Children whose parents have experienced periods of major depression are several times as likely to suffer from the condition themselves at some point in their lives, and new research supports the belief that this predisposition stems from functional differences in their brains.
The amygdala and nucleus accumbens regulate, respectively, the brain's response and reward systems. When people encounter angry, threatening and otherwise upsetting stimuli, the amygdala activates the often subconscious fight-or-flight response, releasing adrenaline and related hormones that may prompt defensive reactions (facial expressions, protective hand gestures) that also disrupt the normal thought process. The nucleus accumbens processes the dopamine and serotonin neurotransmitters in order to regulate pleasurable stimulation such as that provided by sex, food, drugs and music as well as certain elements of learned fear responses.
These structures function differently in patients with major depressive disorders. When, for example, depressive patients view unpleasant images, their amygdalas respond in more dramatic ways than those of patients who have not experienced clinical depression. This reaction manifests itself in the form of more severe discomfort and negative interpretations of the stimuli in question. Affected patients also interpret encouraging stimuli in less positive ways, failing to be moved by images of happy people or promises of monetary rewards. The study involved 39 children aged 10-19, 17 of whom were defined as high-risk subjects whose parents had experienced some form of major depressive disorder and had spent time at clinics specializing in mood disorders. Researchers collected magnetic resonance images of the subject's brains as they viewed a random series of images of human faces displaying emotions that fell somewhere on the continuum between happiness and exaggerated fear.
Results were very much as researchers expected: in a nearly opposite fashion, high-risk children displayed the greatest degree of activity in both the amygdala and the nucleus accumbens when viewing the most extremely frightened faces, while low-risk children responded enthusiastically to images of joyous, satisfied faces and seemed unphased by the expressions of fear exaggerated to near-comic levels. In a related test, high-risk subjects also proved more impulsive and subject to distraction: in some cases, subjects were asked to denote their degree of fear or describe the width of the depicted face's nose by pressing a corresponding button. While the amygdala activity levels of the low-risk group did not change when performing these tasks, the high-level subjects' brain scans showed a decline in activity. This observation implies that their anxiety over frightened faces was impulsive and subject to rapid change - that their emotional states were less stable than those of their peers. In one sense this result shows promise as it could lead to treatments based on the principle of distracting patients from their negative emotions.
Perhaps the most telling aspect of this study: while a majority of the high-risk subjects had been diagnosed with anxiety disorder, researchers excluded kids who'd already been diagnosed with major depressive disorder or reported the use of any psychotropic drugs. It would seem that the genetic roots of depression are even deeper than we've suspected, and that the brains of those whose lineage leaves them prone to mental illness truly function in different ways. Separate tests conducted among the subjects who had not been diagnosed with any disorder yielded similar results. The study's major limitation was the restriction of pictured emotions to fear and happiness. Additional studies including images of depressed, angry or shameful faces may further clarify and reinforce the findings of this study.
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