权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

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

基本信息

批准号：
9231489
负责人：
Ronald L Simons
金额：
$ 56万
依托单位：
UNIVERSITY OF GEORGIA
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-03-01 至 2019-02-28
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9231489
关键词：
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 Exposure to Family Family health status Fostering Funding Health behavior Individual Inflammation Institute of Medicine (U.S.)Interruption Intervention 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 Prevention Preventive Intervention Process Psychosocial Stress Public Health Race Reaction 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 epidemiology study experience health disparity improved indexing low socioeconomic status peer predictive marker prospective public health relevance racism response segregation social stressor vigilance

项目摘要

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，有强有力的证据表明，炎症(INF)和代谢综合征(MS)代表着失调的生物系统，它们预测与年龄相关的慢性疾病的发生，如心血管疾病、2型糖尿病、类风湿性关节炎、癌症和痴呆症。虽然大量的研究结果表明，心理社会压力是INF和MS的一个主要决定因素，但一些关键问题仍然没有得到回答。首先，我们不知道敏感期(早期生物编程)、压力积累、社会图式或错配模型是否最能解释INF和MS的发展。其次，我们几乎没有关于一个发育期内最关键的应激源范围的信息。对童年压力的研究通常只是简单地评估低SES或暴露在严酷的父母教养之下，这些测量通常需要回顾报告。关于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成人压力来源的反应。而且，无论关注的是童年还是成人的逆境，人们对种族相关的压力因素，如种族隔离、感知到的种族主义、歧视和内在化的种族主义等影响生物失调的方式的考虑有限。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儿童、青少年或成人的有害影响知之甚少关于INF和MS的压力源过去研究的最后一个限制是，除了少数例外，它集中在白人样本上，而非裔美国人显示出几乎每种慢性病的比率都要高得多，在INF的生物标记物和MS的大多数指标上得分更高。为了解决这些悬而未决的问题和限制，这项申请寻求资金，以增加INF和MS的生物标记物，以及关于压力和健康行为的电话采访数据，这些数据是根据家庭和社区健康研究(FACHS)样本收集的18年纵向数据，样本约为700名非裔美国人(现在28岁)。具体地说，我们计划追求以下具体目标：1)确定在儿童、青春期和成年期经历的与SE和种族相关的压力源集群，这些压力源最能预测成年INF和MS。2)使用这些压力指数来测试关于来自不同发育阶段的压力源组合影响生物失调的方式的相互竞争的模型。3)调查儿童时期支持性养育和种族社会化的经历，和/或成年期间支持性关系和宗教信仰的经历在多大程度上是促进中枢性和多发性硬化症的健康生物标志物的调节因素。医学研究所规定，这种努力应基于对目标人群进行的纵向流行病学研究的结果。目前，还没有前瞻性的调查确定阻止压力的社会决定因素转化为非裔美国人的生物脆弱性的保护性因素。拟议研究的结果将确定保护过程，并作为以经验为基础的健康差异预防干预措施的基础。