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发育编程:为后代引发疾病易感性。

Developmental Programming: Priming Disease Susceptibility for Subsequent Generations.

作者信息

Messer L C, Boone-Heinonen J, Mponwane L, Wallack L, Thornburg K L

机构信息

School of Community Health, College of Urban and Public Affairs, Portland State University, Portland, OR, USA.

Department of Public Health and Preventive Medicine, Oregon Health & Science University, Portland, OR, USA.

出版信息

Curr Epidemiol Rep. 2015 Mar 1;2(1):37-51. doi: 10.1007/s40471-014-0033-1.

Abstract

Racial and/or ethnic minorities carry the highest burden of many adverse health outcomes intergenerationally We propose a paradigm in which developmental programming exacerbates the effects of racial patterning of adverse environmental conditions, thereby contributing to health disparity persistence. Evidence that developmental programming induces a heightened response to adverse exposures ("second hits") encountered later in life is considered. We evaluated the evidence for the second hit phenomenon reported in animal and human studies from three domains (air, stress, nutrition). Original research including a gestational exposure and a childhood or adulthood second hit exposure was reviewed. Evidence from animal studies suggest that prenatal exposure to is associated with an exaggerated reaction to postnatal air pollution exposure, which results in worse health outcomes. It also indicates offspring exposed to prenatal produce an exaggerated response to subsequent stressors, including anxiety and hyper-responsiveness of the hypothalamic-pituitary-adrenal axis. Similarly, prenatal and postnatal induce synergistic effects on weight gain, metabolic dysfunction, and atherosclerotic risk. second hits (e.g., gestational air pollution followed by childhood stressor) were also considered. Suboptimal gestational environments induce exaggerated offspring responses to subsequent environmental and social exposures. These developmental programming effects may result in enhanced sensitivity of ongoing, racially patterned, adverse exposures in race/ethnic minorities, thereby exacerbating health disparities from one generation to the next. Empirical assessment of the hypothesized role of priming processes in the propagation of health disparities is needed. Future social epidemiology research must explicitly consider synergistic relationships among social environmental conditions to which gestating females are exposed and offspring exposures when assessing causes for persistent health disparities.

摘要

种族和/或少数族裔在代际间承受着许多不良健康后果的最大负担。我们提出了一种范式,即发育编程会加剧不利环境条件的种族模式影响,从而导致健康差距持续存在。文中考虑了发育编程会引发对生命后期遇到的不良暴露(“二次打击”)产生增强反应的证据。我们评估了动物和人类研究在三个领域(空气、压力、营养)中报告的二次打击现象的证据。对包括孕期暴露和儿童期或成年期二次打击暴露的原始研究进行了综述。动物研究的证据表明,产前暴露于[此处原文缺失具体物质]与出生后空气污染暴露的过度反应有关,这会导致更差的健康结果。这也表明,暴露于产前[此处原文缺失具体物质]的后代对随后的应激源会产生过度反应,包括下丘脑 - 垂体 - 肾上腺轴的焦虑和反应过度。同样,产前和产后[此处原文缺失具体物质]对体重增加、代谢功能障碍和动脉粥样硬化风险产生协同作用。也考虑了二次打击(例如,孕期空气污染后接着是儿童期应激源)。孕期环境不佳会使后代对随后的环境和社会暴露产生过度反应。这些发育编程效应可能会导致少数种族/族裔对持续存在的、具有种族模式的不良暴露更加敏感,从而加剧代际间的健康差距。需要对启动过程在健康差距传播中的假设作用进行实证评估。未来的社会流行病学研究在评估持续存在的健康差距的原因时,必须明确考虑孕期女性所接触的社会环境条件与后代暴露之间的协同关系。

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