Here's the abstract of the Caspi study I mentioned, published in Science in 2003:
In a prospective-longitudinal study of a representative birth cohort, we tested why stressful experiences lead to depression in some people but not in others. A functional polymorphism in the promoter region of the serotonin transporter (5-HTT) gene was found to moderate the influence of stressful life events on depression. Individuals with one or two copies of the short allele of the 5-HTT promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by his or her genetic makeup. Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Caspi, Avshalom; Sugden, Karen; Moffitt, Terrie E.; Taylor, Alan; Craig, Ian W.; Harrington, HonaLee; McClay, Joseph1; Mill, Jonathan1; Martin, Judy3; Braithwaite, Antony4; Poulton, Richie3 Science. Vol 301(5631), Jul 2003, pp. 386-389 ________________________________________ From: [EMAIL PROTECTED] [EMAIL PROTECTED] Sent: Tuesday, March 25, 2008 10:03 AM To: Teaching in the Psychological Sciences (TIPS) Subject: Re:[tips] The Gene Illusion I said: >> >I wonder if Mike could favour us with a high-quality research study or > >two published in a peer-reviewed journal which provides evidence of such > >gene-environment interactions. Surely his belief must be based on > >evidence. Mike Palij obligingly replied: > The classic study that answers Stephens request is the discovery of > phenylketonuria or PKU, the genetic defect that prevents the metabolism > of phenylalanine and leads to development of mental retardation. Ah, yes, excellent example. How could I have forgotten that one, which is indeed a classic. But it is a specialized choice and far from our current discussion of social and genetic factors in the development of children into adults. The defective gene impairs a biochemical pathway. Consequently phenylalanine, which is an abundant component of everyone's diet, becomes harmful. It is extraordinarily difficult to provide a diet which is free of this substance, and only a severely abnormal and artificial one will do. Kids hate it so much that it becomes a major challenge to keep them on it. By analogy, I would concede that a social environment as abnormal as a severely-phenylalanine-low diet is could have lasting effects, and you wouldn't even have to specify a particular genotype. But to do it, you might have to raise the kid with wolves. How about a particular genotype and a particular type of environment which kids might be exposed to which is not artificially constructed and imposed, as the low-phenylalanine diet is. If we have to reach back to the PKU diet developed in the 1950's for an example, what does this tell us about how many more relevant gene-social environment examples have been identified since then? Stephen ----------------------------------------------------------------- Stephen L. Black, Ph.D. Professor of Psychology, Emeritus Bishop's University e-mail: [EMAIL PROTECTED] 2600 College St. Sherbrooke QC J1M 1Z7 Canada Subscribe to discussion list (TIPS) for the teaching of psychology at http://flightline.highline.edu/sfrantz/tips/ ----------------------------------------------------------------------- --- To make changes to your subscription contact: Bill Southerly ([EMAIL PROTECTED]) --- To make changes to your subscription contact: Bill Southerly ([EMAIL PROTECTED])
