Wells Jonathan C K, Chomtho Sirinuch, Fewtrell Mary S
Childhood Nutrition Research Centre, Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK.
Proc Nutr Soc. 2007 Aug;66(3):423-34. doi: 10.1017/S0029665107005691.
There is now compelling evidence that growth patterns in early life are associated with risk of the metabolic syndrome in adulthood, although the relative importance of prenatal v. postnatal growth for such associations remains controversial. Body composition may play a key role in the 'programming' of such diseases, through itself being programmed by early growth, and perhaps also by being a mediator of the programming process. Early studies reporting positive associations between birth weight and adult BMI suggested a tendency for large babies to become obese adults. Such findings appeared contradictory to the many studies linking low birth weight with increased risk of the metabolic syndrome. Recent studies now indicate that birth weight is strongly predictive of later lean mass, and has a much weaker association with later fatness. Studies that link low birth weight with a more central adipose distribution in later life remain controversial, and require confirmation using more sophisticated methodologies. Findings for infant growth rate appear population-specific, with infant weight gain predicting subsequent lean mass in developing countries, but predicting subsequent fat mass and obesity in industrialised populations. Further studies are required on this issue, to ensure that appropriate public health policies are recommended for countries across the range of economic development. Although the links between early growth and later disease risk implicate early-life nutrition, either in utero or during infancy, few prospective studies have explored the influence of early diet on later body composition. Many studies have associated breast-feeding with a reduced prevalence of obesity categorised by BMI; however, the few studies directly evaluating childhood fatness provide little support for this hypothesis. Recent advances in the ability to measure body composition during the infant period offer a major opportunity to improve the understanding of the nutritional programming of body composition and its contribution, or lack thereof, to subsequent disease risk.
现在有令人信服的证据表明，早期生活中的生长模式与成年后患代谢综合征的风险相关，尽管产前生长与产后生长在这种关联中的相对重要性仍存在争议。身体成分可能在这类疾病的“编程”中起关键作用，这是由于其自身受早期生长的“编程”，或许还作为编程过程的一个介质。早期研究报告出生体重与成人BMI之间存在正相关，这表明大婴儿有成为肥胖成人的倾向。这类发现似乎与许多将低出生体重与代谢综合征风险增加相联系的研究相矛盾。现在的最新研究表明，出生体重能有力地预测后期的瘦体重，而与后期肥胖的关联则弱得多。将低出生体重与晚年更集中的脂肪分布相联系的研究仍存在争议，需要使用更复杂的方法加以证实。婴儿生长速率的研究结果似乎因人群而异，婴儿体重增加在发展中国家能预测随后的瘦体重，但在工业化人群中则预测随后的脂肪量和肥胖。关于这个问题需要进一步研究，以确保为处于不同经济发展水平的国家推荐适当的公共卫生政策。尽管早期生长与后期疾病风险之间的联系暗示了子宫内或婴儿期的早期营养，但很少有前瞻性研究探讨早期饮食对后期身体成分的影响。许多研究将母乳喂养与按BMI分类的肥胖患病率降低联系起来；然而，少数直接评估儿童肥胖情况的研究几乎没有为这一假设提供支持。婴儿期测量身体成分能力的最新进展为增进对身体成分营养编程及其对后续疾病风险的贡献（或缺乏贡献）的理解提供了一个重要契机。
