心血管

任何时期出现心理问题均增心血管代谢风险

作者:小田 译 来源:金宝搏网站登录技巧 日期:2015-10-21
导读

         鉴于心血管代谢性疾病起源于儿童期的新认识,美国学者们对儿童期至成年期心理问题是否影响心血管代谢风险进行了评估,结果表明,在生命的任何时间点出现心理问题均与心血管代谢风险较高有关。研究结果首次揭示了即使成年期心理问题有所缓解,其增加的心血管代谢风险仍存在;提示早期情感发育可能是终身心血管健康最初预防和改善的目标。

        既往研究显示,成年期心理问题可能导致心血管和代谢性疾病,鉴于心血管代谢性疾病起源于儿童期的新认识,美国学者们对儿童期至成年期心理问题是否影响心血管代谢风险进行了评估,结果表明,在生命的任何时间点出现心理问题均与心血管代谢风险较高有关。研究结果首次揭示了即使成年期心理问题有所缓解,其增加的心血管代谢风险仍存在;提示早期情感发育可能是终身心血管健康最初预防和改善的目标。相关论文近期在线发表于《美国心脏病学会杂志》(J Am Coll Cardiol.)。

        该研究共纳入了来自英国出生队列研究中的6714例受试者,这些受试者在45岁时重复评估了关于心理困扰和生物医学调查。识别不同时期的心理问题(无心理问题、仅存在儿童期心理问题、仅存在成年期心理问题、持续的心理问题)。通过包括免疫、心血管和代谢系统功能的9项生物标记综合信息评估心血管代谢风险。用协变量校正线性回归模型评估心理问题和心血管代谢风险间的相关性。

        结果显示,与那些无心理问题的受试者相比,仅存在儿童期心理问题、仅存在成年期心理问题、持续的心理问题这三类人群的心血管代谢风险均较高,P值分别为0.0002、0.007和< 0.0001。

        参考文献:Ashley Winning, et al. J Am Coll Cardiol. 2015;66(14):1577-1586. doi:10.1016/j.jacc.2015.08.021

Psychological Distress Across the Life Course and Cardiometabolic Risk
Findings From the 1958 British Birth Cohort Study

Commentary by Dr. Valentin Fuster
Ashley Winning, ScD, MPH∗; M. Maria Glymour, ScD, MS†; Marie C. McCormick, MD, ScD∗; Paola Gilsanz, ScD, MPH∗; Laura D. Kubzansky, PhD, MPH∗
[-] Author Information
∗ Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
† Department of Epidemiology and Biostatistics, University of California San Francisco School of Medicine, San Francisco, California
J Am CollCardiol. 2015;66(14):1577-1586. doi:10.1016/j.jacc.2015.08.021

Abstract
Background  Research suggests cardiovascular and metabolic diseases are influenced by psychological distress in adulthood; however, this research is often limited to adult populations and/or a snapshot measure of distress. Given emerging recognition that cardiometabolic diseases have childhood origins, an important question is whether psychological distress earlier in life influences disease development.
Objectives  This study sought to assess whether life course patterns of psychological distress assessed from childhood through adulthood predict biomarkers of cardiometabolic risk in adulthood and whether effects of sustained distress differ from more limited exposure.
Methods  The sample (n = 6,714) consists of members of the 1958 British Birth Cohort Study who completed repeated measures of psychological distress and a biomedical survey at age 45 years. Psychological distress profiles over the life course (no distress, childhood only, adulthood only, or persistent distress) were identified from 6 assessments between ages 7 and 42 years. Cardiometabolic risk was assessed by combining information on 9 biomarkers of immune, cardiovascular, and metabolic system function. Covariate adjusted linear regression models were used to assess associations between distress profiles and cardiometabolic risk.
Results  Compared with those with no distress, cardiometabolic risk was higher among people with psychological distress in childhood only (β = 0.11, SE = 0.03, p = 0.0002), in adulthood only (β = 0.09, SE = 0.03, p = 0.007), and persistent across the life course (β = 0.26, SE = 0.04, p < 0.0001).
Conclusions  Psychological distress at any point in the life course is associated with higher cardiometabolic risk. This is the first study to suggest that even if distress appears to remit by adulthood, heightened risk of cardiometabolic disease remains. Findings suggest early emotional development may be a target for primordial prevention and for promoting lifelong cardiovascular health.
 

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