Thomas B J, Jarrett R J
Int J Obes. 1982;6 Suppl 1:83-9.
In this paper the general concepts of the relationship between body weight, food intake and susceptibility to vascular disease are re-examined in the light of recent evidence. Several studies suggest that the traditional view of the relationship between mortality and adiposity as direct and linear are mistaken and that the relationship is 'U' shaped with minimal mortality at 'average' rather than 'ideal' weight. Furthermore, the notion that higher levels of food energy intake may be responsible for the enhanced susceptibility to arterial disease are also challenged by those in the lower than the upper ranges of total caloric intake. This may account for some of the anomalous inverse relationships found within countries between food (including fat) intake and arterial disease deaths, findings which have stood for years in irreconcilable contrast with the direct relationship between fat intake and cardiovascular mortality between countries. These apparently paradoxical relationships may be explained by the further unexpected finding of low order but highly significant inverse correlations between food energy intake and adiposity. This has supported the notion of a spectrum of energy conservation/dissipation with the energy conserver storing fat even on low intakes and the dissipator expending a high intake yet remaining lean. Adaptive responses to excess intake and to food deprivation may also be involved in this constitutional variation in energy handling.
本文根据最近的证据重新审视了体重、食物摄入量与血管疾病易感性之间关系的一般概念。几项研究表明，传统上认为死亡率与肥胖之间是直接线性关系的观点是错误的，这种关系呈“U”形，在“平均”而非“理想”体重时死亡率最低。此外，食物能量摄入量较高可能导致动脉疾病易感性增加的观点，也受到了总热量摄入量处于较低范围人群的质疑。这可能解释了在一些国家内部发现的食物（包括脂肪）摄入量与动脉疾病死亡之间存在的异常负相关关系，这些发现多年来一直与国家之间脂肪摄入量与心血管死亡率之间的正相关关系形成不可调和的对比。这些明显矛盾的关系可能由食物能量摄入量与肥胖之间低水平但高度显著的负相关这一进一步的意外发现来解释。这支持了能量守恒/消耗谱的概念，即能量保守者即使在低摄入量时也储存脂肪，而能量消耗者消耗高摄入量但仍保持消瘦。对过量摄入和食物匮乏的适应性反应也可能参与了这种能量处理的体质差异。
