1 MRC Lifecourse Epidemiology Unit, University of Southampton , Southampton General Hospital, Tremona Road, Southampton SO16 6YD , UK.
2 Epidemiology Research Unit, CSI Holdsworth Memorial Hospital , Mysore , South India.
Philos Trans R Soc Lond B Biol Sci. 2019 Apr 15;374(1770):20180123. doi: 10.1098/rstb.2018.0123.
An association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently 'programmes' organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomized trials of maternal nutritional interventions during pregnancy have so far had limited follow-up of the offspring. Moreover, interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high-risk individuals in mid-life, DOHaD concepts offer a 'primordial' preventive strategy to reduce disease in future generations by improving fetal and infant development. This article is part of the theme issue 'Developing differences: early-life effects and evolutionary medicine'.
低出生体重与成年人心血管疾病和糖尿病风险增加相关,这导致了健康与疾病的发育起源(DOHaD)假说,该假说提出,早期发育过程中的营养不良会永久性地“编程”器官结构和代谢,导致对后期心血管代谢疾病的易感性。由母体妊娠期糖尿病引起的高出生体重也与后期糖尿病有关,这表明胎儿营养过剩也具有编程效应。出生后因素(体重过度增加/肥胖、吸烟、不良饮食和缺乏身体活动)与胎儿暴露相互作用,增加了疾病风险。动物研究表明,母体或早期产后饮食改变后,后代会出现永久性代谢效应,但人类的证据主要限于观察性和准实验性情况,如母体饥荒暴露。对妊娠期间母体营养干预的随机试验对后代的随访时间有限。此外,干预通常在妊娠早期之后开始,因此错过了关键的围孕期或早期妊娠事件,如表观遗传变化、胎盘形成和胎儿器官发生。最近和正在进行的预孕期干预试验,以及为长期后代随访提供动力的试验,将解决这些问题。虽然目前针对心血管代谢疾病的预防策略侧重于中年高危人群,但 DOHaD 概念提供了一种“原始”的预防策略,通过改善胎儿和婴儿的发育,减少后代的疾病。本文是“发展差异:生命早期效应和进化医学”主题问题的一部分。