In addition to cumulative updated intake, we also examined associations for BCAA intake at baseline and after a 0- to 4-year lag (simple updated intake), which represents the intake obtained from the most recent FFQ prior to each follow-up cycle ( 27). Cumulative updated exposure was estimated by calculating the average exposure from all available follow-up questionnaires up to the most recent follow-up questionnaire cycle ( 27). We calculated cumulative updated average of dietary intakes and lifestyle factors such as BMI or physical activity to better represent long-term patterns and reduce within-person variation. End of follow-up was May 31, 2012, for NHS, May 31, 2013, for NHS II, and January 31, 2012, for HPFS. Person-time was calculated from the date of return of the baseline questionnaire to the date of diagnosis of colorectal cancer, the date of death or end of follow-up, whichever came first. For nonresponders who died of colorectal cancer, we also contacted the next-of-kin to obtain permission to review medical records and confirm a diagnosis of colorectal cancer as described above. Information on deaths was gathered from the National Death Index, state vital statistics records, the postal system, and the report from next-of-kin ( 25, 26), and cause of deaths was confirmed by study physicians who reviewed death certificates and medical records. Proximal colon cancers were defined as cancers located in the cecum, ascending, and transverse colon, distal cancers as those in the descending and sigmoid colon, and rectal cancers as those located in the recto-sigmoid and rectum. Study physicians blinded to exposure status reviewed medical records to confirm a diagnosis of colorectal cancer and extract information on stage, location, and histology. When participants reported a new diagnosis of colorectal cancer on their biennial questionnaires, we asked the participant or the next-of-kin for permission to obtain medical records and pathologic reports. The individual branch chain amino acids valine, leucine, and isoleucine were also highly correlated with each other (all partial Spearman correlation coefficients adjusted for age were 0.99). Although correlations are not available for BCAA intake per se, total BCAA intake was highly correlated with animal protein intake (all partial Spearman correlation coefficients adjusted for age were >0.90), but not with vegetable protein intake (correlations ranging between −0.1 and 0.1 in all three cohorts). In brief, de-attenuated Spearman correlation coefficients between FFQ and dietary records were 0.56 for animal and 0.66 for vegetable protein ( 24). The reproducibility and validity of FFQs to estimate protein intake were examined previously ( 21–23). Total BCAA intake (from now on referred to as “BCAA intake”) was calculated by summing intakes of valine, leucine, and isoleucine. These nutrient intakes were energy adjusted using the residual method ( 20). The contribution of each food to nutrient intake was calculated by multiplying the frequency of consumption of each food by its nutrient content and summing up the nutrient intakes from all foods. Participants answered how often they, on average, consumed a specified amount of food during the previous year. As this is the first prospective study to examine the association between BCAA intake and colorectal cancer, our findings warrant investigation in other cohorts.ĭietary intake was assessed repeatedly with validated semiquantitative food frequency questionnaires (FFQ) every 4 years, starting in 1980 for NHS, 1989 for NHS II, and 1986 for HPFS. We did not find evidence that higher dietary BCAA intake is associated with higher risk of colorectal cancer. However, after including dairy calcium to the models, BCAA intake was no longer associated with risk of colorectal cancer. In multivariable adjusted models, we observed a weak inverse association between BCAA intake and colorectal cancer. After up to 28 years of follow-up, 1,660 cases were observed in NHS, 306 in NHS II, and 1,343 in HPFS. Pooled HRs were obtained using random effect models. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards regression models. Validated food frequency questionnaires were administered every 4 years and follow-up questionnaires on lifestyle biennially. We investigated the association between dietary intake of BCAAs with colorectal cancer risk in three prospective cohorts: the Nurses' Health Study I, NHS II ( n = 92,984), and the Health Professionals Follow-up Study. Branched-chain amino acids (BCAA) are essential amino acids, and emerging evidence suggests that BCAAs may mediate pathways related to cancer progression, possibly due to their involvement in insulin metabolism.
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