Mild Traumatic Brain Injury, Hibernation, Type 2 Diabetes Common Etiopathophysiology Biomarkers and Function

Abstract

The link between diabetes and traumatic brain injury (TBI) is an area worthy of exploration. TBI is caused by bumps, blow, jolt, or penetrating injury to the head. Even mild (mTBI) and moderate TBI frequently results in chronic cognitive, emotional and behavioral symptoms, which impact long-term outcome and functioning. Traumatic brain injury is associated with neuroendocrinopathies including hypothalamic, pituitary, adrenal, gonadal (HPAG axis), pancreatic and other hormonal dysfunctions. Increases in cortisol, cholesterol, and weight gain that can occur with some TBI can all survivors may contribute to Metabolic Syndrome and Type II diabetes. In addition, many patients with TBI find physical activity, proper eating and sleeping difficult. They also often experience anxiety and stress, which contribute to hormonal dysregulation. Taking a proactive approach in lifestyle to avoid becoming diabetic and careful monitoring to address issues can improve the quality of life of patients with TBI and prevent the likelihood of developing metabolic syndrome and Type II diabetes. We also show endocrine data of several different species in different phases or types of hibernation which can be informative.