Studies of twins and families suggest that genes play a role in the origin of anxiety disorders. But heredity alone can't explain what goes awry. Experience also plays a part. In Post Traumatic Stress Disorder (PTSD), for example, trauma triggers the anxiety disorder; but genetic factors may explain why only certain individuals exposed to similar traumatic events develop full-blown PTSD. Researchers are attempting to learn how genetics and experience interact in each of the anxiety disorders—information they hope will yield clues to prevention and treatment.

Several parts of the brain are key actors in a highly dynamic interplay that gives rise to fear and anxiety. Much research centers on the amygdala, an almond-shaped structure deep within the brain. The amygdala is believed to serve as a communications hub between the parts of the brain that process incoming sensory signals and the parts that interpret them. It can signal that a threat is present, and trigger a fear response or anxiety. It appears that emotional memories stored in the central part of the amygdala may play a role in disorders involving very distinct fears, like phobias, while different parts may be involved in other forms of anxiety.

Other research focuses on the hippocampus, another brain structure that is responsible for processing threatening or traumatic stimuli. The hippocampus plays a key role in the brain by helping to encode information into memories. Studies have shown that the hippocampus appears to be smaller in people who have undergone severe stress because of child abuse or military combat. This reduced size could help explain why individuals with PTSD have flashbacks, deficits in explicit memory, and fragmented memory for details of the traumatic event.

Also, research indicates that other brain parts called the basal ganglia and striatum are involved in obsessive-compulsive disorder.

By learning more about brain circuitry involved in fear and anxiety, scientists may be able to devise new and more specific treatments for anxiety disorders. For example, it someday may be possible to increase the influence of the thinking parts of the brain on the amygdala, thus placing the fear and anxiety response under conscious control. In addition, with new findings about neurogenesis (birth of new brain cells) throughout life, perhaps a method will be found to stimulate growth of new neurons in the hippocampus in people with PTSD.

How individuals respond to their environment and how the environment responds to them is a very important part of human behavior. Studies are researching the impact of stress, life changes, social factors and other influences on the development of anxiety disorders. The jury is still out, but one thing is certain, the answer requires much study and will take time. The good news is that science has developed many successful treatments for these illnesses.

Causes of Depression
Substantial evidence from neuroscience, genetics, and clinical investigation shows that depressive illnesses are disorders of the brain. However, the precise causes of these illnesses continue to be a matter of intense research.

Modern brain-imaging technologies are revealing that in depression, neural circuits responsible for the regulation of moods, thinking, sleep, appetite, and behavior fail to function properly, and that critical neurotransmitters-chemicals used by nerve cells to communicate-are out of balance. Genetics research indicates that risk for depression results from the influence of multiple genes acting together with environmental or other nongenetic factors. Studies of brain chemistry and the mechanisms of action of antidepressant medications continue to inform our understanding of the biochemical processes involved in depression.

Very often, a combination of genetic, cognitive, and environmental factors is involved in the onset of a depressive disorder. Trauma, loss of a loved one, a difficult relationship, a financial problem, or any stressful change in life patterns, whether the change is unwelcome or desired, can trigger a depressive episode in vulnerable individuals. Later episodes of depression may occur without an obvious cause.