We found that SES and MS, both alone and in combination, were associated with the prevalence of depression. Lower SES increased the likelihood of depression, and this relationship was strongest among individuals with the lowest level of education or household income. MS and two MS components (lower HDL-C and higher TG) were significantly associated with an increased likelihood of depression, after adjusting for other potential risk factors. There was also a trend toward a positive association between depression and two other MS components (increased waist circumference and FBS). Additionally, participants with the combination of MS and lower SES had an increased likelihood of depression, when compared with individuals with a higher SES and no MS.
Previous studies reported that depressive disorder is more prevalent among people with a lower SES [17, 29–31]. Our results are in agreement with these observations. Data from the Alameda County Study, a community-based longitudinal study of psychological and social factors and their role in health and well-being in almost 7,000 adults from Alameda County, California [32], demonstrated a graded relationship between SES and both prevalent and incident depression. Among participants who were not depressed at the beginning of the study, those with < 9 years of education were almost 2-fold more likely to develop depression during the next 9 years than those with at least a high school education (OR = 1.86, 95% CI 1.36–2.55). Participants with 9–11 years of education were also significantly more likely to become depressed (OR = 1.53, 95% CI 1.16–2.02) [33]. The Alameda County Study, which defined SES by household income tertiles, yielded results similar to ours: 19% of lower-income respondents reported numerous depressive symptoms, but only approximately 11% of higher-income respondents reported these symptoms [32]. A meta-analysis evaluating socioeconomic inequality in depression noted that low-SES individuals had an elevated likelihood of depression (OR = 1.81, p < 0.001) [17]. Based on the “health-related selection theory” and “social causation hypothesis,” Wardle et al. reported that economic deprivation partially explained the reciprocal association between SES and health behaviors [34].
Our results showed an association between depression and MS. These findings are consistent with those of previous studies [35–38]. A longitudinal study found that participants with MS at baseline were 2-fold more likely to develop depressive symptoms during follow-up than healthy matched controls [35]. In a cohort of healthy middle-aged females in the Healthy Women Study, MS predicted the development of depressive symptoms over a 6-year follow-up period [36]. In another population-based study, females with MS during childhood had higher levels of depressive symptoms in adulthood, and the severity of these symptoms increased in proportion to the duration of MS [37]. In 5,698 individuals from the Northern Finland 1966 Birth Cohort Study, MS was not associated with depression when assessed at the age of 31 years [39].
We also found that depression was associated with several MS components (waist circumference, HDL-C, TG, and FBS), although only the associations with lower HDL-C and higher TG remained significant after controlling for covariates in logistic regression analysis. Several previous studies evaluated associations between MS components and depression [3, 36, 38]. The Netherlands Study of Depression and Anxiety found that higher Inventory of Depressive Symptomatology scores were associated with a higher number of MS-related abnormalities, larger waist circumference, higher HDL-C, higher TG, and lower SBP [3]. Of five MS components evaluated in a study conducted in the United Kingdom, central obesity, high TG, and low HDL-C were predictive of depressive symptoms [36]. In a study from India, waist circumference was positively correlated with the severity of depressive symptoms measured using the Hamilton Depression Rating scale (r = 0.291, p = 0.003) [38]. Whether MS components are more predictive of depressive disorders than MS itself is unclear [40]. Further research is required to confirm our findings and define the role of MS components as risk factors for depression.
In the present study, we found that the risk of depression was 4-fold higher among participants with MS and a lower SES than in those without MS and a higher SES. We observed similar trends in all three models. Two previous studies reported the prevalence of depression and its comorbidities according to SES [41, 42]. In the MultiCare Cohort Study, lower SES was associated with a higher prevalence of chronic conditions, such as cardiovascular and metabolic disorders (CMDs), as well as the composite outcome of depression, anxiety, somatoform disorders, and pain. The number of CMDs was associated with the level of education (-0.17 CMDs for medium level and − 0.26 CMDs for high level, when compared with a low education level) and income (-0.27 CMDs per unit on a logarithmic scale). SES was inversely related to the composite outcome including depression in both males and females, although the association was stronger in females [41]. In the other study, which was a population-based study of adult females in the United States Buffalo–Niagara region, the likelihood of depression plus obesity was higher in more educated women than in less educated women (OR = 2.15, 95% CI 1.27–3.62) [42]. By contrast, the combination of education level and MS was more strongly associated with depression in males than in females in our study. These findings suggest the existence of important sex differences for the combined role of education level and MS on the development of depression. It is also possible that men underestimate their negative affective states because of differences in cognitive appraisal, accessibility of memories, or reliance on implicit beliefs, stereotypes, or cultural differences [43]. This, in turn, may mask the true nature of the associations between depression, SES, and MS. Sex differences in the association between MS and depression may also have physiological mechanisms, but this requires further investigation [5]. Numerous studies have reported lower rates of depression among participants with a higher SES or MS [17, 29–33]. However, little is known about the combined effects of SES and MS on depression. To our knowledge, there have been no previous reports regarding the association between depression and the combination of MS and SES.
The current study suggests that SES is an important factor in depression; however, the mechanism underlying its role remains unclear. The relationships between depression, SES, and MS may be at least partly explained by autonomic nervous system changes. In animal models, neuroendocrine system responses to SES have included hyperexcitation of the sympathetic system, hypersecretion of cortisol, and increased visceral fat. These changes are similar to those found in MS, and they have been suggested to occur in depression as well [44]. Furthermore, subordinate rats (which are a model for social stress, as may occur in humans with a low SES) have elevated levels of plasma insulin and leptin and display overeating behavior [24, 45]. Depression has also been associated with changes in inflammatory and hemostatic markers, including increased platelet aggregation, fibrinogen levels, and white blood cell counts [1, 46, 47]. As inflammatory and hemostatic processes also play important roles in MS, depression may be linked to MS and its components through these processes [1]. Further research in this area is warranted.
The present study had some limitations. First, we were unable to determine whether there is a causal relationship between depression and MS and/or low SES, because of the study’s cross-sectional design. Prospective studies are required to establish whether a causal relationship exists. Second, information bias was unavoidable because the study was based on a questionnaire. Third, the presence of depression was based on self-reported data. However, the lifetime prevalence of self-reported depression (2.2%) in this population was similar to the 2.7% prevalence reported in a previous Korean study in which depression was assessed using a well-validated questionnaire [48]. Our findings should be verified using more comprehensive assessments of depression. Fourth, our focus on five metabolic factors may represent an oversimplification of the extremely complex pathophysiologic processes leading to atherosclerosis. High cholesterol and BP may interact synergistically with other, non-conventional risk factors in the development of atherosclerosis.
Despite these limitations, this study has several strengths, including the use of data from a large population of apparently healthy subjects with a low prevalence of chronic disease (92.8% of the overall study population had no chronic disease). Additionally, because of considerable variation in MS components among individuals, we were able to analyze various MS components, in addition to MS itself. Finally, this study included an assessment of several variables, such as disease history, health behavior, education, and household income, as well as the interaction between MS and SES.
In conclusion, this study showed that SES and MS, both alone and in combination, were associated with the presence of depression. Both SES and MS may play important roles in this mood disorder. If replicated in longitudinal studies, these findings may have important healthcare policy implications for primary care physicians, nurses, and community mental health professionals. Future research should explore whether improvements in SES and MS reduce the likelihood of depression.