Article

Heritability Studies in the Postgenomic Era: The 'Fatal Flaw' is Conceptual

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Abstract

In our recent paper “Pulling Back the Curtain on Heritability Studies: Biosocial Criminology in the Postgenomic Era,” we scrutinized heritability studies in criminology (Burt & Simons 2014). Drawing on recent advances in the life sciences, and echoing the calls of prominent scholars, we called for an end to heritability studies in criminology and recognition of the dubious nature of existing heritability estimates. We argued that heritability studies are futile for two reasons: (1) heritability studies suffer from serious methodological flaws with the overall effect of making estimates inaccurate and biased toward inflated heritability and deflated shared environmental influences, and, more importantly, (2) the conceptual biological model on which heritability studies depend—that of identifiably separate effects of genes vs. the environment on phenotype variance—is unsound. As we discussed, profound scientific advances over the past decade, most clearly manifest in epigenetics, demonstrate that genes and environments are enmeshed in a bidirectional, interactional relationship that defies any attempt to demarcate separate contributions to phenotype variance. Thus, heritability studies attempt the impossible. In this short rejoinder , we address Barnes et al. ’ s response to our piece. We attempt to clarify our arguments and correct misinterpretations or misunderstandings, including the misguided idea that the unsound (conceptual) biological model can be mitigated or refuted with statistics or algebra, and conclude by reiterating that biosocial criminology needs to move beyond heritability studies and the outdated, false gene-centric conceptual framework.

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... For example, in their study of five anxietyrelated traits (after a GWAS finding of "no common genetic variants of large effects that contribute to the heritability of these traits"), Trzaskowski and colleagues (2013) reported an average GCTA heritability estimate of 10%, which they noted is less than one fifth of the average twin-study heritability estimate of 55%. Similarly, comparing GCTA and twin study estimates, Trzaskowski, Dale, and Plomin (2013: 1048) concluded: "Behavioral problems in childhood [which included health-related phenotypes such as depression]-whether rated by parents, teachers, or children themselves-show no significant genetic influence using GCTA, even though twin study estimates of heritability are substantial in the same sample…" Thus, GCTA studies provide further evidence that something is awry in the high behavioral genetic heritability estimates of adverse health phenotypes (Burt & Simons 2015). ...
... Indeed, the more we learn about development, the less meaningful seems any attempt to estimate genetic (vs. environmental) contributions to phenotype variance-and the less important (Burt & Simons 2015). ...
... Heritability studies and estimates of adverse health outcomes have gained a lot of traction and attention in recent years based in part on the belief that they are undergirded by rigorous, state-of-the art science. 19 There is value in showing how this work does not measure up to that billing both methodologically and theoretically (Burt & Simons 2015). Although I, among others, find fault in the heritability model, I hope that those who read this critique take it in the spirit of constructive criticism in which it was offered. ...
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Purpose: Heritability studies attempt to estimate the contribution of genes (vs. environments) to variation in phenotypes (or outcomes of interest) in a given population at a given time. The current chapter scrutinizes heritability studies of adverse health phenotypes, emphasizing flaws that have become more glaring in light of recent advances in the life sciences and manifest most visibly in epigenetics. Design/methodology/approach: Drawing on a diverse body of research and critical scholarship, this chapter examines the veracity of methodological and conceptual assumptions of heritability studies. Findings: The chapter argues that heritability studies are futile for two reasons: (1) heritability studies suffer from serious methodological flaws with the overall effect of making estimates inaccurate and likely biased toward inflated heritability, and, more importantly, (2) the conceptual (biological) model on which heritability studies depend—that of identifiably separate effects of genes vs. the environment on phenotype variance—is unsound. As discussed, contemporary bioscientific work indicates that genes and environments are enmeshed in a complex (bidirectional, interactional), dynamic relationship that defies any attempt to demarcate separate contributions to phenotype variance. Thus, heritability studies attempt the biologically impossible. The emerging research on the importance of microbiota is also discussed, including how the commensal relationship between microbial and human cells further stymies heritability studies. Originality/value: Understandably, few sociologists have the time or interest to be informed about the methodological and theoretical underpinnings of heritability studies or to keep pace with the incredible advances in genetics and epigenetics over the past several years. The present study aims to provide interested scholars with information about heritability and heritability estimates of adverse health outcomes in light of recent advances in the biosciences.
... Behavioral genetics shares with many other scientific disciplines the goal of learning about the various factors that shape human beings and about what such knowledge implies for the possibility of positive change. However, the particular way in which behavioral genetics has traditionally raised and answered those questions is the subject of continuing controversy (Barnes et al., 2014;Burt & Simons, 2014;Burt & Simons, 2015;Moffitt & Beckely, 2015;Wright et al., 2017). ...
... A more fundamental charge is sometimes leveled at variance partitioning in the context of developmental causes, a charge that has been considered by a number of critics to be the fatal flaw of behavioral genetics (Burt & Simons, 2014;Burt & Simons, 2015;Moore, 2003). This "interactionist challenge" states that the development of organismic traits is a process of interacting causes that are inextricably entangled, such that their individual causal contributions cannot be separated, let alone quantified. ...
... For example, in their recent challenge to behavioral genetics, Burt and Simons (Burt & Simons, 2015) put the case as follows: ...
Preprint
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Two markedly different concepts of heritability co-exist in the social and life sciences. Behavioral genetics has popularized a highly technical, quantitative concept: heritability as the proportion of genetic variance relative to the total phenotypic variance of a trait in a population. At the same time, a more common biological notion simply refers to the transmission of phenotypic traits across generations via the transmission of genes. It is argued here that the behavioral-genetic concept is of little use overall, while the common biological concept is overly narrow and implies a false view of the significance of genes in development. By appropriately expanding heritability into a general causal concept based on its role in evolution, we will arrive at a new view of development, heritability, and evolution that recognizes the importance of non-genetic inheritance and the causal parity of all determinants of phenotypic traits.
... In addition, as we noted in our comments on the original article by Burt and Simons (2014), they misquoted and mischaracterized scholars, a trend that they continue in their rejoinder (Burt and Simons, 2015). A simple example occurs in the first sentence of their rejoinder, where they allege that they follow in the footsteps of "renowned behavioral geneticists (e.g., Rutter, 1997;Turkheimer, 2011a)" and call for an end to heritability studies. ...
... Unfortunately, our mathematical proofs had no discernable effect on the opinions of Burt and Simons. They reacted (Burt and Simons, 2015) by accusing us of "wrangling over the methodological assumptions and statistical minutiae of the twin-study model," which they said "is a waste of scientific energy and attention". Regarding the validity of the EEA, one of the core criticisms leveled against twin studies in their original article (2014), Burt and Simons concluded in the online supplement to their rejoinder (2015) that we are going to have to "agree to disagree." ...
... Having moved away from their earlier mathematical assertions, Burt and Simons (2015) now pivot to the position that the "fatal flaw" in heritability studies is conceptual, not mathematical (the subtitle of their rejoinder is "The Fatal Flaw Is Conceptual"). They even chastised us for interpreting the "crux" of their case as being methodological when it was really conceptual. ...
Article
KEYWORDS: biosocial, assumptions, twinsIn their initial article, Burt and Simons (2014) laid out a range of specific criticismsof twin-based research. They argued that violations of the statistical assumptions thatunderpin this line of work result in upwardly biased estimates of heritability and down-wardlybiasedestimatesofenvironmentaleffects.AccordingtoBurtandSimons,thefind-ingsgeneratedfrombehavioralgeneticapproachesare“biologicallynonsensical”andare“misguided.” Indeed, Burt and Simons stated, without qualification, that an entire classof statistical models used to analyze twin data are “seriously flawed.” Because behavioralgenetic designs suffer from “fatal flaws,” they argued, twin-based research designs andtheir associated statistical methods should be put to an “end in criminology.”We examined their assertions carefully. We found that Burt and Simons (2014) cherry-picked the studies they cited in support of their position regarding the biasing impact ofthe equal environments assumption (EEA), something they openly admit in the onlinesupporting information of their rejoinder (Burt and Simons, 2015, this issue). Specifically,theystate,“wefocusedonarticlesthatshowedthattheEEAisnotavalidassumption”tosupport their claim that heritability estimates from behavioral genetic studies are chron-ically overestimated as a result of violations of this assumption. In fact, they relied pri-marily on a single source (Joseph, 1998, 2004, 2006, 2010) for their critique. Notably, wefound that they failed to cite the vast majority of the more than 60 studies that tested forviolations of the EEA—a body of work that is inconsistent with their claims.
... However, the particular way behavioral genetics has traditionally raised and answered those questions has been the subject of continuing controversy. Indeed, the pages of Criminology have hosted one of the latest instalments of this debate (Barnes et al. 2014;Burt & Simons 2014;Burt & Simons 2015;Moffitt & Beckely 2015;Wright et al. 2017), and we believe it is fair to say that it did not end in mutual understanding. ...
... Fortunately, to follow these considerations requires neither very specific nor particularly modern knowledge of biology (contrary to some recent critiques of behavioral genetics that stress the importance of molecular biological knowledge such as epigenetics [e.g. Burt & Simons 2015;Charney et al. 2012]). They all follow from basic insights that were available, in principle, to scholars for at least a century. ...
... A more fundamental charge is sometimes leveled at variance partitioning in the context of developmental causes, one that has been considered by a number of critics to be the final nail in the coffin of behavioral genetics (Burt & Simons 2014;Burt & Simons 2015;Moore 2003). This "interactionist challenge" states that the development of organismic traits is a process of interacting causes that are inextricably entangled, such that their individual causal contributions cannot be separated, let alone quantified. ...
Preprint
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The concept of heritability in behavioral genetics is different from the more standard concept used in biology. The former is a statistical measure of the proportion of genetic variance relative to the total phenotypic variance of a trait in a population, the latter refers to the transmission of phenotypic traits across generations via the transmission of an underlying causal substrate (genes). It will be argued that the behavioral-genetic concept is a generally useless quantity, while the standard biological concept is overly narrow and implies a false picture of the significance of genes in development. By suitably expanding standard heritability into a general causal concept based on its role in evolution, we will arrive at a general view of development that recognizes the causal parity of all determinants of phenotypic traits and shows why the behavioral genetic dichotomy of genes vs environment is fundamentally misguided. Some implications for criminology and the social sciences will be addressed.
... Heritability studies suggest a genetic predisposition to antisocial behaviour and to callous/unemotional traits (Berg et al., 2013), although the notion of heritability is suspect (Burt & Simons, 2015;Vreeke, 2000), and how any predisposition translates into psychopathic personality characteristics is unknown (Berg et al., 2013;Glenn & Raine, 2014). We can entertain the possibility that Philby had a genetic predisposition, given descriptions of his father, although any such precursor cannot be disentangled from their interpersonal relationship. ...
Chapter
Henri Nouwen (1932-1996) was a charismatic Roman Catholic priest, psychologist, academic, public speaker, and spiritual guide. He was one of the most prolific and influential spiritual writers of the previous century. Although he died more than 25 years ago, increasing numbers of followers continue to seek guidance through his literary legacy. There is a wealth of biographical sources that invite research into Nouwen’s life. Despite his success and exceptional talents, the data suggests that his personality, life and career were complex and troubled. Colleagues described him as temperamental, anxious, obsessive, needy, and self-centered. Nouwen was transparent about his shortcomings and strived to live his spiritual life through his personal struggles. This psychobiographical case study used a career development lens to investigate Nouwen’s attempts to establish an identity and give meaning to his existence. The findings indicate that although Nouwen tried out a range of career options, he failed to experience an optimal level of satisfaction or happiness. The study contributes to a number of areas, namely, the legacy of Nouwen, identity and meaning-making in socio-cultural contexts, the career development of extraordinary individuals, and the use of career development theory in psychobiographical research.
... 277) when evaluating scientific claims. This is not something that criminologists-along with scholars in most academic disciplines-have been very good at historically (Burt & Simons, 2015;Kulig, Pratt, & Cullen, 2017). Thus, it should not be surprising that such skepticism has yet to make its way into the digit ratio literature, where the widespread presence of null results for the 2D:4D ratio has done little to dampen scholars' faith in its predictive validity (see, e.g., Kilmek, Galbarczyk, Nenko, & Jasienska, 2016;Manning, Kildiff, Cook, Crewther, & Fink, 2014;Ribeiro, Neave, Morais, & Manning, 2016). ...
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The search for reliable risk factors is a staple among both scholars and policymakers concerned with structuring interventions designed to reduce aggressive and violent behavior. Within this line of work, strong claims have recently been made regarding the predictive capacity of a potential physical biomarker of criminogenic risk: the 2D:4D digit ratio, a purported indirect indicator of exposure to fetal testosterone. The results of studies assessing the link between the digit ratio and problematic behavior are, however, mixed. Accordingly, in the present study we subject this literature (N=32 studies; 361 effect size estimates) to a meta-analysis using multilevel modeling techniques. Our results reveal that the overall mean effect size of the 2D:4D digit ratio to measures of aggressive and violent behavior is weak but statistically significant (mean r=0.036, p<0.05). Moderator analyses confirm that these weak effects are generally consistent (and often non-significant) across a variety of methodological conditions (e.g., different outcome measures, different kinds of samples). We conclude with a call for caution against placing emphasis on the 2D:4D digit ratio as a reliable risk factor for aggressive and violent behavior.
... Relevant in this context is also that the widely reported estimates of heritability of intelligence and other complex social behaviors drawn from behavioral genetics often obscure the degree to which these estimates may encompass environmental mediation (e.g., Stenberg, 2013). The field of behavior genetics that produces heritability estimates based in adoption design is fraught with conceptual and methodological flaws in its core procedures (e.g., Burt & Simons, 2015;Charney, 2012;Joseph, 2010;Richardson & Norgate, 2005). Moreover, although the term "heritability" evokes a connection through transmission of genes between parent and offspring, its technical meaning involves no reference to measurable genetic factors (Taylor, 2007) and "the only practical application of a heritability coefficient is to predict the results of a program of selective breeding" (Wahlsten, quoted in Joseph, 2010, p. 558). ...
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... There is no evidence whatsoever that a unit of difference between 14 and 15 on the CES depression scale is the same as that between 19 and 20 on that scale. This is a very real problem since virtually all of the twin research on personality is based on these types of rank order scales but has been incorrectly interpreted as measuring quantitative trait differences [9][10][11]. It is not surprising that studies analyzing actual genomic data related to cognitive and personality traits have often reported much lower genetic associations than the "heredity" implied by these models [12,13]. ...
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Callous-unemotional behavior (CU) is currently under consideration as a subtyping index for conduct disorder diagnosis. Twin studies routinely estimate the heritability of CU as greater than 50%. It is now possible to estimate genetic influence using DNA alone from samples of unrelated individuals, not relying on the assumptions of the twin method. Here we use this new DNA method (implemented in a software package called Genome-wide Complex Trait Analysis, GCTA) for the first time to estimate genetic influence on CU. We also report the first genome-wide association (GWA) study of CU as a quantitative trait. We compare these DNA results to those from twin analyses using the same measure and the same community sample of 2,930 children rated by their teachers at ages 7, 9 and 12. GCTA estimates of heritability were near zero, even though twin analysis of CU in this sample confirmed the high heritability of CU reported in the literature, and even though GCTA estimates of heritability were substantial for cognitive and anthropological traits in this sample. No significant associations were found in GWA analysis, which, like GCTA, only detects additive effects of common DNA variants. The phrase 'missing heritability' was coined to refer to the gap between variance associated with DNA variants identified in GWA studies versus twin study heritability. However, GCTA heritability, not twin study heritability, is the ceiling for GWA studies because both GCTA and GWA are limited to the overall additive effects of common DNA variants, whereas twin studies are not. This GCTA ceiling is very low for CU in our study, despite its high twin study heritability estimate. The gap between GCTA and twin study heritabilities will make it challenging to identify genes responsible for the heritability of CU.
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Background Twin studies have shown that anxiety in a general population sample of children involves both domain-general and trait-specific genetic effects. For this reason, in an attempt to identify genes responsible for these effects, we investigated domain-general and trait-specific genetic associations in the first genome-wide association (GWA) study on anxiety-related behaviours (ARBs) in childhood. Methods The sample included 2810 7-year-olds drawn from the Twins Early Development Study (TEDS) with data available for parent-rated anxiety and genome-wide DNA markers. The measure was the Anxiety-Related Behaviours Questionnaire (ARBQ), which assesses four anxiety traits and also yields a general anxiety composite. Affymetrix GeneChip 6.0 DNA arrays were used to genotype nearly 700,000 single-nucleotide polymorphisms (SNPs), and IMPUTE v2 was used to impute more than 1 million SNPs. Several GWA associations from this discovery sample were followed up in another TEDS sample of 4804 children. In addition, Genome-wide Complex Trait Analysis (GCTA) was used on the discovery sample, to estimate the total amount of variance in ARBs that can be accounted for by SNPs on the array. Results No SNP associations met the demanding criterion of genome-wide significance that corrects for multiple testing across the genome (p<5×10<sup>−8</sup>). Attempts to replicate the top associations did not yield significant results. In contrast to the substantial twin study estimates of heritability which ranged from 0.50 (0.03) to 0.61 (0.01), the GCTA estimates of phenotypic variance accounted for by the SNPs were much lower 0.01 (0.11) to 0.19 (0.12). Conclusions Taken together, these GWAS and GCTA results suggest that anxiety – similar to height, weight and intelligence − is affected by many genetic variants of small effect, but unlike these other prototypical polygenic traits, genetic influence on anxiety is not well tagged by common SNPs.
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Epigenetics is a burgeoning area of biomedical research into the mechanisms by which genes are regulated—how the activity of producing proteins is run. If genetics is concerned with how genetic variation produces differences in body and behavior, epigenetics concerns how similar genetics can produce different outcomes. Though molecular epigenetic research is highly biochemical in nature, it is of interest to sociologists because some epigenetic changes are environmentally induced and persist, potentially across the life span, or into the next generation. Further, much epigenetic research tracks mechanisms by which social forces—from pollution, to nutrition, to mothering, to traumatic experience—become molecularly embodied, affect gene expression, and induce durable changes in behavior and health. We begin with an introduction to the science of environmental epigenetics focused on articulating the logic of experimentation and explanation in this field. Turning to sociologists’ key interests, we review the ...
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The science of genetics is undergoing a paradigm shift. Recent discoveries, including the activity of retrotransposons, the extent of copy number variations, somatic and chromosomal mosaicism, and the nature of the epigenome as a regulator of DNA expressivity, are challenging a series of dogmas concerning the nature of the genome and the relationship between genotype and phenotype. According to three widely held dogmas, DNA is the unchanging template of heredity, is identical in all the cells and tissues of the body, and is the sole agent of inheritance. Rather than being an unchanging template, DNA appears subject to a good deal of environmentally induced change. Instead of identical DNA in all the cells of the body, somatic mosaicism appears to be the normal human condition. And DNA can no longer be considered the sole agent of inheritance. We now know that the epigenome, which regulates gene expressivity, can be inherited via the germline. These developments are particularly significant for behavior genetics for at least three reasons: First, epigenetic regulation, DNA variability, and somatic mosaicism appear to be particularly prevalent in the human brain and probably are involved in much of human behavior; second, they have important implications for the validity of heritability and gene association studies, the methodologies that largely define the discipline of behavior genetics; and third, they appear to play a critical role in development during the perinatal period and, in particular, in enabling phenotypic plasticity in offspring. I examine one of the central claims to emerge from the use of heritability studies in the behavioral sciences, the principle of minimal shared maternal effects, in light of the growing awareness that the maternal perinatal environment is a critical venue for the exercise of adaptive phenotypic plasticity. This consideration has important implications for both developmental and evolutionary biology.
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Sex differences in the genetic and environmental influences on childhood conduct disorder and adult antisocial behavior were examined in a large community sample of 6,383 adult male, female, and opposite-sex twins. Retrospective reports of childhood conduct disorder (prior to 18 years of age) were obtained when participants were approximately 30 years old, and lifetime reports of adult antisocial behavior (antisocial behavior after 17 years of age) were obtained 8 years later. Results revealed that either the genetic or the shared environmental factors influencing childhood conduct disorder differed for males and females (i.e., a qualitative sex difference), but by adulthood, these sex-specific influences on antisocial behavior were no longer apparent. Further, genetic and environmental influences accounted for proportionally the same amount of variance in antisocial behavior for males and females in childhood and adulthood (i.e., there were no quantitative sex differences). Additionally, the stability of antisocial behavior from childhood to adulthood was slightly greater for males than females. Though familial factors accounted for more of the stability of antisocial behavior for males than females, genetic factors accounted for the majority of the covariation between childhood conduct disorder and adult antisocial behavior for both sexes. The genetic influences on adult antisocial behavior overlapped completely with the genetic influences on childhood conduct disorder for both males and females. Implications for future twin and molecular genetic studies are discussed.
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SNPs discovered by genome-wide association studies (GWASs) account for only a small fraction of the genetic variation of complex traits in human populations. Where is the remaining heritability? We estimated the proportion of variance for human height explained by 294,831 SNPs genotyped on 3,925 unrelated individuals using a linear model analysis, and validated the estimation method with simulations based on the observed genotype data. We show that 45% of variance can be explained by considering all SNPs simultaneously. Thus, most of the heritability is not missing but has not previously been detected because the individual effects are too small to pass stringent significance tests. We provide evidence that the remaining heritability is due to incomplete linkage disequilibrium between causal variants and genotyped SNPs, exacerbated by causal variants having lower minor allele frequency than the SNPs explored to date.
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In the past century, nearly all of the biological sciences have been directly affected by discoveries and developments in genetics, a fast-evolving subject with important theoretical dimensions. in this rich and accessible book, Paul Griffiths and Karola Stotz show how the concept of the gene has evolved and diversified across the many fields that make up modern biology. By examining the molecular biology of the 'environment', they situate genetics in the developmental biology of whole organisms, and reveal how the molecular biosciences have undermined the nature/nurture distinction. Their discussion gives full weight to the revolutionary impacts of molecular biology, while rejecting 'genocentrism' and 'reductionism', and brings the topic right up to date with the philosophical implications of the most recent developments in genetics. Their book will be invaluable for those studying the philosophy of biology, genetics and other life sciences.
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KEYWORDS: biosocial, assumptions, twinsIn their initial article, Burt and Simons (2014) laid out a range of specific criticismsof twin-based research. They argued that violations of the statistical assumptions thatunderpin this line of work result in upwardly biased estimates of heritability and down-wardlybiasedestimatesofenvironmentaleffects.AccordingtoBurtandSimons,thefind-ingsgeneratedfrombehavioralgeneticapproachesare“biologicallynonsensical”andare“misguided.” Indeed, Burt and Simons stated, without qualification, that an entire classof statistical models used to analyze twin data are “seriously flawed.” Because behavioralgenetic designs suffer from “fatal flaws,” they argued, twin-based research designs andtheir associated statistical methods should be put to an “end in criminology.”We examined their assertions carefully. We found that Burt and Simons (2014) cherry-picked the studies they cited in support of their position regarding the biasing impact ofthe equal environments assumption (EEA), something they openly admit in the onlinesupporting information of their rejoinder (Burt and Simons, 2015, this issue). Specifically,theystate,“wefocusedonarticlesthatshowedthattheEEAisnotavalidassumption”tosupport their claim that heritability estimates from behavioral genetic studies are chron-ically overestimated as a result of violations of this assumption. In fact, they relied pri-marily on a single source (Joseph, 1998, 2004, 2006, 2010) for their critique. Notably, wefound that they failed to cite the vast majority of the more than 60 studies that tested forviolations of the EEA—a body of work that is inconsistent with their claims.
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There is growing evidence that the complexity of higher organisms does not correlate with the ‘complexity’ of the genome (the human genome contains fewer protein coding genes than corn, and many genes are preserved across species). Rather, complexity is associated with the complexity of the pathways and processes whereby the cell utilises the deoxyribonucleic acid molecule, and much else, in the process of phenotype formation. These processes include the activity of the epigenome, noncoding ribonucleic acids, alternative splicing and post-translational modifications. Not accidentally, all of these pro- cesses appear to be of particular importance for the human brain, the most complex organ in nature. Because these processes can be highly environmentally reactive, they are a key to understanding behavioural plasticity and highlight the importance of the developmental process in explaining behavioural outcomes.
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The Limits of Family Influence: Genes, Experience, and Behavior. David C. Rowe. New York: Guilford Press. 1994. 232 pp. ISBN 0-89862-132-1. $30 cloth. In The Limits of Family Influence, David Rowe carefully delineates the basic view of genetic and environmental effects on children's characteristics espoused by behavior geneticists such as Scarr, Plomin, Loehlin, and Willerman. The thesis of this quite readable book is that variations in shared family environment have little influence on individual trait development. The book challenges many long-held assumptions about socialization, arguing that variables such as social class, single parenthood, parental warmth, and divorce have little effect on personality. Perhaps more than any other treatment of the "nature-nurture" war, The Limits of Family Influence attempts to drive home the distinction between experiences that family members share (operating to make them alike) and experiences that are unique to each family member. In doing so, the book also tries to establish the point that it is not the much-maligned heritability estimate that social policy makers should concern themselves with in making decisions about programs for children and families; rather, it is the proportion of variance attributable to shared family environments--not h sup 2 but c sup 2 . Rowe begins his assault on the bulk of social science research by identifying weaknesses in the psychological theories that undergirded many research efforts--namely, Freudianism, early behaviorism, and social learning theory. He then carefully sets out the behavior genetics research paradigm. The chapter, "Separating Nature and Nurture," is probably as lucid a treatment of this paradigm as can be found anywhere. What follows are extensive treatments of the behavior genetics research on personality factors and intelligence. An entire chapter is devoted to showing how differences in children, previously identified as having been caused by environmental variables such as social class, ethnicity, and parental warmth, may reflect underlying genetic differences in those individuals. Although Rowe does an excellent job of explicating the behavior geneticist's position on environmental influences, The Limits of Family Influence has limitations. First, it offers little that is new. Thus, it is not likely to persuade those whose views of environmental action correspond more closely to the views of Gottlieb or Lerner or Sameroff or Wachs, and so forth. Second, the view of environmental action attacked by Rowe is no longer the dominant view of "environmentalists." Most environmentalists now describe environmental action as complex and dynamic, one in which the child is constantly active. …
Book
Behavior genetics has always been a breeding ground for controversies. From the “criminal chromosome” to the “gay gene,” claims about the influence of genes like these have led to often vitriolic national debates about race, class, and inequality. Many behavior geneticists have encountered accusations of racism and have had their scientific authority and credibility questioned, ruining reputations, and threatening their access to coveted resources. In Misbehaving Science, Aaron Panofsky traces the field of behavior genetics back to its origins in the 1950s, telling the story through close looks at five major controversies. In the process, Panofsky argues that persistent, ungovernable controversy in behavior genetics is due to the broken hierarchies within the field. All authority and scientific norms are questioned, while the absence of unanimously accepted methods and theories leaves a foundationless field, where disorder is ongoing. Critics charge behavior geneticists with political motivations; champions say they merely follow the data where they lead. But Panofsky shows how pragmatic coping with repeated controversies drives their scientific actions. Ironically, behavior geneticists’ struggles for scientific authority and efforts to deal with the threats to their legitimacy and autonomy have made controversy inevitable—and in some ways essential—to the study of behavior genetics.
Article
A considerable challenge in evolutionary genetics is to understand the genetic mechanisms that facilitate or impede evolutionary adaptation in natural populations. For this, we must understand the genetic loci contributing to trait variation and the selective forces acting on them. The decreased costs and increased feasibility of obtaining genotypic data on a large number of individuals have greatly facilitated gene mapping in natural populations, particularly because organisms whose genetics have been historically difficult to study are now within reach. Here we review the methods available to evolutionary ecologists interested in dissecting the genetic basis of traits in natural populations. Our focus lies on standing genetic variation in outbred populations. We present an overview of the current state of research in the field, covering studies on both plants and animals. We also draw attention to particular challenges associated with the discovery of quantitative trait loci and discuss parallels to studies on crops, livestock, and humans. Finally, we point to some likely future developments in genetic mapping studies.
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This volume collects essays written by John Dupré during his time as Director of the ESRC centre for Genomics in Society, and reflects his interest in the implications of emerging ideas in biology for philosophy. Particular interests include: epigenetics and related areas of molecular biology that have eroded the exceptional status of the gene, and presented the genome as fully interactive with the rest of the cell; developmental systems theory which, especially in the light of epigenetics, provides a space for a vision of evolution that takes full account of the fundamental importance of developmental processes; and microbiology, the elephant in the room of contemporary philosophy of biology. The emphasis on the importance of microbes is perhaps the most distinctive theme of the essays, and one that is shown to subvert such basic biological assumptions as the organization of biological kinds on a branching Tree of Life, and the simple traditional conception of the biological organism. These topics are understood in the context of a view of science, partly taken from earlier work, but developed further in some of the present essays, as realistically grounded in the natural order, but at the same time pluralistic and inextricably integrated within a social and normative context. Topics to which these philosophical and scientific ideas are addressed include the nature of the organism, the limits of neo-Darwinian evolutionary theory, the significance of genomics, the biological status of human races, and the evolutionary and developmental plasticity of human nature.
Article
Classically derived estimates of heritability from twin models have been plagued by the possibility of genetic-environmental covariance. Survey questions that attempt to measure directly the extent to which more genetically similar kin (such as monozygotic twins) also share more similar environmental conditions represent poor attempts to gauge a complex underlying phenomenon of GE-covariance. The present study exploits a natural experiment to address this issue: Self-misperception of twin zygosity in the National Longitudinal Survey of Adolescent Health (Add Health). Such twins were reared under one "environmental regime of similarity" while genetically belonging to another group, reversing the typical GE-covariance and allowing bounded estimates of heritability for a range of outcomes. In addition, we examine twins who were initially misclassified by survey assignment-a stricter standard-in three datasets: Add Health, the Minnesota Twin Family Study and the Child and Adolescent Twin Study in Sweden. Results are similar across approaches and datasets and largely support the validity of the equal environments assumption.
Article
Nature and nurture do not operate independently of each other, and, to an important degree, genetic effects on behavior come about because they either influence the extent to which the individual is likely to be exposed to individual differences in environmental risk or they affect how susceptible the individual is to environmental adversities. The time has come for an explicit research focus on the forms of interplay between genes and environment and on how this interplay is involved in the causal mechanisms for the origins of antisocial behavior and for its persistence or desistance over time. Molecular genetics has an even greater potential than quantitative genetics for understanding environmental risk mechanisms and the interplay between nature and nurture.
Article
Reviews the book, Genes and behavior: Nature-nurture interplay explained by M. Rutter (see record 2006-01387-000). Surveying developments in behavior genetics, Michael Rutter provides an integrative synthesis in writing that is both important and timely. The book aims to offer a nontechnical account of the "various ways in which genetic influences on behavior may be important." To do so, Rutter reviews what is known of environmental influences and how genes and environments might work across development. The book is effectively organized. A first group of five chapters is devoted to quantifying the strength of genetic and environmental influences and illustrating study designs that do so. A second group of three chapters discusses specific genes known to influence behavior outcomes and offers a readable discussion of how such genes might actually work during behavioral development. Before a final summary, there are two provocative chapters; one discussing the role of GE interaction and correlation, and another focused on what environments can do to gene expression. This highly readable and largely nontechnical book provides the reader with insightful understanding of contemporary behavior genetic research. It deserves to be widely read. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
Nature and nurture do not operate independently of each other, and, to an important degree, genetic effects on behavior come about because they either influence the extent to which the individual is likely to be exposed to individual differences in environmental risk or they affect how susceptible the individual is to environmental adversities. The time has come for an explicit research focus on the forms of interplay between genes and environment and on how this interplay is involved in the causal mechanisms for the origins of antisocial behavior and for its persistence or desistance over time. Molecular genetics has an even greater potential than quantitative genetics for understanding environmental risk mechanisms and the interplay between nature and nurture. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
The author argues that it is what children experience outside the home, in the company of their peers, that matters most. Parents don't socialize children: children socialize children. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
Using the “classical twin method,” political scientists John Alford, Carolyn Funk, and John Hibbing conclude that political ideologies are significantly influenced by genetics, an assertion that has garnered considerable media attention. Researchers have long used human twins in attempts to assess the degree of genetic influence on various behavioral traits. Today, this methodology has been largely replaced in favor of contemporary molecular genetic techniques, and thus heritability studies have seen a diminishing role in behavioral genetic research of the twenty-first century. One important reason the twin method has been superseded is that it depends upon several questionable assumptions, the most significant of which is known as the equal environments assumption. Alford, Funk, and Hibbing argue that this crucial assumption, and thus their conclusion, holds up under empirical scrutiny. They point to several studies in support of this assumption. Here, we review the evidence presented and conclude that these attempts to test the equal environments assumption are weak, suffering significant methodological and inherent design flaws. Furthermore, much of the empirical evidence provided by these studies actually argues that, contrary to the interpretation, trait-relevant equal environments assumptions have been violated. We conclude that the equal environments assumption remains untenable, and as such, twin studies are an insufficient method for drawing meaningful conclusions regarding complex human behavior.
Article
There is a trend among behavioral scientists to view ever more complex attitudes or systems of belief as in some sense genetically determined (or “heritable”). Consistent with this trend is the recent article of Alford, Funk, and Hibbing titled “Are Political Orientations Genetically Transmitted?” in which the authors claim to have demonstrated that when it comes to the transmission of political ideologies, genes count for more than environment. Their article has received an enormous amount of attention among political scientists and in the popular press. I critically evaluate the research technique on the basis of which the authors' support their claims and argue that it suffers from significant methodological flaws. Such flaws notwithstanding, I demonstrate that the authors' data do not clearly support their conclusions. I then question the cogency, from an historical and theoretical perspective, of proposing the existence of “liberal” and “conservative” “phenotypes” and “genotypes.” My argument has implications beyond the findings of Alford, Funk, and Hibbing, and applies to all studies that claim to have demonstrated the heritability of complex and politically relevant attitudes.
Article
Unaccounted population stratification can lead to spurious associations in genome-wide association studies (GWAS) and in this context several methods have been proposed to deal with this problem. An alternative line of research uses whole-genome random regression (WGRR) models that fit all markers simultaneously. Important objectives in WGRR studies are to estimate the proportion of variance accounted for by the markers, the effect of individual markers, prediction of genetic values for complex traits, and prediction of genetic risk of diseases. Proposals to account for stratification in this context are unsatisfactory. Here we address this problem and describe a reparameterization of a WGRR model, based on an eigenvalue decomposition, for simultaneous inference of parameters and unobserved population structure. This allows estimation of genomic parameters with and without inclusion of marker-derived eigenvectors that account for stratification. The method is illustrated with grain yield in wheat typed for 1279 genetic markers, and with height, HDL cholesterol and systolic blood pressure from the British 1958 cohort study typed for 1 million SNP genotypes. Both sets of data show signs of population structure but with different consequences on inferences. The method is compared to an advocated approach consisting of including eigenvectors as fixed-effect covariates in a WGRR model. We show that this approach, used in the context of WGRR models, is ill posed and illustrate the advantages of the proposed model. In summary, our method permits a unified approach to the study of population structure and inference of parameters, is computationally efficient, and is easy to implement.
Article
The equal-environments assumption (EEA) in twin studies of psychiatric disorders assumes that the family environment which contributes to risk for a disorder is equally correlated between monozygotic (MZ) and dizygotic (DZ) twin pairs. In a study of psychiatric disorders in female twins, Kendler and colleagues (1993) have demonstrated the utility of a test of the EEA which includes a specified family environmental factor defined by using measures of perceived zygosity. We tested the EEA assumption among 3155 male—male twin pair members of the Vietnam Era Twin Registry for the following DSM-III-R lifetime disorders: alcohol dependence, marijuana dependence, any illicit drug dependence, nicotine dependence, major depression, and posttraumatic stress disorder. The majority of MZ (81.6%; n = 1593) and DZ (90.2%; n = 1086) twin pairs agreed with the investigator''s assigned zygosity. The best-fitting model for each of these disorders did not allow for a specified family environmental influence. These results support the usefulness of perceived zygosity in tests of the EEA. In male twin pairs, perceived zygosity has little impact on twin similarity for common psychiatric disorders.
Article
Although G×E studies are typically based on the assumption that some individuals possess genetic variants that enhance their vulnerability to environmental adversity, the differential susceptibility perspective posits that these individuals are simply more susceptible to environmental influence than others. An important implication of this model is that those persons most vulnerable to adverse social environments are the same ones who reap the most benefit from environmental support. The present study tested several implications of this proposition. Using longitudinal data from a sample of several hundred African Americans, we found that relatively common variants of the dopamine receptor gene and the serotonin transporter gene interact with social environmental conditions to predict aggression in a manner consonant with differential susceptibility. When the social environment was adverse, individuals with these genetic variants manifested more aggression than other genotypes, whereas when the environment was supportive they demonstrated less aggression than other genotypes. Further, we found that these genetic variants interact with environmental conditions to foster various cognitive schemas and emotions in a manner consistent with differential susceptibility and that a latent construct formed by these schemas and emotions mediated the effect of gene by environment interaction on aggression.
Article
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Article
In his essay, "Genes and Ideologies," Evan Charney wrangles with the question of the role of genes in the formation of political attitudes via a critique of Alford, Funk, and Hibbing's 2005 American Political Science Review article. Although critical evaluations are necessary, his essay falls short of what is required of a scientific critique on both empirical and theoretical grounds. We offer a comment on his essay and further contend that it is naïve to proceed on the assumption that a barrier exists between the biological and social sciences, such that the biological sciences have nothing to offer the social sciences. If we look beyond our discipline's current theoretical models we may find a more thorough, and not just competing, explanation of political behavior.
Article
Several recent studies have argued that human genetic variation conforms to a model of isolation by distance, whereas others see a predominant role for long-range migrations and bottlenecks. It is unclear whether either of these views fully describes the global pattern of human genetic variation. In this article, we use a coalescent-based simulation approach to compare the pattern of neutral genetic variation predicted by these views to the observed pattern estimated from neutral autosomal microsatellites assayed in 1,032 individuals from 53 globally-distributed populations. We find that neither view predicts every aspect of the observed pattern of variation on its own, but that a combination of the two does. Specifically, we demonstrate that the observed pattern of global gene identity variation is consistent with a history of serial population fissions, bottlenecks and long-range migrations associated with the peopling of major geographic regions, and gene flow between local populations. This history has produced a nested pattern of genetic structure that is inconsistent with the existence of independently evolving biological races. We consider the implications of our findings for methods that apportion variation into within- and between-group components and for medical genetics.
Article
To evaluate the equal environments assumption (EEA) of the twin method for mother-reported symptoms of child and adolescent emotional and behavioral problems. Four emotional and behavioral problem scales (symptoms of separation anxiety disorder, attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder) and four environmental similarity measures (sharing friends, sharing classes, dressing alike, and perceived zygosity) were assessed by telephone interviews with the biological mothers of 1,948 female adolescent and young adult twin pairs. The effect of environmental similarity on the magnitude of the monozygotic and dizygotic twin correlations and on the parameter estimates from genetic model-fitting was examined for each symptom scale. The measures of environmental similarity were not strongly or consistently related to the similarity of twins for mother-reported emotional and behavioral problems. On average, controlling for environmental similarity did not substantially affect estimates of genetic and environmental influences. These results lend support for the validity of the EEA and suggest that estimates of genetic and environmental influences obtained from twin studies of mother-reported child and adolescent emotional and behavioral problems are not unduly biased by the greater environmental similarity of monozygotic than dizygotic twins.
Article
In this research note, DeFries-Fulker (DF) regression analysis is reframed in model-fitting terms, where an individual's expected score is modeled as a function of their co-twin's proband status. This more flexible implementation of the DF model allows DZ-O twins to be incorporated in a sex-limitation model. Brief simulation results are presented along with the Mx scripts used.
Article
A central sociological problem is the extent to which genetics and the environment influence human behavior. Studies of twins are a core method in attempts to disentangle and to determine the comparative strength of genetic and environmental influences on psychosocial outcomes. A critical assumption of twin studies is that both monozygotic "identical" twins and dizygotic "fraternal" twins share common social environments. Therefore, any greater similarity of monozygotic than dizygotic twins is attributed to genetic influences. This paper tests the equal environment assumption by examining the extent to which greater concordance of adolescent monozygotic compared to dizygotic twins results from social, as well as genetic, influences. Bivariate comparisons indicate that monozygotic twins show greater similarity than dizygotic twins in socially-based characteristics including physical attractiveness, time spent in each other's company, the overlap in friendship networks, and friends' use of alcohol. Multivariate analyses indicate that measures of the social environment sometimes reduce or eliminate apparent genetic effects. In comparison with genetic indicators, social variables are usually stronger predictors of depression and alcohol use and abuse. These findings suggest that past twin studies could overstate the strength of genetic influences because some similarities in behavior among monozygotic compared to dizygotic twins stem from social influences.
Article
The aims of this study were to examine the genetic contribution on physical activity (PA) within a nationwide population of young adult male twin pairs from Sweden and to investigate the equal environment assumption (EEA) in relation to PA. Information on PA was collected by questionnaires in 1998 and 2002 and the impact of genetic factors was estimated by structural equation modeling (SEM). The study included 1,022 pairs of twins and the best fitting SEM-model gave a heritability of 49% (95% CI, 40-56%) for total PA and all PA dimensions showed genetic contributions between 40% and 65%. Non-shared environmental factors were also important, whereas shared environmental factors did not contribute to PA behaviors. The EEA was investigated with a linear regression model, examining if the twins contact frequency predicted within-pair differences in PA, and further by a simulation study. We found no support for violation of the EEA.
Article
explicitly the chief programmatic fallacy committed by those who argue so strongly for the importance of heritability measures for human traits. The fallacy is that a knowledge of the heritability of some trait in a population provides an index of the efficacy of environmental or clinical intervention in altering the trait either in individuals or in the population as a whole. This fallacy, sometimes propagated even by geneticists, who should know better, arises from the confusion between the technical meaning of heritablility and the everyday meaning of the word. A trait can have a heritability of 1.0 in a population at some time, yet this could be completely altered in the future by a simple environmental change. If this were not the case, ‘inborn errors of metabolism’ would be forever incurable, which is patently untrue. But the misunderstanding about the relationship between heritability and phenotypic plasticity is not simply the result of an ignorance of genetics on the part of psychologists and electronic engineers. It arises from the entire system of analysis of causes through linear models, embodied in the analysis of variance and covariance and in path analysis. It is indeed ironic that while Morton and his colleagues dispute the erroneous programmatic conclusions that are drawn from the analysis of human phenotypic variation, they nevertheless rely heavily for their analytic techniques on the very linear models that are responsible for the confusion. I would like to look rather closely at the problem of the analysis of causes in human genetics and to try to understand how the underlying model of this analysis moulds our view of the real world. I will begin by saying some very obvious and elementary things about causes, but I will come thereby to some very annoying conclusions.
Human biodiversity and the egalitarian fiction In The Nurture Versus Biosocial Debate in Criminology
  • John Wright
  • Mark Paul
  • M Alden Morgan Kevin
  • J C Beaver
  • Brian B Barnes
  • Boutwell
Wright, John Paul, and Mark Alden Morgan. 2014. Human biodiversity and the egalitarian fiction. In The Nurture Versus Biosocial Debate in Criminology, eds., Kevin M. Beaver, J.C. Barnes, and Brian B. Boutwell. Thousand Oaks, CA: Sage.