Depression And Rheumatoid Arthritis

Psychological alterations are frequent among patients with diseases such as rheumatoid arthritis (RA), ankylosing spondylitis or psoriatic arthritis, due to the chronic pain they cause and the disability they cause. Dr. William Julio.

William Julio, MD, FAPA
Latin Agency for News Medicine and Public Health

Rheumatologists could substantially lessen the symptoms of depression in their patients by determining the root cause of their depression. Likewise, prevent pain and disability, reduce systemic inflammation, designing and implementing programs based on medical evidence to mitigate the effects of depression in rheumatoid arthritis.


It has been recognized that depression is prevalent among patients with Rheumatoid Arthritis (RA). This article reviews both the social context and the biological state of the disease in people with RA, as this disease affects both physically and psychologically. Understanding socioeconomic factors, individual patient characteristics, and biological causes for depression in RA can lead to a more complete paradigm, with the goal of achieving interventions to eliminate depression in patients with RA.

It is recognized that depression is prevalent among patients with Rheumatoid Arthritis (RA). This article reviews both the social context and the biologic disease state of a person with RA as this illness affects both physically and psychologically. Understanding the socioeconomic factors, individual patient characteristics and biological causes of depression in RA can lead to a more comprehensive paradigm for targeting interventions to eliminate depression in RA.

Depression, Rheumatoid Arthritis
Depression, Rheumatoid Arthritis

The condition of rheumatoid arthritis (RA) is a multifactorial, chronic and inflammatory disease that primarily affects the joints, with a prevalence of between 0.5% to 1%. Pain, fatigue, and disability, which can be considered stressors, are common challenges that could subsequently lead to psychological distress.

Depression commonly co-occurs with RA in a range of 13% to 20% or greater, based on clinical evaluations. Studies using self-report measures of depressive symptoms suggest considerably higher ranges (eg 40%), although symptom levels may be subclinical. Longitudinal studies suggest a cumulative risk for depression and intermittent recurrences over time (eg 40% over 9 years). The prevalence of depression in RA is well above that reported in the general community or primary care, but similar to other chronic conditions. Depression in RA is associated with high levels of illness, pain, fatigue, disability, use of medical services, but also with lower compliance with therapy and increased suicide risk and mortality.

As with most complex biological systems, the relationship between depression and RA is multifactorial: in some cases it is likely that depression is mediated by the socioeconomic outcomes of RA. In other cases, depression may be due to disability from RA. Regardless of the initiating factors, the contributing socioeconomic, functional, and biological consequences of RA can perpetuate depressive symptoms. Understanding the component mechanisms of depression in RA is critical for effective treatment.

The terms socioeconomic status (SE), social class, and socioeconomic position are widely used in health research, pointing out the importance of these factors in health outcomes. A low ES is generally associated with high psychiatric morbidity, depression, and mortality. Poor coping skills, life events, exposure to stressors, and weak social support are some examples of risk factors for depression that are more prevalent in groups with low ES. Regarding the direction of the association of SS and depression, the most consistent results support the idea of ​​causality (low SS increases the risk of depression) weighing selection (depression hinders social mobility), although both directions can operate simultaneously. There is a substantial amount of research linking ES, depression, and RA. However, despite the consensus of experts that ES is multifactorial, most studies of ES in patients with depression and / or RA use a single socioeconomic variable in a single period and level.

Being female and being young are factors that are associated with depression and with confusing the relationship between SS and depression in RA. As women have a higher prevalence of RA and depression, ignoring gender would falsely increase the magnitude of other variables associated with depression.

Comorbidities and pain are commonly associated with both RA and depression. Not surprisingly, pain has been indicated as a mechanism along the causal pathway for depression and those with RA. Furthermore, depression can confuse self-reports of pain. Alternatively, pain in an RA patient and comorbid depression can cause the physical symptoms of RA to be incorrectly attributed to depression.

There is conflicting evidence as to whether the activity of the RA condition as measured by rheumatologist documentation of joint inflammation and pain may or may not affect depression. Some studies show a positive correlation between depression and the activity of the RA condition, while others do not. Taking this one step further, it has been shown that loss of valued activities, beyond functional impairment, leads to depression. This suggests that depression in RA may not be caused by the acute clinical manifestation of the RA disease, but rather caused by long-term disability and joint damage associated with arthritis resulting in loss of valued activities.

With regard to the treatment of the RA condition, it is not unexpected that patients who have a clinical remission are less likely to remain depressed, compared to those who do not achieve a remission. A common element in the proposed mechanism, linking the patient and the characteristics of the RA condition with depression, is the ability to adapt to the burden of the RA condition and its treatment. Positive coping mechanisms, social support (eg being married), and having a sense of control over the RA condition are associated with fewer depressive symptoms.

More recent studies have shown that systematic inflammation, measured by acute phase reactants and pro-inflammatory cytokines, is often associated with the development of depression, and it has been suggested that systemic inflammation may be associated with, cause, or contribute to depressive symptoms during chronic inflammation disorders. In patients with RA, there is conflicting evidence regarding acute phase reactants and high sensitivity of C-reactive protein, and their relationship with depression. The hypothesis that systemic inflammation contributes to a high prevalence of depressive symptoms in RA patients is supported by the following observations. First, inflammatory cytokines and acute phase reactants are increased in depressive symptoms in patients without RA. Second, elevated levels of cytokines such as IL-6 and TNF-α can predict that a response to treatment of depression symptoms will not occur. Third, there is evidence that anti-inflammatory therapies have clinical benefit in reducing depressive symptoms. Fourth, medications such as traditional and biological antirheumatic modifying drugs have been suggested to influence the relationship between inflammation and depression in patients with RA.

None of the factors associated with RA exist in a vacuum. For example, there is a significant interaction between SS and disability in patients with RA and comorbid depression. The association of disability with depression was stronger for people with low ES compared to those with high ES. The assumption that disability and SS have independent consequences for depression in RA patients does not hold. One potential explanation for this is that, at each level of functioning, people with low ES may not have the supportive resources to function as well as those with high ES, leading to even higher levels of depression. RA affects people both physically and physiologically, and by focusing on the social, individual, contextual, and biological causes for depression, rheumatologists can consider a more comprehensive paradigm. This is true for other autoimmune conditions as well, such as systemic lupus erythematosus, where a low ES is associated with disparities in the health characteristics of patients, levels of systemic inflammation, and a high prevalence of depression.

Public health research goals should be maintained in order to develop policies and interventions to reduce the disparities associated with SS, depression, and RA. In addition, the rapid advances in immunology could lead to accumulating more persuasive data related to systemic inflammation in RA and its serious negative health implications. Rheumatologists must consider depression as a consequence of both the social context and biological factors of the depressive condition in RA, in order to assess which aspect contributes the most to depression in patients with RA. Rheumatologists could substantially reduce the symptoms of depression in their patients by determining the root cause of depression, preventing pain and disability, decreasing systemic inflammation, as well as designing and implementing programs based on medical evidence to mitigate the effects of depression in RA. This involves moving beyond associations to establish causal relationships that, in turn, may lead to new and targeted therapies for depression in RA patients.

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