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: 8792241
• 负责人: Ronald L Simons
• 金额: $ 55.81万
• 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/8792241
• 关键词: Accounting; Address; Adolescence; Adolescent; Adult; African American; Age; Age-Years; Arthritis; Biological; Biological Markers; Cardiovascular Diseases; Charge; Child Rearing; Childhood; Chronic; Chronic Disease; Cognitive; Communities; Data; Dementia; Development; Discrimination; Disease; Distress; Environment; Epidemiology; Exposure to; Family; Family health status; Fostering; Funding; Health; 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; 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; racism; response; segregation; social; stressor; vigilance

DESCRIPTION (provided by applicant): 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 application 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 SE- 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.

描述（由申请人提供）：近年来，已有强有力的证据表明炎症（INF）和代谢综合征（MS）代表了预测慢性年龄相关疾病（如心血管疾病、2型糖尿病、类风湿性关节炎、癌症和痴呆）发作的失调生物系统。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，但一些关键问题仍然没有答案。首先，我们不知道是否敏感期（早期生物编程），压力积累，社会示意图，或不匹配模型最好的发展INF和MS。第二，我们几乎没有信息的范围内的发展时期的压力是最关键的。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养育，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，但通常没有考虑到童年压力可能会缓和对成人压力源的反应。而且，无论重点是童年或成年逆境，种族相关的压力，如种族隔离，感知种族主义，歧视和内化的种族主义影响生物失调的方式一直受到限制。第三，我们对父母支持、种族社会化、社会支持或宗教信仰等因素在多大程度上减少了儿童、青少年或成年人的有害影响知之甚少。 过去研究的最后一个限制是，除了少数例外，它集中在白色样本上，而非裔美国人显示出几乎每种类型慢性疾病的显著更高的比率，并且在INF的生物标志物和MS的大多数指标上得分更高。为了解决这些未回答的问题和限制，本申请寻求资金来添加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，与家庭和社区健康研究（FACHS）收集的大约700名非洲裔美国人（现在28岁）样本的18年纵向数据进行比较。具体来说，我们计划追求以下具体目标：1）确定在儿童期，青春期和成年期经历的SE和种族相关的压力源的集群，最好地预测成人INF和MS。2）使用这些压力指数来测试竞争模型，关于来自不同发育阶段的压力源联合收割机影响生物失调的方式。和，3）调查在何种程度上的支持性养育和种族社会化的经验，在儿童期，和/或支持性关系和宗教信仰在成年期，是调节因素，促进健康的生物标志物INF和MS。医学研究所规定，这种努力应以针对目标人群的纵向流行病学研究结果为基础。目前，还没有前瞻性的调查，确定的保护性因素，中断翻译的社会决定因素的压力到生物脆弱性的非洲裔美国人。拟议研究的结果将确定保护过程，并作为基于医疗保健的健康差异预防干预措施的基础。