Heritability, heterogeneity, and group differences
Idea: As conventionally interpreted, heritability indicates the fraction of variation in a trait associated with "genetic differences." A high value indicates a strong genetic contribution to the trait and "makes the trait a potentially worthwhile candidate for molecular research" that might identify the specific genetic factors involved. I contest the conventional interpretation and contend that there is nothing reliable that anyone can do on the basis of estimates of heritability for human traits. While some have moved their focus to cases in which measurable genetic and environmental factors are involved, others see the need to bring genetics into the explanation of differences among the averages for groups, especially racial groups.
Common readings = Taylor 2013a (skepticism about the estimation and interpretation of heritability used to push back at Davey-Smith's (2011) account of the "gloomy prospect" for social epidemiology); Moffitt 2005 (Interaction of measured genes and measured environments)
There are many supplementary readings. Get the overall idea, concepts, and evidence first for these articles, going back to go through the equations only if you have time and aptitude/perseverance.
a. Heritability & critique
Heritability is a quantity derived from analysis of variation in traits of humans, other animals, or plants in ways that take account of the genealogical relatedness of the individuals whose traits are observed. Such "quantitative genetic" analysis does not require any knowledge of the genes or "measurable genetic factors" involved.
Turkheimer is "on the left" of behavioral genetics, being much less gung ho about the implications of its findings. Here he gives a clear overview of what the field has shown.
Plomin articulates the confident consensus of behavior genetics, namely, that they've debunked the supposed environmentalist orthodoxy in social science that says that everything is social and have established a basis for connecting with molecular genetics to identify the actual genetic factors.
Rutter, a senior psychological researcher (who once worked with Brown on social determinants of mental illness), tries to moderate the "polarizing claims" and "unwarranted extrapolations."
Taylor 2013 casts doubt on the findings that underlie both Turkheimer and Plomin's articles by exposing problems with the concepts and methods used to arrive at those findings. Taylor (2010) ends with a nudge towards methods that use measured genetic factors as well as measured environmental factors (the latter being the staple of social epidemiology). Taylor (2013a) uses the same line of critique to push back at Davey-Smith's (2011) account (from session 8) of the "gloomy prospect" for social epidemiology.
b. Interaction of measured genes and measured environments
Moffitt 2005 provides a review of what's involved in trying to identify interactions between measured genetic and environmental factors. (Use Taylor 2010 to get clear about the difference between this kind of interaction and the classical genotype x environment interaction in quantitative genetics.) Caspi 2002 is one of two 2002 papers that caused a lot of splash. Young 2006 describes failure to replicate the findings. Davey-Smith 2009 picks up on the current consensus that the 2002 studies have been hard to replicate and invokes Mendelian randomization as a way to strengthen causal inference about interactions between measured genetic and environmental factors. Rosenquist et al. report a "significant gene-by-birth-cohort interaction, which adds a previously unidentified dimension to gene-by-environment interaction research."
c. Data & models about heritability & change (or lack of it)
Dickens 2001 provides a resolution of the paradox that heritability of IQ test scores is reported to be high, but there has been a large increase in average IQ test scores from one generation to the next. We know that genes haven't changed from one generation to the next, so Dickens' account is also exposing a flaw in the logic that because heritability of IQ test scores is high within racially defined groups and because there is a large difference in average IQ test scores between whites and blacks, genetic factors are probably involved in that difference.
Rushton 2005 however thinks that 30 years of research has validated that idea.
Taylor 2010 refers to Dickens 2001, but gives a somewhat different spin on its implications.
Notes and annotations from 2007 course
Common readings and cases: Moffitt 2005 (Interaction of measured genes and measured environments), Taylor 2010 (skepticism about the estimation and interpretation of heritability)
Supplementary Reading: Caspi 2002, Davey-Smith 2009, Dickens 2001, Plomin 2006, Rushton 2005, Rutter 2002, Turkheimer 2000
- Caspi, A., J. McClay, et al. (2002). "Role of Genotype in the Cycle of Violence in Maltreated Children." Science 297(5582): 851-854.
- Davey-Smith, G. (2009). "Mendelian randomization for strengthening causal inference in observational studies: Application to gene by environment interaction." Perspectives on Psychological Science, in press.
- Davies, G., A. Tenesa, et al. (2011). "Genome-wide association studies establish that human intelligence is highly heritable and polygenic." Molecular Psychiatry: 1-10.
- Dickens, W. T. and J. R. Flynn (2001). "Heritability estimates versus large environmental effects: The IQ paradox resolved." Psychological Review 108(2): 346-369.
- Moffitt, T. E., A. Caspi, et al. (2005). "Strategy for investigating interactions between measured genes and measured environments." Archives of General Psychiatry 62(5): 473-481.
- Plomin, R. and K. Asbury (2006). "Nature and Nurture: Genetic and Environmental Influences on Behavior." The Annals of the American Academy of Political and Social Science 600(1): 86-98.
- Rosenquist, J. N., S. F. Lehrer, et al. (2014). "Cohort of birth modifies the association between FTO genotype and BMI." PNAS.
- Rushton, J. P. and A. R. Jensen (2005). "Thirty years of research on race differences in cognitive ability." Psychology, Public Policy, and Law 11: 235-294.
- Rutter, M. (2002). "Nature, nurture, and development: From evangelism through science toward policy and practice." Child Development 73(1): 1-21.
- Taylor, P. J. (2010). "Three puzzles and eight gaps: What heritability studies and critical commentaries have not paid enough attention to." Biology & Philosophy, 25:1-31. (DOI 10.1007/s10539-009-9174-x).
- Taylor, P. J. (2013a). "Heterogeneity, not randomness, sets challenges for quantitative genetics and epidemiology: A response to Davey Smith's "gloomy prospect." Ms.
- Taylor, P. J. (2013). "Five Fundamental Gaps In Nature-Nurture Science." Ms.
- Turkheimer, E. (2000). "Three laws of behavior genetics and what they mean." Current Directions in Psychological Science 9(5): 160-164.
- Young, S. E., A. Smolen, et al. (2006). "Interaction between MAO-A genotype and maltreatment in the risk for conduct disorder: failure to confirm in adolescent patients." The American Journal of Psychiatry 163(6): 1019-1025.
Annotations on common readings
Annotated additions by students
(In alphabetical order by author's name with contributor's initials and date at the end.)
ROBERT PLOMIN and KATHRYN ASBURY. Nature and Nurture: Genetic and Environmental Influences on Behavior. ANNALS, AAPSS, 600, July 2005
“The appropriate conjunction between the words nature and nurture is not versus but and (Plomin et al.)”. Plomin and Asbury argue that genetics, environment, and the interplay between them influences development of individual differences in behaviors, and thus characterizes mental health status and cognitive abilities. Previous research have evinced that genetics and environment each account for roughly half of the variance responsible for behavioral traits. Plomin and Asbury cites twin and adoption studies on schizophrenia as providing overwhelming evidence for genetic transmission of a behavioral disposition; espousing the existence of a 45% schizophrenic concordance rate among monozygotic (mz) twin pairs, which dwarfs a 17% schizophrenic concordance rate among dizygotic twins pairs. It is posited that the discordance in schizophrenia among pairs of genetic clones (mz twins) is wholly mediated by environmental factors.
In this article, it is noted that one important manifestation of genetic research has been the conceptualization of the nature of nurture (the reality and implication of nonshared environment). Plomin and Asbury contend that environmental research, employing genetically sensitive designs, have consistently found environments that affect behavioral development culpable for producing differences among children in the same family; defying conventional theories of socialization. Sibling similarities are proposed to be strongly rooted in their genes rather than their shared environment. “Environments can be considered as extended phenotypes, reflecting genetic differences between individuals as they select, modify, and construct their own experience of the world (Plomin et al.),” through a process termed genotype-environment correlation. Plomin and Asbury assert the aforementioned as being the reason why environmental measures cannot be assumed to be un-confounded. The authors support a paradigmatic shift, disbanding passive models of how the environment affects individuals in favor of models that recognize the active role we play in constructing our personal milieu. The difficulty of identifying nonshared environmental factors that account for large amounts of variance is conceded. Plomin and Asbury surmise that happenstance (featuring random noise, idiosyncratic experiences etc.) contributes to nonshared environment. Furthermore, over the life course small differences in experience might lead to large differences in outcome.
The authors’ assertion is that most life scientists are concerned with generalities of the genome, but medical and behavioral scientists are more interested in variations in the genome that are responsible for hereditary differences (as they possess a unique causal status in explaining illness and behavior). Plomin and Asbury aver that ignoring individuality (due in part to fears of evoking sentiments of unequal humanity) renders the utopian ideal of optimizing the development of each person (through individual-level interventions) less feasible.
Plomin and Asbury predict that behavioral genomics will have an impact on many institutions in society (altering their philosophy and organizational structure). Etiological diagnoses, individualized treatment programs, and early prediction of problems (allowing for potential preventative interventions) are noted as being future ramifications of this field. (SY)