Abstract PR-02: Dietary fat intake and risk of ovarian cancer in the NIH-AARP Diet and Health Study
Authors: Blank Madeleine M. , Wentzensen Nicolas , Hollenbeck Al , Schatzkin Arthur , Park Yikyung 
Published: May 2012

Abstract
Dietary fat is known to change estrogen levels and has been postulated to increase risk of ovarian cancer. However, previous studies of dietary fat and ovarian cancer have reported inconsistent results. Therefore, we investigated whether total, saturated, monounsaturated, polyunsaturated, animal, or vegetable fat intake is associated with risk of ovarian cancer in a large prospective cohort study, the NIH-AARP Diet and Health Study. We assessed dietary intake with a 124-item food frequency questionnaire and other risk factors at baseline in 1995–1996. Cancer ascertainment was accomplished with matching of the participants to the state cancer registry database. We defined cases as invasive, first primary epithelial ovarian cancer. The relative risks (RR) and 95% confidence interval (CI) were estimated using the Cox proportional hazard model, with multivariate adjustment for age, race, education, body mass index, parity, use of oral contraceptive and menopausal hormone therapy, and total energy intake. During follow-up through 2003, we identified 482 ovarian cancer cases (253 serous tumor and 229 nonserous tumor). We found that total fat intake was significantly positively associated with risk of ovarian cancer. Women in the highest, compared to the lowest, quintile of total fat intake had a 43% increased risk of ovarian cancer (RRQ5 vs. Q1=1.43, 95% CI, 1.07–1.92; Ptrend=0.02). The association did not differ by cancer subtypes: both serous and nonserous tumors were related to an increased risk of ovarian cancer. Comparing the highest versus the lowest quintile of total fat intake, RR was 1.49 (95% CI:0.99–2.24. p trend=0.19) for serous tumor and 1.37 (95% CI:0.90–2.08, p trend=0.04) for nonserous tumor. When types of fat were examined, we found that polyunsaturated fat intake was associated with an increased risk of ovarian cancer when comparing the highest and lowest quintiles of intake (RRQ5 vs. Q1, 1.46; 95% CI, 0.99–2.17; Ptrend=0.05). Monounsaturated and saturated fat intakes were unassociated with risk of ovarian cancer. Animal fat intake was related to a slight increased risk, while vegetable fat intake was unrelated. When we tested for interactions by use of oral contraceptive and menopausal hormone therapy, parity, and body mass index, we observed no significant interactions. However, total fat intake was associated with ovarian cancer risk only in women who have never used oral contraceptives (RRQ5 vs. Q1=1.81, 95% CI:1.24–2.66; Ptrend&lt;0.01), in those who were nulliparous (RRQ5 vs. Q1=2.18, 95% CI:1.05–4.50; Ptrend= 0.02), or in women who used menopausal hormone therapy for more than 5 years (RRQ5 vs. Q1=1.79, 95% CI:1.03–3.11; Ptrend= 0.13). In summary, we found that total fat intake was significantly related to an increased risk of ovarian cancer. Risk attributable to sources and types of fats and interactions by oral contraceptive, parity, and menopausal hormone therapy warrants further investigation.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):PR-02.