Kral T V E, Berkowitz R I, Stunkard A J, Stallings V A, Brown D D, Faith M S
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Int J Obes (Lond). 2007 Jul;31(7):1061-7. doi: 10.1038/sj.ijo.0803551. Epub 2007 Feb 20.
This study compared 4-year changes in daily energy density (ED; kcal/g) in children born at different risk for obesity, characterized the stability of ED and examined associations between ED and child body composition.
Prospective cohort study to measure habitual dietary ED of children who are born at different risk for obesity.
Children who were born at high risk (n=22) or low risk (n=27) for obesity based on maternal pre-pregnancy weight.
Three-day food records were collected from children's mothers at child ages 3, 4, 5 and 6 years. Three categories of ED were computed (food only, food and milk, and food and all beverages) and body composition assessed at each year.
The mean (+/-s.e.m.) ED increased over time across all children (linear trend: P<0.003): 2.18+/-0.07 to 2.32+/-0.06 kcal/g (food only); 1.66+/-0.07 to 1.82+/-0.06 kcal/g (food and milk); and 1.24+/-0.04 to 1.37+/-0.05 kcal/g (food and all beverages). Intraindividual coefficients of variation were smaller than those previously reported for adults. Weight indices were not correlated with dietary ED (P>0.05).
Dietary ED increased in young children, irrespective of their predisposition to obesity, between the ages of 3 and 6 years. The genes that promote childhood obesity may not exert their influence through dietary ED, which may be more strongly influenced by environmental factors.
本研究比较了不同肥胖风险出生儿童的每日能量密度(ED;千卡/克)在4年中的变化,描述了能量密度的稳定性,并研究了能量密度与儿童身体成分之间的关联。
前瞻性队列研究,以测量不同肥胖风险出生儿童的习惯性饮食能量密度。
根据母亲孕前体重,分为肥胖高风险组(n = 22)和低风险组(n = 27)的儿童。
在儿童3、4、5和6岁时,收集其母亲记录的3天食物摄入量。计算三类能量密度(仅食物、食物加牛奶、食物加所有饮料),并每年评估身体成分。
所有儿童的平均(±标准误)能量密度随时间增加(线性趋势:P<0.003):仅食物:从2.18±0.07千卡/克增至2.32±0.06千卡/克;食物加牛奶:从1.66±0.07千卡/克增至1.82±0.06千卡/克;食物加所有饮料:从1.24±0.04千卡/克增至1.37±0.05千卡/克。个体内变异系数小于先前报道的成年人。体重指数与饮食能量密度无相关性(P>0.05)。
3至6岁儿童的饮食能量密度增加,无论其肥胖易感性如何。促进儿童肥胖的基因可能不是通过饮食能量密度发挥作用,饮食能量密度可能受环境因素影响更大。