New York Obesity Nutrition Research Center, St. Luke's Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, NY, USA; Mount Sinai Adolescent Health Center, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Physiol Behav. 2013 Aug 15;120:106-13. doi: 10.1016/j.physbeh.2013.07.009. Epub 2013 Aug 1.
Weight loss dieting remains the treatment of choice for the vast majority of obese individuals, despite the limited long-term success of behavioral weight loss interventions. The reasons for the near universal unsustainability of behavioral weight loss in [formerly] obese individuals have not been fully elucidated, relegating researchers to making educated guesses about how to improve obesity treatment, as opposed to developing interventions targeting the causes of weight regain. This article discusses research on several factors that may contribute to weight regain following weight loss achieved through behavioral interventions, including adipose cellularity, endocrine function, energy metabolism, neural responsivity, and addiction-like neural mechanisms. All of these mechanisms are engaged prior to weight loss, suggesting that these so called "anti-starvation" mechanisms are activated via reductions in energy intake, rather than depletion of energy stores. Evidence suggests that these mechanisms are not necessarily part of a homeostatic feedback system designed to regulate body weight, or even anti-starvation mechanisms per se. Although they may have evolved to prevent starvation, they appear to be more accurately described as anti-weight loss mechanisms, engaged with caloric restriction irrespective of the adequacy of energy stores. It is hypothesized that these factors may combine to create a biological disposition that fosters the maintenance of an elevated body weight and works to restore the highest sustained body weight, thus precluding the long-term success of behavioral weight loss. It may be necessary to develop interventions that attenuate these biological mechanisms in order to achieve long-term weight reduction in obese individuals.
尽管行为减肥干预的长期成功率有限，但减肥节食仍然是绝大多数肥胖者的首选治疗方法。[以前]肥胖者的行为减肥几乎普遍不可持续的原因尚未完全阐明，这使得研究人员只能猜测如何改善肥胖症治疗，而不是开发针对体重反弹原因的干预措施。本文讨论了一些可能导致通过行为干预减肥后体重反弹的因素的研究，包括脂肪细胞性、内分泌功能、能量代谢、神经反应性和类似成瘾的神经机制。所有这些机制在减肥之前就已经被激活，这表明这些所谓的“抗饥饿”机制是通过减少能量摄入而不是耗尽能量储存来激活的。有证据表明，这些机制不一定是旨在调节体重的体内平衡反馈系统的一部分，甚至不一定是抗饥饿机制本身。尽管它们可能是为了防止饥饿而进化的，但它们似乎更准确地被描述为抗减肥机制，与热量限制有关，而与能量储存的充足性无关。据推测，这些因素可能会结合起来，形成一种促进维持较高体重的生物倾向，并努力恢复最高持续体重，从而排除行为减肥的长期成功。可能有必要开发干预措施来减弱这些生物机制，以实现肥胖者的长期体重减轻。
