What Causes Generalized Anxiety Disorder? The exact causes of Generalized Anxiety Disorder (GAD) are not fully understood, but research suggests there may be several factors which contribute to its development. It’s complex and difficult to pinpoint exactly what would push one person into having GAD and not another, but several areas have been identified as relevant, particularly studies of the brain which show how people process emotion.
It’s been shown that genetics and family history play a part with 40% of people with GAD also having close relatives with the disorder. But it’s also the case that there is some element of anxiety being ‘learned’ from growing up with anxious role models and unconsciously internalizing their responses and behavior.
Environmental factors and circumstances may also lead to GAD, such as trauma, divorce, bereavement and personal or family illness. Studies also suggest that caffeine, drugs, alcohol and nicotine can cause symptoms of anxiety and make existing anxiety worse. There’s a host of other influences in everyday life which can contribute too, such as pollution and diet.
There are theories that GAD results from an imbalance in brain chemistry and abnormal functioning in nerve cell pathways. The brain areas which deal with thought and emotion rely on chemicals called neurotransmitters to send information across the nerve cells and if these pathways are disrupted, problems with mood and anxiety can result. Some of the chemicals highlighted in anxiety disorders are gamma-aminobutyric acid (GABA), serotonin, dopamine, and epinephrine. Of these, serotonin has been proven to be particularly important in creating feelings of well-being; a reduction of it is linked to anxiety. Imbalances of stress hormones such as cortisol also play a role in whether a person will develop GAD.
Research using brain magnetic resonance imaging technology (MRI) and neuro-chemical techniques has highlighted that the amygdala plays distinct roles in most anxiety disorders, not just GAD. The amygdala is an almond-shaped structure deep inside the brain and is thought to be a ‘communications hub’, processing incoming information and sensory signals before alerting the rest of the brain to a perceived threat and triggering a fear or anxiety response. If a fear threat is picked up, the amygdala coordinates this with bodily functions and alters heart-rate, blood pressure and physical responses, which is why anxiety produces such unpleasant symptoms. It’s thought that in people with GAD, the amygdala has become highly sensitive and thus it reacts with a high-stress response.
This relationship between brain circuitry, the amygdala and anxiety was investigated in a study by Stanford University School of Medicine in 2010 and revealed conclusively that people with GAD have abnormalities in the way their brain unconsciously controls emotions.
First author of the study, Amit Etkin, MD, PHD reported on clinical findings which suggested that adult GAD patients initially register negative stimuli in a normal way but then have difficulty in how they control negative feelings afterward. The study involved twenty-four healthy participants and seventeen with Generalized Anxiety Disorder who were all given the same task to view pictures of people looking happy or fearful with the words ‘happy’ and ‘fear’ written on the images. Subjects then had to use a button box to identify the expression on each face. The images and words did not always match; some happy faces had the word ‘fear’ written on and vice versa which created a conflict and confusion of emotion in participants.
Findings showed that both the GAD and healthy participants were able to identify the expressions, but healthy participants were able to react more quickly to expressions and words that didn’t match if the previous image was also incongruent. This showed that some emotion regulation processes were activated and that people were adapting to the conflicting messages on the screen. However, in the GAD subjects, there was no reaction time effect and in the most anxious people, the reaction time worsened when there were two incongruent images in a row. The MRI scans also showed that in the healthy participants faced with conflicting images and words, a section of the brain called the pregenual anterior cingulate ‘lit up’ and inhibited the amygdala from reacting with the stress response. In the GAD patients, this didn’t happen, proving that there was a definite disruption to the brain’s circuitry.
These findings bode well for improvements in diagnosis and treatment of Generalized Anxiety Disorder. It’s possible that medications and therapy can now be better used in future to specifically target the fear response in the brain.
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