Depression is one of the leading causes of disability worldwide, and around a third of patients do not recover fully with standard treatment. Scientists suspect that inflammation plays a part in some cases, yet the evidence is muddied because most studies involve people already taking antidepressants. A new study from Egypt suggests that a common inflammation marker sits lower in depressed patients who have never been treated.
Researchers at Ain Shams University in Cairo compared 120 outpatients with major depressive disorder in a cross-sectional study. The findings appear in The Open Psychology Journal. Of the patients, 47 had never taken medication for their condition, while 73 had received it in the past.
Patients aged 18–65 were chosen at random from the Institute of Psychiatry at Ain Shams University Hospital and the Abbasia Hospital for Mental Health, between March 2020 and June 2021. People with recent infections, inflammatory diseases, surgery or injuries were excluded, as were those taking drugs that affect inflammation. Each patient gave a fasting blood sample, and clinicians confirmed the diagnosis with a structured interview and rated depression, anxiety and physical symptoms.
C-reactive protein, known as CRP, is a substance made by the liver when the body is inflamed, and doctors often measure it in routine blood tests. A treatment-naive patient is someone who has never received medication for their condition. The never-treated group was younger, with an average age of about 29 compared with about 38.
Patients who had never been treated had a significantly lower average CRP level, at 1.5 mg/L compared with 2.7 mg/L. Almost all patients were within the normal range, and only two, both in the medication group, had levels above 5 mg/L.
CRP also followed the course of the illness. Levels rose with the number of depressive episodes and with the number of years a person had been ill. The never-treated group averaged two episodes and about three years of illness, against almost five episodes and ten years in the medication group. CRP was not linked to depression severity, anxiety or physical symptom scores, which were similar in both groups.
The medication group was mixed. Forty patients had stopped taking medication before the study, while others were on SSRIs, SNRIs or other drugs. The authors offer two readings of the result: higher CRP may reflect the natural course of repeated episodes, or it may be a response to antidepressants.
The study cannot tell these apart, which matters if inflammation markers are ever to guide treatment. The study has clear limits. It captured one moment in time, so it cannot show cause, and it had no healthy comparison group. It did not compare types of antidepressant, and CRP shifts with infection, injury and body weight. Treated patients were also older and had been ill for longer, which makes the two groups hard to compare.
Earlier research has found that CRP tends to be higher in people with depression than in healthy people, though often still within the normal range, as here. Findings on antidepressants and CRP are mixed, with some studies reporting rises and others falls. The authors call their work preliminary and say it needs replication, so it is a first hint rather than proof.
