- Interleukin-1β levels are significantly associated with depression severity, but not suicidal ideation and behaviour
- Tumor necrosis factor-α is significantly associated with suicidal ideation and behaviour
Evidence Rating Level: 2 (Good)
Depression affects around 8% of the total adult American population. The pathophysiology underlying this common mental health disorder remains under investigation. Previous research has shown inflammation to be associated with depression. However, further research remains to be conducted to clarify the specific inflammatory markers associated with depression.
This cohort study conducted in China measured the plasma cytokines of 82 participants. Participants over the age of 18 and confirmed DSM-V diagnosis of depression by a psychiatrist were included. Individuals comorbid with another mental health disorder like schizophrenia and bipolar disorder, who had an infection or antibiotics use in the past 3 months, or who have an autoimmune disorder or are on immunosuppressive therapy were excluded. Specifically, 14 plasma cytokines were measured at baseline by drawing venous blood samples in the morning after a period of fasting the night before. Participant’s depression severity was also gathered at baseline using the Patient Health Questionnaire-9 (PHQ-9). Depression severity was followed up at 1, 2, and 3 months. Participant’s suicidal ideation and behaviour was also assessed at the 3-month mark using the Hamilton Depression Rating Scale (HDRS). The participant’s age, BMI, education, social support, and depression treatment were also taken into consideration during data analysis and interpretation. The primary outcome measured depression severity.
The results showed that interleukin-1β (IL-1β) levels were significantly associated with depression severity at all monthly follow-ups, even when adjusted for by considering external factors (age, BMI, education, antidepressant drug, and baseline PHQ-9). Tumor necrosis factor-α was significantly associated with suicidal ideation and behaviour, while IL-1β was not. A limitation of this study is the lack of a healthy control group. Certainly, gathering data on inflammatory markers from healthy individuals would allow researchers to accurately compare differences and make further comments on the pathophysiological association between specific cytokines and depression. Nevertheless, the study offers deeper insight into the physiology underlying depression and provides education on specific inflammatory markers that could potentially be targeted in future therapy.
Click here to read this study in BMC Psychiatry
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