Inflammation as a potential causal mechanism explaining the association between depression and executive functioning.

• In Event: Poster Session 03
  In Poster Session: PS 03 Topic - Developmental Psychopathology

Abstract

Executive functioning is disrupted during a depressive episode and deficits persist when depression is in remission (Snyder, 2013). A better understanding of why executive functioning is impaired in depression is needed – adiposity and inflammation are two partially overlapping candidate mechanisms that may explain why executive functioning is impaired in depression. First, we examine in a population-representative sample of adults whether the combination of depression and elevated immune markers is differentially associated with worse executive functioning across the adult lifespan. Next, we investigate in a prospective, longitudinal sample of adolescents whether adiposity and/or inflammatory biomarkers prospectively predict increases in depressive symptoms and decreases in performance on tasks of executive functioning.
Study 1 examines the baseline assessment of a population-representative sample of 43,896 adults aged 18-93 years and tests whether the combination of depression and an inflammatory biomarker, C-reactive protein (CRP), is differentially associated with worse executive functioning. Study 2 examines 288 adolescents aged 16 years who were assessed annually over 3 years and tests whether elevated body mass index (BMI) and/or inflammatory biomarkers, including CRP and interleukin-6, are prospectively associated with increases in depressive symptoms and decreases in four measures of executive functioning within a structural equation modelling framework.
In Study 1, elevated CRP (B = -0.67, p<.001), depression (B = -3.70, p<.001), and their combination (B = -1.10, p<.001) were associated with worse executive functioning [coefficients are unstandardized; mean executive functioning score = 81.81 (SD=26.04)], following adjustment for relevant covariates. In Study 2, higher BMI was prospectively associated with higher levels of IL-6 (b = 0.33, p<.001) and depressive symptoms (b = 0.10, p=.03). Importantly, interleukin-6 was consistently associated with worse executive functioning (b = -.13, p=.01) and BMI was indirectly associated with worse executive functioning via interleukin-6 – results were not replicated in CRP.
The combination of depression and inflammation is differentially associated with poorer executive functioning; however, it is unlikely that inflammation is a depression-specific cause of executive dysfunction and instead, it likely that elevated inflammatory physiology is dysregulated across multiple physical and mental health disorders. Inflammatory physiology is implicated in the pathogenesis of cognitive functioning in depression and adiposity may contribute to the development of such a pro-inflammatory state. Notably, the associations of inflammation and adiposity with both depression and executive dysfunction are observable early in life. Further research is needed that evaluate the degree to which modifiable lifestyle and socioeconomic factors, such as diet, sedentary behavior, exposure to environmental toxins, stressful life events, contribute to a pro-inflammatory and/or adipose phenotype.

Authors

• Naoise Mac Giollabhui, Temple University
  Presenting Author

• Catharina Hartmann, Accare
  Non-Presenting Author

• Lauren M Ellman, Temple University
  Non-Presenting Author

• Christopher L Coe, University of Wisconsin-Madison,
  Non-Presenting Author

• Lyn Y Abramson, University of Wisconsin-Madison,
  Non-Presenting Author

• Lauren B Alloy, Temple University
  Non-Presenting Author