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Association between dietary inflammatory potential and risk of breast cancer: findings from the Sister Study
Author(s) -
PARK YONGMOON,
Shivappa Nitin,
Petimar Joshua,
Steck Susan,
Hébert James,
Sandler Dale
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.168.1
Subject(s) - medicine , breast cancer , hazard ratio , quartile , oncology , cancer , confidence interval , estrogen receptor , confounding , proportional hazards model , body mass index , gynecology
Background It has recently been suggested that the inflammatory potential of diet may influence the risk of breast cancer. However, few studies have investigated associations for pre‐versus post‐menopausal breast cancer or considered effect modification by obesity. Methods Energy adjusted‐Dietary Inflammatory Index (E‐DII) TM was calculated for 49,731 Sister Study cohort participants who completed a validated 146‐item food frequency questionnaire at enrollment in 2003–2009. Women aged 35 to 74 years in the U.S. and Puerto Rico were eligible if they had a sister who had been diagnosed with breast cancer. High DII scores represent a more pro‐inflammatory diet. Cox proportional hazards models were used to estimate multivariable‐adjusted hazard ratios (HR) and 95% confidence intervals (CIs) for breast cancer risk by E‐DII quartiles, after adjusting for potential confounders including known risk factors for breast cancer. Breast cancer subtypes were based on estrogen receptor (ER) and progesterone receptor (PR) status. Time‐varying menopausal status was considered. Results During follow‐up (mean, 7.6 years), 2,155 breast cancers were diagnosed at least 1 year after enrollment. E‐DII scores were not associated with overall or invasive breast cancer (HR highest vs. lowest quartile : 1.11 [95% CI, 0.96–1.29]; 1.14 [95% CI, 0.95–1.35], respectively), although there was a positive association between E‐DII scores and ER‐PR‐breast cancer (HR highest vs. lowest quartile : 1.69 [95% CI, 1.02–2.80], P trend = 0.06). E‐DII scores were associated with increased risk of postmenopausal breast cancer (HR highest vs. lowest quartile : 1.20 [95% CI, 1.01–1.42], P trend = 0.04) and ER‐PR‐invasive postmenopausal breast cancer (HR highest vs. lowest quartile : 2.06 [95% CI, 1.19–3.58], P trend = 0.01). E‐DII scores were not associated with breast cancer in premenopausal women. Obese women (i.e., those with a body mass index ≥30 kg/m 2 ) had increased risk of overall and invasive breast cancer with increasing E‐DII scores (HR highest vs. lowest quartile : 1.42 [95% CI, 1.07–1.90], P trend = 0.04; 1.54 [95% CI, 1.11–2.13], P trend = 0.02, respectively), which was not observed in non‐obese women. Similarly, E‐DII was more strongly associated with breast cancer among women with waist circumference ≥ 88 cm. Conclusion Our findings suggest that dietary inflammatory potential may differentially influence the risk of breast cancer by menopausal status, breast cancer subtype, and adiposity phenotypes. Support or Funding Information This research was supported by the Intramural Research Program of the National Institutes of Health, the National Institute of Environmental Health Sciences (Z01‐ES044005).