Fetal origins of adult disease:: strength of effects and biological basis
Fetal origins of adult disease:: strength of effects and biological basis
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DOI：
10.1093/ije/31.6.1235
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发表时间：
2002-12-01
影响因子：
7.7
通讯作者：
Osmond, C
中科院分区：
文献类型：
--
作者：
Barker, DJP;Eriksson, JG;Osmond, C
背景低出生体重一直被证明与冠心病(CHD)及其生物学危险因素有关。低出生体重的影响会因婴儿生长缓慢和童年时体重快速增加而增加。为了量化发育过程在冠心病发生中的重要性，有必要确定胎儿、婴儿和儿童的发育对晚年主要病理事件-死亡、住院治疗和药物需求的影响。方法对1924-1944年在赫尔辛基大学医院出生的13517名男性和女性进行纵向研究，记录出生时和儿童时期的身体尺寸，记录死亡、住院和开出慢性病药物处方。结果出生时和婴儿期体型较小，随后3岁至11岁体重加速增加，预测冠心病累积发病率有很大差异。结论冠心病和2型糖尿病可能起源于发育可塑性和代偿性生长两种广泛存在的生物学现象。
Background Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication.Methods Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented.Results The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension.Conclusions Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.