Health inequalities have been associated with social class for centuries: in 1842, the average lifespan for a ‘gentleman’ was 45 years, whereas for ‘labourers’ it was 16 years (Smith, Carroll, Rankin, & Rowan, 1992). Specifically, people from low socioeconomic status (SES) have higher odds of developing depression and anxiety than middle or high economic status groups. (Lorant et al., 2003). This effect is seen across different definitions of depression and across different measures of SES (Everson, Maty, Lynch, & Kaplan, 2002).
Lorant et al.’s meta-analysis suggests that this relationship is more due to causation than selection; low SES increases the risk of depression, rather than depression leads to decreased social status. For this reason, that is what I shall be focussing on, although the selection mechanism has been studied in its own right. This literature review will focus on depression, although anxiety will also be considered in some cases, as negative emotions tend to cluster together, meaning that anxiety and depression are often experienced simultaneously (Clark & Watson, 1991).
However, no one theory fully explains the phenomenon (Adler et al., 1994).
Most research into the psychosocial link between social rank and depressive disorders looks at the idea of poverty-related stress being the mediating factor (C. L. Hammen, 2015). People from low SES experience more stress, both acute and chronic. This is compounded by the fact that this population interprets ambiguous events as more stressful, compared to people from a higher status (Chen & Matthews, 2001). The effect of these stressors has been measured in a wide range of studies.
Acute stressors, such as high job demands, being a victim of crime and short-term financial strain, are predictive of a depressive episode, especially in women and the elderly (Glass, Stanislav, & Berkman, 1997). Chronic stressors, such as poor working conditions, financial difficulties and health problems, have a major impact depression in women, both on their own, and in combination with acute stressors. In fact, they amplify the effect of acute stressors when experienced together (C. Hammen, Kim, Eberhard, & Brennan, 2009). Other studies have replicated these findings with groups of both genders. (Ensel & Lin, 1996).
People from low social rank do not experience just chronic or acute stress: they often experience both together, for example the chronic stress of living in a neighbourhood with a high crime rate, and the acute stress of a burglary. Therefore, the findings by Hammen et al. (2009) are critical, as the cumulative effect they revealed explains why the same acute stressor in a person of high SES’s life does not have the same effect.
Although there are many studies on the effects of stress on depression, there are widely varying conclusions, although the majority of studies in the last 15 years point to low SES being a predictor for depression. For example, a meta-analysis of 27 studies, examining stress as a mediating pathway between SES and depression uncovered 9 studies that used stress as an explanatory mechanism, but 5 that had little or no role of stress, and 3 reported no significant relationship. (Matthews et al., 2010). These results may be partly explained by methodological weaknesses. First, the definition of stress is very variable and depends on the individual and their circumstances. Anything can be stressful to someone if they are in a certain situation, so using a questionnaire to look for ‘stressful life events’ will not account for all possible stressors. Secondly, most of these studies used a self-reported diagnosis of depression, which has implications in that people from lower SES have decreased health literacy and are less likely to see a doctor, so this may not be entirely accurate. (CITE)Thirdly, several of the studies only include patients in the sample, which, especially in countries without universal healthcare, mean that the poorest patients are not represented (Holzer, Shea, Swanson, & Leaf, 1986). Finally, the definition of psychiatric disorders, depression in particular, varies widely, especially in older research papers (Lorant et al., 2003).
Research suggests that there are physiological mechanisms that mediate the relationship between low SES and increased incidence of anxiety and depression. A study of 132 adolescents showed that the epigenetic effect of low SES impacted brain function and behaviour, through the modulation and methylation of gene promotors, particularly the serotonin transporter gene. Methylation of this gene is associated with depression and other stress-related disorders (Swartz, Hariri, & Williamson, 2016). These results have been replicated in other studies. (Cicchetti, Rogosch, & Sturge-Apple, 2007). Furthermore, low SES and the stress that comes with that status, influences neuroplasticity, which in turn affects patterns of emotional expression and emotional regulation, as well as the body’s response to stress. The body has higher baseline glucocorticoid levels and increased allostatic load on areas such as the prefrontal cortex and hippocampus, which downregulate the stress response and the amygdala, which is responsible for the emotions. In this way, low SES can be linked to depression and anxiety.
While these studies are valuable in that they illustrate some mechanisms that may be involved in the pathway of disease, they are not pathological mechanisms in their own right, and cannot offer the whole explanation. Swartz et al.’s study on epigenetics barely acknowledges the role of the environment in influencing the expression of the serotonin transporter gene, but this is the interaction that causes the effect between SES and depression that we are looking for. Similarly, elevated baseline glucocorticoid in response to chronic stress is a valuable pathway, but in itself does not cause depression.
It is obvious that the link between these two complex conditions is multifactorial, individual and only partially understood. Although a lot of the research focusses on stress and the way that it manifests itself in the brain, there are many other researched mechanisms as to how low SES leads to depression. Furthermore, both of these conditions, low SES and depression are hard to define and test, meaning that not all research is comparable. However, it is clear that there is a causation mechanism between SES, stress and depression, which has strong implications for future research and public health policy.