Gluckman Peter D, Hanson Mark A, Morton Susan M B, Pinal Catherine S
Liggins Institute, University of Auckland, Grafton, Private Bag 92019, Auckland, New Zealand.
Biol Neonate. 2005;87(2):127-39. doi: 10.1159/000082311. Epub 2004 Nov 24.
The hypothesis that there is a developmental component to subsequent adult disease initially arose from epidemiological findings relating birth size to either indices of disease risk or actual disease prevalence in later life. While components of the epidemiological analyses have been challenged, there is strong evidence that developmental factors contribute to the later risk of metabolic disease--including insulin resistance, obesity, and heart disease--as well as have a broader impact on osteoporosis, depression and schizophrenia. We suggest that disease risk is greater when there is a mismatch between the early developmental environment (i.e., the phase of developmental plasticity) versus that experienced in mature life (i.e., adulthood), and that nutritional influences are particularly important. It is also critical to distinguish between those factors acting during the developmental phase that disrupt development from those influences that are less extreme and act through regulated processes of epigenetic change. A model of the relationship between the developmental and mature environment is proposed and suggests interventional strategies that will vary in different population settings.
认为后续成人疾病存在发育因素这一假说最初源于流行病学研究结果，这些结果将出生时的大小与疾病风险指标或晚年实际疾病患病率联系起来。虽然流行病学分析的某些部分受到了质疑，但有强有力的证据表明，发育因素会导致日后患代谢性疾病（包括胰岛素抵抗、肥胖症和心脏病）的风险增加，同时对骨质疏松症、抑郁症和精神分裂症也有更广泛的影响。我们认为，当早期发育环境（即发育可塑性阶段）与成年后的经历（即成年期）不匹配时，疾病风险会更高，而且营养影响尤为重要。区分发育阶段中干扰发育的因素与那些不太极端且通过表观遗传变化的调节过程起作用的影响因素也至关重要。本文提出了一个发育环境与成熟环境之间关系的模型，并提出了在不同人群环境中会有所不同的干预策略。
