User:Mwright0131/sandbox

Up to 25% of general practice patients are diagnosed with co-morbid anxiety and depression. The comorbidity of these disorders are explained by either shared genetics to both anxiety and depression or from one disorder increasing the likelihood of developing the other. Anxiety and depression may also coincide due to the neurological relationship of hormones, neurotransmitters,and HPA dysregulation. Hormones are your body's chemical messengers, and travel through your bloodstream to help control how certain cells and organs do their work. Their behavior is altered when a person struggles with Mixed Anxiety-Depressive Disorder (MADD), including the corticotropin-releasing hormone (CRH). CRH is involved with regulating the stress response and is dysregulated in MADD, as an increased amount of CRH in cerebrospinal fluid has been reported in both anxiety and depression. However, other neurotransmitters and hormones controlled by your HPA (hypothalamic-pituitary-adrenal axis) are regulated differently in the two disorders. The HPA is a neuroendocrine unit comprised of the hypothalamus, pituitary gland, and adrenal glands, which plays key roles in maintaining homeostasis and the body's response to stress. Cortical areas of the brain such as the OFC (orbito-frontal cortex) demonstrate altered activity patterns in patients with MADD. The OFC is found in the prefrontal cortex of the brain, just above your eye sockets, and shares connections with sensory areas as well as limbic system structures involved in emotion and memory. This area is linked to an overproduction of a neurotransmitter called serotonin in patients with MADD.