Strep infections are known to trigger autoimmune disorders, affecting millions worldwide (Aran et al 2011). Recently, researchers from Stanford University found an association between post-strep autoantibodies and an enzyme involved in insulin degradation and insulin resistance (Aran et al 2011). The autoantibodies attack the enzyme and decrease insulin degradation and correlate with higher insulin levels and insulin resistance.
Aran et al (2011) have shown these post-strep autoantibodies are also associated with metabolic syndrome, which is characterized by a multitude of metabolic risk factors for cardiovascular disease and type 2 diabetes (T2D) including but not limited to hypertension, insulin resistance, hormonal imbalance, prothrombotic and proinflammatory state (Aran et al 2011). Metabolic syndrome is a leading cause of morbidity and mortality in the developed world (Aran et al 2011).
Metabolic syndrome, T2D and depression often occur together (Wolkowitz et al 2011 and Gragnoli 2014). In fact, depression increases the risk of T2D by 60% (Mezuk et al 2008) and conversely, researchers have also shown T2D is associated with an increase in the risk of major depressive disorder (Gragnoli 2014).
Research out of the Department of Psychiatry at the University of California – San Francisco indicates that although major depressive disorder (MDD) is typically a mental illness, pathology associated with MDD is evident in cells and organs throughout the body. Major depressive disorder is often associated with developing serious medical conditions such as cardiovascular disease, stroke, dementia, osteoporosis, diabetes, insulin resistance, and the metabolic syndrome (Wolkowitz et al 2011).
In their research article, Wolkowitz et al (2011) discuss mediators (e.g., hormones, steroids, insulin levels) that are dysregulated in MDD and may contribute to the depressed state itself and the associated medical conditions. The authors state that by studying these new mediators not only could new targets be found to treat depression and its associated conditions but it could also help reclassify MDD as a multi-system disorder rather than one confined to just the brain. These data are in line with a growing body of evidence linking infections, immunity, depression, and metabolism.
Aran A, Weiner K, Lin L, Finn LA, Greco MA, et al. (2010) Post-Streptococcal Auto-Antibodies Inhibit Protein Disulfide Isomerase and Are Associated with Insulin Resistance. PLoS ONE 5(9): e12875.
Aran A, Lin L, Finn LA, Weiner K, Peppard P, et al. (2011) Post-Streptococcal Antibodies Are Associated with Metabolic Syndrome in a Population-Based Cohort. PLoS ONE 6(9): e25017.
Gragnoli C. Hypothesis of the neuroendocrine cortisol pathway gene role in the comorbidity of depression, type 2 diabetes, and metabolic syndrome. The Application of Clinical Genetics 2014:7 43–53
Mezuk B, Eaton WW, Albrecht S, Golden SH. Depression and type 2 diabetes over the lifespan: a meta-analysis. Diabetes Care. 2008;31(12): 2383–2390.
Wolkowitz OM, Reus VI, Mellon SH. Of sound mind and body: depression, disease, and accelerated aging. Dialogues Clin Neurosci. 2011;13(1):25-39.
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