Principal Investigator: Heather A. Eliassen
Endometrial cancer is the most common cancer of the female reproductive organs, and its incidence is projected to surpass colorectal cancer incidence and become the third leading type of cancer in US women by 2030. Despite being the female malignancy most highly related to excess body weight, very few dietary risk factors have been implicated in endometrial cancer etiology. Diets modulating biological pathways of inflammation and insulin response may influence endometrial cancer incidence. Therefore, to capture the biologically relevant aspects of these diets for endometrial cancer two scores to assess long-term inflammatory and insulinemic potential of usual diets in two large prospective cohort studies, the Nurses’ Health Studies. Interestingly, our subgroup analysis suggested an interaction between body mass index and the inflammatory potential of diet in type 1 endometrial cancer incidence with a stronger positive association in overweight women. In other words, pro-inflammatory diets (rich in sugar-sweetened beverages, refined grains and red and processed meat) may aggravate inflammatory and insulin-related pathological pathways, especially among overweight women who may already be in a condition of increased inflammation, thus leading to higher risk of developing type 1 endometrial cancer.
Background: Whilst unopposed estrogen exposure is considered the major driver of endometrial carcinogenesis, it is unclear whether diets with inflammatory or insulinemic potential are associated with risk of endometrial cancer.
Methods: We followed 48,526 women from the Nurses’ Health Study (NHS, 1984-2016) and 87,323 women from the NHS II (1989-2017). Using repeated measures of FFQs, we calculated empirical dietary inflammatory pattern (EDIP) and empirical dietary index for hyperinsulinemia (EDIH) scores based on circulating biomarkers of inflammation or C-peptide, respectively. Cox regression models were used.
Results: We documented 1,468 cases over 32 years of follow-up. Women in the highest EDIP or EDIH quintile had 1.66 (95% CI, 1.40, 1.97) and 1.57 times (95% CI, 1.33, 1.86) higher risk of endometrial cancer, respectively, compared to women in the lowest quintile. However, additional adjustment for BMI attenuated the associations. In subgroup analyses, we observed a significant interaction by BMI, where a significant direct association with EDIP was evident in overweight women (HRQ5vs.Q1 1.47; 95% CI 0.92, 2.35; p-trend=0.02).
Conclusions: Higher dietary inflammatory or insulinemic potential was associated with increased endometrial cancer incidence, nonetheless this association was not independent of adiposity. Furthermore, among overweight women, greater EDIP was directly associated with risk, even after adjusting for BMI.
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