Social Determinants of Inflammation and Metabolic Syndrom among African Americans

非裔美国人炎症和代谢综合征的社会决定因素

• 批准号: 8621298
• 负责人: Ronald L Simons
• 金额: $ 61.79万
• 依托单位: UNIVERSITY OF GEORGIA
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-03-01 至 2018-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8621298
• 关键词: Accounting; Address; Adolescence; Adolescent; Adult; African American; Age; Age-Years; Arthritis; Biological; Biological Markers; Cardiovascular Diseases; Charge; Childhood; Chronic; Chronic Disease; Cognitive; Communities; Data; Dementia; Development; Discrimination; Disease; Distress; Environment; Epidemiology; Exposure to; Family; Family health status; Fostering; Funding; Health behavior; Individual; Inflammation; Institute of Medicine (U.S.); Investigation; Life Cycle Stages; Malignant Neoplasms; Measurement; Measures; Metabolic; Metabolic syndrome; Minority Groups; Modeling; Neighborhoods; Non-Insulin-Dependent Diabetes Mellitus; Onset of illness; Parenting behavior; Physiological; Preparation; Preventive Intervention; Process; Psychosocial Stress; Public Health; Race; Reaction; Relative (related person); Reporting; Research; Rheumatoid Arthritis; Risk; Sampling; Schools; Social support; Socialization; Societies; Stress; Target Populations; Telephone Interviews; Testing; Translations; Weather; Work; age related; base; biological systems; community health study; experience; health disparity; improved; indexing; peer; programs; prospective; public health relevance; racism; response; segregation; social; stressor; vigilance

PROJECT SUMMARY In recent years, strong evidence has accrued indicating that inflammation (INF) and metabolic syndrome (MS) represent dysregulated biological systems that predict onset of chronic, age-related diseases such as cardiovascular disease, type 2 diabetes, rheumatoid arthritis, cancer, and dementia. Although a wealth of findings has indicated that psychosocial stress is a major determinant of INF and MS, a number of crucial questions remain unanswered. First, we do not know whether sensitive period (early biological programming), stress accumulation, social schematic, or mismatch models best account for the development of INF and MS. Second, we have little information regarding the range of stressors within a developmental period that are most critical. Studies of childhood stress usually simply assess low SES or exposure to harsh parenting, and these measurements typically entail retrospective reports. Research on the effect of adult stress sometimes includes community context but usually fails to consider the way that childhood stress may moderate reactions to adult stressors. And, whether the focus is childhood or adult adversity, there has been limited consideration of the way that race-related stressors such as segregation, perceived racism, discrimination, and internalized racism impact biological dysregulation. Third, we know little about the extent to which factors such as parental support, racial socialization, social support, or religiosity operate to reduce the deleterious impact of childhood, adolescent, or adult stressors on INF and MS. A final limitation of past research is that it has focused, with a few exceptions, on White samples whereas African Americans display significantly higher rates of almost every type of chronic illness and score higher on biomarkers of INF and most indictors of MS. In order to address these unanswered questions and limitations, this proposal seeks funding to add biomarkers of INF and MS, as well as telephone interview data regarding stress and health behaviors, to the 18 years of longitudinal data that has been collected on the Family and Community Health Study (FACHS) sample of roughly 700 African Americans (now 28 years of age). Specifically, we plan to pursue the following specific aims: 1) identify the cluster of SES- and race-related stressors experienced in childhood, adolescence, and adulthood that best predict adult INF and MS. 2) Use these stress indices to test competing models regarding the manner in which stressors from various developmental periods combine to influence biological dysregulaton. And, 3) investigate the extent to which the experience of supportive parenting and racial socialization during childhood, and/or supportive relationships and religiosity during adulthood, are moderating factors that promote healthy biomarkers for INF and MS. There are few, if any, efficacious preventive interventions that address the causes of health disparities. The Institute of Medicine prescribes that such efforts be based on the results of longitudinal, epidemiological research with target populations. Currently, there are no prospective investigations that identify the protective factors that interrupt the translation of social determinants of stress into biological vulnerabilities for African Americans. The results of the proposed research will identify protective processes and serve as the basis for empirically-based, health disparities preventive interventions.

项目摘要 近年来，强有力的证据表明，炎症（INF）和代谢综合征 (MS)代表失调的生物系统，预测慢性，年龄相关疾病的发病，如 心血管疾病、2型糖尿病、类风湿性关节炎、癌症和痴呆。虽然大量的 研究结果表明，心理社会压力是INF和MS的主要决定因素， 问题仍然没有答案。首先，我们不知道是否敏感期（早期生物编程）， 压力累积、社会图式或失配模型最能解释INF和MS的发展。 第二，我们几乎没有关于发展期内最重要的压力源范围的信息。 很危险儿童压力的研究通常只是评估低社会经济地位或暴露于严厉的父母，这些 测量通常需要回顾性报告。对成人压力影响的研究有时包括 社区背景，但通常没有考虑到儿童压力可能会缓和对成人的反应， 压力源而且，无论关注的焦点是童年还是成年的逆境， 与种族有关的压力因素，如种族隔离，种族主义，歧视和内化的种族主义 影响生物失调。第三，我们对诸如父母的因素在多大程度上 支持，种族社会化，社会支持，或宗教信仰的运作，以减少有害的影响，童年， 过去研究的最后一个限制是，它集中在一个 少数例外，在白色样本，而非洲裔美国人显示出显着更高的比率，几乎每一个 慢性疾病的类型和得分较高的生物标志物INF和大多数指标的MS。 这些未回答的问题和局限性，该提案寻求资金，以增加INF和MS的生物标志物， 以及关于压力和健康行为的电话采访数据，到18年的纵向数据， 家庭和社区健康研究（FACHS）收集了大约700名非洲人的样本。 美国人（现在28岁）。具体而言，我们计划实现以下具体目标：1）确定 童年、青春期和成年期经历的一系列与SES和种族相关的压力源是最好的 2）使用这些压力指数来测试竞争模型， 来自不同发育阶段的应激源联合收割机影响生物失调。第三，调查 在童年时期得到支持性父母养育和种族社会化的经历的程度，和/或 成年期的支持性关系和宗教信仰，是促进健康的调节因素。 INF和MS的生物标志物。即使有，也很少有有效的预防干预措施来解决原因 健康差距。医学研究所规定，这种努力应基于以下结果： 针对目标人群的纵向流行病学研究。目前，没有前景 调查，确定保护因素，中断翻译的社会决定因素的压力 非裔美国人的生物脆弱性拟议研究的结果将确定 保护过程并作为基于经验的健康差异预防干预措施的基础。