基于生活环境、健康和疾病在分子水平上密切相关的核心理念,健康和疾病的发育起源(developmental origins of health and disease,DOHaD)理论为健康与疾病间的关联研究提供了全新视角。该理论通过多学科、多领域的知识互通,追溯不同的...基于生活环境、健康和疾病在分子水平上密切相关的核心理念,健康和疾病的发育起源(developmental origins of health and disease,DOHaD)理论为健康与疾病间的关联研究提供了全新视角。该理论通过多学科、多领域的知识互通,追溯不同的生活经历如何影响生命全过程中的健康和疾病风险。成人期疾病的敏感窗口期不再局限于妊娠前和妊娠期,分娩期至成年早期也成为暴露因素发挥作用的重要时段。母源性/父源性因素、环境因素、新生儿出生状况、儿童期代谢情况等能够通过影响表观遗传、代谢和免疫调控、氧化应激等,改变发育程序并对子代远期健康产生正向或负向影响。因此,为实现健康促进,需要同步推进早期生命阶段预防、后期随访及健康干预的关口前移,以期有效降低成年期疾病风险,提升生命全周期健康水平。综述DOHaD领域最新研究进展对阐明人类发展早期阶段发生的不良事件影响健康和疾病模式及发现有效干预措施具有积极意义。展开更多
传统观念认为,成人疾病的发生主要由遗传和成人期生活环境所致。然而,近几年来国际学术界通过大量的流行病学调查结果,提出＂健康与疾病发育起源（Developmental Origins of Health andDisease,DOHaD）＂新概念。学者提出,虽然多种代谢...传统观念认为,成人疾病的发生主要由遗传和成人期生活环境所致。然而,近几年来国际学术界通过大量的流行病学调查结果,提出＂健康与疾病发育起源（Developmental Origins of Health andDisease,DOHaD）＂新概念。学者提出,虽然多种代谢性疾病（如脂肪肝、展开更多
人类研究和动物实验阐述了"成人疾病胎儿起源"的发生机理以及宫内不良环境与成人后疾病的关联。不仅如此,大量的流行病学资料也证明,出生后发育可塑期同样有着"规划"的功能。学者们将慢性疾病程序化的敏感时期从宫...人类研究和动物实验阐述了"成人疾病胎儿起源"的发生机理以及宫内不良环境与成人后疾病的关联。不仅如此,大量的流行病学资料也证明,出生后发育可塑期同样有着"规划"的功能。学者们将慢性疾病程序化的敏感时期从宫内延续至婴儿期甚至儿童期,形成"健康和疾病的发育起源"(Developmental Origins of Adult Health and Disease)学说,其中心内容是(1)胎儿营养不良;(2)胎儿期较多暴露于皮质醇激素;(3)遗传易感性;(4)出生后的快速生长。虽然许多流行病学研究结果可以部分验证提出的假说,但仍不能完全清楚地阐明出生体重与成人后疾病关系的具体机理。展开更多
Background: Antenatal betamethasone treatment is widely used for the prevention of neonatal respiratory distress syndrome in preterm infants and substantially reduces neonatal mortality and morbidity. Fetal exposure t...Background: Antenatal betamethasone treatment is widely used for the prevention of neonatal respiratory distress syndrome in preterm infants and substantially reduces neonatal mortality and morbidity. Fetal exposure to excess glucocorticoids has been proposed as one of the core mechanisms of the fetal origins of adult disease hypothesis. We assessed whether antenatal exposure to betamethasone for the prevention of neonatal respiratory distress syndrome affects cardiovascular risk factors at 30 years of age. Methods: We followed up at age 30 years 534 individuals whose mothers participated in a doubleblind, placebo-controlled, randomised trial of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome. Mothers received two doses of betamethasone or placebo given by intramuscular injection 24 h apart. Follow-up assessments included anthropometry; measurement of blood pressure, blood lipids (after overnight fasting), and early morning cortisol levels; and a 75 g oral glucose tolerance test. Findings: There were no differences between those exposed to betamethasone and to placebo in body size, blood lipids, blood pressure, plasma cortisol, prevalence of diabetes, or history of cardiovascular disease. After a 75 g oral glucose tolerance test, participants exposed to betamethasone had higher plasma insulin concentrations at 30 min (60.5 vs 52.0 mIU/L; ratio of geometric means 1.16 95%CI 1.03 to 1.31 , p=0.02) and lower glucose concentrations at 120 min (4.8 vs 5.1 mmol/L; difference -0.26 mmol/L -0.53 to 0.00 , p=0.05) than did those exposed to placebo. Interpretation: Antenatal exposure to betamethasone might result in insulin resistance in adult offspring, but has no clinical effect on cardiovascular risk factors at 30 years of age. Thus, obstetricians should continue to use a single course of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome.展开更多
文摘基于生活环境、健康和疾病在分子水平上密切相关的核心理念,健康和疾病的发育起源(developmental origins of health and disease,DOHaD)理论为健康与疾病间的关联研究提供了全新视角。该理论通过多学科、多领域的知识互通,追溯不同的生活经历如何影响生命全过程中的健康和疾病风险。成人期疾病的敏感窗口期不再局限于妊娠前和妊娠期,分娩期至成年早期也成为暴露因素发挥作用的重要时段。母源性/父源性因素、环境因素、新生儿出生状况、儿童期代谢情况等能够通过影响表观遗传、代谢和免疫调控、氧化应激等,改变发育程序并对子代远期健康产生正向或负向影响。因此,为实现健康促进,需要同步推进早期生命阶段预防、后期随访及健康干预的关口前移,以期有效降低成年期疾病风险,提升生命全周期健康水平。综述DOHaD领域最新研究进展对阐明人类发展早期阶段发生的不良事件影响健康和疾病模式及发现有效干预措施具有积极意义。
文摘人类研究和动物实验阐述了"成人疾病胎儿起源"的发生机理以及宫内不良环境与成人后疾病的关联。不仅如此,大量的流行病学资料也证明,出生后发育可塑期同样有着"规划"的功能。学者们将慢性疾病程序化的敏感时期从宫内延续至婴儿期甚至儿童期,形成"健康和疾病的发育起源"(Developmental Origins of Adult Health and Disease)学说,其中心内容是(1)胎儿营养不良;(2)胎儿期较多暴露于皮质醇激素;(3)遗传易感性;(4)出生后的快速生长。虽然许多流行病学研究结果可以部分验证提出的假说,但仍不能完全清楚地阐明出生体重与成人后疾病关系的具体机理。
文摘Background: Antenatal betamethasone treatment is widely used for the prevention of neonatal respiratory distress syndrome in preterm infants and substantially reduces neonatal mortality and morbidity. Fetal exposure to excess glucocorticoids has been proposed as one of the core mechanisms of the fetal origins of adult disease hypothesis. We assessed whether antenatal exposure to betamethasone for the prevention of neonatal respiratory distress syndrome affects cardiovascular risk factors at 30 years of age. Methods: We followed up at age 30 years 534 individuals whose mothers participated in a doubleblind, placebo-controlled, randomised trial of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome. Mothers received two doses of betamethasone or placebo given by intramuscular injection 24 h apart. Follow-up assessments included anthropometry; measurement of blood pressure, blood lipids (after overnight fasting), and early morning cortisol levels; and a 75 g oral glucose tolerance test. Findings: There were no differences between those exposed to betamethasone and to placebo in body size, blood lipids, blood pressure, plasma cortisol, prevalence of diabetes, or history of cardiovascular disease. After a 75 g oral glucose tolerance test, participants exposed to betamethasone had higher plasma insulin concentrations at 30 min (60.5 vs 52.0 mIU/L; ratio of geometric means 1.16 95%CI 1.03 to 1.31 , p=0.02) and lower glucose concentrations at 120 min (4.8 vs 5.1 mmol/L; difference -0.26 mmol/L -0.53 to 0.00 , p=0.05) than did those exposed to placebo. Interpretation: Antenatal exposure to betamethasone might result in insulin resistance in adult offspring, but has no clinical effect on cardiovascular risk factors at 30 years of age. Thus, obstetricians should continue to use a single course of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome.
