4.5 Article

Longitudinal associations between biomarkers of inflammation and changes in depressive symptoms in patients with type 1 and type 2 diabetes

Journal

PSYCHONEUROENDOCRINOLOGY
Volume 91, Issue -, Pages 216-225

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2018.02.032

Keywords

Inflammation; Biomarkers; Type 1 diabetes; Type 2 diabetes; Depression

Funding

  1. German Federal Ministry of Education and Research (BMBF) [FKZ 01G10809, FKZ 01GI1107]
  2. German Federal Ministry of Health (BMG)
  3. Ministry of Culture and Science of the State North Rhine-Westphalia
  4. German Federal Ministry of Education and Research (BMBF)

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Background: Depressive disorders represent a frequent comorbidity of type 1 diabetes (T1D) and type 2 diabetes (T2D). Subclinical inflammation increases the risk of depressive symptoms in the general population, but the relationship appears complex and bidirectional, and longitudinal data from patients with diabetes are lacking. Therefore, this study aimed to analyse associations between changes in depressive symptoms and changes in biomarkers of inflammation in patients with T1D and T2D and to investigate the hypothesis that higher baseline levels of biomarkers of inflammation are related to a less pronounced reduction of depressive symptoms over time. Methods: Depressive symptoms and systemic levels of six biomarkers of inflammation were assessed in 168 individuals with T1D and 103 individuals with T2D who participated in baseline and 1-year follow-up examinations. Data were obtained from two matching randomised controlled trials addressing diabetes distress and depressive symptoms. Longitudinal associations between biomarkers and depressive symptoms were estimated using linear regression models adjusting for multiple confounders. Results: In patients with T2D, reductions in depressive symptoms were associated with reductions in high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-18 and IL-1 receptor antagonist (IL-1RA) (P <= 0.016), whereas no associations were seen for IL-6, CCL2 and adiponectin. Higher CCL2 levels at baseline were associated with lower subsequent reduction in depressive symptoms (P = 0.018). Neither baseline levels nor changes in biomarkers in subclinical inflammation were associated with changes in depressive symptoms in patients with T1D. Conclusions: Reductions of depressive symptoms were longitudinally associated with reductions in biomarkers of inflammation in patients with T2D. Higher baseline CCL2 levels were related with lower reduction of depressive symptoms in this group. No such associations were observed in patients with T1D, suggesting that risk factors and pathomechanisms linking inflammation and depression may differ between diabetes types.

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