Schaffner, Kenneth F (2006). “Behavior: Its Nature and Nurture, Part 1” in Parens, Eric, Chapman, Audrey R, and Press, Nancy (eds.) Wrestling with Behavioral Genetics. Baltimore: Johns Hopkins University Press, 3-39.
Schaffner attempts to provide an overview of various concepts of behavioral causation with an emphasis on explaining the genetic component. The following are thoughts and questions that may help piece together the puzzle to ultimately form a thesis concerning ethical issues of genetic screening for complex behavioral traits. This is more like free association but its purpose is to get thoughts out. How does moral relativism play into our discussion? Schaffner speaks to genetic and environmental causation but how do psychological factors play into the equation? What about behavior as a phenomenological factor rather than a trait? By calling behavior a trait, are we not presupposing a form of reductionism to genetics? In more touchy-feely language, am I not more than what my genetics, environment, and a G x E interaction dictate? We need to check out Rawls? He is used as an argument for genetic enhancement and intervention. Hat is the effect of environment on evolution? What about environmental heritability? How will w divide up quantitative versus molecular approaches to behavioral genetics? Schizophrenia too genetic to study? Depression too environmental? We may want to stick with ASPD due to the link to criminality. We may also want to explore thresholds of risk to help draw the line if we are not going to reject any intervention or enhancement?
In the first dialogue, Schaffner appeals to Lewontin on red blood cell phosphatase activity to explain environmental and genetic variation. He mentions on pp. 13 a study in which all phenotypic variation is due to environmental factors. What about Stotz’s claim that the gene also acts as an environment, i.e., what is the effect of the rest of the genome on the trait? Have Jim show you the math concerning the heritability of having a brain being zero (pp. 16). We need to explore problems with the equal environment assumption if we are to argue against the benefit of genetic testing o n ASPD. What is the best argument for behavior being genetically linked (broad)? The problem with the fearful mice experiment is that what if a mouse ate some bad cheese and had diarrhea? Would it be classified as fearful? How to distinguish?
Rowe and Jacobson (1999) developed criteria for factors deemed shared environmental effect
1. Near universals in culture do not count.
2. Environmental exposure must be common to all siblings.
3. The environmental exposure must have directional effect on the trait in question.
4. The environmental exposure must change the trait in a constant direction in order for it to be shared.
Problem with (1) if environment does have an effect on gene frequency. Problem with (2) is that how do you define common experience? Problem with (3, 4) is how do you tease out other effects (both genetic and environmental)? Even Schaffner realizes this difficulty since he places this idea as a “term of art”. He seems to agree with the “gloomy prospect” of possibly never being able to tease out environmental effects in the narrow, non-shared sense. Has anyone looked at DNA from 100 years ago compared to now? If there is a significant difference (problems with qualifying significance) would that not point to environmental inheritance or would it be argued as genetic? Problems with models. What the simplest and most complex model for behavioral genetics?
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