Associations of dietary patterns with kidney cancer risk, kidney cancer-specific mortality and all-cause mortality among postmenopausal women.

BACKGROUND: The empirical dietary index for hyperinsulinemia (EDIH) and empirical dietary inflammatory pattern (EDIP) are novel measures of dietary quality associated with insulin hypersecretion or chronic inflammation, respectively, whereas the Healthy Eating Index (HEI-2015) measures adherence to the Dietary Guidelines for Americans (DGA). We evaluated associations of EDIH, EDIP and HEI-2015 on the risk of both kidney cancer development and mortality. METHODS: We calculated the dietary scores from baseline food frequency questionnaires among 115,830 participants aged 50-79 years in the Women's Health Initiative. Multivariable-adjusted Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (95%CI) for kidney cancer risk, kidney cancer-specific mortality and all-cause mortality, per 1-standard deviation increment in dietary pattern scores. RESULTS: Higher EDIH was associated with greater risk of kidney cancer development [HR, 1.12; 95%CI, (1.01,1.23)], kidney cancer-specific death [1.22(0.99,1.48)], and all-cause mortality, [1.05(1.02,1.08)]. Higher HEI-2015 was associated with lower risk of kidney cancer development, [0.85(0.77, 0.94)], kidney cancer-specific death, [0.84(0.69,1.03)] and all-cause mortality, [0.97(0.95,1.00)]. However, EDIP was not significantly associated with outcomes. Associations did not differ by BMI categories. CONCLUSIONS: Low-insulinemic dietary patterns and higher quality diets, are worthy of testing in dietary pattern intervention trials for kidney cancer prevention and improved survivorship.

Assessment of dietary carotenoid intake and biologic measurement of exposure in humans.

Carotenoids are a diverse family of phytochemicals with over 1000 different carotenoids present in nature. A human diet containing a variety of plant foods typically includes approximately 50 different carotenoids, although six (α-carotene, ß-carotene, ß-cryptoxanthin, lycopene, lutein, and zeaxanthin) comprise over 90% of total carotenoid intake. Most carotenoids do not meet the definition of a nutrient, but several can be cleaved to form vitamin A and are important contributors to vitamin A nutriture and prevention of vitamin A deficiency. Large epidemiologic studies suggest that diets rich in total or specific carotenoids are associated with a reduced risk of several diseases including various types of cancer, cardiovascular disease, cognitive disorders, and age-related macular degeneration. However, accurate measurement of dietary intake is challenging and current methods of dietary assessment, including food frequency questionnaires, diet records and 24-h recalls, have strengths and limitations regarding estimating carotenoid intake. Additionally, carotenoid bioavailability from the diet is influenced by many variables including food processing and cooking, meal composition, and individual characteristics of the host including age, digestive efficiency, nutritional status and genetic polymorphisms. Carotenoids are deposited in many human tissues and can be measured using a variety of techniques including high performance liquid chromatography (HPLC) and mass spectrometry (MS). Continued research is necessary to improve dietary intake assessment and establish biologically relevant dose-response relationships in the context of individual variability to advance our understanding of diet, disease risk, and health promotion.