Sandman Curt A, Davis Elysia P
333 City Drive West, Suite 1200, Department of Psychiatry & Human Behavior, University of California, Irvine, Orange, CA 92868, USA.
Department of Pediatrics, University of California, CA, USA.
Future Neurol. 2010;5(5):675-690. doi: 10.2217/fnl.10.35. Epub 2010 Sep 21.
The developmental origins of disease or fetal programming model predicts that early exposures to threat or adverse conditions have lifelong consequences that result in harmful outcomes for health. The vast majority of the studies in support of the programming model in human beings are retrospective and most relied on surrogate measures of early experience such as birth weight or preterm birth. Recently, a small number of prospective studies have been reported that have documented the developmental consequences of exposures to stressful intrauterine conditions. These studies of gestational stress have clearly shown that fetal exposures to psychosocial and/or biological markers of adversity have significant and largely negative consequences for fetal, infant and child neurological development. Fetal exposure to stress, especially early in gestation, results in delayed fetal maturation and impaired cognitive performance during infancy and results in decreased brain volume in areas associated with learning and memory in children. The accumulating evidence supports the conclusion that fetal exposure to stress profoundly influences the nervous system, with consequences that persist into childhood and perhaps beyond.
疾病的发育起源或胎儿编程模型预测，早期暴露于威胁或不利条件会产生终身后果，进而导致对健康有害的结果。绝大多数支持人类编程模型的研究都是回顾性的，并且大多数依赖于早期经历的替代指标，如出生体重或早产。最近，有少量前瞻性研究报告，记录了暴露于压力性宫内环境的发育后果。这些关于孕期压力的研究清楚地表明，胎儿暴露于逆境的心理社会和/或生物学标志物对胎儿、婴儿和儿童的神经发育具有重大且主要为负面的影响。胎儿暴露于压力，尤其是在孕期早期，会导致胎儿成熟延迟、婴儿期认知能力受损，并导致儿童与学习和记忆相关区域的脑容量减少。越来越多的证据支持这样的结论，即胎儿暴露于压力会深刻影响神经系统，其后果会持续到童年，甚至可能更久。
