Measuring the impact of structural inequality on the structure of the brain.
Measuring the impact of structural inequality on the structure of the brain.
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DOI：
10.1073/pnas.2306076120
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发表时间：
2023-06-20
影响因子：
11.1
通讯作者：
Sheridan, Margaret A.
中科院分区：
文献类型：
--
作者：
Sheridan, Margaret A.
在他们最近的论文中，Zugman et al. (1)通过跨国比较，在捕捉性别不平等与大脑结构之间的关系方面取得了重大进展。作者探讨了国家层面的性别不平等与个人层面的神经结构性别差异之间的关联。该分析很好地利用了在各种国家环境中获得的类似神经数据。这篇论文代表了研究结构不平等的生物学嵌入的工作向前迈出了真正有趣的一步，同时也是合作和开放科学倡议价值的一个很好的例子。2010年，赫茨曼和博伊斯提出，社会不平等可能“深入皮肤”，影响长期健康和福祉（2）。这一概念被称为生物嵌入，是社会不平等导致健康结果差异的一种机制。生物嵌入已经形成了社会经济地位，种族，以及在较小程度上，性别和健康结果之间的关联的解释模型。生物嵌入已被提出作为观察的一种解释，即在不同的国家和时间，社会经济地位和几乎所有的健康结果之间都有很强的关联，包括全因发病率和死亡率（3）。在跨国比较中，研究人员观察到，经济上更平等的社会等级（基尼系数较低）的富裕国家的健康结果的社会梯度不如那些社会梯度相对较低的国家，如美国。在人口总体水平上观察到的这些健康梯度，几乎可以肯定是由许多因素解释的。即使在实行社会化医疗的社会，经济资源也使人们能够直接购买保健服务。此外，经济资源可用于增加休闲时间，进入支持福祉的社交网络，以及购买可用于解决健康缺陷的教育。生物嵌入的概念是对社会等级制度对健康影响的这些基于资源的解释的补充。在生物嵌入的概念中，探讨了两种主要的可能性：第一，社会不平等聚集了直接影响生物发展的逆境的可能性，第二，不平等本身的经历可以塑造生物学，从而塑造健康结果。这两种可能性的证据是广泛的，并已在相对独立的研究，虽然交叉的文献。大量的工作表明，逆境的经历，如直接暴露于人际暴力或缺乏父母照顾，特别是在幼儿时期，对大脑发育有长期影响。最近的随机研究表明，大脑结构的长期变化是由早期社会活动引起的。
In their recent paper, Zugman et al.(1) have made significant trides in capturing the relationship between gender inequality and brain structure through a cross-country comparison. The authors explore the association between gender inequality at the country level and gender differences in neural structure at the individual level. The analysis is an excellent use of similar neural data acquired across a variety of country settings. This paper represents a truly interesting step forward in work examining the biologic embedding of structural inequality, while also serving as an excellent example of the value of collaborative and open science initiatives. In 2010, Hertzman and Boyce proposed that social inequality could “get under the skin” impacting long-term health and well-being (2). This concept, known as biologic embedding, is one mechanism through which social inequality leads to differences in health outcomes. Biologic embedding has shaped explanatory models for the association between socioeconomic status, race, and, to a lesser degree, gender, and health outcomes.Biologic embedding has been proposed as one explanation for the observation that across country settings and time, strong associations have been observed between socioeconomic status and almost every health outcome, including all-cause morbidity and mortality (3). In cross-country comparisons, researchers have observed that wealthy countries with more economically equal social hierarchies (lower Gini coefficients) have less strong social gradients of health outcomes than those, like the United States with relatively unmitigated social gradients (4). These gradients in health, observed at the aggregate level of the population, are almost certainly explained by a wide number of factors. Economic resources confer direct access to purchasing health care even in societies with socialized medicine. In addition, economic resources can be used to increase leisure, access social networks which support well-being, and purchase education which can be used to address health deficits. The concept of biologic embedding is in addition to these resource-based explanations of the impact of social hierarchy on health. Within the concept of biologic embedding, two primary possibilities have been explored: first, the possibility that social inequality aggregates exposure to adversities which directly impact biologic development, and second, that the experience of inequality itself can shape biology and thus health outcomes. Evidence for both possibilities is extensive and has been studied in relatively separate, albeit intersecting pieces of literature. A vast body of work has demonstrated that experiences of adversity such as direct exposure to interpersonal violence or lack of parental care, particularly when experienced in early childhood, have long-term impacts on brain development (5). Recent randomized studies indicate that long-term changes in brain structure are caused by early social
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DOI：
10.1136/bmj.b4471
发表时间：
2009-11-10
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Kondo N;Sembajwe G;Kawachi I;van Dam RM;Subramanian SV;Yamagata Z
通讯作者：
Yamagata Z
影响因子：
14.2
作者：
Martinez, Adali;de la Rosa, Rosemarie;Mujahid, Mahasin;Thakur, Neeta
通讯作者：
Thakur, Neeta
影响因子：
3.3
作者：
Ellis, Bruce J.;Sheridan, Margaret A.;McLaughlin, Katie A.
通讯作者：
McLaughlin, Katie A.
影响因子：
16.6
作者：
Weissman, David G.;Hatzenbuehler, Mark L.;Cikara, Mina;Barch, Deanna M.;McLaughlin, Katie A.
通讯作者：
McLaughlin, Katie A.
影响因子：
5.2
作者：
McEwen BS;Gianaros PJ
通讯作者：
Gianaros PJ