Eriksson Johan G, Forsén Tom J
National Public Health Institute, Department of Epidemiology and Health Promotion, Helsinki, Finland.
Ann Med. 2002;34(3):157-61.
Coronary heart disease (CHD) originates early in life and numerous studies have shown inverse associations between body size at birth and CHD in adult life. Recently it has been shown that the increased risk for CHD associated with a small body size at birth is modified by growth during childhood. The greatest risk for CHD is noted in individuals with small body size at birth and who 'catch-up' in weight and body size during childhood. An increase in body weight and body mass index during the first year of life is however associated with a reduced risk of CHD. These recent findings add to the evidence that optimizing early growth is an important area in primary prevention of CHD. There are several potential mechanisms explaining the association between a non-optimal early growth and CHD. Behavioral, physiological, hormonal and genetic factors influence growth. Although socio-economic factors influence the risk of CHD, the association between slow fetal growth and CHD is not caused by confounding socio-economic factors. Biological programming - the process whereby a stimulus during critical periods of development has long lasting or lifelong effects on metabolism - is proposed to mediate the effects between early growth and adult diseases.
冠心病(CHD)在生命早期就已发病,众多研究表明,出生时的体型与成年后的冠心病之间存在负相关。最近有研究表明,出生时体型较小所带来的冠心病风险增加会因儿童期的生长而改变。冠心病风险最高的是那些出生时体型小且在儿童期体重和体型“追赶”上来的个体。然而,出生后第一年体重和体重指数的增加与冠心病风险降低有关。这些最新发现进一步证明,优化早期生长是冠心病一级预防的一个重要领域。有几种潜在机制可以解释早期生长不理想与冠心病之间的关联。行为、生理、激素和遗传因素都会影响生长。虽然社会经济因素会影响冠心病风险,但胎儿生长缓慢与冠心病之间的关联并非由社会经济因素的混杂所致。生物编程——即在发育关键期的刺激对新陈代谢产生长期或终身影响的过程——被认为是介导早期生长与成人疾病之间影响的机制。