Elevated C-reactive Protein as a Predictive Marker of Clinical Depression and Anxiety

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2024

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Abstract

Previous research has documented an association between elevated peripheral blood inflammation and depression diagnosis and symptom severity1. We investigated the association between inflammation and depression as well as anxiety symptom severity and response to treatment by assessing patients reporting depressive and anxiety symptoms for a period of three to six weeks, with quantified anxiety and depressive symptoms being documented weekly. The depressive and anxiety symptom severities were quantified using the Montgomery-Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Rating Scale (HAM-A), respectively. The sample included 472 patients (55% male, mean age = 27.5 years, mean duration of stay = 69.4 days, mean baseline MADRS score = 26.1, mean baseline HAM-A score = 19.6), of which 195 individuals reported depressive symptoms, while 198 individuals reported anxiety symptoms. Three blood samples per individual were collected and assessed to detect any elevated inflammatory responses as measured with blood serum levels of C-Reactive protein (CRP). The samples from each group of interest underwent a high-sensitivity assay for CRP levels during the pre-treatment and post-treatment periods. The relationship between patients’ baseline CRP levels/inflammatory responses collected at admission was cross-referenced with their response to treatment during the course stay at a psychiatric rehabilitation clinic as measured with reported symptom severity over time to determine if inflammation was a predictive marker of depression and anxiety treatment responses. We found that elevated CRP levels were positively associated with depressive treatment response as measured with ratings of reduction in depression symptom severity levels over time using the MADRS (p=0.004). In contrast, elevated CRP levels were not significantly associated with anxiety treatment response as measured with ratings of anxiety symptom severity levels over time using the HAM-A (p=0.109). Specifically, high CRP levels at admission correlated with less reduction in depressive symptoms over time, as if the effects of mental health rehabilitation treatment for depression were dampened by increased levels of inflammation as measured with CRP levels at the start of treatment. These findings suggest that baseline CRP levels at admission are a predictive marker for lingering depressive symptom severity over time even in people receiving treatment, but less so for anxiety symptom severity. Numerous limitations regarding the sample pool and the type of treatment administered were present in this study, including the lack of inclusion of healthy controls to account for the effects of low to no inflammation. Race and gender, factors that influence baseline inflammatory levels, were not controlled for when measuring CRP levels in the reported findings. Limitations regarding the structure and sensitivity of the outcome measure scales may have also skewed the reported MADRS and HAM-A scores. Future studies need to control for these limitations in order to better understand the association between inflammation and mental disorder treatment response as measured with symptom severity.

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