Sørensen Thorkild I A
Institute of Preventive Medicine, Copenhagen University Hospitals, Centre for Health and Society, Copenhagen DK1357K, Denmark.
Proc Nutr Soc. 2009 Feb;68(1):43-54. doi: 10.1017/S0029665108008847. Epub 2008 Dec 15.
Use of the energy balance equation for understanding the causation of obesity is discussed. Its basis on the thermodynamic laws is expressed in mathematical models for body-weight changes. Only a very small net energy surplus per time unit constitutes the energy deposition during weight gain, making measurements of its components difficult. The physical laws provide exact quantitative relationships between energy intake, energy expenditure and deposition of energy, but cannot disentangle the initiating and driving forces of the energy imbalance, which may also be an active storage of fat in adipose tissue. These and various other limitations of the energy balance model warrant cautiousness in using the model in studies of obesity causation. Weight gain may be self-promoting and mathematical feedback models allowing estimation of such effects show that they are realistic. Predisposition and susceptibility should be distinguished, and susceptibility as a modifiable predisposition, the genetic and environmental contribution to predisposition and its usefulness as targets for prevention and treatment are discussed. Current progress in unravelling genetic predisposition, the complex genetically-determined mechanisms, the slower progress in unravelling the environmental influences, the different nature of genetic and environmental influences, the possible pathways of environmental influences and the environmental influences as mediators of genetic effects are addressed. The evidence behind the prevailing concept of the 'obesogenic' environment is critically analysed. Finally, particular opportunities for the identification of the causes of the obesity epidemic by detailed analysis of an observed irregular development of the epidemic over long time periods are presented, and evidence for predisposition as a result of postnatal environmental influences is inferred from these studies.
讨论了利用能量平衡方程来理解肥胖成因的问题。其基于热力学定律的原理在体重变化的数学模型中得以体现。在体重增加期间,每次能量净剩余量非常小才构成能量沉积,这使得对其组成部分的测量变得困难。物理定律给出了能量摄入、能量消耗与能量沉积之间精确的定量关系,但无法厘清能量失衡的起始和驱动因素,而能量失衡也可能是脂肪在脂肪组织中的主动储存。能量平衡模型的这些以及其他各种局限性,使得在肥胖成因研究中使用该模型时需谨慎。体重增加可能具有自我促进作用,允许对这种效应进行估计的数学反馈模型表明它们是现实可行的。应区分易感性和倾向性,并且作为一种可改变的倾向性来讨论易感性、遗传和环境对倾向性的贡献及其作为预防和治疗靶点的有用性。阐述了在揭示遗传易感性方面的当前进展、复杂的遗传决定机制、在揭示环境影响方面进展较慢的情况、遗传和环境影响的不同性质、环境影响的可能途径以及作为遗传效应介导因素的环境影响。对“致肥胖”环境这一流行概念背后的证据进行了批判性分析。最后,提出了通过详细分析长期观察到的肥胖流行的不规则发展来确定肥胖流行原因的特殊机会,并从这些研究中推断出由出生后环境影响导致易感性的证据。