Stress and cardiovascular disease.

P Björntorp
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Abstract

The statistical associations between stress and cardiovascular and other prevalent diseases have not been explained. Perceived stress, resulting in an uncontrollable defeat reaction, has been shown by James Henry (Henry 1993) to be followed by specific endocrine abnormalities, including sensitization of the hypothalamo-pituitary-adrenal (HPA) axis, and inhibited sex steroid and growth hormone secretions. With an elevated waist/hip circumference ratio (WHR)--a simple, surrogate, measurement of intraabdominal, visceral fat masses--combined with insulin resistance, similar endocrine perturbations are found. Based on considerable evidence, such endocrine abnormalities seem to be followed by accumulation of intraabdominal, visceral fat masses and insulin resistance, both powerful risk factors for cardiovascular disease, diabetes and stroke. A postulated chain of events is therefore that the endocrine perturbations are primary factors, followed by visceral fat accumulation, insulin resistance and other risk factors dependent on the hyperinsulinemia following insulin resistance. This highlights the importance of elucidating the cause(s) to the endocrine abnormalities. These are identical to those described by Henry (1993) to follow a stress reaction of a defeat type. Findings of several psychosocial and socio-economic handicaps might provide a basis for such a reaction, supported by experimental studies in primates. Furthermore, depression, anxiety, alcohol consumption and smoking, all known activators of the HPA axis, are also often found. The low sex steroid and growth hormone secretions might be secondary to the hypersensitive HPA-axis. They could also be caused by other factors, and are, each alone, capable of causing both visceral fat accumulation and insulin resistance. Visceral fat accumulation is only an indirect, surrogate measurement of the underlying endocrine abnormalities, but is useful for screening purposes on a population basis. Developments of novel techniques for sensitive, yet simple measurements of HPA axis activity under undisturbed conditions seem to allow a better definition of pathogenetic factors. Utilizing such methods, subgroups of the syndrome including visceral fat accumulation, insulin resistance and other associated risk factors (Metabolic Syndrome), are beginning to emerge. A more detailed information on noxious factors in society leading to a defeat reaction to perceived stress, endocrine abnormalities and the Metabolic Syndrome, with increased risk for prevalent disease may hopefully be developed by these new methods.

压力和心血管疾病。
压力与心血管疾病和其他流行疾病之间的统计关联尚未得到解释。詹姆斯·亨利(Henry 1993)发现,感知到的压力会导致无法控制的失败反应,随之而来的是特定的内分泌异常,包括下丘脑-垂体-肾上腺(HPA)轴的敏感化,以及性类固醇和生长激素分泌的抑制。腰臀围比(WHR)升高——一种测量腹内内脏脂肪团的简单替代方法——与胰岛素抵抗相结合,可发现类似的内分泌紊乱。根据大量证据,这种内分泌异常似乎伴随着腹腔内、内脏脂肪堆积和胰岛素抵抗,这两者都是心血管疾病、糖尿病和中风的重要危险因素。因此,一个假定的事件链是内分泌紊乱是主要因素,其次是内脏脂肪堆积、胰岛素抵抗和其他依赖于胰岛素抵抗后高胰岛素血症的危险因素。这突出了阐明内分泌异常原因的重要性。这些与Henry(1993)描述的失败类型的压力反应相同。一些社会心理和社会经济障碍的发现可能为这种反应提供了基础,并得到了灵长类动物实验研究的支持。此外,抑郁、焦虑、饮酒和吸烟,这些已知的下丘脑轴激活物也经常被发现。低性类固醇和生长激素分泌可能继发于敏感的hpa轴。它们也可能是由其他因素引起的,而且每一种因素都能引起内脏脂肪堆积和胰岛素抵抗。内脏脂肪堆积只是潜在内分泌异常的间接替代测量,但对人群的筛查目的是有用的。在不受干扰的条件下,对HPA轴活性进行敏感而简单的测量的新技术的发展似乎可以更好地定义致病因素。利用这些方法,包括内脏脂肪堆积、胰岛素抵抗和其他相关危险因素(代谢综合征)在内的综合征亚群开始出现。通过这些新方法,我们有望对社会中导致对感知压力、内分泌异常和代谢综合征的失败反应的有害因素提供更详细的信息,这些因素会增加患流行疾病的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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