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Social causation or social selection? The longitudinal interrelationship between poverty and depressive symptoms in China.

社会因果关系还是社会选择?中国贫困与抑郁症状的纵向相互关系。

  • 影响因子:3.71
  • DOI:10.1016/j.socscimed.2020.112848
  • 作者列表:"Jin Y","Zhu D","He P
  • 发表时间:2020-02-19
Abstract

RATIONALE:To our knowledge, no prior studies have investigated these bidirectional pathways between poverty and depressive symptoms to identify potential mechanisms. OBJECTIVE:This study aimed to investigate the interrelationship between poverty and depressive symptoms by examining two causal theories: social causation, which claims that the condition of poverty causes mental health disorders, and social selection, which suggests that those with poor mental health are more likely to drift into poverty. METHOD:We obtained data from 17,250 adults aged 45 years or above from the China Health and Retirement Longitudinal Studies, first conducted in 2011-2012. Participants were tracked for 4 years, with baseline measurements taken as well as two 2-year follow-up visits. Structural equation models were used to examine the pathways in two directions at baseline, 2-year follow-up and 4-year follow-up. RESULTS:We found significant total effects and indirect effects of poverty on depressive symptoms at baseline, which were mediated through deterioration of household living conditions, decrease in social participation, and decline in life satisfaction. In the opposite direction, depressive symptoms directly led individuals to drift into poverty at baseline and at follow-up. CONCLUSIONS:This study suggested that social causation and social selection may operate concurrently. Proactive interventions, especially ones focusing on modifiable protective factors that our findings identified as mediators in the link between poverty and depression, are urgently needed to break the vicious cycle of poverty and depression and create a virtuous cycle of increasing returns.

摘要

理由: 据我们所知,之前没有研究调查贫困和抑郁症状之间的这些双向途径来确定潜在的机制。 目的: 本研究旨在通过检验两种因果理论来探讨贫困和抑郁症状之间的相互关系: 社会因果关系,声称贫困状况导致精神卫生障碍,以及社会选择, 这表明那些有贫穷精神卫生的人更容易陷入贫困。 方法: 我们从 17,250-2011 首次进行的中国健康和退休纵向研究中获得了 2012 名 45 岁或以上成年人的数据。对参与者进行了 4 年的跟踪,进行了基线测量以及两次 2 年的随访。使用结构方程模型在基线、 2 年随访和 4 年随访时检查两个方向的通路。 结果: 我们发现基线时贫困对抑郁症状有显著的总效应和间接效应,这些效应是通过家庭生活条件恶化、社会参与减少和生活满意度下降来介导的。相反的方向是,抑郁症状直接导致个体在基线和随访时陷入贫困。 结论: 本研究提示社会因果关系和社会选择可能同时运作。积极的干预措施,特别是那些关注我们的发现被确定为贫困和抑郁之间联系的调解人的可改变的保护因素, 迫切需要打破贫困和抑郁的恶性循环,创造回返增加的良性循环。

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发表时间:2020-01-24
来源期刊:Molecular psychiatry
DOI:10.1038/s41380-020-0649-0
作者列表:["Li C","Meng F","Garza JC","Liu J","Lei Y","Kirov SA","Guo M","Lu XY"]

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影响因子:5.83
发表时间:2020-01-22
DOI:10.1523/JNEUROSCI.0786-19.2019
作者列表:["Torretta S","Rampino A","Basso M","Pergola G","Di Carlo P","Shin JH","Kleinman JE","Hyde TM","Weinberger DR","Masellis R","Blasi G","Pennuto M","Bertolino A"]

METHODS::Multiple schizophrenia (SCZ) risk loci may be involved in gene co-regulation mechanisms, and analysis of coexpressed gene networks may help to clarify SCZ molecular basis. We have previously identified a dopamine D2 receptor (DRD2) coexpression module enriched for SCZ risk genes and associated with cognitive and neuroimaging phenotypes of SCZ, as well as with response to treatment with antipsychotics. Here we aimed to identify regulatory factors modulating this coexpression module and their relevance to SCZ. We performed motif enrichment analysis to identify transcription factor (TF) binding sites in human promoters of genes coexpressed with DRD2. Then, we measured transcript levels of a group of these genes in primary mouse cortical neurons in basal conditions and upon overexpression and knockdown of predicted TFs. Finally, we analyzed expression levels of these TFs in dorsolateral prefrontal cortex (DLPFC) of SCZ patients. Our in silico analysis revealed enrichment for NURR1 and ERR1 binding sites. In neuronal cultures, the expression of genes either relevant to SCZ risk (Drd2, Gatad2a, Slc28a1, Cnr1) or indexing coexpression in our module (Btg4, Chit1, Osr1, Gpld1) was significantly modified by gain and loss of Nurr1 and Err1. Postmortem DLPFC expression data analysis showed decreased expression levels of NURR1 and ERR1 in patients with SCZ. For NURR1 such decreased expression is associated with treatment with antipsychotics. Our results show that NURR1 and ERR1 modulate the transcription of DRD2 coexpression partners and support the hypothesis that NURR1 is involved in the response to SCZ treatment.SIGNIFICANCE STATEMENT In the present study, we provide in silico and experimental evidence for a role of the TFs NURR1 and ERR1 in modulating the expression pattern of genes coexpressed with DRD2 in human DLPFC. Notably, genetic variations in these genes is associated with SCZ risk and behavioral and neuroimaging phenotypes of the disease, as well as with response to treatment. Furthermore, this study presents novel findings on a possible interplay between D2 receptor-mediated dopamine signaling involved in treatment with antipsychotics and the transcriptional regulation mechanisms exerted by NURR1. Our results suggest that coexpression and co-regulation mechanisms may help to explain some of the complex biology of genetic associations with SCZ.

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影响因子:6.22
发表时间:2020-01-17
DOI:10.1038/s41386-020-0614-2
作者列表:["Chadha R","Meador-Woodruff JH"]

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