In our last installment, we discussed a familiar finding from the National Comorbidity Survey Replication (NCS-R): the peak age of onset for any mental health disorder is about 14 years. In an attempt to explain these data, we are exploring some of the known developmental changes in the teenaged brain at the level of gene, cell, and behavior.
We discussed in the last column a number of issues, ranging from alterations in gray matter volume to changes in adolescent executive function. Does a more complete understanding of these maturational processes provide enough hints to explain the NCS-R data?
Here we will attempt to answer this question. Three psychopathologies will be examined: affective disorders, anxiety disorders, and risk-taking activities-behaviors that may underlie substance abuse issues. As we go through some fairly recent findings, there may be an intellectual temptation to explain the NCS-R findings in terms of mutational (genetic) alterations inside otherwise normally functioning adolescent-related developmental processes.
As we will discover, demonstrating that this is indeed the biological basis for their numbers has proved to be surprisingly elusive. The relationship between the onset of psychiatric disorders and the typical changes seen in the developing brain of adolescents is complex, indirect, and not well understood. There is some evidence that certain disorders exist because of an exaggeration of otherwise typically functioning processes. But these are only hints. We are only in the beginning stages of our understanding of the relationship between adolescence and mental health. To date, no genetic anomalies have been shown to be responsible for the peak onset findings revealed by NCS-R in any mental health–related disorder.
ANXIETY AND DEPRESSION
Major depression is a serious and commonly experienced fact of life for many adolescents. Puzzling to some researchers, the adolescent-onset form often carries the most severe, most disabling symptoms of any form of human depression. Anxiety-related symptoms often precede the disorder, acting like a harbinger, and often first presenting in childhood.
Are there any cellular or even molecular explanations for these data? Unruly and wildly fluctuating hormonal changes are usually invoked to account for some of the risk associated with the adolescent-related affective disorders. That invocation may be well founded, with some of the strongest data coming from epidemiological investigations.
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