Abstract
Chronic low-grade inflammation represents a likely intermediary in the relation between carbohydrate nutrition and both type 2 diabetes and cardiovascular disease. This study assessed the prospective association between carbohydrate quantity and quality [dietary glycemic index (GI), glycemic load (GL), and added sugar, fiber, and whole-grain intake] during puberty, a potentially critical period for later disease, and low-grade inflammation in younger adulthood. The analysis was based on 205 participants (113 girls and 92 boys) from the DONALD (Dortmund Nutritional and Anthropometric Longitudinally Designed) study with at least 2 3-d weighed dietary records during puberty (girls: 9–14 y, boys: 10–15 y) and blood samples in younger adulthood (18–36 y). Multivariable linear regression models were used to analyze the associations between carbohydrate nutrition and circulating concentrations of pro- and anti-inflammatory immune mediators [high-sensitivity C-reactive protein (hs-CRP), interleukin (IL) 6, IL-18, and adiponectin]. A higher intake of carbohydrates during puberty (P-trend = 0.005), particularly from higher-GI food sources (P-trend = 0.01), was prospectively related to higher concentrations of IL-6 in younger adulthood, independently of baseline BMI and early life, socioeconomic, and other nutritional factors. Furthermore, a higher dietary GL (P-trend = 0.002) and a lower intake of whole grains (P-trend = 0.01) were independently associated with higher IL-6 concentrations in adults. Dietary GI and added sugar and fiber intakes were not independently associated with IL-6 (P-trend ≥ 0.09). Carbohydrate nutrition during puberty was not independently related to hs-CRP, IL-18, and adiponectin concentrations (all P-trend > 0.1). During puberty, a higher intake of carbohydrates from higher-GI food sources and lower whole-grain consumption prospectively predict greater IL-6 concentrations in young adulthood. These data support the hypothesis that diet during puberty influences later inflammation and metabolic dysfunction.
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