Abstract

Finding biological predictors and novel mechanisms underlying negative symptoms of schizophrenia is of significant importance given the lack of effective treatments. Increasing data support a role for metabolic dysfunction and inflammation in reward processing deficits in psychiatric illness. Herein, we found an interaction between lipids and inflammation as a predictor of worse negative symptom severity in individuals with schizophrenia. Future studies may seek to further elucidate this relationship and thereby reveal novel treatment targets for negative symptoms.

Highlights

  • There is increased focus on the interaction of inflammatory and metabolic pathways in psychiatric disorders[1,2,3,4]

  • We have recently demonstrated that markers of altered glucose metabolism were associated with decreased functional connectivity in reward circuitry, an effect that was only seen in individuals with increased inflammation in patients with depression[2]

  • We examined negative symptoms and non-fasting levels of plasma lipid markers as well as plasma concentrations of two of the most commonly altered cytokines in patients with schizophrenia: tumor necrosis factor (TNF) and interleukin-6 (IL-6), which have both been shown to be associated with negative symptoms[13,14]

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Summary

METHODS

Health Care System (Atlanta VAHCS) as part of two different parent studies. Negative symptoms, both total score and PANSS total score. As the inflammatory markers were run at different times, the concentrations were mean-centered (the batch effect was LDL ln TNF (mean-centered). Accounted for as a covariate in analyses) Median splits for both the metabolic and inflammatory markers were calculated in order to ln IL-6 (mean-centered). BMI body mass index, PANSS positive and negative syndrome scale, LDL low-density lipoprotein, ln TNF natural log of tumor necrosis factor, ln IL-6 natural log of interleukin-6. Determine the relationship between the interaction of metabolic and inflammatory markers with negative symptom severity including the following covariates: age, sex, race, smoking, body mass index (BMI), batch effect, and time between blood samples for metabolic and inflammatory markers. A replication sample including 58 individuals with schizophrenia was used to replicate the findings from the primary sample (see Supplementary Materials)[14]

AUTHOR CONTRIBUTIONS
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