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55th Annual BGA Meeting in Atlanta, Georgia

Student travel fund, behavior genetics.

Founded in 1970, the Behavior Genetics Association (BGA) is an international society. Behavior genetics has a strong tradition in twin and family study designs, and more recently gene-finding studies.

The purpose of the BGA is to promote the scientific study of the interrelationship of genetic mechanisms and behavior, both human and animal; to encourage and aid the education and training of research workers in the field of behavior genetics; and to aid in the dissemination and interpretation to the general public of knowledge concerning the interrelationship of genetics and behavior, and its implications for health and human development and education.

We welcome scientists who share our interest in the interrelationships between genes and traits/behavior, both in humans and non-human animals.

BGA Banquet, London, England, 29 June 2024

** In memoriam of Professor Peter McGuffin CBE FMedSci **

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behaviour genetics

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• National Center for Biotechnology Information - PubMed Central - Behavioral Genetics and Child Temperament
• Academia - Behaviour Genetics : An Overview
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behaviour genetics , the study of the influence of an organism’s genetic composition on its behaviour and the interaction of heredity and environment insofar as they affect behaviour. The question of the determinants of behavioral abilities and disabilities has commonly been referred to as the “nature-nurture” controversy.

The relationship between behaviour and genetics , or heredity, dates to the work of English scientist Sir Francis Galton (1822–1911), who coined the phrase “nature and nurture.” Galton studied the families of outstanding men of his day and concluded, like his cousin Charles Darwin , that mental powers run in families. Galton became the first to use twins in genetic research and pioneered many of the statistical methods of analysis that are in use today. In 1918 British statistician and geneticist Ronald Aylmer Fisher published a paper that showed how Gregor Mendel ’s laws of inheritance applied to complex traits influenced by multiple genes and environmental factors.

The first human behavioral genetic research on intelligence and mental illness began in the 1920s, when environmentalism (the theory that behaviour is a result of nongenetic factors such as various childhood experiences) became popular and before Nazi Germany’s abuse of genetics made the notion of hereditary influence abhorrent . Although genetic research on human behaviour continued throughout the following decades, it was not until the 1970s that a balanced view came to prevail in psychiatry that recognized the importance of nature as well as nurture. In psychology , this reconciliation did not take hold until the 1980s. Much behavioral genetic research today focuses on identifying specific genes that affect behavioral dimensions, such as personality and intelligence , and disorders, such as autism, hyperactivity, depression , and schizophrenia.

Quantitative genetic methods are used to estimate the net effect of genetic and environmental factors on individual differences in any complex trait , including behavioral traits. In addition, molecular genetic methods are used to identify specific genes responsible for genetic influence. Research is carried out in both animals and humans; however, studies using animal models tend to provide more-accurate data than studies in humans because both genes and environment can be manipulated and controlled in the laboratory.

By mating related animals such as siblings for many generations, nearly pure strains are obtained in which all offspring are genetically highly similar. It is possible to screen for genetic influence on behaviour by comparing the behaviour of different inbred strains raised in the same laboratory environment. Another method, known as selective breeding , evaluates genetic involvement by attempting to breed for high and low extremes of a trait for several generations. Both methods have been applied to a wide variety of animal behaviours, especially learning and behavioral responses to drugs , and this research provides evidence for widespread influence of genes on behaviour.

Because genes and environments cannot be manipulated in the human species, two quasi-experimental methods are used to screen for genetic influence on individual differences in complex traits such as behaviour. The twin method relies on the accident of nature that results in identical (monozygotic, MZ) twins or fraternal (dizygotic, DZ) twins. MZ twins are like clones , genetically identical to each other because they came from the same fertilized egg. DZ twins, on the other hand, developed from two eggs that happened to be fertilized at the same time. Like other siblings, DZ twins are only half as similar genetically as MZ twins. To the extent that behavioral variability is caused by environmental factors, DZ twins should be as similar for the behavioral trait as are MZ twins because both types of twins are reared by the same parents in the same place at the same time. If the trait is influenced by genes, then DZ twins ought to be less similar than MZ twins. For schizophrenia , for example, the concordance (risk of one twin’s being schizophrenic if the other is) is about 45 percent for MZ twins and about 15 percent for DZ twins. For intelligence as assessed by IQ tests, the correlation, an index of resemblance (0.00 indicates no resemblance and 1.00 indicates perfect resemblance), is 0.85 for MZ twins and 0.60 for DZ twins for studies throughout the world of more than 10,000 pairs of twins. The twin method has been robustly defended as a rough screen for genetic influence on behaviour.

The adoption method is a quasi-experimental design that relies on a social accident in which children are adopted away from their biological (birth) parents early in life, thus cleaving the effects of nature and nurture. Because the twin and adoption methods are so different, greater confidence is warranted when results from these two methods converge on the same conclusion—as they usually do. An influential adoption study of schizophrenia in 1966 by American behavioral geneticist Leonard Heston showed that children adopted away from their schizophrenic biological mothers at birth were just as likely to become schizophrenic (about 10 percent) as were children reared by their schizophrenic biological mothers. A 20-year study begun in the 1970s in the United States of intelligence of adopted children and their biological and adoptive parents showed increasing similarity from infancy to childhood to adolescence between the adopted children and their biological parents but no resemblance between the adopted children and their adoptive parents.

In contrast to traditional molecular genetic research that focused on rare disorders caused by a single genetic mutation , molecular genetic research on complex behavioral traits and common behavioral disorders is much more difficult because multiple genes are involved and each gene has a relatively small effect. However, some genes identified in animal models have contributed to an improved understanding of complex human behavioral disorders such as reading disability, hyperactivity, autism , and dementia .

Celebrating a Century of Research in Behavioral Genetics

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• Published: 20 January 2023
• Volume 53 , pages 75–84, ( 2023 )

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A century after the first twin and adoption studies of behavior in the 1920s, this review looks back on the journey and celebrates milestones in behavioral genetic research. After a whistle-stop tour of early quantitative genetic research and the parallel journey of molecular genetics, the travelogue focuses on the last fifty years. Just as quantitative genetic discoveries were beginning to slow down in the 1990s, molecular genetics made it possible to assess DNA variation directly. From a rocky start with candidate gene association research, by 2005 the technological advance of DNA microarrays enabled genome-wide association studies, which have successfully identified some of the DNA variants that contribute to the ubiquitous heritability of behavioral traits. The ability to aggregate the effects of thousands of DNA variants in polygenic scores has created a DNA revolution in the behavioral sciences by making it possible to use DNA to predict individual differences in behavior from early in life.

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Introduction

Although the history of heredity and behavior can be traced back to ancient times (Loehlin 2009 ), the first human behavioral genetic research was reported in the 1920s, which applied quantitative genetic twin and adoption designs to assess genetic influence on newly developed measures of intelligence. The 1920s also marked the beginning of single-gene research that led to molecular genetics. The goal of this review is to outline 100 years of progress in quantitative genetic and molecular genetic research on behavior, a whistle-stop tour of a few of the major milestones in the journey. The review focuses on human research even though non-human animal research played a major role in the first 50 years (Maxson 2007 ). It uses intelligence as a focal example because intelligence was the target of much human research, even though a similar story could be told for other areas of behavioral genetics such as psychopathology.

The Two Worlds of Genetics

The most important development during this century of behavioral genetic research has been the synthesis of the two worlds of genetics, quantitative genetics and molecular genetics. Quantitative genetics and molecular genetics both have their origins in the 1860s with Francis Galton (Galton 1865 , 1869 ) and Gregor Mendel (Mendel 1866 ), respectively. Not much happened until the 1900s when Galton’s insights led to methods to study genetic influence on complex traits and when Mendel’s work was re-discovered. The two worlds clashed as Mendelians looked for 3:1 segregation ratios indicative of single-gene traits, whereas Galtonians assumed that Mendel’s laws of heredity were specific to pea plants because they knew that complex traits are distributed continuously.

Antipathy between the two worlds of genetics followed because of the different goals of Mendelians and Galtonians. Mendelians, the predecessors of molecular geneticists, wanted to understand how genes work, which led to the use of induced mutations and a focus on dichotomous traits that were easily assessed such as physical characteristics rather than behavioral traits. In contrast, Galtonians, whose descendants are quantitative geneticists, used genetics as a tool to understand the etiology of naturally occurring variation in complex traits selected for their intrinsic interest and importance, with behavioral traits, especially intelligence, high on the list. The resolution to the conflict could be seen in Ronald Fisher’s 1918 paper, which showed that Mendelian inheritance is compatible with quantitative traits if the assumption is made that several genes affect a trait (Fisher 1918 ). Nonetheless, the two worlds of genetics went their own way for most of the century.

The synthesis of the two worlds of genetics began in the 1980s with the technological advances of DNA sequencing, polymerase chain reaction, and DNA microarrays that enabled genome-wide association (GWA) studies of complex traits. In addition to finding DNA variants associated with complex traits, GWA genotypes led to three far-reaching advances in genetic research. First, GWA genotypes were used to estimate directly the classical quantitative genetic parameters of heritability and genetic correlation, which could be called quantitative genomics . Second, the results of GWA studies were used to create polygenic scores that predict individual differences for complex traits. Third, GWA genotypes facilitated new approaches to causal modeling of the interplay between genes and environment. Together, when applied to behavioral traits, these advances could be called behavioral genomics . This synthesis of the two worlds of genetics, the journey from behavioral genetics to behavioral genomics, is the overarching theme of this whistle-stop tour celebrating a century of research in behavioral genetics. (See Fig.  1 .) The itinerary begins with milestones in quantitative genetics and then molecular genetics, concluding with behavioral genomics.

Synthesis of the two worlds of genetics: from behavioral genetics to behavioral genomics.

Quantitative Genetics

The first 50 years of quantitative genetic research, from 1920 to 1970, started off well with family studies (Jones 1928 ; Thorndike 1928 ), twin studies (Holzinger 1929 ; Lauterbach 1925 ; Merriman 1924 ; Tallman 1928 ) and adoption studies (Burks 1928 ; Freeman et al. 1928 ) using the recently devised IQ test. However, this nascent research was squelched with the emergence of Nazi eugenic policies (McGue 2008 ). The void was filled with behaviorism (Watson 1930 ), which led to environmentalism, the ‘blank slate’ view that we are what we learn (Pinker 2003 ).

Nonetheless, a few studies of IQ appeared in the 1930 and 1940 s, such as the first study of identical twins reared apart (Newman et al. 1937 ) and the first adoption study that assessed birth parents (Skodak and Skeels 1949 ). Both indicated substantial genetic influence on IQ, as did a review of all available IQ data (Woodworth 1941 ).

In 1960, the field-defining book, Behavior Genetics (Fuller and Thompson 1960 ), was published. It mostly reviewed research on nonhuman animals. In their preface, the authors noted that “we considered omitting human studies completely” (p. vi); even their chapter on cognitive abilities primarily reviewed nonhuman research. An earlier influential review began by saying, “In the writer’s opinion, the genetics of behavior must be worked out on species that can be subjected to controlled breeding. At the present time this precludes human subjects” (Hall 1951 ).

In 1963, a milestone review was published in Science of 52 family, twin and adoption studies of IQ (Erlenmeyer-Kimling and Jarvik 1963 ). Although the studies were very small by modern standards and heritability was not calculated, the average results from the different designs suggested substantial heritability. For example, the average MZ and DZ twin correlations were 0.87 and 0.53, respectively, suggesting a heritability of 68%. However, despite being published in Science , the paper was largely ignored; it was cited only 22 times in five years.

The pace of behavioral genetic research picked up in the 1960s, once again primarily research on non-human animals (Lindzey et al. 1971 ; McClearn 1971 ), although some twin studies on cognitive abilities were also published (Nichols 1965 ; Schoenfeldt 1968 ). However, the first 50 years of quantitative genetic research ended badly with the publication in 1969 of Arthur Jensen’s paper, How Much Can We Boost IQ and Scholastic Achievement? (Jensen 1969 ). The paper touched on ethnic differences, which made it one of the most controversial papers in the behavioral sciences, with 900 citations in the first five years and more than 6200 citations in total.

1970 was a watershed year marking the second 50 years of behavioral genetic research. It was the year that the Behavior Genetics Association was launched and the first issue of its journal, Behavior Genetics , was published. Another 1970 milestone was the publication of the foundational paper for model-fitting analysis of quantitative genetic designs (Jinks and Fulker 1970 ).

The 1970s and 1980s yielded most of the major discoveries for quantitative genetics as applied to behavioral traits, discoveries that are listed as landmarks in the following paragraphs. Nonetheless, in the aftermath of Jensen’s 1969 paper, behavioral genetic research, especially on intelligence, was highly controversial (Scarr and Carter-Saltzman 1982 ). Most notably, Leon Kamin severely criticized the politics as well as science of behavioral genetic research on intelligence in his book, The Science and Politics of I.Q. (Kamin 1974 ). He concluded that “There exist no data which should lead a prudent man to accept the hypothesis that I.Q. test scores are in any degree heritable” (p. 1). The book was cited more than 2000 times and stoked antipathy towards genetic research. It also impugned the motivation of genetic researchers, saying that they are ‘committed to the view that those on the bottom are genetically inferior victims of their own immutable defects’ (p. 2).

All Traits are Heritable

Despite this hostility, genetic research grew exponentially in the 1970s and created a seismic shift from the prevailing view that behavioral traits like intelligence are not “in any degree heritable”. In 1978, a review of 30 twin studies of intelligence yielded an average heritability estimate of 46% (Nichols 1978 ). Moreover, the conclusion began to emerge that all traits show substantial heritability. This conclusion, which has been called the first law of behavioral genetics (Turkheimer 2000 ), was first observed in 1976 in a twin study of cognitive data for 3000 twin pairs, which also included extensive data on personality and interests for 850 twin pairs (Loehlin and Nichols 1976 ). The authors noted “the curious uniformity of identical-fraternal differences both within and across trait domains” (p. 89). A 2015 meta-analysis of all published twin studies showed that behavioral traits are about 50% heritable on average (Polderman et al. 2015 ). Demonstrating the ubiquitous importance of genetics was the fundamental accomplishment of behavioral genetics.

No Traits are 100% Heritable

The flip side of the finding of 50% heritability was just as important: no traits are 100% heritable. It is ironic that, after a century of environmentalism, genetic research provided the strongest evidence for the importance of the environment; previous environmental research was confounded because it ignored genetics. Moreover, investigating environmental influences in genetically sensitive designs led to two of the most important discoveries about the environment: nonshared environment and the nature of nurture.

Nonshared Environment

Quantitative genetic research showed that environmental influences work very differently from the way they were assumed to work. A second discovery by Loehlin and Nichols ( 1976 ) was that salient environmental influences are not shared by twins growing up in the same family: “Environment carries substantial weight in determining personality – it appears to account for at least half the variance – but that environment is one for which twin pairs are correlated close to zero” (p. 92). This phenomenon has come to be known as nonshared environment (Plomin and Daniels 1987 ).

Loehlin and Nichols suggested that cognitive abilities are an exception to the rule that environmental influences make children in a family different from, not similar to, one another. Their twin study suggested that about 25% of the variance of cognitive abilities could be attributed to shared environment. A direct test of shared environmental influence is the correlation between adoptive siblings, genetically unrelated children adopted into the same family. Seven small studies of adoptive siblings yielded an average IQ correlation of 0.25, which seemed to precisely confirm the twin estimate (McGue et al. 1993 ).

However, in 1978, a study of 100 pairs of adoptive siblings reported an IQ correlation of -0.03 (Scarr and Weinberg 1978 ). This is a good example of the progressive nature of behavioral genetic research (Urbach 1974 ). Scarr and Weinberg noted that previous studies involved children, whereas theirs was the first study of post-adolescent adoptive siblings aged 16 to 22, and they hypothesized that the effect of shared environmental influence on cognitive development diminishes after adolescence as young adults make their own way in the world. Their hypothesis was confirmed in two additional studies of post-adolescent adoptive siblings that yielded an average IQ correlation of -0.01 (McGue et al. 1993 ). Evidence that shared environmental influence declines after adolescence to negligible levels for cognitive abilities has also emerged from twin studies (Briley and Tucker-Drob 2013 ; Haworth et al. 2010 ). However, one of the biggest mysteries about nonshared environment remains: what are these environmental influences that make children growing up in the same family so different (Plomin 2011 )?

The Nature of Nurture

Another milestone was the revelation that environmental measures widely used in the behavioral sciences, such as parenting, social support, and life events, show genetic influence (Plomin and Bergeman 1991 ), with heritabilities of about 25% on average (Kendler and Baker 2007 ). This finding emerged in the 1980s as measures of the environment were included in quantitative genetic designs, which also led to the discovery that associations between environmental measures and psychological traits are significantly mediated genetically (Plomin et al. 1985 ). The nature of nurture is one of the major directions for research in behavioral genomics, as discussed later.

Heritability Increases During Development

Another milestone in the 1970s was the Louisville Twin Study in which mental development of 500 pairs of twins was assessed longitudinally and showed that the heritability of intelligence increases from infancy to adolescence (Wilson 1983 ). In light of the replication crisis in science (Ritchie 2021 ), a cause for celebration is that this counterintuitive finding of increasing heritability of intelligence – from about 40% in childhood to more than 60% in adulthood -- has consistently replicated, as seen in cross-sectional (Haworth et al. 2010 ) and longitudinal (Briley and Tucker-Drob 2013 ) mega-analyses.

In 1977, a landmark paper showed how univariate analysis of variance can be extended to multivariate analysis of covariance in a model-fitting framework (Martin and Eaves 1977 ). They applied their approach to cognitive abilities and found an average genetic correlation of 0.52, indicating that many genes affect diverse traits, called pleiotropy . Subsequent studies also yielded genetic correlations greater than 0.50 between diverse cognitive abilities (Plomin and Kovas 2005 ).

In the 1970s and 1980s, bigger and better studies made most of the major quantitative genetic discoveries, going far beyond merely estimating heritability. But it was not all smooth sailing. Most notably, The Bell Curve resurrected many of the issues that followed Jensen’s 1969 paper (Herrnstein and Murray 1996 ). Nonetheless, by the 1990s, quantitative genetic research had convinced most scientists of the importance of genetics for behavioral traits, including intelligence (Snyderman and Rothman 1990 ). One symbol of this change was that the 1992 Centennial Conference of the American Psychological Association chose behavioral genetics as one of two themes that best represented the past, present, and future of psychology (Plomin and McClearn 1993 ). Then, just as quantitative genetic discoveries began to slow, the synthesis with molecular genetics began, which led to the DNA revolution and behavioral genomics.

Molecular Genetics

During its first 50 years, molecular genetics focused on single-gene disorders. In 1933, a Nobel prize was awarded to Thomas Hunt Morgan for mapping genes responsible for single-gene mutations in fruit flies (Morgan et al. 1923 ), but human mapping was stymied because only a few single-gene markers such as blood types were available – variants in DNA itself were not available for another fifty years. Research on single-gene effects discovered in pedigree studies only incidentally involved behavioral traits. For example, phenylketonuria, the most common single-gene metabolic disorder, was discovered in 1934 (Folling 1934 ) and shown to be responsible for 1% of the population institutionalized for severe intellectual disability.

In the 1940s, it became clear that DNA is the mechanism of heredity, culminating in the most famous paper in biology which proposed the double-helix structure of DNA (Watson and Crick 1953 ). An important milestone for human behavioral genetics was the discovery in 1959 that the most common form of intellectual disability, Down syndrome, was due to a trisomy of chromosome 21 (Lejeune et al. 1959 ).

In 1961, the genetic code was cracked showing that three-letter sequences of the four-letter alphabet of DNA coded for the 20 amino acids (Crick et al. 1961 ). Just as with quantitative genetics, the 1970s was a watershed decade that ushered in the second 50 years, the genomics era.

The Genomics Era

The era of genomics began in the 1970s when methods were developed to sequence DNA’s nucleotide bases (Sanger et al. 1977 ). In 2003, fifty years after the discovery of the double helix structure of DNA, the Human Genome Project identified the sequence of 92% of the three billion nucleotide bases in the human genome (Collins et al. 2003 ).

In the 1980s, the first common variants in DNA itself were discovered, restriction fragment length polymorphisms (RFLPs) (Botstein et al. 1980 ). RFLPs enabled linkage mapping for single-gene disorders and were the basis for DNA fingerprinting, which revolutionized forensics (Jeffreys 1987 ). Polymerase chain reaction (PCR) was also developed which facilitated genotyping by rapidly amplifying DNA fragments (Mullis et al. 1986 ). In the 1980s, these developments increased the pace of linkage mapping of single-gene disorders, many of which had cognitive consequences, such as phenylketonuria (Woo et al. 1983 ) and Huntington disease (Gusella et al. 1983 ). In the 1990s, DNA sequencing revealed thousands of single-nucleotide polymorphisms (SNPs), the most common DNA variant (Collins et al. 1997 ).

In the 1990s, linkage was also attempted for complex traits that did not show single-gene patterns of transmission, such as reading disability (Cardon et al. 1994 ), but these were unsuccessful because linkage, which traces chromosomal recombination between disease genes and DNA variants within families, is unable to detect small effect sizes (Plomin et al. 1994 ). Researchers then pivoted towards allelic association in unrelated individuals, which is much more powerful in detecting DNA variants of small effect size. An early example of association was an allele of the apolipoprotein E gene on chromosome 19 that was found in 40% of individuals with late-onset Alzheimer disease as compared to 15% in controls (Corder et al. 1993 ).

The downside of allelic association is that an association can only be detected if a DNA variant is itself the functional gene or very close to it. For this reason, and because genotyping each DNA variant was slow and expensive, the 1990s became the decade of candidate gene studies in which thousands of studies reported associations between complex behavioral traits and a few ‘candidate’ genes, typically neurotransmitter genes thought to be involved in behavioral pathways. However, these candidate-gene associations failed to replicate because these studies committed most of the sins responsible for the replication crisis (Ioannidis 2005 ). For example, when 12 candidate genes reported to be associated with intelligence were tested in three large samples, none replicated (Chabris et al. 2012 ).

Genome-wide Association

In 1996, an idea emerged that was the opposite of the candidate-gene approach: using thousands of DNA variants to systematically assess associations across the genome in large samples of unrelated individuals (Risch and Merikangas 1996 ). However, genome-wide association (GWA) seemed a dream because genotyping was slow and expensive.

The problem of genotyping each DNA variant in large samples was solved in the 2000s by the commercial availability of DNA microarrays, called SNP chips , which genotype hundreds of thousands of SNPs for an individual quickly, accurately, and inexpensively. SNP chips paved the way for GWA analyses. In 2007, the first major GWA analysis included 2000 cases for each of seven major disorders and compared SNP allele frequencies for these cases with controls (The Wellcome Trust Case Control Consortium 2007 ). Replicable associations were found but they were few in number and extremely small in effect size. Hundreds of GWA reports appeared in the next decade with similarly small effect sizes across the behavioral and biological sciences (Visscher et al. 2017 ), including cognitive traits such as educational attainment (Rietveld et al. 2013 ) and intelligence in childhood (Benyamin et al. 2014 ) and adulthood (Davies et al. 2011 ).

These GWA studies led to the realization that the biggest effect sizes were much smaller than anyone anticipated. For case-control studies, risk ratios were less than 1.1, and for dimensional traits, variance explained was less than 0.001. This meant that huge sample sizes would be needed to detect these miniscule effects, and thousands of these associations would be needed to account for heritability, which is usually greater than 50% for cognitive traits. Ever larger GWA samples scooped up more of these tiny effects. Most recently, a GWA meta-analysis with a sample size of 3 million netted nearly four thousand independent significant associations after correction for multiple testing, but the median effect size of these SNPs accounted for less than 0.0001 of the variance (Okbay et al. 2022 ).

A century after Fisher’s 1918 paper, the discovery of such extreme polygenicity (Boyle et al. 2017 ; Visscher et al. 2021 ) was a turning point in the voyage from behavioral genetics to behavioral genomics. GWA genotypes brought the two worlds of genetics together by making it possible to use GWA genotypes to create three sets of tools to investigate highly polygenic traits: quantitative genomics, polygenic scores, and causal modeling (see Fig.  1 ). When applied to behavioral traits, these tools constitute the new field of behavioral genomics.

Quantitative Genomics

What good are SNP associations that account for such tiny effects? The molecular genetic goal of tracking effects from genes to brain to behavior is daunting when the effects are so small. However, in contrast to this bottom-up approach from genes to behavior, the top-down perspective of behavioral genetics answered this question by using GWA genotypes to estimate quantitative genetic parameters of heritability and genetic correlations, which could be called quantitative genomics . The journey picked up speed as quantitative genomics led to three new milestones.

Genome-wide Complex Trait Analysis (GCTA). In 2011, the first new method was devised to estimate heritability and genetic correlations since twin and adoption designs in the early 1900s. GCTA (originally called GREML) uses GWA genotypes for large samples of unrelated individuals to compare overall SNP similarity to phenotypic similarity pair by pair for all pairs of individuals (Yang et al. 2011 ). The extent to which SNP similarity explains trait similarity is called SNP heritability because it is limited to heritability estimated by the SNPs on the SNP chip. Genetic correlations are estimated by comparing each pair’s SNP similarity to their cross-trait phenotypic similarity.

SNP heritability estimates are about half the heritability estimated by twin studies (Plomin and von Stumm 2018 ). This ‘missing heritability’ occurs because SNP heritability is limited to the common SNPs genotyped on current SNP chips, which also creates a ceiling for discovery in GWA research. Most SNPs are not common, and rare SNPs appear to be responsible for much of the missing heritability, at least for height (Wainschtein et al. 2022 ). Importantly, quantitative genomic estimates of genetic correlations are not limited in this way and thus provide estimates of genetic correlations similar to those from twin studies (Trzaskowski et al. 2013 ).

Linkage Disequilibrium Score (LDSC) Regression. In 2015, a second quantitative genomic method, LDSC, was published which estimates heritability and genetic correlations from GWA summary effect size statistics for each SNP, corrected for linkage disequilibrium between SNPs (Bulik-Sullivan et al. 2015 ). LDSC estimates of heritability and genetic correlations are similar to GCTA estimates, although GCTA estimates are generally more accurate (Evans et al. 2018 ; Ni et al. 2018 ). The advantage of LDSC is that it can be applied to published GWA summary statistics in contrast to GCTA which requires access to GWA data for individuals in the GWA study.

Genomic Structural Equation Modeling (Genomic SEM). In 2019, a third quantitative genomic analysis completed the arc from quantitative genetics to quantitative genomics by combining quantitative genetic structural equation model-fitting, routinely used in twin analyses, to LDSC heritabilities and genetic correlations (Grotzinger et al. 2019 ). Genomic SEM provides insights into the multivariate genetic architecture of cognitive traits (Grotzinger et al. 2019 ) and psychopathology (Grotzinger et al. 2022 ).

The second answer to the question about what to do with SNP associations that have such small effect sizes is the creation of polygenic scores.

Polygenic Scores

A milestone that marks the spot where the DNA revolution began to transform the behavioral sciences is polygenic scores. Rather than using GWA genotypes to estimate SNP heritabilities and genetic correlations, polygenic scores use GWA genotypes to create a single score for each individual that aggregates, across all SNPs on a SNP chip, an individual’s genotype for each SNP (0, 1 or 2) weighted by the SNP’s effect size on the target trait as indicated by GWA summary statistics. In 2001, polygenic scores were introduced in plant and animal breeding (Meuwissen et al. 2001 ) and later in cognitive abilities (Harlaar et al. 2005 ) and psychopathology (Purcell et al. 2009 ). GWA summary statistics needed to create polygenic scores are now publicly available for more than 500 traits, including dozens for psychiatric disorders and other behavioral traits including cognitive traits (PGS Catalog 2022 ).

The most predictive polygenic scores in the behavioral sciences are for cognitive traits, especially educational attainment and intelligence. Early GWA studies of cognitive traits were underpowered to detect the small effects that we now know are responsible for heritability (Plomin and von Stumm 2018 ). In 2013, a landmark was a GWA study of educational attainment with a sample size exceeding 100,000 (Rietveld et al. 2013 ). A polygenic score derived from its GWA summary statistics predicted 2% of the variance of educational attainment in independent samples. The finding that the biggest effects accounted for only 0.0002 of the variance of educational attainment made it clear that much larger samples would be needed to scoop up more of the tiny effects responsible for the twin heritability estimate of about 40%. In the past decade, the predictive power of polygenic scores for educational attainment has increased with increasing sample sizes from 2% (Rietveld et al. 2013 ) to 5% (Okbay et al. 2016 ) to 10% (Lee et al. 2018 ) to 14% in a GWA study with a sample size of three million (Okbay et al. 2022 ). The current polygenic score for intelligence, derived from a GWA study with a sample of 280,000, predicted 4% of the variance (Savage et al. 2018 ), but, together, the polygenic scores for educational attainment and intelligence predicted 10% of the variance of intelligence test scores (Allegrini et al. 2019 ).

The next milestone will be to narrow the gap between heritability explained by polygenic scores and SNP heritability. A more daunting challenge will be to break through the ceiling of SNP heritability to reach the heritability estimated by twin studies. Reaching both of these destinations will be facilitated by even larger GWA studies and whole-genome sequencing (Wainschtein et al. 2022 ).

Polygenic scores are unique predictors because inherited DNA variations do not change systematically during life – there is no backward causation in the sense that nothing in the brain, behavior or environment changes inherited differences in DNA sequence. For this reason, polygenic scores can predict behavioral traits from early in life without knowing anything about the intervening pathways between genes, brain, and behavior.

Polygenic scores have brought behavioral genetics to the forefront of research in many areas of the life sciences because polygenic scores can be created in any sample of unrelated individuals for whom GWA genotype data are available. No special samples of twins or adoptees are needed, nor is it necessary to assess behavioral traits in order to use polygenic scores to predict them.

Although the implications and applications of polygenic scores derive from its power to predict behavioral traits without regard to explanation (Plomin and von Stumm 2022 ), another milestone on the road to behavioral genomics has been the leverage provided by GWA genotypes for causal modeling.

Causal Modeling

A final milestone on the journey from behavioral genetics to behavioral genomics is a suite of new approaches that use GWA genotypes in causal models that attempt to dissect sources of genetic influence on behavioral traits (Pingault et al. 2018 ). Although traditional quantitative genetic models are causal models, GWA genotypes have enhanced causal modeling in research on assortative mating (Border et al. 2021 ; Yengo et al. 2018 ), population stratification (Abdellaoui et al. 2022 ; Lawson et al. 2020 ), and Mendelian randomization (Richmond and Davey Smith 2022 ).

An explosion of research on genotype-environment correlation was ignited by a 2018 paper in Science on the topic of the nature of nurture (Kong et al. 2018 ). The study included both parent and offspring GWA genotypes and showed that a polygenic score computed from non-transmitted alleles from parent to offspring influenced offspring educational attainment; these indirect effects were dubbed genetic nurture . GCTA has also been used to investigate genotype-environment correlation (Eilertsen et al. 2021 ). Although a great strength of behavioral genomics is its ability to investigate genetic influence in samples of unrelated individuals, combining GWA genotypes with traditional quantitative genetic designs has also enriched causal modeling (McAdams et al. 2022 ), for example, by comparing results within and between families (Brumpton et al. 2020 ; Howe et al. 2022 ).

This whistle-stop tour has highlighted some of the milestones in a century of research in behavioral genetics. The progress is unmatched in the behavioral sciences and its discoveries have been transformative. The most exciting development is the synthesis of quantitative genetics and molecular genetics into behavioral genomics. The energy from this fusion will propel the field far into the future.

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Plomin, R. Celebrating a Century of Research in Behavioral Genetics. Behav Genet 53 , 75–84 (2023). https://doi.org/10.1007/s10519-023-10132-3

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Postgrad growth area: Behavioral genetics

Psychologists who link genes to behavior are in hot demand.

By Cassandra Willyard

Print version: page 14

Seven years ago, with the completion of the Human Genome Project, scientists ushered in a new era for research. After sequencing nearly every gene in the human body, they now have a wealth of new tools and information to learn more about humans than ever before.

These new tools have led to great demand for behavioral geneticists, who work to decipher the intricate ways that the environment and genes interact to influence human behavior and cause disease. A couple of decades ago, twin sets and large families were the only way to explore the role of genes in such complex human traits as intelligence. Today, researchers also have silicon chips and powerful sequencing machinery that allow them to conduct sophisticated searches for the multitude of genetic variants that may influence a single trait. They can even look at the human epigenome, the network of chemical tags that control gene expression.

The ways that behavior, genes and environment interact are often incredibly complex, but it's an exciting intellectual challenge, and jobs in the field abound, says Michael Neale, PhD, a behavioral genetics professor at Virginia Commonwealth University in Richmond, Va.

"Good people are very highly sought after," he adds.

Why it's hot

Behavioral genetics is in the midst of a technological revolution. A decade ago, researchers focused on one or two regions of the genome. With the new DNA chips — thumbnail-size pieces of silicon that allow researchers to assess the presence or absence of given variants — "it's easy to measure a couple of million single base pair changes," Neale says.

The rapidly falling price of these DNA chips means that researchers will soon be able to sequence a person's entire genome for less than $1,000. "Once we can do that, we'll have radically higher power to analyze the inheritance of behavioral and psychological traits," says Geoffrey Miller, PhD, an evolutionary psychologist at the University of New Mexico, who uses behavioral genetics methods in his research. That means researchers will have a better chance of uncovering rare variants and copy number variants associated with given behavioral traits or psychological disorders.

With these powerful new tools, behavioral geneticists are on the cusp of revolutionizing our understanding of human personality and intelligence and figuring out which genes influence our risk for mental illnesses. That's attracting the attention of major funders, including the National Institutes of Health. Since 2000, the NIH's Center for Scientific Review has had a study section devoted to reviewing behavioral genetics grant applications. In a commentary in the May 19 issue of the Journal of the American Medical Association, National Institute of Mental Health Director Thomas Insel, MD, and co-author Philip Wang, MD, DrPH, emphasized the importance of genetics and epigenetics in understanding the biological basis for mental illnesses.

The field is heating up in more quantifiable ways as well. Although the number of submissions to the journal Behavior Genetics increased only slightly last year, the journal's impact continues to rise: The number of PDF downloads, for example, climbed from 66,362 in 2008 to 105,222 in 2009, according to Janice Stern, the journal's publishing editor at Springer Science + Business Media.

What you can do

Most psychologists who work in behavioral genetics end up in academia. According to Michael Stallings, PhD, a professor at the University of Colorado's Institute for Behavioral Genetics in Boulder, 75 percent of the PhDs who have graduated with certificates in behavioral genetics from his institute have found jobs in universities.

Within academia, options abound. "This area of research spans so many different areas and disciplines," says Danielle Dick, PhD, an assistant professor of psychiatry at Virginia Commonwealth University who conducts behavioral genetics research. She has received job offers from programs in clinical psychology, general psychology, developmental psychology and genetics.

Many behavioral geneticists hope to learn more about the complex relationship between genes and addiction. But researchers are also trying to answer questions related to development, personality, cognition, language acquisition, music ability and much more. Behavioral geneticists also search for genetic variants linked to such complex diseases as Alzheimer's, childhood obesity, Type 2 diabetes and schizophrenia.

Some behavioral geneticists find jobs in the private sector, often at drug companies that are trying to use genotyping to identify people who are likely to respond well to drugs. Genome-testing companies, such as 23andMe, are also interested.

In the future, behavioral geneticists may even work in clinical settings. Once researchers have a better understanding of how genes influence addiction risk or mental health, genetic counselors may be able to offer families guidance.

Earnings outlook

Salaries vary widely by location and experience, but an informal survey of experts in the field yielded the following ranges: Postdocs earn anywhere from $40,000 to $60,000 a year. Assistant professors typically make in the $60,000 to $80,000 range. Those who go on to become associate professors can make $80,000 and up. Full professors can "wind up north of $200,000, if you're doing well," Neale says.

According to APA's 2010 annual salary survey , assistant professors in doctoral psychology departments earned a median salary of $63,000, associate professors earned $72,000 and full professors brought in $104,300.

Not surprisingly, salaries tend to be higher in the private sector. One of Stallings's students went on to work for a drug company. Five years out of graduate school, she's earning $100,000 a year.

How to get there

A few institutions offer graduate training in behavioral genetics. At the University of Colorado–Boulder, for example, students can earn a certificate in behavioral genetics in addition to their psychology degree. Researchers like Neale and Dick at the Virginia Institute for Psychiatric and Behavioral Genetics, part of Virginia Commonwealth University, also accept graduate students through a variety of departments.

However, any psychology doctoral degree can lay the foundation for a career in behavioral genetics. But be sure to take courses in neuroscience and genetics on top of your required psychology classes, Stallings says. Also, pay attention in your advanced math and statistics classes. "It's one of these areas where your ability to prove your statistical aptitude is sort of a requirement for entry into the field," Miller says.

After graduating, most budding behavioral geneticists seek additional research experience as a postdoc in a behavioral genetics lab. Collecting DNA may be simple these days, but it's only the first step. "You have to really understand gene function and gene structure to interpret your results," Dick says.

Because there are only a handful of such labs, competition for postdoctoral positions can be fierce. Stand out by having strong publications, math skills and perhaps even computer programming expertise, says Stallings. It also helps to network at the annual Behavior Genetics Association meeting, he adds.

Pros and cons

Like to work in teams? Then behavioral genetics may be a good choice for you. "This is big science," Miller says. "It's not something you can do effectively as a solo researcher." So, be prepared to have your name appear next to 12 others when you publish. Another plus: Behavior genetics papers tend to end up in high-profile journals, Miller says, and a Science or Nature paper looks pretty good on your curriculum vitae.

Another advantage to the field is that behavior geneticists tend to work with large data sets, which provide researchers with a lot of statistical power, allowing them to come to less ambiguous conclusions.

Once you've published your findings, however, they may be hotly debated. "People are still sometimes uncomfortable with finding that particular psychological traits are influenced by genes," Miller says. Also, because the studies are often extremely technical, explaining your work to the public and the media can be challenging. A given behavior might be linked to dozens of genes and have an environmental component, as well, says Neale.

For Dick, the pace of discovery makes such frustrations fade into the background. "What we were doing six months ago is different than what we're doing today," she says. "And there are few areas in psychology where you can say that."

Cassandra Willyard is a writer in New York. 

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Behavioral Genomics

The first systematic studies of whether human behaviors are hereditary were conducted over 100 years ago by Sir Francis Galton, Charles Darwin's cousin. Galton was interested in determining whether human abilities, such as intelligence, could be inherited, and he realized that in order to do this, he must distinguish between those behaviors that were innate and those that were influenced by the environment . To make this distinction, Galton studied the behavioral characteristics of genetically identical twins who were raised in different environments. If twins who had similar traits at birth became dissimilar when reared under differing conditions, these results would support the idea that environment was the primary influence on human behavior. Using this method, Galton deduced that nature (genetics) rather than nurture (environment) played a significant role in behavior (Galton, 1874).

Galton's twin studies and other research involving inherited abilities made him a pioneer in the field of behavioral genetics. Today, modern behavioral geneticists have the same basic goal as Galton: to understand the genetic and environmental contributions to individual variations in behavior. However, current theories support the role of both genes and environment in behavioral outcomes (Robinson, 2004).

Can Single Genes Determine Our Actions?

Many people know about single-gene disorders , but few people know that these conditions are actually far less common than the numerous disorders and nondisease phenotypes that result from the intricate interplay between multiple genes and the environment. Furthermore, even with single-gene disorders (in which a mutation in just one gene manifests as disease), it is often the case that modifier genes at other loci contribute to the severity of the disease phenotype . Thus, sensational reports suggesting that scientists have found the individual gene responsible for a particular behavioral trait (be it alcoholism, sexual orientation, or another complex phenotype) are misleading. In reality, specific animal behaviors—including those of humans—are the result of multiple genes interacting with numerous environmental factors. Awareness of this complexity has shifted researchers' focus from individual genes to entire genomes, thus giving rise to the field of behavioral genomics .

From Behavioral Genetics to Behavioral Genomics

The candidate gene approach.

Traditionally, research efforts involving the potential impact of genes on inherited disorders have been advanced using the " candidate gene " approach, in which investigators ask whether a specific allele is more common in subjects who display a particular trait or behavior than in those subjects who do not (Fitzpatrick et al. , 2005). For a gene to be considered as affecting behavior, some a priori knowledge is usually required, including either pathological mechanisms (in the case of disorders) or how a specific gene affects similar behaviors in other organisms. The latter information can sometimes be obtained from one or more of the numerous databases detailing the genomes of a variety of species , including humans, mice, chickens, fruit flies, honeybees, worms, and zebrafish.

After a gene is selected as a "candidate," its expression pattern (most often in the brain) in subjects who display the behavior of interest is compared to that in subjects who do not display the behavior. This comparison can be performed under natural conditions (i.e., without manipulation) in order to gather correlative data regarding the gene and the behavior. However, a more causal link can be established if expression of the gene is manipulated via transgenic or knock-in/knock-out techniques and the resulting behavior is observed. Indeed, these techniques have been essential in determining the genes associated with adaptive behaviors that are evolutionarily conserved in diverse species (e.g., foraging and reproduction ), and they have also helped pinpoint genes associated with neurobehavioral disorders like autism.

Large-Scale Approaches

Unfortunately, a candidate-gene-by-candidate-gene approach is often inefficient. Thus, investigators are increasingly turning to the enormous amount of data available through the genome sequencing of many organisms. Use of this information allows researchers to adopt a more unbiased approach, simultaneously examining up to thousands of genes at once. Genomic tools also allow scientists to associate genetic variants, including single nucleotide polymorphisms (SNPs), with specific behaviors or even with different gene expression patterns using microarray comparisons. Often, the genes identified through these large-scale genomic approaches are designated as candidate genes, and the effects of these candidates are then verified through more traditional approaches wherein individual genes and their functions are examined.

Candidate Genes for Adaptive Behaviors

As previously mentioned, various techniques have been used to successfully identify genes associated with a number of adaptive behaviors. Such behaviors include courtship and mating, foraging, and social interaction, all of which have been evolutionarily conserved.

Courtship and Mating

Male courtship in the fruit fly Drosophila melanogaster was one of the first behaviors for which researchers found strong evidence for specification by a gene—namely, the so-called "fruitless" gene (abbreviated fru ). In male fruit flies, courtship is a complex, ritualistic behavior that involves many visual, olfactory, gustatory, tactile, and acoustic cues, as well as intricate motor output directed toward attracting a suitable mate (i.e., a female that has not recently mated). During courtship, the male fruit fly orients to the female, taps her with his forelegs, sings a courtship-specific song by vibrating one wing, probes the female's genitalia, and then curves his abdomen to mate (Figure 1; Hall, 1994).

The fruitless gene first emerged as a candidate gene for sexual behavior when it was discovered that male flies with fru mutations were sterile due to defective performance of courtship and copulation (Gill, 1963). Years later, the mutated gene present in these flies was cloned, and the protein that it encodes was identified as a transcription factor (Ito et al. , 1996; Ryner et al. , 1996). Researchers have also determined that the fru gene is spliced differentially in males and females and that this gene generates various sex-specific messenger RNAs (Demir & Dickson, 2005; Kyriacou, 2005). Interestingly, not only does the male pattern of splicing elicit male courtship behavior, but it also influences sexual orientation, as evidenced by the finding that male splicing in otherwise normal females generated male behavior (e.g., singing) that was directed toward other females (Figure 2; Demir & Dickson, 2005). Functional conservation of the fru gene has only been shown in one other species, the malaria mosquito Anopheles gambiae (Gailey et al. , 2006), and a mammalian homologue for fru does not exist. Even so, fru is a good example of how genes can specify aspects of a complex inborn behavior.

Once the for gene was associated with foraging behavior in fruit flies, it was used as a candidate gene to study similar behaviors in other species. For example, the fruit fly for gene shows high sequence homology to the Amfor gene in honeybees. Changing Amfor expression can alter the foraging behavior of a honeybee, thereby transforming the bee from a "nurse" (a bee that cares for the young) to a "forager" (a bee that leaves the hive to find pollen and nectar). Like the rover fruit fly, the forager honeybee has higher levels of the PKG enzyme than do nurse bees (Ben-Shahar et al. , 2002). Researchers have also noted that an orthologue of for , called egl-4 , is associated with food-related behavior in the roundworm C. elegans (Fujiwara et al. , 2002). Taken together, these findings suggest that for could be used as a candidate gene for behaviors concerning food acquisition in other species.

Social Interaction

Researchers began their inquiry into these genes using voles, which are small rodents that look like mice, because there are two particular vole species that differ greatly in terms of social behavior . Specifically, prairie voles ( Microtus ochrogaster ) are affiliative and monogamous (i.e., each vole has only one mate), and both parents provide care for their young, whereas montane voles ( Microtus montanus ) are comparatively asocial, polygamous (i.e., each vole has multiple mates), and nonpaternal. In male prairie voles, living and/or mating with a female causes AVP release in the brain, and paternal and pair-bonding behavior is triggered. However, these behaviors can be disrupted by blocking the V 1a receptor for AVP with an antagonist. Thus, comparing AVP receptor expression between these two vole species was proposed as a useful way to determine which genes contribute to social behavior.

Indeed, prairie and montane voles have markedly different patterns of binding to the V 1a receptors within their brains (Figure 3; Young et al. , 1999). The polygamous montane vole has much more binding in the lateral septum of the brain than the prairie vole, whereas the monogamous prairie vole has a higher intensity of binding in the diagonal band of Broca, a brain area involved in appetitive reward (Young et al. , 1999; Insel & Young, 2000). Furthermore, elevating the expression of the V 1a receptor in the brains of promiscuous voles increased the pair-bonding behavior of males to females (Lim et al. , 2004). Thus, the social behavior of these two species of voles seems to be due to variations in gene expression of the V 1a receptor.

Candidate Genes for Human Disorders

Neurobehavioral disorders are debilitating psychiatric conditions that include depression, bipolar disorder, schizophrenia, and autism. Currently, diagnosis of these diseases is based primarily on clinical symptoms that vary immensely depending on the individual. This phenotypic variability makes effective treatment paradigms difficult to establish. For this reason, scientists have been searching for candidate genes that may influence the onset of these neuropsychiatric pathologies (Glatt & Freimer, 2002). Identifying these candidate genes is difficult, because there are often no clear biomarkers associated with a particular disease against which predictions about the effects of a gene could be tested. Despite such limitations, researchers have associated numerous genes with some neurobehavioral disorders, including autism and schizophrenia. In addition, microarray technology and new SNP-based, whole-genome association methods have helped combat these difficulties to some extent (Glatt & Freimer, 2002; Sutcliffe, 2008).

Autism is a severe neurobehavioral disorder characterized by impaired social skills and repetitive and stereotyped interests and behavior. Autism includes mental retardation in up to 70% of cases (Fombonne, 2003), and it affects many brain areas. Twin studies and examinations of family history suggest that the heritability of autism is roughly 90% (Freitag, 2007; Sutcliffe, 2008). Genetic aspects of the disorder have been substantiated by the identification of chromosomal translocations, inversions, and large deletions or duplications, which are more prevalent in individuals who have more severe cognitive problems. For example, several recent large-scale studies collectively screened almost 2,000 families with autism for recurrent copy number variations, which are small losses or gains in DNA . The consortium of researchers involved in these studies found that copy number variation in a gene called neurexin is linked to the presence of autism. The researchers also found a region on chromosome 11 that might contain sequences that are involved in the disorder (Autism Genome Project Consortium, 2007). Similarly, Weiss and colleagues (2008) found that a microdeletion and microduplication on chromosome 16p11.2 increased susceptibility for the disorder in 1% of cases. Other studies using DNA microarrays have identified many more copy number variations that can be sporadic or inherited and appear to be major genetic risk factors for autism in 10% to 20% of cases (Morrow et al. , 2008; Sutcliffe, 2008).

Table 1 summarizes the genes that have been implicated in autism thus far (Sutcliffe, 2008). Although these genes are diverse, most researchers suggest that they may be linked by a common mechanism, namely dysregulation of gene expression that occurs after neural activity (Morrow et al. , 2008). It is also evident that studying all of these genes, as well as the genes that they regulate and are regulated by, requires the large-scale analysis techniques employed in genomics.

Table 1: Putative and Known Autism-Related Genes

Adhesion Fragile X mental retardation 1 Neuroligin 3 Neuroligin 4 Neurexin 1 SH3 and multiple ankyrin repeat domains 3 Contactin-associated protein-like 2 Protocadherin 10 Contactin 3 Na /H exchanger isoform 9 Na /H exchanger isoform 6 Deleted in autism 1 Ataxin 2-binding protein 1 Fragile X mental retardation 1 Methyl CpG binding protein 2 Deleted in autism 1 Protocadherin 10 Na /H exchanger isoform 9 Ataxin 2-binding protein 1 Ubiquitin protein ligase E3A Fragile X mental retardation 1 Methyl CpG binding protein 2 Na /H exchanger isoform 6 Ataxin 2-binding protein 1 Ubiquitin protein ligase E3A Engrailed homeobox 2 Serotonin transporter (SERT, 5-HTT) Met proto-oncogene (c-Met, HGFR) Na channel, voltage-gated, type VII Ring finger protein 8

Table adapted from Sutcliffe, 2008

Schizophrenia

Schizophrenia is a neuropsychiatric illness in which individuals have impaired perceptions of reality (e.g., hallucinations, delusions, and disorganized thoughts). As with autism, genetic implications for this disorder arose from twin studies. For instance, such studies show that 45% of identical twins who are adopted by different families will both be schizophrenic. Furthermore, if one sibling within a family has been diagnosed with schizophrenia, the other siblings have a 10-time greater chance of also developing the disorder (Plomin et al. , 1994).

Identifying the genetic components of schizophrenia is complicated by the difficulties associated with diagnosing the disease itself, as different doctors often use different criteria to make the same diagnosis. Thus, when they perform studies of schizophrenia, investigators must be particularly careful to look at large populations of individuals with and without the illness, to ensure that all subjects have been diagnosed using the same criteria.

Recently, about 15% of patients with schizophrenia were found to have mutations in a large set of genes, many of which are important for brain development (Walsh et al. , 2008). Disturbances have also been found in the expression of genes related to synaptic function, energy metabolism , and oligodendrocyte function (Bray, 2008). These findings implicate hundreds of potential gene candidates and suggest that each person with the disorder could have a different genetic cause. Thus, despite the power of whole-genome analysis to link diseases to genes, considerable work is often required to separate the "wheat" from the "chaff" in such data sets.

Genetic Components of Human Behavior and Disease

The genetic components of the behaviors and disorders described in the previous sections are by no means comprehensive. Moreover, genes have also been linked to many other diverse traits and diseases, including addiction (e.g., alcohol and tobacco), handedness, bipolar disorder, depression, and dyslexia. With genome sequencing costs plummeting and new discoveries about the genes and environmental factors that affect behavior being made each day, it seems certain that in the years to come, we will develop an even better understanding of why we behave the way we do.

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• v.22(7); 2021 Dec 31

Challenges Faced by Behavioral Genetic Studies: Researchers Perspective from the MENA Region

Omar f. khabour.

1 Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan;

Ahmed A. Abu-Siniyeh

2 Department of Clinical Laboratory Sciences, Faculty of Science, The University of Jordan, Amman, Jordan;

Karem H. Alzoubi

3 Department of Pharmacy Practice and Pharmacotherapeutics, University of Sharjah, Sharjah, UAE;

4 Department of Clinical Pharmacy, Jordan University of Science and Technology, Irbid, 22110 Jordan;

Nihaya A. Al-Sheyab

5 Faculty of Nursing, Maternal and Child Health Department, Jordan University of Science and Technology, Irbid, 22110, Jordan;

6 Charles Perkins Centre and Faculty of Nursing and Midwifery, The University of Sydney, Sydney, Australia

Associated Data

Data will be made available upon reasonable request through email to the corresponding author [KHA].

Behavioral genetic studies are important for the understanding of the contribution of genetic variations to human behavior. However, such studies might be associated with some ethical concerns.

In the current study, ethical challenges related to studies of genetic variations contributing to human behavior were examined among researchers. To achieve the study purpose, the Middle East and North Africa (MENA) region researchers were taken as an example, where the after- mentioned ethical challenges were discussed among a group of researchers, who were the participants of an online forum. Discussions and responses of the participants were monitored and were later qualitatively analyzed.

Discussions revealed that several ethical challenges, including subjects’ recruitment, the difficulty of obtaining informed consents, and issues of privacy and confidentiality of obtained data as information leakage, in this case, will lead to social stigma and isolation of the participants and their immediate family members. Jordanian social and cultural norms, faith, and the tribal nature of the population were raised as a major challenge that might face conducting behavioral genetic studies in the Arab populations of the MENA. The lack of regulation related to the conduction of genetic studies, misunderstanding, and misuse of genetic information are other challenges. A full explanation of genetic research and the current and future possible benefits/risks of such research could be potential solutions.

In conclusion, the MENA populations are tackled with major challenges in relation to conducting research studies in genetics/antisocial behavior field/s. Establishment of guidelines related to genetic studies, capacity building, increasing public awareness about the importance of genetic testing, and enhancing responsible conduct of research will facilitate the conduct of such sensitive studies in the future in the region.

1. INTRODUCTION

Antisocial behaviors are defined as angry, hostile, or aggressive acts that harm and lack consideration for others' comfort or violate their rights in which the aggressor usually has no regret for what he or she has committed [ 1 , 2 ]. Such kind of condition has a variety of symptoms, which begins in preschool-aged children and continues through adulthood [ 3 ]. It has been found that around 50 percent of the adults who suffer from antisocial behavior symptoms have acquired these behaviors since they were in elementary school, and those symptoms persisted until adulthood. Symptoms included unashamed disrepute, disregard for others, scarcity of ethical behavior, offensive to others without a sign of bother for the other, irritability, and aggression [ 4 ].

The etiology of antisocial behavior is heterogeneous, so that each condition is different from the other and the notion of the causes of antisocial behavior relies on different factors such as environmental, biological, and genetic factors [ 5 ]. Different biological factors have an implication in developing antisocial behavior, such as brain damage during pregnancy, brain hypoxia in the womb or birth, or neuropsychological dysfunction and psychosocial influences [ 6 ]. A number of studies also showed that environmental factors have a major role in the creation of antisocial behavior, especially during childhood [ 7 ]. Examples of such factors include; the person exposed to domestic violence and abused in his home, his parents being drug users, was abused during his childhood either sexually, physically, or emotionally or an unstable home environment [ 5 , 7 ].

As shown by various studies, genes have an impact on childhood antisocial and aggressive behavior during childhood, and scientists have recognized specific genetic associations with antisocial behavior [ 8 , 9 ]. Even with an increasing understanding of the genetic bases of human behavior, a cautious approach is warranted either in making inferences about a given individual or in considering changes to the legal system that might now take a defendant's experience and disposition into account [ 10 , 11 ]. In fact, antisocial behavior had a clear genetic component and was shown to be influenced by certain genetic polymorphisms [ 12 ]. Polymorphisms in four genes have been found to be associated with an increased vulnerability for antisocial and impulsive behavior in response to aversive environmental conditions [ 13 ]. These genes include 1) MAOA that codes for monoamine oxidase A enzyme, which has an important implication in dopamine, noradrenaline, and serotonin metabolism [ 14 ]; 2) SLC6A4 gene codes for the serotonin transporter SLC6A4, which plays an important role in controlling serotonin levels in the synaptic cleft [ 15 ]; 3) COMT gene codes for catechol-O-methyltransferase), which is the main regulator of dopamine levels in synapses [ 16 ]; 4) DRD4 gene codes for the dopamine D4 receptor, which is a G protein-coupled receptor that is highly expressed in the cerebellum and plays a significant role in dopaminergic synapses [ 17 ]. In a genome-wide study of antisocial behavior in a large combined sample, it has been shown that a large number of genetic variants play a role in antisocial behavior and several variants show gender-specific effects on antisocial behavior in males and females [ 18 ]. In the current study, the ethical challenges face by genetic studies that examine genetic variations contributing to antisocial behavior were discussed in this study by taking the Middle East and North Africa (MENA) researchers as an example.

2.1. Study Design

In the current study, a descriptive qualitative approach was used to explore the research ethics of genetic variations contributing to antisocial behavior by taking MENA researchers as an example. Researchers from MENA participated in the study as a part of the Responsible Conduct of Research (RCR) training program, which was hosted by the online learning platforms of Jordan University of Science and Technology and the University of California at San Diego, CA, USA. This program was funded by The National Institute of Health/Fogarty International Center to enhance the RCR in the MENA region. Twenty-eight researchers were the study participants, including 18 from Jordan, 2 from Tunisia, 2 from Morocco, and one from each of the following countries: Egypt, Yemen, Iraq, Sudan, Algeria, and Gaza-Strip/Palestinian Authority. The majority of participants were faculty members (PhD holders, n=24) and 4 were MSc research assistants.

The opinions of the scientists (n=28) were collected through an online discussion forum. The forum was opened for a total of two weeks, with enough time provided by the moderator for each of the questions to motivate online discussion. The posts in the discussion (n=118) were used as a tool for qualitative analysis and were categorized into six ethical themes 1) subjects recruitment, 2) informed consent process, 3) privacy and confidentiality, 4) nature of the population (culture, norms, and regulations), 5) interpretation of the findings, and 6) Risks and benefits. An expert qualitative researcher monitored forum discussions. This process included promoting the study participants to be involved in the discussion using some provocative statements and probe questions such as “good point that needs more elaboration ….”, “could you explain more…”, etc. Such a monitoring process is effective in improving the validity of the collected data and study findings [ 19 ]. To reduce bias, a different researcher other than the one who monitored the discussion forum transcribed the collected data into different domains. In detail , the moderator was responsible for posting the main questions and probing when needed, and then he directed and facilitated the online discussion. Participation in the online discussions was voluntary and participants were informed that they have the right to withdraw at any point without penalties. All discussions in the forum were transcribed verbatim for analysis. Researchers conducted the analysis process in its original English to maintain fidelity of the results, which could be lost by early and inaccurate translation. Preliminary analysis was conducted after the end of the online discussion on the forum to get a general impression of the data. Analysis of the transcribed data was undertaken manually through the coding process and generating categories and themes by two independent researchers, who then met to overcome any inconsistency in the categorization of themes and subthemes and reach a consensus.

2.2. Ethical Approval

The Institutional Review Board (IRB) at the Jordan University of Science and Technology (IRB-JUST) approved this study. The IRB applies the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. Participants gave informed consent before they participated in the forum.

Participants were asked about their opinion concerning ethical challenges for studies that examine genetic variations contributing to antisocial behavior in the Arabic populations. A total of 6 challenges were raised/discussed by the participants (Table ​ 1 1 ). The order of challenges according to number of participants who raised/discussed them is privacy and confidentiality > risks and benefits > culture/norms/regulations > informed consent > interpretations of the findings > Subjects’ recruitments (Table ​ 1 1 ). Details about challenges are presented below:

Main challenges of conduction of antisocial genetic research in the MENA region

Subjects' recruitment	4 (14.2)
Informed consent	9 (32.1)
Privacy and confidentiality	16 (57.1)
Nature of the population: culture, norms and regulations	12 (42.9)
Interpretation of the findings	7 (25.0)
Risks and benefits	15 (53.6)

3.1. Subjects' Recruitment

Several participants pointed to a challenge in recruiting subjects for this kind of research due to the sensitivity of the topic and the lack of awareness and knowledge of such studies and their test results.

Among suggested solutions to this challenge are creating more awareness about genetic studies, proper genetic counseling, and highlighting potential benefits.

One participant stated that “participants always concentrate on the direct benefit of research”.

Another participant said, “The lack of interest of the participants in such studies will pose an obstacle in recruiting”. However, one participant suggested a solution for the recruitment challenge: “Development of effective interventions based on genetic testing could promote motivation to participate.”

3.2. Informed Consent Process

Participants discussed the reasons why informed consent in genetic studies in Arab populations is difficult to obtain, and whether this difficulty (if any) applies only to antisocial studies or for all types of research, and how this problem can be solved?

Three members agreed that “the hardest part is achieving the consent form”.

One participant stated that “……. As the information gained from genetic testing will be retraced to the whole family, thus, submitting the consent will be very hard to achieve …”.

Most members also stressed that informed consent is required and participants need to have a full explanation of the current and future possible benefits/risks of such research in order to convince the population of signing the consent form.

For example, one member stated, “I think genetic counseling is one way to deliver information. I think an explanation and understanding of some of the human behavior by participants would encourage them to accept informed consent and participation in such studies.”

Another member said “The main ethical challenge in antisocial studies is the high risk of stigma and its devastating consequences that need to be stated in the consent form.”

3.3. Privacy and Confidentiality

Others highlighted matter of privacy and confidentiality of medical information of the study participants as the leakage in most cases would lead to stigmatizing related individuals, including socially isolating them and creating negative psychological effects on them.

A female member (S.A) said “Confidentiality breach and disclosure of such information generated by genetic studies can associate some families with some genetic diseases (even if rare) in the form of the social stigma that can lead to isolation and all psychological consequences……”

Such information might be used inappropriately by private insurance companies by depriving/ refuse to cover persons from stigmatized families.”

One male member pointed to the shared nature of genetic information and highlighted that breaching confidentiality can also harm the relatives of participants.

The member stated “….. Being afraid of breaching confidentiality and privacy…..These genetic findings might affect negatively the carrier (relatives of the person who has the genetic condition.”

3.4. Nature of the Population: Culture, Norms, and Regulations

Two participants stressed the importance of Jordanian social norms, culture, faith, and the tribal nature of the population, which might form an obstacle in conducting antisocial genetic-related studies in the Arab populations, including Jordan.

One member stated, “The culture and norms of the Jordanian community could be a major barrier for such genetic tests as people not prepared and are threatened by antisocial consequences”.

Another example: “societies in the Middle East should be prepared to accept the results of genetic studies, this needs a time that is not short. Researchers should play a great effective role in this, simplified lectures, debates, and discussions involving different spectra of the society, implanting the culture of “no discrimination” and even “Drama” and social media can participate in changing the ideas of the societies.”

Another two members stated that “If the study holds conflict with participants’ religious beliefs then it will be almost impossible to recruit the required population”.

Examples related to the lack of regulation related to the conduction of genetic study as an obstacle are “The question of who should be entitled to have the right to access and use such stigmatizing information/records related to families in the population”.

“There is a need to have regulations monitoring the process of such studies due to the fear of having a social misunderstanding of the real purpose behind conducting such studies.”

3.5. Interpretation of the Findings

Misunderstanding and misuse of genetic information are highlighted by several as major challenge s .

For example:

“If such studies proved a direct relation of the “warrior gene” to antisocial behavior then violent individuals will try to get away with punishment by blaming it all on their bad genes”. “Authorities might blame the genes for all antisocial behavior and crimes and disregard other criminating factors.”

“Members/families (in Jordan) that would be diagnosed carrying variants/genes related to causing antisocial behavior will be highly stigmatized, due to the fact that antisocial behavior is always connected to mental illness in Jordanian society”.

“Such research will end up being a tool for destroying others’ lives by stigmatizing them with a specific genetic trait which states that this person has the potential possibility of committing a specific antisocial behavior, consequently condemning them for what they might do and not for what they did”.

3.6. Risks and Benefits

Major discussions related to antisocial genetic research were focused on issues related to benefits/risks from the conduction of such studies. Two members shared opposite opinions concerning whether genetic polymorphisms would increase the possibility of an individual to have an untreatable genetic disorder. Meanwhile, one member recommended that it is not worth it to tell the subject that they hold a good possibility to an untreatable genetic disorder, whereas the other said that knowing such a possibility will create extra awareness within that subject, who in turn will avoid specific behavior which will prevent further and future complications.

One member stated, “If a patient is susceptible to develop an untreatable disease, s/he may benefit from avoiding other factors that could contribute to increasing the risk, the management can be provided early and some complications may be prevented.”

Another member stated, “Do you think that research aiming at genetic testing for the susceptibility for behavioral and cognitive disorders is a waste of money and resources or could it lead to preventative approaches?”

Two members stated that, “Financials should be aimed towards the other affecting factors such as environmental factors and dysfunctional families for that they are easier to identify”, One member mentioned that “Genetic testing of the behavioral disorders is not a waste of money for that preventive measures can be taken should the genetic susceptibility be identified”.

More examples: “Genetic testing for study purposes could reveal certain genetic predispositions for some disease which predisposes participants to social stigma, social isolation, and psychological problems in eastern communities ( e.g. Jordan)”.

“Revealing information about the existence and relation of a gene to the antisocial behavior among a specific population will create a stigmatizing effect which in turn will negatively affect such population, and therefore researchers should think twice when it comes to conducting such research in Jordan”.

4. DISCUSSION

The behavioral genetics is an important topic in genetics, which focuses on investigating the link between genes and criminal and aggressive behaviors and their relations with the surrounding environment [ 20 ]. During the last years, growing pieces of evidence exposed the significant impact of both genes and the environment on an individual’s antisocial behavior that changed the views toward antisocial behavior concepts. Moreover, understanding the causes of antisocial behavior would set the stage for prevention interventions that could significantly reduce the crime rate [ 21 ]. In the current study, a group of MENA researchers examined ethical challenges related to studies of genetic variations contributing to antisocial behavior in the Arab populations. The main challenges discussed included the recruitment of subjects, informed consent process, risks and benefits, privacy and confidentiality, and interpretations of findings and culture.

The first challenge discussed by the researchers is related to recruitments of subjects due to the sensitivity of the topic and lack of awareness about genetic testing in the Arab populations. In a study that was conducted on genetic factors that contribute to epilepsy, the decline-to-participate rate among eligible subjects was about 84%, which has been attributed to confidentiality and lack of compensation [ 22 ]. The recruitment of subjects to cancer genetic studies and clinical trials for genetic diseases was also a challenge [ 23 , 24 ]. Thus, enhancing the awareness of the MENA populations about the importance of genetic studies can improve the recruitment of participants in such studies.

The second main challenge was a violation of a patient’s confidentiality and privacy by genetic testing. In a study that investigated the attitudes of healthcare professionals toward behavioral genetic testing for antisocial behavior, the majority of study participants were against genetic testing unless treatment was obtainable. Participants were worried about probable harm, such as exposing patient’s confidentiality that may lead to social stigma and racial discrimination [ 25 ]. Similar findings were reported in previous studies that highlighted the potential of genetic data in exposing personal/family information such as one's parent, sibling, and children [ 26 - 28 ]. Maintaining participants’ confidentiality and privacy will enhance the trust in researchers and will ultimately increase participation in genetic studies.

A different challenge that the researchers raised is related to the risks and benefits of the study. Some of the researchers doubted concerning applications of the findings and if interventions are available for subjects at risk of antisocial behavior. In a previous study, disagreement regarding the usefulness of such studies was reported. Some participants indicated that genetic testing could provide an early indication for parents about the problems children may face in the near future, which enables them to take their preventative decision early. On the other hand, some participants were concerned about potential risks for such testing that include misinterpretation of the findings, false positives, false negatives, and the danger of stigmatization that potentially comes along with a positive test result [ 29 , 30 ]. With respect to the interpretation of data, which was also discussed by researchers in the current study, it is worth to mention that environmental risk factors have also been identified in influencing antisocial behavior. Actually, environmental factors tend to contribute largely to antisocial outcomes when compared to genetic ones. This is because variations in the environment seem to significantly affect an individual's gene expression via mechanisms that involve epigenetic changes. This will complicate the understanding and prediction of an individual's behavior [ 31 , 32 ].

Social norms, culture, faith, and the tribal nature of the Arab populations of the MENA might be a major difficulty in conducting antisocial genetic related studies. It is not an easy task to convince people to accept the results of genetic studies, especially if the study holds conflict with participants’ religious beliefs that will complicate participation in such a study. Another obstacle that may face genetic studies is stigmatizing the family diagnosed by carrying variants/genes related to causing antisocial behavior because antisocial behavior is always linked to psychological illness among the Jordanian community. The informed consent process was also among the challenges discussed by the researchers. The informed consent was also highlighted as a challenge in several previous studies [ 33 , 34 ]. There is a necessity to comprehend people’s beliefs, awareness, and responses toward genetic testing, which may fill the gap by explaining and clearing vague, concern, and knowledge in such research [ 35 ]. The shortage of expertise in the area of genetic counseling and the absence of regulations in most of the countries in the region will pose difficulties in resolving such a challenge.

The MENA populations are tackled with major challenges in providing comprehensive and up-to-date health services in the field of genetics [ 36 ]. These obstacles include lack of resources, a limited number of trained persons in the area of genetic testing and counseling, a misperception that genetic testing is too expensive to conduct, lack of regulations, and fear of families who have been diagnosed with a certain genetic disorder to be stigmatized within their community. Establishment of guidelines related to genetic studies, capacity building, increasing public awareness about the importance of genetic testing, and enhancing responsible conduct of research will facilitate the conduction of such sensitive studies in the future in the region.

Social behaviors are expected to be affected by strong environmental factors. In fact, the impact of the environment on gene expression via epigenetic mechanisms is well established [ 37 - 40 ]. In recent reviews, epigenetic regulation of genes involved in neuroendocrine, serotonergic and oxytocinergic pathways and their role in modulating personality and vulnerability to proactive and reactive aggressive behavior were discussed [ 41 , 42 ]. Thus, behavioral genetics and epigenetics are important areas in research that help uncover the fine interaction between genes and environment and the subsequent molecular pathways that contribute to aggression in the populations.

Among the limitations of the current study is that the majority of participants were from Jordan. The study was part of a fellowship that was conducted in Jordan. It is worth mentioning that most of the MENA countries share language, culture, religions… etc. , and these countries suffer from the same issues regarding scientific research as explained above. Thus, the study represents the MENA region to some extent. However, expanding the study to have good representations of MENA countries is strongly recommended.

The MENA populations are tackled with major challenges in relation to conducting research studies in genetics/antisocial behavior field/s. Establishment of guidelines related to genetic studies, capacity building, increasing public awareness about the importance of genetic testing, and enhancing responsible conduct of research will facilitate the conduct of such sensitive studies in the future in the region.

ACKNOWLEDGEMENTS

Declared none.

ETHICS APPROVAL AND CONSENT TO PARTICIPATE

The Institutional Review Board (IRB) at the Jordan University of Science and Technology, Jordan (IRB-JUST) approved this study.

HUMAN AND ANIMAL RIGHTS

No animals were used in this study. For the proceduces on humans the IRB applies the ethical standards as laid down in the 1964 Declaration of Helsinki and its later amendments.

CONSENT FOR PUBLICATION

Participants gave informed consent before they participated in the forum.

AVAILABILITY OF DATA AND MATERIALS

Work on this project was supported by grant # 5R25TW010026-02 from the Fogarty International Center of the U.S. National Institutes of Health.

CONFLICT OF INTEREST

The authors declare no conflict of interest, financial or otherwise.

Emotional RNC speech about son’s fentanyl death tells only part of the story: David F. Kisor

• Updated: Aug. 16, 2024, 5:40 a.m.
• | Published: Aug. 16, 2024, 5:39 a.m.

Anne Fundner speaks about her son's fentanyl overdose death during the Republican National Convention Tuesday, July 16, 2024, in Milwaukee. In a guest column today, Dr. David F. Kisor, an Ohio expert in the emerging field of pharmacogenomics, writes that, beyond the political focus on fentanyl, the public should also be aware of discovery of a genetic variant that makes 3% to 4% of individuals extraordinarily more susceptible to dying from fentanyl exposure because of their difficulty in metabolizing the drug. (AP Photo/Matt Rourke) AP Photo/Matt Rourke

• Guest Columnist, cleveland.com

AVON LAKE, Ohio -- On Tuesday, July 16, at the Republican National Convention, a California mother, Anne Fundner, described the tragic death of her 15-year-old son , who died of a fentanyl overdose after unsuspectingly ingesting the drug. This is an all-too-common occurrence.

Nationally, there were nearly 108,000 drug overdose deaths in 2022 , with a large majority being attributed to synthetic opioids, mainly fentanyl. In Ohio, over the five-year span of 2018-2022, there was an average of nearly 4,800 drug overdose deaths annually, placing Ohio consistently in the top five states in terms of overdose numbers, a distinction not desired.

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