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James Brody
April 5th, 2006, 03:51 PM
from Journal Watch: Psychiatry. http://psychiatry.jwatch.org/

Genes vs. environment: a distinction given us by the great Frank Galton. Modern evaders point out the uselessness of genes without environments and compare development to a rectangle that needs both length and width.

The analogy fails however.

One assumption, passing into the night, was that genes could not be changed and, therefore, environments were our effective tool. Environmental determinism dominated academia. (Neat way to justify teaching jobs! If equal outcomes do not appear, then we need more teachers. Einstein had not yet told us clearly the futility of continuing to do more of whatever doesn't work. And Feynman's astute observation, that education best succeeds when it increases variability of outcomes, had not been made.)

Subsidiary assumption: we are all alike genetically in the things that count. Clearly no longer tenable despite its early endorsement by EP leaders Cosmides & Tooby.

Popular belief trails applications, not faiths. As humans gain skill with genes, the popular acceptance of those methods grows, particularly in the biomedical fields. Eugenics is very much the cement of so many human interactions, even when concealed under the banner of "sexual selection."

Meanwhile, I've copied Dr. Silver's review because it's pass-worded at the source.

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Poststroke Depression: It's Not Just the Brain, It's the Genes

Studies have demonstrated the relation among stroke, lesion location, and the development of major depression. An unrelated line of research has revealed an association between a functional polymorphism on the promoter region linked to the serotonin transporter gene (5-HTTLPR) and the susceptibility to depression, especially in the presence of severe life stress. Now, researchers examine the relation between stroke and the 5-HTTLPR polymorphism. The investigators performed genotyping, conducted semistructured psychiatric interviews, and obtained family histories of mood disorders.

Subjects were 26 stroke patients with mood disorders and 25 nondepressed stroke patients (mean age in both groups, 60). Patients were excluded if they had severe cognitive problems, or if depression was present before the stroke and continued afterwards. The presence of at least one short allele was significantly associated with poststroke depression. In addition, the depressed group had significantly higher rates of personal major depression and/or anxiety disorder, as well as of family histories of major depression and/or bipolar disorder. In a regression analysis, genotype did not influence the effect of personal or family history on the presence of depression.

Comment: The 5-HTTLPR genotype might affect vulnerability to depression by directly influencing serotonin function or by increasing vulnerability to stress (see Journal Watch Psychiatry Jan 12 2005). It would be useful to study whether lesion location and this polymorphism interact to increase vulnerability to depression.

Jonathan Silver, MD

Published in Journal Watch Psychiatry April 5, 2006

Source
Ramasubbu R et al. Serotonin transporter gene promoter region polymorphism associated with poststroke major depression. J Neuropsychiatry Clin Neurosci 2006; 18:96-9.