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Inflammatory potential of diet and risk of pancreatic cancer in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
Zheng, J, Merchant, AT, Wirth, MD, Zhang, J, Antwi, SO, Shoaibi, A, Shivappa, N, Stolzenberg-Solomon, RZ, Hebert, JR, Steck, SE
International journal of cancer. 2018;(12):2461-2470
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Abstract
Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet. We aimed to examine the association between the inflammatory potential of diet, assessed with the Dietary Inflammatory Index (DII®), and pancreatic cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial prospective cohort. Our study included 101,449 participants aged 52-78 years at baseline who completed both baseline questionnaire and a diet history questionnaire. Energy-adjusted DII (E-DII) scores were computed based on food and supplement intake. Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with participants in the lowest E-DII quintile (most anti-inflammatory scores) as referent. After a median 8.5 years of follow-up, 328 pancreatic cancer cases were identified. E-DII scores were not associated with pancreatic cancer risk in the multivariable model (HRQ5vsQ1 = 0.94; 95% CI = 0.66-1.35; p-trend = 0.43). Time significantly modified the association (p-interaction = 0.01). During follow up <4 years, there was suggestive evidence of an inverse association between E-DII and pancreatic cancer (HRQ5vsQ1 = 0.60; 95% CI = 0.35-1.02; p-trend = 0.20) while there was a significant positive trend in the follow up ≥4 years (HRQ5vsQ1 = 1.31; 95% CI = 0.83-2.08; p-trend = 0.03). Similar results were observed for E-DII from food only. Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk; however, heterogeneous results were obtained with different follow-up times. These divergent associations may result from the influences of undetected disease in the short-term.
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The Effect of Iron Fortification on Iron (Fe) Status and Inflammation: A Randomized Controlled Trial.
Ma, J, Sun, Q, Liu, J, Hu, Y, Liu, S, Zhang, J, Sheng, X, Hambidge, KM
PloS one. 2016;(12):e0167458
Abstract
BACKGROUND Iron deficiency (ID) is common in toddlers in developing countries. Iron fortified or meat-based complementary foods may be effective to prevent ID. OBJECTIVE Our objective was to compare iron status at 18 months and growth from 6 to 18 months in rural poor toddlers fed 3 different complementary foods. METHODS The study was nested within a larger trial in which 6-month-old infants were randomized to receive 50g/d meat (MG), an equi-caloric fortified cereal supplement (FG) or local cereal supplement (LG) for 1 year. Hb, sTfR, HsCRP, ferritin and AGP were measured in 410 blood samples collected by a random sampling (MG, 137; FG, 140; LG, 133); calprotectin was measured in feces. Body iron = -[log (sTfR ×1000/ferritin)-2.8229] /0.1207. ID = ferritin<12ug/L. RESULTS The toddlers in FG had the significantly highest levels in serum ferritin and body iron (P = 0.043, 0.004), and the rates of both ID and iron deficiency anemia (IDA) were the lowest in FG (P = 0.010, 0.021). The rate of systemic inflammation in FG was 30.71%, which was the highest among three groups (P = 0.042). No intervention effects on either the rates of ID and IDA or iron stores (serum ferritin and body iron) were shown in MG. The change in length-for-age z scores (LAZ) from 6 to 18 months among three groups was significantly different (P = 0.021) and a smaller decrease of LAZ in MG and a larger decrease of LAZ in FG were observed. CONCLUSION Iron fortified cereal improved iron status of poor rural toddlers but was also associated with systemic inflammation which was likely to impair their growth.