Abstract：
Status inequality is hypothesised to increase socioeconomic inequalities in health by creating an environment in which social cohesion erodes and social comparisons intensify. Such an environment may cause systemic chronic inflammation. Although these are often-used explanations in social epidemiology, empirical tests remain rare.
We analysed data from the West of Scotland Twenty-07 Study. Our sample consisted of 1977 participants in 499 small residential areas. Systemic chronic inflammation was measured by high-sensitivity C-reactive protein (hs-CRP; <10 mg/L). An area-level measurement of status inequality was created using census data and contextual-level social cohesion was measured applying ecometrics. We estimated linear multilevel models with cross-level interactions between socioeconomic position (SEP), status inequality, and social cohesion adjusted for age and gender. Our main analysis on postcode sector-level was re-estimated on three smaller spatial levels.
The difference in hs-CRP between disadvantaged and advantaged SEPs (0.806 mg/L; p = 0.063; [95%CI: -0.044; 1.656]) was highest among participants living in areas where most residents were in advantaged SEPs. In these status distributions, high social cohesion was associated with a shallower socioeconomic gradient in hs-CRP and low social cohesion was associated with a steeper gradient. In areas with an equal mix of SEPs or most residents in disadvantaged SEPs, the estimated difference in hs-CRP between disadvantaged and advantaged SEPs was -0.039 mg/L (p = 0.898; [95%CI: 0.644; 0.566]) and -0.257 mg/L (p = 0.568; [95%CI: 1.139; 0.625]) respectively. In these status distributions, the gradient in hs-CRP appeared steeper when social cohesion was high and potentially reversed when social cohesion was low. Results were broadly consistent when using area-levels smaller than postcode sectors.
Inequalities in hs-CRP were greatest among participants living in areas wherein a majority of residents were in advantaged SEPs and social cohesion was low. In other combinations of these contextual characteristics, inequalities in systemic chronic inflammation were not detectable or potentially even reversed.
We analysed data from the West of Scotland Twenty-07 Study. Our sample consisted of 1977 participants in 499 small residential areas. Systemic chronic inflammation was measured by high-sensitivity C-reactive protein (hs-CRP; <10 mg/L). An area-level measurement of status inequality was created using census data and contextual-level social cohesion was measured applying ecometrics. We estimated linear multilevel models with cross-level interactions between socioeconomic position (SEP), status inequality, and social cohesion adjusted for age and gender. Our main analysis on postcode sector-level was re-estimated on three smaller spatial levels.
The difference in hs-CRP between disadvantaged and advantaged SEPs (0.806 mg/L; p = 0.063; [95%CI: -0.044; 1.656]) was highest among participants living in areas where most residents were in advantaged SEPs. In these status distributions, high social cohesion was associated with a shallower socioeconomic gradient in hs-CRP and low social cohesion was associated with a steeper gradient. In areas with an equal mix of SEPs or most residents in disadvantaged SEPs, the estimated difference in hs-CRP between disadvantaged and advantaged SEPs was -0.039 mg/L (p = 0.898; [95%CI: 0.644; 0.566]) and -0.257 mg/L (p = 0.568; [95%CI: 1.139; 0.625]) respectively. In these status distributions, the gradient in hs-CRP appeared steeper when social cohesion was high and potentially reversed when social cohesion was low. Results were broadly consistent when using area-levels smaller than postcode sectors.
Inequalities in hs-CRP were greatest among participants living in areas wherein a majority of residents were in advantaged SEPs and social cohesion was low. In other combinations of these contextual characteristics, inequalities in systemic chronic inflammation were not detectable or potentially even reversed.
摘要：
背景：假设地位不平等通过创造一种社会凝聚力侵蚀和社会比较加剧的环境来增加健康方面的社会经济不平等。这样的环境可引起全身性慢性炎症。尽管这些是社会流行病学中经常使用的解释，实证检验仍然很少见。
方法：我们分析了来自苏格兰西部二十-07研究的数据。我们的样本包括499个小住宅区的1977年参与者。通过高敏C反应蛋白（hs-CRP；<10mg/L）测量系统性慢性炎症。使用人口普查数据创建了地区级别的地位不平等度量，并使用生态计量学测量了上下文级别的社会凝聚力。我们估计了具有社会经济地位(SEP)之间跨水平相互作用的线性多水平模型，地位不平等，社会凝聚力根据年龄和性别进行了调整。我们对邮政编码部门级别的主要分析是在三个较小的空间级别上重新估计的。
结果：处于不利地位的SEP和处于有利地位的SEP之间的hs-CRP差异（0.806mg/L;p=0.063;[95CI：-0.044;1.656]）在居住在大多数居民处于有利SEP地区的参与者中最高。在这些状态分布中，高社会凝聚力与hs-CRP较浅的社会经济梯度相关,低社会凝聚力与较陡的梯度相关.在SEP组合相等的地区或处于不利地位的SEP中的大多数居民，弱势和优势SEP之间hs-CRP的估计差异分别为-0.039mg/L(p=0.898;[95CI:0.644;0.566])和-0.257mg/L(p=0.568;[95CI:1.139;0.625]).在这些状态分布中，当社会凝聚力较高时,hs-CRP的梯度呈现更陡,而当社会凝聚力较低时,hs-CRP的梯度可能逆转.使用小于邮政编码扇区的区域级别时，结果大致一致。
结论：生活在大多数居民处于优势SEP且社会凝聚力较低地区的参与者中，hs-CRP的不平等程度最大。在这些上下文特征的其他组合中，全身性慢性炎症的不平等无法检测到,甚至有可能逆转.
方法：我们分析了来自苏格兰西部二十-07研究的数据。我们的样本包括499个小住宅区的1977年参与者。通过高敏C反应蛋白（hs-CRP；<10mg/L）测量系统性慢性炎症。使用人口普查数据创建了地区级别的地位不平等度量，并使用生态计量学测量了上下文级别的社会凝聚力。我们估计了具有社会经济地位(SEP)之间跨水平相互作用的线性多水平模型，地位不平等，社会凝聚力根据年龄和性别进行了调整。我们对邮政编码部门级别的主要分析是在三个较小的空间级别上重新估计的。
结果：处于不利地位的SEP和处于有利地位的SEP之间的hs-CRP差异（0.806mg/L;p=0.063;[95CI：-0.044;1.656]）在居住在大多数居民处于有利SEP地区的参与者中最高。在这些状态分布中，高社会凝聚力与hs-CRP较浅的社会经济梯度相关,低社会凝聚力与较陡的梯度相关.在SEP组合相等的地区或处于不利地位的SEP中的大多数居民，弱势和优势SEP之间hs-CRP的估计差异分别为-0.039mg/L(p=0.898;[95CI:0.644;0.566])和-0.257mg/L(p=0.568;[95CI:1.139;0.625]).在这些状态分布中，当社会凝聚力较高时,hs-CRP的梯度呈现更陡,而当社会凝聚力较低时,hs-CRP的梯度可能逆转.使用小于邮政编码扇区的区域级别时，结果大致一致。
结论：生活在大多数居民处于优势SEP且社会凝聚力较低地区的参与者中，hs-CRP的不平等程度最大。在这些上下文特征的其他组合中，全身性慢性炎症的不平等无法检测到,甚至有可能逆转.
