Higher levels of inflammation associated with specific depressive symptoms


A new ELSA study published in Translational Psychiatry has found that elevated levels of inflammation are associated with the development of somatic symptoms (e.g. feeling sad, lonely, and depressed) but not cognitive-affective symptoms (e.g. sleep problems, lack of energy) in people with a genetic risk for depression.

Depression is a leading cause of disability worldwide and with around one third of patients failing to respond to conventional antidepressants, understanding the complex nature of depression is vital, as Philipp Frank, author of the study explains:

“Depression is a highly heterogenous disorder with varying types of symptom expressions. This variability can make treatment difficult, and thus far, a lot of people with depression do not get better after being treated with antidepressant medication.

“Our findings show that certain genes increase the risk of developing both depressive symptoms and elevated levels of inflammation. However, inflammation seems to be important primarily for the manifestation of somatic but not cognitive-affective symptoms. Therefore, future trials are needed to test whether anti-inflammatory drugs may be particularly useful for people with somatic depression profile.”

The study, which used data from 3,510 people aged 50 and over is unique, as co-author Dorina Cadar (Senior Research Fellow at UCL) explains: “This is the first study to investigate the underlying mechanisms between genetic susceptibility and symptomatic typology of depressive symptoms in a representative sample of English adult population.

“Understanding that inflammatory markers could exacerbate the genetic predisposition in the manifestation of somatic rather than cognitive symptoms represents an important avenue that needs to be considered in personalised treatment and future drug development."


Frank P, Ajnakina O, Steptoe A and Cadar D. Genetic Susceptibility, Inflammation and Specific Types of Depressive Symptoms: Evidence from the English Longitudinal Study of Ageing. Translational Psychiatry 2020 May 12;10:140.doi: 10.1038/s41398-020-0815-9 [Download]

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