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BackgroundThe relation between carbohydrate intake and risk of ischemic heart disease (IHD) has not been fully explored in Asian populations known to have high-carbohydrate diets.ObjectiveWe assessed whether intakes of total carbohydrates, different types of carbohydrates, and their food sources were associated with IHD mortality in a Chinese population.DesignWe prospectively examined the association of carbohydrate intake and IHD mortality in 53,469 participants in the Singapore Chinese Health Study with an average follow-up of 15 y. Diet was assessed by using a semiquantitative food-frequency questionnaire. HRs and 95% CIs were calculated by using a Cox proportional hazards analysis.ResultsWe documented 1660 IHD deaths during 804,433 person-years of follow-up. Total carbohydrate intake was not associated with IHD mortality risk [men: HR per 5% of energy, 0.97 (95% CI: 0.92, 1.03); women: 1.06 (95% CI: 0.99, 1.14)]. When types of carbohydrates were analyzed individually, starch intake was associated with higher risk [men: 1.03 (95% CI: 0.99, 1.08); women: 1.08, (95% CI: 1.02, 1.14)] and fiber intake with lower risk of IHD mortality [men: 0.94 (95% CI: 0.82, 1.08); women: 0.71 (95% CI: 0.60, 0.84)], with stronger associations in women than men (both P-interaction < 0.01). In substitution analyses, the replacement of one daily serving of rice with one daily serving of noodles was associated with higher risk (difference in HR: 26.11%; 95% CI: 10.98%, 43.30%). In contrast, replacing one daily serving of rice with one of vegetables (-23.81%; 95% CI: -33.12%, -13.20%), fruit (-11.94%; 95% CI: -17.49%, -6.00%), or whole-wheat bread (-19.46%; 95% CI: -34.28%, -1.29%) was associated with lower risk of IHD death.ConclusionsIn this Asian population with high carbohydrate intake, the total amount of carbohydrates consumed was not substantially associated with IHD mortality. In contrast, the shifting of food sources of carbohydrates toward a higher consumption of fruit, vegetables, and whole grains was associated with lower risk of IHD death.

Deficiencies in methyl donor status may render DNA methylation changes and DNA damage, leading to carcinogenesis. Epidemiological studies reported that higher dietary intake of choline is associated with lower risk of pancreatic cancer, but no study has examined the association of serum choline and its metabolites with risk of pancreatic cancer. Two parallel case–control studies, one nested within the Shanghai Cohort Study (129 cases and 258 controls) and the other within the Singapore Chinese Health Study (58 cases and 104 controls), were conducted to evaluate the associations of baseline serum concentrations of choline, betaine, methionine, total methyl donors (i.e., sum of choline, betaine and methionine), dimethylglycine and trimethylamine N‐oxide (TMAO) with pancreatic cancer risk. In the Shanghai cohort, odds ratios and 95% confidence intervals of pancreatic cancer for the highest quartile of choline, betaine, methionine, total methyl donors and TMAO were 0.27 (0.11–0.69), 0.57 (0.31–1.05), 0.50 (0.26–0.96), 0.37 (0.19–0.73) and 2.81 (1.37–5.76), respectively, compared to the lowest quartile. The corresponding figures in the Singapore cohort were 0.85 (0.23–3.17), 0.50 (0.17–1.45), 0.17 (0.04–0.68), 0.33 (0.10–1.16) and 1.42 (0.50–4.04). The inverse associations of methionine and total methyl donors including choline, betaine and methionine with pancreatic cancer risk in both cohorts support that DNA repair and methylation play an important role against the development of pancreatic cancer. In the Shanghai cohort, TMAO, a gut microbiota‐derived metabolite of dietary phosphatidylcholine, may contribute to higher risk of pancreatic cancer, suggesting a modifying role of gut microbiota in the dietary choline‐pancreatic cancer risk association. What's new? Over half of all pancreatic cancers aren't associated with known risk factors. In this prospective study, the authors examined serum levels of three nutrients (choline, methionine, and betaine) that have been associated with reduced oxidative DNA damage and epigenetic changes such as methylation. They found that, as predicted, higher serum levels of these nutrients were correlated with lower pancreatic cancer risk. They also found that certain compounds associated with gut microbiota increased this risk. These results identify novel etiological factors that may guide future prevention strategies for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Background: Vitamin B6 is an important enzymatic cofactor in pathways relevant for the development of pancreatic cancer. In order to evaluate vitamin B6 as a preventive factor for pancreatic cancer, a biomarker approach is needed to overcome the limitations inherent in self-reported dietary information.Methods: To determine whether levels of serum B6 vitamers, including pyridoxal 5'-phosphate (PLP), pyridoxal (PL), 4-pyridoxic acid (PA), and the PA/(PLP + PL) ratio (PAr), were associated with risk of pancreatic cancer, two nested case-control studies of 187 incident pancreatic cancer cases and 258 individually matched controls were conducted within two prospective cohorts of 81,501 participants in Shanghai, China, and Singapore. PLP, PL, and PA were quantified in pre-diagnostic serum samples. Odds ratios and 95% confidence intervals (CIs) were calculated using conditional logistic regression with adjustment for potential confounders.Results: The median (5th-95th percentiles) concentrations of serum PLP among control subjects of the Shanghai and Singapore cohorts were 25.7 (10.0-91.7) nmol/L and 58.1 (20.8-563.0) nmol/L, respectively. In pooled analyses, high serum PLP was associated with a reduced risk of pancreatic cancer (P for trend = 0.048); the adjusted odds ratio for the highest category of PLP (>52.4 nmol/L) was 0.46 (95% CI 0.23, 0.92) compared to vitamin B6 deficiency (<20 nmol/L). No associations were found for serum PL, PA, or PAr with pancreatic cancer risk.Conclusions: Higher concentrations of PLP may protect against the development of pancreatic cancer. The protective effect may be more apparent in populations with low concentrations of circulating vitamin B6. [ABSTRACT FROM AUTHOR]

One potential mechanism by which physical activity may protect against breast cancer is by decreasing mammographic density. Percent mammographic density, the proportion of dense breast tissue area to total breast area, declines with age and is a strong risk factor for breast cancer. The authors hypothesized that women who were more physically active would have a greater decline in percent mammographic density with age, compared with less physically active women. The authors tested this hypothesis using longitudinal data (1996–2004) from 722 participants in the Study of Women's Health Across the Nation (SWAN), a multiethnic cohort of women who were pre- and early perimenopausal at baseline, with multivariable, repeated-measures linear regression analyses. During an average of 5.6 years, the mean annual decline in percent mammographic density was 1.1% (standard deviation = 0.1). A 1-unit increase in total physical activity score was associated with a weaker annual decline in percent mammographic density by 0.09% (standard error = 0.03; P = 0.01). Physical activity was inversely associated with the change in nondense breast area (P < 0.01) and not associated with the change in dense breast area (P = 0.17). Study results do not support the hypothesis that physical activity reduces breast cancer through a mechanism that includes reduced mammographic density. [ABSTRACT FROM PUBLISHER]