COPING STYLE STRESS RESPONSIVENESS AND LIPIDS
COPING STYLE STRESS RESPONSIVENESS AND LIPIDS
批准号:
3365729
负责人:
Raymond Niaura
金额:
$29.99万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1992
资助国家:
美国
项目状态:
已结题
起止时间:
1992-05-01 至 1995-04-30
关键词:
apolipoproteins blood lipid blood lipoprotein blood tests body physical activity body weight catecholamines cholesterol coping dietary lipid enzyme activity epinephrine gender difference human subject interview lipid metabolism lipoprotein lipase low density lipoprotein norepinephrine nutrition related tag personality personality tests physiologic stressor pituitary adrenal axis psychological stressor psychological tests questionnaires repression saturated fatty acids serum stress triglycerides urinalysis
中文摘要
压制性应对代表了一种针对威胁信息的策略
以远离威胁或最小化…为特征的
负面情绪。然而,当受到压力时,压抑的铜牌会表现出
与非抑制物相比,生理反应增强。我们自己的
初步数据表明,压抑性应对也与
脂蛋白谱异常,尤其是男性与女性相比。
我们推测这些异常与补药的升高有关。
交感-肾上腺和垂体-肾上腺活动增加
生理应激反应和酶活性降低
与脂类和脂蛋白的代谢有关。此外,我们假设
应对方式对血脂的影响不能用
相对体重、体脂分布、饱和膳食摄入量
脂肪和胆固醇或体力活动。最后,我们预计应对
风格对脂蛋白谱的影响将在一年内保持稳定,并且
压抑性应对可能与有害的血脂变化有关
在压力大的时候。为了检验这些假设,190名男性和女性
根据应对方式进行分类的医科学生将被评估
测定血脂、脂蛋白、尿皮质醇和
儿茶酚胺,一年内四次:无应激基线期间两次
在紧张的学术考试期间,我有过两次这样的经历。饮食摄入量,
体重、身高和腹内脂肪分布,以及体力活动
将与血脂测量同时进行测量。研究对象将
还可以测试对各种药物的急性心血管反应性
行为应激源(言语、心算、镜面追踪、等距
运动),以及脂蛋白脂肪酶和肝脏酶的活性
甘油三酯脂肪酶在研究开始时和一年后再次。
我们预计男性抑制者的总数将会增加
低密度脂蛋白-胆固醇、甘油三酯、非酯化脂肪酸、载脂蛋白B
尿皮质醇浓度和排泄量的增加,
去甲肾上腺素、肾上腺素与心血管反应
压力,与非抑制物相比。个人身份识别
心理特征和心理生理机制
对脂蛋白异常的易感性将对
了解动脉粥样硬化的风险以及预防和治疗
疾病。
英文摘要
Repressive coping represents a strategy against threatening information
characterized by a general orientation away from threat or minimization of
negative emotions. However, when stressed, repressive copers display
increased physiological responsiveness compared to nonrepressors. Our own
preliminary data suggests that repressive coping is also associated with
abnormal lipoprotein profiles, particularly in males compared to females.
We hypothesize that these abnormalities are related to elevations in tonic
sympathetic-adrenal and pituitary-adrenal activity, to increased
physiological stress-responsiveness, and to decreased activity of enzymes
related to metabolism of lipids and lipoproteins. Further, we hypothesize
that effects of coping style on lipids are not explained by differences in
relative body weight, body fat distribution, dietary intake of saturated
fat and cholesterol or physical activity. Finally, we expect that coping
style effects on lipoprotein profiles will be stable over one year, and
that repressive coping may be associated with detrimental lipid changes
during periods of stress. To test these hypotheses, 190 male and female
medical students, classified according to coping style, will be assessed
for levels of serum lipids and lipoproteins and urinary cortisol and
catecholamines, four times over one year: twice during stress-free baseline
periods and twice during stressful academic examinations. Dietary intake,
weight, height and intra-abdominal fat distribution, and physical activity
will be measured concurrent with the lipid measurements. Subjects will
also be tested for acute cardiovascular responsiveness to a variety of
behavioral stressors (speech, mental arithmetic, mirror tracing, isometric
exercise), and for activity of the enzymes lipoprotein lipase and hepatic
triglyceride lipase at the beginning of the study and again one year later.
We expect that male repressors will show increased total and
LDL-cholesterols, triglycerides, nonesterified fatty acids, apoliprotein B
concentrations, and concommitant increases in urinary cortisol,
norepinephrine, epinephrine, and cardiovascular responsiveness during
stress, compared to nonrepressors. Identification of individual
psychological characteristics and psychophysiological mechanisms which
predispose toward lipoprotein abnormalities will have implications for
understanding risks for, and prevention and treatment of, atherosclerotic
diseases.
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