Generalized anxiety disorder (GAD) is a chronic and disabling disorder with a low rate of full remission. It has been commonly assumed that pathologic anxiety is a continuing chronic course of early-onset illness, a perspective that is changing with current research. In a recent cross-sectional study of almost 2000 community-dwelling elderly people aged 65 or over, the prevalence of GAD was 11%, with a quarter of individuals reporting their first episode after age 50. While most cases of symptomatic GAD in the elderly are recurrent, only about a third receive appropriate medical attention including some with comorbid major depression and disabling phobias. The factors most associated with pure GAD are female sex, having cognitive impairment, lower body mass index, low report affective support in childhood, and taking a high number of prescription medications independently of other mental health factors, such as psychotropic medication use, major depression, and phobia. It appears that GAD in later life does not represent the continuing chronic course of early-onset illness but has a clinical presentation distinct from GAD in younger population with age-specific predictors such as metabolic disorders and chronic diseases including adiposity, respiratory disorders, arrhythmia, heart failure, and cognitive impairment. And although anxiety disorders can be triggered by stressful life events, adverse life events including early ones, may predict elderly-onset GAD. One often overlooked biologic vulnerability factor in elderly GAD is dysfunction of the adrenergic and noradrenergic stress systems. Similar abnormalities in those two have been reported in two other stress-related psychiatric disorders, posttraumatic stress disorder and panic disorder.
The mechanism of heightened anxiety is purportedly related to increased plasma levels of norepinephrine after stress, in conjunction with increased signal transduction of adrenaline, noradrenaline and to a lesser extent dopamine. There may also be heightened activity in the hypothalamic-pituitary-adrenal (HPA) axis in others with evidence of neuroendocrine dysfunction or overt brain injury. Effective therapy of GAD combines pharmacologic, psychotherapy, and mindful based meditation. Its favorable impact on increased circulating levels of adrenocorticotropic hormone, proinflammatory cytokine levels, and other stress markers for GAD, providing indirect substantiation of a neuropsychiatric mechanism of GAD in some individuals.