Computational modeling of human metabolism, body weight and composition

我们继续开发和测试我们的人体新陈代谢和体重动力学的数学模型。 我们应用我们的成人模型来客观地测量能量摄入量的变化，并与自我报告的摄入量变化进行比较，在一年的减肥干预期间，受试者随机分为低碳水化合物饮食和低脂肪饮食。我们发现，自我报告的能量摄入变化表明，在3个月、6个月和12个月时，热量限制处于相对持续的状态，每天500至600千卡，两种饮食之间没有显著差异。然而，基于客观模型的能量摄入量变化估计显示，卡路里摄入量早期大幅下降&800千卡/天，随后在年底指数回升至比基线低100千卡/天。考虑到自我报告的体力活动并没有对结果产生实质性影响。随着时间的推移，对卡路里摄入量变化的客观、基于模型的估计与自我报告的测量之间的差异逐渐增大。我们的结果表明，在干预的早期阶段，遵循低碳水化合物饮食的指导导致了比低脂肪饮食更大的卡路里限制，但这些饮食差异并不持续。 我们最近还模拟了所谓的“蛋白质杠杆”在美国肥胖症流行中的潜在作用，即减少食物供应中的蛋白质比例，从而导致补偿 增加总能量摄入量，试图保持绝对蛋白质消耗量的目标量。根据联合国粮食及农业组织发布的粮食资产负债表，尽管美国粮食供应的绝对蛋白质含量自1970年代初以来有所增加，但由于可用碳水化合物和脂肪的增加幅度更大，来自蛋白质的可用卡路里比例下降了1%。我们的数学模型表明，根据蛋白质杠杆模型，即使食物中蛋白质的比例如此微小的下降，也有可能导致能量摄入的相对较大的增加。因此，虽然蛋白质杠杆效应不太可能完全解释肥胖症的流行，但其潜在贡献不应被忽视。 最后，我们扩展了我们的儿童生长数学模型，模拟了从出生到成年的能量平衡动态，并应用我们的模型估计了不准确测量的婴儿配方奶粉对婴儿体重和肥胖的潜在影响。

We continue to develop and test our mathematical models of human metabolism and body weight dynamics. We applied our adult model to objectively measure energy intake changes in comparison with self-reported intake changes during a 1-year weight-loss intervention with subjects randomized to low-carbohydrate versus low-fat diets. We found that self-reported changes in energy intake indicated a relatively persistent state of calorie restriction of 500 to 600 kcal/d at 3, 6, and 12 months with no significant differences between the diets. However, the objective model-based estimates of energy intake change demonstrated large early decreases in calorie intake > 800 kcal/d followed by an exponential return to 100 kcal/d below baseline at the end of the year. Accounting for self-reported physical activities did not materially affect the results. Discrepancies between the objective, model-based estimates of calorie intake changes and the self-reported measurements became progressively greater over time. Our results indicated that instructions to follow the low-carbohydrate diet resulted in greater calorie restriction than the low-fat diet in the early phases of the intervention, but these diet differences were not sustained. We also recently modeled the potential role of so-called "protein leverage" on US obesity prevalence whereby decreasing the protein fraction of the food supply leads to compensatory increases in total energy intake in an attempt to maintain a target amount of absolute protein consumed. According to food balance sheets published by the Food and Agriculture Organization of the United Nations, while the absolute protein content of the US food supply has increased since the early 1970s, the fraction of available calories from protein has decreased by 1% because of greater increases in available carbohydrate and fat. Our mathematical model indicated that even such a small decrease in the protein fraction of the food supply has the potential to result in relatively large increases in energy intake according to the protein leverage model. Therefore, while the protein leverage effect is unlikely to fully explain the obesity epidemic, its potential contribution should not be ignored. Finally, we extended our mathematical model of childhood growth to simulate the energy balance dynamics from birth through adulthood and applied our model to estimate the potential effect on infant body weight and adiposity of inaccurately measured infant formula.