Generalised anxiety disorder (GAD) is an anxiety disorder characterized by excessive, uncontrollable and often irrational worry, that is, apprehensive expectation about events or activities.  This excessive worry often interferes with daily functioning, as individuals with GAD typically anticipate disaster, and are overly concerned about everyday matters such as health issues, money, death, family problems, friendship problems, interpersonal relationship problems, or work difficulties.  GAD is the most common cause of disability in the workplace in the United States.
Individuals often exhibit a variety of physical symptoms, including
- numbness in hands and feet
- muscle tension
- muscle aches
- difficulty swallowing
- excessive stomach acid buildup
- stomach pain, vomiting
- bouts of breathing difficulty
- difficulty concentrating
- hot flashes
- rashes, and
- inability to fully control the anxiety
(ICD-10). Especially the last point, the perceived inability and the sense of loss of control often leads into a vicious cycle of anxiety, anxiety begetting yet more anxiety.
Two percent of the adult population experience GAD in Europe and the US in a given year.   Globally about 4% are affected at some point in their life.  GAD is seen in women twice as much as men. GAD is also common in individuals with a history of substance abuse and a family history of the disorder.  Once GAD develops, it may become chronic, but can be managed or eliminated with proper treatment.
Where does it come from?
In most psychiatric conditions three factors are implicated, especially so in GAD:
- biology (e.g. genes)
- psychology (e.g. one’s experiences and strategies to deal with stressors)
- social environment
About a third of the variance for generalized anxiety disorder has been attributed to genes. Individuals with a genetic predisposition for GAD are more likely to develop GAD, especially in response to a life stressor. 
Antidpressants, especially the serotonin reuptaker inhibitors (SSRIs), are on the medication side the first line of treatment. Benzodiazepines, such as Alprazolam (Xanax®), can be of help in the short-run. However, long-term use of benzodiazepines can worsen underlying anxiety, with evidence that reduction of benzodiazepines can lead to a lessening of anxiety symptoms.  Similarly, long-term alcohol use is associated with anxiety disorders,  with evidence that prolonged abstinence can result in a disappearance of anxiety symptoms. Still, it can take up to two years for anxiety symptoms to return to baseline in about a quarter of people recovering from alcoholism. Sometimes anxiety pre-exists alcohol or benzodiazepine dependence, but the dependence acts to keep the anxiety disorders going and often progressively making them worse.
Tobacco smoking has also been established as a risk factor for developing anxiety disorders, as has excessive caffeine usage has been linked to anxiety. 
Generalized anxiety disorder has been linked to disrupted functional connectivity of the amygdala and its processing of fear and anxiety.  Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal and accessory basal nuclei). The basolateral complex processes the sensory-related fear memories and communicates their threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices. Another area, the adjacent central nucleus of the amygdala, controls species-specific fear responses in its connections to the brainstem, hypothalamus and cerebellum areas. In those with generalized anxiety disorder, these connections seem less functionally distinct, and there is greater gray matter in the central nucleus. Another difference is that the amygdala areas have decreased connectivity with the insula and cingulate areas that control general stimulus salience, while having greater connectivity with the parietal cortex and prefrontal cortex circuits that underlie executive functions. The latter suggests a compensation strategy for dysfunctional amygdala processing of anxiety. This is consistent with cognitive theories that suggest the use in this disorder of attempts to reduce the involvement of emotions with compensatory cognitive strategies.
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