growth and tumors can occur independent of the commonly assumed cause: excess estrogens or xenoestrogens (such as plastics).
The male and female mice were fed a diet with high levels of Linoleic acid (in the form of 10,12,CLA) believed to induce a state of metabolic dysfunction mimicking metabolic syndrome as it is seen in humans. Estrogen blocking medication was given to the females so that only the estrogen-independent effects of obesity and diabetes type II were evaluated (elevated cholesterol, blood sugar and insulin resistance.)
It is well established that estrogen is responsible for stimulating breast growth, and it has long been suspected that outside sources (hormones in meat, xenoestrogens, etc.) are partially responsible for early breast development and an increased risk for breast cancer in adulthood. We now know that early onset diabetes and obesity-related changes can also increase breast cancer risk, even in the absence of estrogen.
These findings are significant, because they establish additional independent risk factors for breast cancer, one of the leading cancers among women. Metabolic syndrome (characterized by central obesity, hypertension, high blood sugar and fats) is already suspected of playing a role in certain pathologies related to estrogen imbalance; we know that adipocytes (fat cells) which accumulate in obesity synthesize their own estrogen and other hormones. Based on this understanding, it has been theorized that metabolic syndrome’s relationship to breast cancer may result primarily from changes in estrogen levels.
We must now acknowledge metabolic syndrome, and even obesity or diabetes type II on their own, as independent risk factors in the development of breast cancer (primarily in early development, but likely in all age groups). An increase in estrogen levels, secondary to obesity, is no less concerning based on this research and should not be overlooked. Rather, these individual findings in a patient (obesity, insulin resistance, high estrogen exposure) should be viewed as multiple, individual factors which combine to produce a greater overall risk.
Dr. Kaley Bourgeois
Studies:
1. Grace E. Berryhill, et al. Diet-induced metabolic change induces estrogen-independent allometric mammary growth. PNAS. September, 2012.
2. Starche, S., Vollmer, G. Is there an estrogenic component in the metabolic syndrome? Genes & Nutrition, Vol. 1, pp. 177-188. 2006