Background and Purpose-Lay people often mention stress as one of the most important risk factors for stroke. Stress might trigger a cerebrovascular event directly or could be associated with higher levels of blood pressure or an unfavorable lifestyle. To examine these possibilities, we analyzed the association between self-reported stress frequency and intensity and risk of stroke. Methods-Data from the second examination, 1981 to 1983, of participants in the Copenhagen City Heart Study were analyzed with Cox regression after a mean of 13 years of follow-up. A total of 5604 men and 6970 women were included, and 929 first-ever strokes occurred, of which 207 (22%) were fatal within 28 days after onset of symptoms. The stress frequency categories were never/hardly ever, monthly, weekly, or daily. The stress intensity categories were never/hardly ever, light, moderate, or high. Results-Subjects with high stress intensity had almost a doubled risk of fatal stroke compared with subjects who were not stressed (relative risk [RR], 1.89; 95% CI, 1.11 to 3.21). Weekly stress was associated with an RR of 1.49 (95% CI, 1.00 to 2.23). There was no significant effect of stress in analyses of nonfatal strokes. Subjects who reported to be stressed often were more likely to have an adverse risk factor profile. Conclusions-Self-reported high stress intensity and weekly stress were associated with a higher risk of fatal stroke compared with no stress. However, there were no significant trends, and the present data do not provide strong evidence that self-reported stress is an independent risk factor for stroke.

Objective To assess the relation between self reported intensity and frequency of stress and first time incidence of primary breast cancer. Design Prospective cohort study with 18 years of follow-up. Setting Copenhagen City heart study, Denmark. Participants The 6689 women participating in the Copenhagen City heart study were asked about their perceived level of stress at baseline in 1981-3. These women were followed until 1999 in the Danish nationwide cancer registry, with < 0.1% loss to follow-up. Main outcome measure First time incidence of primary breast cancer. Results During follow-up 251 women were diagnosed with breast cancer. After adjustment for confounders, women with high levels of stress had a hazard ratio of 0.60 (95% confidence interval 0.37 to 0.97) for breast cancer compared with women with low levels of stress. Furthermore, for each increase in stress level on a six point stress scale an 8% lower risk of primary breast cancer was found (hazard ratio 0.92, 0.85 to 0.99). This association seemed to be stable over time and was particularly pronounced in women receiving hormone therapy. Conclusion High endogenous concentrations of oestrogen are a known risk factor for breast cancer, and impairment of oestrogen synthesis induced by chronic stress may explain a lower incidence of breast cancer in women with high stress. Impairment of normal body function should not, however, be considered a healthy response, and the cumulative health consequences of stress may be disadvantageous.

Background: Psychological stress and alcohol are both suggested as risk factors for stroke. Further, there appears to be a close relation between stress and alcohol consumption. Several experimental studies have found alcohol consumption to reduce the immediate effects of stress in a laboratory setting. We aimed to examine whether the association between alcohol and stroke depends on level of self-reported stress in a large prospective cohort. Methods: The 5,373 men and 6,723 women participating in the second examination of the Copenhagen City Heart Study in 1981–1983 were asked at baseline about their self-reported level of stress and their weekly alcohol consumption. The participants were followed-up until 31st of December 1997 during which 880 first ever stroke events occurred. Data were analysed by means of Cox regression modelling. Results: At a high stress level, weekly total consumption of 1–14 units of alcohol compared with no consumption seemed associated with a lower risk of stroke (adjusted RR: 0.57, 95% CI: 0.31–1.07). At lower stress levels, no clear associations were observed. Regarding subtypes, self-reported stress appeared only to modify the association between alcohol intake and ischaemic stroke events. Regarding specific types of alcoholic beverages, self-reported stress only modified the associations for intake of beer and wine. Conclusions: This study indicates that the apparent lower risk of stroke associated with moderate alcohol consumption is confined to a group of highly stressed persons. It is suggested that alcohol consumption may play a role in reducing the risk of stroke by modifying the physiological or psychological stress response.