IJE Advance Access published online on July 1, 2008
International Journal of Epidemiology, doi:10.1093/ije/dyn124
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Type A behaviour and risk of coronary heart disease: The JPHC Study
1Public Health, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University. Suita-shi, Osaka, Japan.
2Department of Society, Human Development and Health, Harvard School of Public Health, Boston, MA, USA.
3Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, Tokyo, Japan.
*Corresponding author. Public Health, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University. Suita-shi, Osaka 565-0871, Japan. E-mail: fvgh5640{at}mb.infoweb.ne.jp
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Abstract |
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Background Although numerous studies of type A behaviour and risk of coronary heart disease (CHD) have been reported in the west (with mixed findings), few studies have been carried out in Asian populations.
Methods We examined prospectively the association between type A-behaviour and risk of CHD incidence within a cohort of 86 361 Japanese men and women aged 40–69 years. A total of 669 cases of newly diagnosed CHD occurred between the baseline questionnaire (1990–94) and the end of follow-up in January 2004.
Results We found no overall evidence of an association between type A and CHD incidence. The multivariate hazard ratio (HR) and 95% confidence intervals for CHD incidence in the highest vs lowest level of type A was 1.19 (0.94–1.51) overall. Contrary to expectation, Japanese men with lower levels of type A behaviour (lower levels of impatience, aggressiveness and competitiveness) appeared to be at significantly increased risk of CHD incidence (HR = 1.32; 95% CI 1.02–1.72). In contrast to men, there was insignificant but a tendency for reduced risk of CHD incidence (HR = 0.79, 95% CI 0.46–1.34) for women with lower levels of type A behaviour.
Conclusions Type A behaviour does not predict CHD incidence in the Japanese population. Among males, type B behavioural patterns appear to confer increased CHD risk. Our findings suggest that the cardio-toxic effect of type A behaviour is gender-specific and culturally contingent.
Keywords coronary heart disease, type A behaviour, prospective studies
Accepted 29 May 2008
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Introduction |
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In 1974, Meyer Friedman and Ray Rosenman1 proposed that type A behaviour—consisting of time urgency and free-floating hostility—was an independent risk factor for coronary heart disease (CHD). However, despite the promise of early studies (including a successful intervention study2 to reduce type A and prevent coronary disease recurrence), subsequent negative studies have raised questions about the viability of the type A hypothesis. According to Williams3 ‘a Medline search on type A behaviour in the late 1970s would elicit scores of citations; one in the late 1990s elicits only a few’.
In defence of the continuing relevance of type A, researchers have pointed out that pencil-and-paper assessments of type A behaviour (used in most large-scale cohort studies) yield a much less reliable diagnosis of type A compared with videotaped clinical examinations, which may account for the null findings of some those studies.4 Meantime, in spite of the likely measurement error, epidemiological studies reported as recently as the late 1990s have continued to show type A behaviour—including even time urgency—to be an independent predictor of CHD.5,6 The puzzle of the rise and decline of the type A construct has never been adequately explained. Matthews for example has speculated that type A happened to predict heart attacks during the late 1960s when the disease was more prevalent among upper socio-economic groups (as echoed by the popular stereotype of the ‘executive coronary’), and the behavioural patterns associated with type A (time urgency, competitiveness, aggression) were also more commonly exhibited among the same social groups.7 Based on this, one might further speculate that over time, as time urgency and competitiveness increased and spread throughout the rest of the population, type A lost its ability to predict coronary disease. Although no studies have been carried out to test it, the foregoing theory suggests that the ‘toxicity’ associated with type A is very much dependent on the surrounding cultural context.
Interestingly, the vast majority of studies of type A to date have been carried out in western populations (primarily North America and western Europe), while far fewer studies have been conducted in other cultural contexts. Within Asian populations, the findings of studies on type A have been mixed and contradictory. For example, among Japanese-American men in the Honolulu Heart Program, no significant associations were found between type A scores and prevalence of myocardial infarction or angina pectoris. However, there was a trend for type B individuals to have higher risk of myocardial infarction.8 On the other hand, a more recent case–control study within a Japanese population reported that type A behaviour pattern was positively associated with history of myocardial infarction among both men and women.9 To our knowledge, no prospective study has been reported on type A and coronary disease incidence within an Asian population. The results of such a study—regardless of the findings—may shed further light on the embeddedness of the type A construct within a cultural context. We therefore sought to test the association between coronary prone-behaviour pattern and CHD incidence and prognosis within a large-scale Japanese cohort study.
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Materials and methods |
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Study cohort
The first cohort of the Japan Public Health Center-based Prospective Study (JPHC Study) was initiated in 1990 (Cohort I) while the second cohort was initiated in 1993 (Cohort II) within 11 public health center areas throughout the country.10 The study population of the present study was defined as all residents (n = 116 896) aged 40–59 years for cohort I and 40–69 years for Cohort II at baseline. Of these residents, 220 residents were excluded due to non-Japanese nationality (n = 51), late reports of emigration occurring before the start of the follow-up period (n = 166) and incorrect birth date (n = 3). Therefore, 116 676 residents were remained eligible for the study. A baseline self-administered questionnaire on various lifestyles was given to residents in 1993 and 1994; 95 374 residents responded to the questionnaire and were included in the study cohort. The overall response rate was 82%. The JPHC study was approved by the institutional review board of the National Cancer Center, Tokyo Japan.
Baseline questionnaire survey
A baseline self-administered questionnaire on various lifestyles was given to participants in 1990 for Cohort I and 1993 and 1994 for Cohort II. The questionnaire included personal and family medical history, psychosocial factors such as perceived stress, household structure, and occupation, behaviour pattern, and lifestyle factors such as smoking and alcohol habits, dietary habits and physical activity.
We assessed four aspects of the type A behavioural pattern through self-reports of: competitive drive, speed and impatience, aggressiveness and irritability. A single item was used to assess the level of each: ‘How hasty and impatient do you consider yourself to be? (very, somewhat, or not at all)’, ‘How competitive and eager to excel in everything do you consider yourself to be? (very, somewhat, not at all)’, ‘How aggressive do you consider yourself to be? (very, somewhat, or not at all)’, and ‘How irritable do you consider yourself to be? (very, somewhat, or not at all)’. The above four items were then combined into an overall index of coronary prone-behaviour pattern. Questions were scored from 0 (‘Low’) to 2 for the highest category. Thus, the overall index of coronary prone-behaviour pattern had a possible range from 0 (lowest type A pattern) to 8 (highest type A pattern). The index had acceptable internal consistency reliability (Cronbach alpha coefficient of 0.61). We assessed the content validity of our four-item scale by comparing the items in our study with other established type A instruments such as the Framingham Type A Scale11 and MMPI-2 Type A Scale.5 Side-by-side comparison of individual items revealed that our items matched well with validated instruments in domains such as aggression, irritability, competitiveness and time urgency.12
A total of 86 361 (41 474 men and 44 887 women) participants provided valid responses to the question and were used for the analyses.
Confirmation of CHD
A total of 64 hospitals were registered within the sampling area of the JPHC cohort. All were major hospitals with the capability of treating patients with acute CHD. Physicians blinded to the patent's lifestyle data reviewed the medical records at each hospital. Acute coronary events were included in the study if they occurred after the date of return of the baseline questionnaire and before January 1, 2004.
The details of the surveillance for CHD were described previously.13 Briefly, myocardial infarction was confirmed in the medical records according to the criteria of the MONICA (Monitoring Trends and Determinants of Cardiovascular Disease) project,14 which requires evidence from ECGs, cardiac enzymes and/or autopsy. When such a workup was not performed and here was typical chest pain, a probable diagnosis was made. In the absence of diagnosis of myocardial infarction, deaths that occurred within 1 h from onset of symptoms were regarded as sudden cardiac deaths. Fatal CHD included sudden cardiac deaths or deaths within 28 days after the onset of MI.
Among the study subjects, 6657 died, 6155 moved out of the study areas and 346 were lost to follow-up within the 10-year follow-up period.
Statistical analysis
Person-years in the follow-up period were counted from the date of the return of the baseline survey until one of the following endpoints. For the analysis of CHD incidence, person-years were censored at the date of disease diagnosis, the date of emigration from the study area, the date of death, or the end of study period (December 31, 2003), whichever come first. For persons who were lost to follow-up, the last confirmed date of their presence in the study area was used as the date of censoring. Analysis of covariance and chi-square tests were used to compare sex-specific age-adjusted mean values and proportions of cardiovascular risk factors. The outcomes for this study were defined as newly occurring CHD incidence and deaths during the study period. Hazard ratios (HR) and their 95% confidence intervals (95% CI) were calculated after adjustment for age and other potential confounding factors using Cox proportional-hazards models. Confounding variables included age (years), smoking status (never, former, current), ethanol intake (non- and ex-drinkers, less than weekly, <150 g per week or 
150 g per week), body mass index (kg/m2 in quartiles), sports at leisure time (<1 day per month, 1–3 days per month and 1 day per week), occupation (economically inactive, professional, management, administrative, sales and services, manual labour, farming, forestry and fishery, or others), and perceived stress (less, moderate or high). To check for effect modification, we also stratified analyses according to alcohol intake [non- or lighter-alcohol drinkers (<150 g per week) vs heavier-drinkers (150 g per week)]. We also checked for statistical interactions by using cross-product terms of coronary prone-behaviour pattern and stratifying variables. We tested the assumption of proportional hazards by using both time-dependent covariate method and linear correlation test, and found no violation of proportionality. All analyses were conducted using the SAS statistical package Version 9.1 (SAS Institute Inc., Cary, NC).
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Results |
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During 988 747 person-years of follow-up (average follow-up period: 11.5 years) for the 86 361 subjects (41 474 men and 44 887 women), we documented 669 cases of newly diagnosed CHD (514 men and 155 women), 551 myocardial infarctions (425 men and 126 women) and 118 sudden cardiac deaths (89 men and 29 women). These cases comprised 469 nonfatal (367 men and 102 women) and 200 fatal coronary events (147 men and 53 women).
We separately examined type A behavioural pattern in relation to cardiovascular risk factors among men and women (Table 1). Distributions of type A behavioural pattern score were: score of 0, 1% in both men and women, score of 1, 2% in men and 3% in women, score of 2, 6% in men and 7% in women, score of 3, 12% in men and 15% in women, score of 4, 38% in men and 42% in women, score of 5, 16% in both men and women, score of 6, 12% in men and 9% in women, score of 7, 7% in men and 4% in women, and score of 8, 6% in men and 3% in women. Subjects were categorized into four levels of type A behavioural pattern based on the distribution of our combined index: Very High (scores of 6–8, 25% in men and 16% in women), High (score of 5, 16% in men and 16% in women), Medium (score of 4, 38% in men and 42% in women) or Low (scores of 0–3, 21% in men and 26% in women). Men with very high type A behavioural pattern were more likely to be heavy drinkers (P < 0.001), current smokers (P < 0.001) and hypertensive (P < 0.001), and to engage physical activities (P < 0.001). Men with very high type A behavioural pattern also had higher perceived stress (P < 0.001) as well as higher employment rate (P < 0.001). Women with very high type A behavioural pattern were more likely to be current smokers (P < 0.001) and heavy drinkers (P = 0.002), and reported higher perceived stress (P < 0.001) as well as higher employment rate (P < 0.001).
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Table 2 shows HRs of CHD incidence according the categories of type A behavioural pattern. We show the patterns for the overall cohort, as well as broken out by gender. For overall participants, we found no associations between type A behavioural pattern and CHD incidence. However, among men, we found that those with lower type A behavioural pattern had a 1.4-fold multivariable-adjusted higher risk of CHD incidence (P for linear trend: 0.04). Each standard deviation increment in type A behavioural pattern (1 SD = 1.55) was associated with a significant reduction in the risk of CHD incidence (HR = 0.91; 95% CI 0.84–0.99) among men. Men with lower type A behavioural pattern had also 1.3- to 1.4-fold multivariable-adjusted higher risk of MI incidence and non-fatal MI incidence. These patterns were observed for non-fatal events only. There were no associations between type A behavioural pattern and sudden cardiac deaths or fatal-CHD in men.
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In contrast to men, among women we found no statistically significant associations between type A behavioural pattern and any of the coronary outcomes studied although there was a tendency for reduced risk of CHD incidence (HR = 0.79, 95% CI 0.46–1.34) with lower levels of type A behaviour. P-value for type A x sex interaction term was 0.08.
Table 3 shows the HRs of CHD incidence according to levels of each constituent item that make up the type A behaviour pattern index. For overall participants, low impatience was associated with a 1.4-fold higher multivariable-adjusted risk of CHD incidence and myocardial infarction. Low competitiveness was also associated with 1.7-fold higher risk of fatal CHD for men and women combined. Among men, lower impatience, competitiveness and aggressiveness were each associated with higher risks of CHD incidence, myocardial infarction and non-fatal CHD. We found linear trends between impatience and all of these outcomes (P for linear trend: P = 0.03, P = 0.01 and P = 0.03, respectively). In contrast to men, there were no associations between constituent items of the type A behaviour pattern index and any of the outcomes studied in women.
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We next examined for potential effect modification by stratifying the analyses by alcohol intake [non- or lighter-drinkers (<150 g per week) vs heavier-drinkers (
150 g per week)] (data not shown). We found an interaction between type A and alcohol intake for CHD incidence among men. The excess risk of CHD incidence was stronger in non- or less-alcohol drinkers with lower type A scores (HR = 1.73; 95% CI 1.12–2.69) compared with drinkers (HR = 1.08; 95% CI 0.73–1.59) (P for interaction: P = 0.01). |
Discussion |
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In this large prospective analysis in a Japanese population, we found no overall association between type A behaviour pattern and risk of CHD. If anything, we found an association between type A behaviour and incident non-fatal coronary disease among Japanese men that was in the opposite direction to the one expected based on prior studies conducted in the west. Ours is not the first study to suggest such a pattern in a Japanese population. A previous cross-sectional study reported that Japanese male patients with acute myocardial infarction were less likely to consider themselves as hard driving or competitive.15 Another cross-sectional study found that Japanese men who reported lower anger expression in combination with low levels of stress-coping behaviours (e.g. talking with friends, drinking, physical exercise) had increased risks of high blood pressure.16 In contrast to men, we found insignificant, but a tendency for reduced risk of CHD among women with lower levels of type A behaviour that was similar result from previous studies conducted in western populations.
The hypothesized mechanisms underlying the association between type A behaviour and CHD prognosis include an unhealthy profile of behaviours (such as smoking and heavy alcohol consumption), as well as exaggerated cardiovascular reactivity to stress through neuro-endocrine mechanisms.17 With regard to the latter, the type A is associated with greater negative affective and behavioural responses to stress, including anger, hostility and aggression.12 These affective and behavioural responses in turn activates neuro-endocrine pathways such as the hypothalamic-pituitary-adrenal (HPA)-axis and the sympathetic adrenal-medullary (SAM) axis.17 The long-term activation of these axes in turn induces a sustained increase in cortisol,17 norepinephrine secretion,17 inflammatory proteins,18 platelet abnormalities19 and endothelial dysfunction,20 which may ultimately exacerbate other cardiovascular risk factors such as hypertension,17 heart rate,21 hyperlipidemia,17 diabetes17 and the progression of atherosclerosis.17
Our findings suggest that the toxicity of the type A behaviour pattern is culturally contingent. In Japanese society, especially for male ‘salary-men’, group cohesion is strongly emphasized, while public displays of competitiveness, hostility and aggression are frowned upon and actively discouraged. Within such a context, type B behavioural patterns may imply a high degree of conformity with group values. In turn, ‘not rocking the boast’ may be associated with suppression of frustration and anger, which may be more toxic to the heart than outwardly expressing the same emotions. We speculate that type A Japanese males in our study were possibly able to ‘let off steam’ by venting their frustrations. Within Japanese company culture, such venting frequently takes place after work hours among fellow workers at sake bars, ‘snacks’ and karaoke bars. In our study, the heavier drinking pattern among type A males appeared to accentuate the protective effect on cardiovascular disease of traits such as aggression, competitiveness and irascibility. Although type A males smoked somewhat more than type B males, they were also more likely to engage in other cardio-protective behaviours such as physical activity.
Despite our large sample size and prospective follow-up design, our study is not without limitations. Our assessment of the type A behaviour pattern was not obtained through the ‘gold standard’ video-taped clinical examinations, or previously validated questionnaire instruments. Nonetheless, an item-by-item comparison of our instrument with existing scales such as the Framingham Type A Scale and the MMPI-2 Type A Scale suggested close similarity in items tapping into domains such as aggression, irritability, competitiveness and time urgency. Admittedly, the use of single items to tap each of these domains is likely to have resulted in measurement error and reduced reliability. On the other hand, such measurement error would have attenuated any association between type A behaviour and risk of coronary disease. Instead, we found a suggestion of a significant inverse relationship between type A and coronary disease that was contra-positive to our hypothesis, at least based upon previous studies conducted in western populations. We feel that this unexpected association is noteworthy in spite of the limitations of measurement. Our cohort study also lacked information on other personality and emotional traits which have been previously associated with risk of CHD, such as hostility, depression and anxiety.
Furthermore, the study sample was selected from the areas that were selected to represent the extent of variation in the mortality rate and to consider geographical distribution and feasibility. However, generalization of our results as well as representativeness of our study sample could be limited due to non-respondents to the baseline questionnaire. In view of a previous report, the ‘healthy volunteer effect’ was observed among subjects who responded to our baseline questionnaire.22 Furthermore, the incidence of CHD in the present study population was 63.3 cases per 100 000 people during the follow-up period, whereas 71.2 cases per 100 000 people in the whole JPHC study cohorts including non-respondents to the baseline questionnaire, suggesting that persons with existing disease, unfavorable life-style profiles or low socioeconomic status may have been less willing to response to the questionnaire.
Despite these limitations, to our knowledge, this is one of the few prospective investigations of type A behaviour and CHD incidence reported in an Asian population. Our findings lend weight to the notion that type A is a culturally contingent pattern of behaviour, and that its toxicity depends upon the social milieu within which the behaviour is expressed.
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Appendix |
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Study group members
Members of the Japan Public Health Center-based Prospective Study (JPHC Study, principal investigator: S. Tsugane) Group are: S. Tsugane, M. Inoue, T. Sobue and T. Hanaoka, National Cancer Center, Tokyo; J. Ogata, S. Baba, T. Mannami, A. Okayama and Y. Kokubo, National Cardiovascular Center, Osaka; K. Miyakawa, F. Saito, A. Koizumi, Y. Sano, I. Hashimoto and T. Ikuta, Iwate Prefectural Ninohe Public Health Center, Iwate; Y. Miyajima, N. Suzuki, S. Nagasawa, Y. Furusugi and N. Nagai, Akita Prefectural Yokote Public Health Center, Akita; H. Sanada, Y. Hatayama, F. Kobayashi, H. Uchino, Y. Shirai, T. Kondo, R. Sasaki, Y. Watanabe, Y. Miyagawa and Y. Kobayashi, Nagano Prefectural Saku Public Health Center, Nagano; Y. Kishimoto, E. Takara, T. Fukuyama, M. Kinjo, M. Irei and H. Sakiyama, Okinawa Prefectural Chubu Public Health Center, Okinawa; K. Imoto, H. Yazawa, T. Seo, A. Seiko, F. Ito and F. Shoji, Katsushika Public Health Center, Tokyo; A. Murata, K. Minato, K. Motegi and T. Fujieda, Ibaraki Prefectural Mito Public Health Center, Ibaraki; K. Matsui, T. Abe, M. Katagiri and M. Suzuki, Niigata Prefectural Kashiwazaki and Nagaoka Public Health Center, Niigata; M. Doi, A. Terao, Y. Ishikawa and T. Tagami, Kochi Prefectural Chuo-higashi Public Health Center, Kochi; H. Sueta, H. Doi, M. Urata, N. Okamoto and F. Ide, Nagasaki Prefectural Kamigoto Public Health Center, Nagasaki; H. Sakiyama, N. Onga, H. Takaesu and M. Uehara, Okinawa Prefectural Miyako Public Health Center, Okinawa; F. Horii, I. Asano, H. Yamaguchi, K. Aoki, S. Maruyama, M. Ichii and M. Takano, Osaka Prefectural Suita Public Health Center, Osaka; Y. Tsubono, Tohoku University, Miyagi; K. Suzuki, Research Institute for Brain and Blood Vessels Akita, Akita; Y. Honda, K. Yamagishi and S. Sakurai, Tsukuba University, Ibaraki; M. Kabuto, National Institute for Environmental Studies, Ibaraki; M. Yamaguchi, Y. Matsumura, S. Sasaki and S. Watanabe, National Institute of Health and Nutrition, Tokyo; M. Akabane, Tokyo University of Agriculture, Tokyo; T. Kadowaki, Tokyo University, Tokyo; M. Noda, International Medical Center of Japan, Tokyo; Y. Kawaguchi, Tokyo Medical and Dental University, Tokyo; Y. Takashima, Kyorin University, Tokyo; K. Nakamura, Niigata University, Niigata; S. Matsushima and S. Natsukawa, Saku General Hospital, Nagano; H. Shimizu, Sakihae Institute, Gifu; H. Sugimura, Hamamatsu University, Shizuoka; S. Tominaga, Aichi Cancer Center Research Institute, Aichi; H. Iso, Osaka University, Osaka; M. Iida, W. Ajiki and A. Ioka, Osaka Medical Center for Cancer and Cardiovascular Disease, Osaka; S. Sato, Osaka Medical Center for Health Science and Promotion, Osaka; E. Maruyama, Kobe University, Hyogo; M. Konishi, K. Okada and I. Saito, Ehime University, Ehime; N. Yasuda, Kochi University, Kochi; S. Kono, Kyushu University, Fukuoka.
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Acknowledgements |
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This study was supported by Grants-in-aid for Cancer Research and for the Third Term Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan. Dr Ai Ikeda was also supported by the post-doctoral fellowship program of the Uehara memorial foundation (Tokyo, Japan). The authors thank all staff members in each study area and in the central office for their painstaking efforts to conduct the baseline survey and follow-up. The authors thank Dr Mariko Shiozaki, Osaka University, Graduate School of Medicine, for valuable advices and supports on the manuscript.
Conflict of interest: None declared.
KEY MESSAGES
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References |
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