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Consumption of Total and Individual Sugars, Sugary Foods and Sugary Beverages in Relation to Adiposity‐Related Cancer Risk in the Framingham Offspring Cohort (1991–2013)
Author(s) -
Makarem Nour,
Lin Yong,
Bandera Elisa V.,
Jacques Paul,
Parekh Niyati
Publication year - 2016
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.30.1_supplement.42.1
Subject(s) - medicine , cohort , hazard ratio , framingham heart study , diet and cancer , cohort study , obesity , offspring , overweight , breast cancer , proportional hazards model , cancer , environmental health , framingham risk score , confidence interval , pregnancy , biology , disease , genetics
Objective The purpose of this prospective cohort study was to examine total sugar, sucrose, fructose and usual sugary food and beverage consumption in relation to the risk of adiposity‐related cancers combined and three of the most commonly diagnosed site‐specific cancers (breast, prostate and colorectal) in the Framingham Offspring cohort. Methods The study sample consisted of 3,184 men and women from the Framingham Offspring cohort. This cohort was recruited in 1971–1975, and clinical exams were conducted, on average, every 4 years to collect medical, lifestyle and anthropometric data. The main exposures were intakes of total sugar, fructose, sucrose and sugary foods and beverages. Data on diet was first available in 1991 and was collected using a food frequency questionnaire. The outcomes of interest were combined incidence of adiposity‐related cancers in addition to incidence of breast, prostate and colorectal cancer. Cancers were considered adiposity‐related if identified by the National Cancer Institute and the American Cancer Society as clearly or possibly linked to overweight and obesity. Incident cancers were identified from medical records (n=565) and were documented until 2013. Therefore, the study encompassed a follow‐up period of >20 years. Cox proportional hazards models were used to compute hazard ratios (HR) and 95% confidence intervals (CI) to estimate associations between total sugar, fructose, sucrose and sugary foods and beverages in relation to cancer risk. Results After adjustment for multiple confounders including age, smoking, waist‐to‐hip ratio, reproductive risk factors, energy, alcohol, in addition to antioxidant, fiber, fat and red and processed meat intake, total sugar and sucrose intakes were not associated with risk of adiposity‐related cancers combined or any of the site‐specific cancers. Fructose intake, as percentage of total calories, in the highest versus lowest quintile was associated with >2‐fold increase in prostate (HR: 2.18; 95%CI: 1.23–3.87) and colorectal cancer risk (HR:2.25; 95%CI:1.04–4.86). In general, consumption of sugary foods and beverages was associated with up to 2‐fold higher risk of adiposity‐related cancers and all site‐specific cancers, but associations were only statistically significant for prostate cancer. For prostate cancer, higher total consumption of sugary foods and beverages was associated with 88% higher cancer risk (1.88, 95%CI: 1.03–3.40). Sugary beverage consumption (fruit juice and sugar‐sweetened beverages) in the highest versus lowest quintile was associated with >3‐fold higher prostate cancer risk (HR:3.60, 95%CI:1.85–7.01). In particular, higher fruit juice intake was associated with >2‐fold increase in risk (HR: 2.73; 95%CI:1.45–5.11). Among sugary foods, dessert foods such as chocolate and doughnuts were associated with up to 88% risk of prostate cancer (HR:1.88; 95%CI:1.23–2.87). Conclusions In this cohort of middle‐aged American adults, fructose intake was associated with higher prostate and colorectal cancer risk. Our findings suggest that higher sugary food and beverage intakes increase cancer risk, particularly for prostate cancer. These analyses suggest that avoiding foods and beverages that are rich in sugar may be used as an effective cancer control strategy. Support or Funding Information This research was supported by the American Cancer Society Research Scholar Grant (#RSG‐12‐005‐01‐CNE)

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