The declining trend in cardiovascular mortality rates seen since the mid-1970s in Western countries have been more pronounced for people in higher socioeconomic status (SES) groups. The fact that established risk factors, are limited in explaining the socioeconomic differences in cardiovascular disease (CVD) has opened new fields of research. One such field is the role of SES in the preclinical (asymptomatic) stages of the atherosclerotic disease process. The main purpose of this thesis was to study the relation between SES and preclinical atherosclerosis and to evaluate the potential of a mediating role of health-related behaviours and psychosocial stressors. The study population was derived from the Malmö Diet and Cancer Study (MDCS), a prospective cohort study. Recruitment was carried out between 1991 and 1996. The total participation rate was 40.6% (28,098 of a total of 69,129 individuals). A random 50% of those who entered the MDCS between 1991-1994 (n = 12,445) were invited to take part in a study on the epidemiology of carotid artery disease. A total of 6,103 subjects (96%) accepted the invitation. In 1992 questions assessing psychosocial factors were added to the baseline questionnaire. Since we used these variables in our analyses, only those subjects attending the MDCS between 1992-1994, who accepted the invitation to the carotid artery disease study (n = 4,884), were included in the studies. SES was defined by educational level and occupational status. Ultrasound determined carotid intima-media thickness (IMT), carotid plaque and carotid stenosis were used as markers or indicators of carotid atherosclerosis. Cross-sectionally, adult low SES was associated with increased carotid atherosclerosis, in both men and women. Furthermore, among women, the atherosclerotic process seemed to be affected by low SES in childhood. Adult low SES was also associated with the progression of atherosclerosis in women. Even though low SES seemed to have a substantial impact on health-related behaviours known to affect the atherosclerotic disease process, such behaviours could only partly explain the found SES differences in atherosclerosis. More precise measures of these risk factors might increase their explanatory potential. Differences in psychosocial stressors outside the workplace could not add much to the explanation of the SES differences in atherosclerosis. Regarding psychosocial stressors at work, the specific hypothesis that a working situation characterized by high psychological demands and low decision latitude (“job strain”) would be associated with increased carotid atherosclerosis could not be supported in this study, neither in men nor women. Instead, a more complex pattern of interaction between job demands and job decision latitude was shown. There were generally larger socioeconomic differences in atherosclerosis in women than in men. This might be partly due to methodological problems such as selection bias. However, the results might mirror the true relationship between SES and atherosclerosis in men and women. In conclusion, the results show that low SES has an impact already on the early stages of the cardiovascular disease process, i.e., in preclinical atherosclerosis. Furthermore, the results suggest that a life-course perspective might increase our understanding of the social causes of atherosclerotic disease. The socioeconomic differences found seemed to be partly mediated by health-related behaviours and to a lesser extent by psychosocial stressors outside the workplace.