28 September 2018

Depression sharply increases risk of SLE

Clinical Rheumatology

As if having depression isn’t bad enough, now research has found it more than doubles your risk of developing systemic lupus erythematosus (SLE) in the future. 

“A history of depression was associated with a risk 2.5 times as great as no history of depression in developing SLE,” the US study authors wrote in JAMA Psychiatry.

And the association can’t simply be explained by the higher prevalence of health risk behaviours among people with depression, namely factors such as higher BMI and cigarette smoking which have been shown to be linked with SLE, according to findings from a long-term prospective study.

Even after accounting for these common risk factors the association stayed true, the researchers said after analysing data collected from two cohorts of women participating in the Nurses’ Health Study and the Nurses’ Health Study II over a 20-year period. Similarly, oral contraception and postmenopausal hormone use could not solely account for the increased risk.

The prospective study involved analysing data from almost 200,000 nurses being assessed at regular intervals over two decades for a wide variety of health risk factors, as well as regularly documenting their current health status.

Researchers found the median time from depression to incident SLE was 4.5 years, leading them to suggest the association was more likely causal rather than the depression simply being an early sign of SLE or that SLE was being initially misdiagnosed as depression.

The analysis found the increased risk of developing SLE remained no matter which of three indicators had been used to determine the patient had depression – a clinician’s diagnosis of depression, antidepressant use or whether the patient had depression symptoms as assessed by the Mental Health Inventory. Antidepressant use conferred the highest risk.

In terms of mechanism of action, it has been shown in prospective studies, that concentrations of biomarkers of systemic inflammation are increased in depression. It is also known that individuals susceptible to developing SLE have increased blood concentrations of inflammatory cytokines and chemokines. Consequently, researchers suggest the elevation of inflammatory cells found in people with depression may fuel autoimmunity in pre-SLE states.

“Our findings provide support for the hypothesis that depression is a causal risk factor for developing SLE, perhaps via altered immune function,” they said.

So, practically speaking what does this mean?

The authors suggest their study has two possible clinical implications.

Firstly, for screening. Knowing that this is a potentially high-risk group, it might be worthwhile to screen patients with depression or a strong family history of depression for SLE, improving rates of early detection of the condition.

Secondly, there may be a potential therapeutic intervention.

“Lifestyle interventions to reduce inflammation in persons with depression may reduce the risk of autoimmune disease as well as other negative health sequelae of depression, including cardiovascular disease,” they conclude.

JAMA Psychiatry doi:10.1001/jamapsychiatry.2018.2462