A schematic illustration of the brain’s complex circuitry mediating fear responses and anxiety behavior along with hormonal mechanisms responsible for hyperactivity of the HPA axis in response to a threat. When the brain receives a threat signal, the hypothalamus which is activated by the amygdala triggers the release of CRH. It funnels CRH to activate the Pituitary gland, which ultimately controls the other endocrine glands and body’s hormonal response to stress. This occurs via the action of CRH that stimulates the pituitary synthesis of ACTH as an interconnecting element of the HPA Axis. In turn, ACTH travels down the bloodstream and stimulates the adrenal glands located atop of both kidneys to secrete more stress and threat hormones including Cortisol, Adrenaline, and Noradrenaline and release them into the bloodstream to assist the body in handling threat or stress better resulting in higher levels of cortisol in the blood. However, prolonged high cortisol levels in the bloodstream exacerbate anxiety and interfere with the body’s natural self-repair mechanism. Hence, Cortisol’s far-reaching, systemic effects play numerous roles in the body’s effort to carry out its processes and maintain homeostasis. Correspondingly, these are the hormones, particularly cortisol, involved in the regulation of the HPA system that plays a vital role in anxiety-related disorders.