JAMA子刊:肥胖不是“吃>消耗”这么简单

碳水化合物-胰岛素模型(CIM)认为,高碳水化合物饮食导致餐后高血糖,刺激胰岛素分泌,促进了脂肪储存,使血液中糖、脂等供能分子不足,致使饥饿感和能量摄入增加、降低代谢率,从而导致肥胖;
遗传学、动物实验、行为和观察研究、喂食研究等,均有证据支持CIM;
CIM的饮食建议:减少糖负荷(GL)高的碳水食物,多吃低GL的碳水食物,吃全谷,增加健康高脂食物,蛋白质摄入充足但不过量,代谢综合征患者可用膳食脂肪替代碳水。
延伸阅读

The Carbohydrate-Insulin Model of Obesity: Beyond "Calories In, Calories Out"

肥胖的碳水化合物-胰岛素模型:不止卡路里的摄入和消耗

10.1001/jamainternmed.2018.2933

2018-07-02, Article

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Despite intensive research, the causes of the obesity epidemic remain incompletely understood and conventional calorie-restricted diets continue to lack long-term efficacy. According to the carbohydrate-insulin model (CIM) of obesity, recent increases in the consumption of processed, high-glycemic-load carbohydrates produce hormonal changes that promote calorie deposition in adipose tissue, exacerbate hunger, and lower energy expenditure. Basic and genetic research provides mechanistic evidence in support of the CIM. In animals, dietary composition has been clearly demonstrated to affect metabolism and body composition, independently of calorie intake, consistent with CIM predictions. Meta-analyses of behavioral trials report greater weight loss with reduced-glycemic load vs low-fat diets, though these studies characteristically suffer from poor long-term compliance. Feeding studies have lacked the rigor and duration to test the CIM, but the longest such studies tend to show metabolic advantages for low-glycemic load vs low-fat diets. Beyond the type and amount of carbohydrate consumed, the CIM provides a conceptual framework for understanding how many dietary and nondietary exposures might alter hormones, metabolism, and adipocyte biology in ways that could predispose to obesity. Pending definitive studies, the principles of a low-glycemic load diet offer a practical alternative to the conventional focus on dietary fat and calorie restriction.

First Authors:
David S Ludwig

Correspondence Authors:
David S Ludwig

All Authors:
David S Ludwig,Cara B Ebbeling