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"Genetic psychology" redirects here. For Franz Brentano's concept of genetic psychology, see Genetic psychology (Brentano).

For the journal, see Behavior Genetics (journal). Behavioural genetics, also referred to as behaviour genetics, is a field of scientific research that uses genetic methods to investigate the nature and origins of individual differences in behaviour. While the name "behavioural genetics" connotes a focus on genetic influences, the field broadly investigates the extent to which genetic and environmental factors influence individual differences, and the development of research designs that can remove the confounding of genes and environment. Behavioural genetics was founded as a scientific discipline by Francis Galton in the late 19th century, only to be discredited through association with eugenics movements before and during World War II. In the latter half of the 20th century, the field saw renewed prominence with research on inheritance of behaviour and mental illness in humans (typically using twin and family studies), as well as research on genetically informative model organisms through selective breeding and crosses. In the late 20th and early 21st centuries, technological advances in molecular genetics made it possible to measure and modify the genome directly. This led to major advances in model organism research (e.g., knockout mice) and in human studies (e.g., genome-wide association studies), leading to new scientific discoveries.

Findings from behavioural genetic research have broadly impacted modern understanding of the role of genetic and environmental influences on behaviour. These include evidence that nearly all researched behaviours are under a significant degree of genetic influence, and that influence tends to increase as individuals develop into adulthood. Further, most researched human behaviours are influenced by a very large number of genes and the individual effects of these genes are very small. Environmental influences also play a strong role, but they tend to make family members more different from one another, not more similar.

History[edit]
Selective breeding and the domestication of animals is perhaps the earliest evidence that humans considered the idea that individual differences in behaviour could be due to natural causes. Plato and Aristotle each speculated on the basis and mechanisms of inheritance of behavioural characteristics. Plato, for example, argued in The Republic that selective breeding among the citizenry to encourage the development of some traits and discourage others, what today might be called eugenics, was to be encouraged in the pursuit of an ideal society. Behavioural genetic concepts also existed during the English renaissance, where William Shakespeare perhaps first coined the phrase "nature versus nurture" in The Tempest, where he wrote in Act IV, Scene I, that Caliban was "A devil, a born devil, on whose nature Nurture can never stick".

Modern-day behavioural genetics began with Sir Francis Galton, a nineteenth-century intellectual and cousin of Charles Darwin. Galton was a polymath who studied many subjects, including the heritability of human abilities and mental characteristics. One of Galton's investigations involved a large pedigree study of social and intellectual achievement in the English upper class. In 1869, 10 years after Darwin's On the Origin of Species, Galton published his results in Hereditary Genius. In this work, Galton found that the rate of "eminence" was highest among close relatives of eminent individuals, and decreased as the degree of relationship to eminent individuals decreased. While Galton could not rule out the role of environmental influences on eminence, a fact which he acknowledged, the study served to initiate an important debate about the relative roles of genes and environment on behavioural characteristics. Through his work, Galton also "introduced multivariate analysis and paved the way towards modern Bayesian statistics" that are used throughout the sciences—launching what has been dubbed the "Statistical Enlightenment".

The field of behavioural genetics, as founded by Galton, was ultimately undermined by another of Galton's intellectual contributions, the founding of the eugenics movement in 20th century society. The primary idea behind eugenics was to use selective breeding combined with knowledge about the inheritance of behaviour to improve the human species. The eugenics movement was subsequently discredited by scientific corruption and genocidal actions in Nazi Germany. Behavioural genetics was thereby discredited through its association to eugenics. The field once again gained status as a distinct scientific discipline through the publication of early texts on behavioural genetics, such as Calvin S. Hall's 1951 book chapter on behavioural genetics, in which he introduced the term "psychogenetics", which enjoyed some limited popularity in the 1960s and 1970s. However, it eventually disappeared from usage in favour of "behaviour genetics".

The start of behaviour genetics as a well-identified field was marked by the publication in 1960 of the book Behavior Genetics by John L. Fuller and William Robert (Bob) Thompson. It is widely accepted now that many if not most behaviours in animals and humans are under significant genetic influence, although the extent of genetic influence for any particular trait can differ widely. A decade later, in February 1970, the first issue of the journal Behavior Genetics was published and in 1972 the Behavior Genetics Association was formed with Theodosius Dobzhansky elected as the association's first president. The field has since grown and diversified, touching many scientific disciplines.

Methods[edit]
The primary goal of behavioural genetics is to investigate the nature and origins of individual differences in behaviour. A wide variety of different methodological approaches are used in behavioural genetic research, only a few of which are outlined below.

Animal studies[edit]
Investigators in animal behaviour genetics can carefully control for environmental factors and can experimentally manipulate genetic variants, allowing for a degree of causal inference that is not available in studies on human behavioural genetics. In animal research selection experiments have often been employed. For example, laboratory house mice have been bred for open-field behaviour, thermoregulatory nesting, and voluntary wheel-running behaviour. A range of methods in these designs are covered on those pages. Behavioural geneticists using model organisms employ a range of molecular techniques to alter, insert, or delete genes. These techniques include knockouts, floxing, gene knockdown, or genome editing using methods like CRISPR-Cas9. These techniques allow behavioural geneticists different levels of control in the model organism's genome, to evaluate the molecular, physiological, or behavioural outcome of genetic changes. Animals commonly used as model organisms in behavioural genetics include mice, zebra fish, and the nematode species C. elegans.

Machine learning and A.I. developments are allowing researchers to design experiments that are able to manage the complexity and large data sets generated, allowing for increasingly complex behavioral experiments.

Human studies[edit]
Main article: Human behaviour genetics

See also: Heritability and Quantitative genetics § Pedigree analysis

Some research designs used in behavioural genetic research are variations on family designs (also known as pedigree designs), including twin studies and adoption studies. Quantitative genetic modelling of individuals with known genetic relationships (e.g., parent-child, sibling, dizygotic and monozygotic twins) allows one to estimate to what extent genes and environment contribute to phenotypic differences among individuals.

Twin and family studies[edit]
Main article: Twin studies

The basic intuition of the twin study is that monozygotic twins share 100% of their genome and dizygotic twins share, on average, 50% of their segregating genome. Thus, differences between the two members of a monozygotic twin pair can only be due to differences in their environment, whereas dizygotic twins will differ from one another due to environment as well as genes. Under this simplistic model, if dizygotic twins differ more than monozygotic twins it can only be attributable to genetic influences. An important assumption of the twin model is the equal environment assumption that monozygotic twins have the same shared environmental experiences as dizygotic twins. If, for example, monozygotic twins tend to have more similar experiences than dizygotic twins—and these experiences themselves are not genetically mediated through gene-environment correlation mechanisms—then monozygotic twins will tend to be more similar to one another than dizygotic twins for reasons that have nothing to do with genes.

Twin studies of monozygotic and dizygotic twins use a biometrical formulation to describe the influences on twin similarity and to infer heritability. The formulation rests on the basic observation that the variance in a phenotype is due to two sources, genes and environment. More formally,, where  is the phenotype,  is the effect of genes,  is the effect of the environment, and  is a gene by environment interaction. The  term can be expanded to include additive, dominance , and epistatic genetic effects. Similarly, the environmental term  can be expanded to include shared environment and non-shared environment, which includes any measurement error. Dropping the gene by environment interaction for simplicity (typical in twin studies) and fully decomposing the  and  terms, we now have. Twin research then models the similarity in monozygotic twins and dizygotic twins using simplified forms of this decomposition, shown in the table. The simplified Falconer formulation can then be used to derive estimates of, , and. Rearranging and substituting the  and  equations one can obtain an estimate of the additive genetic variance, or heritability,, the non-shared environmental effect  and, finally, the shared environmental effect. The Falconer formulation is presented here to illustrate how the twin model works. Modern approaches use maximum likelihood to estimate the genetic and environmental variance components.

Genome-wide association studies[edit]
See also: Evolution of the brain § Genetic factors of recent evolution, and Neurogenetics

Behavioural genetics also uses and generates databases that contain genomic, neurological (e.g. neuroanatomy/neuroimaging data) and behavioral (e.g. survey data about lifestyle- and health-related activities) information. Such databases are used in genome-wide association studies (GWAS).

Measured genetic variants[edit]
The Human Genome Project has allowed scientists to directly genotype the sequence of human DNA nucleotides. Once genotyped, genetic variants can be tested for association with a behavioural phenotype, such as mental disorder, cognitive ability, personality, and so on.


 * Candidate Genes. One popular approach has been to test for association candidate genes with behavioural phenotypes, where the candidate gene is selected based on some a priori theory about biological mechanisms involved in the manifestation of a behavioural trait or phenotype. In general, such studies have proven difficult to broadly replicate and there has been concern raised that the false positive rate in this type of research is high.
 * Genome-wide association studies. In genome-wide association studies, researchers test the relationship of millions of genetic polymorphisms with behavioural phenotypes across the genome. This approach to genetic association studies is largely atheoretical, and typically not guided by a particular biological hypothesis regarding the phenotype. Genetic association findings for behavioural traits and psychiatric disorders have been found to be highly polygenic (involving many small genetic effects).
 * SNP heritability and co-heritability. Recently, researchers have begun to use similarity between classically unrelated people at their measured single nucleotide polymorphisms (SNPs) to estimate genetic variation or covariation that is tagged by SNPs, using mixed effects models implemented in software such as Genome-wide complex trait analysis (GCTA). To do this, researchers find the average genetic relatedness over all SNPs between all individuals in a (typically large) sample, and use Haseman–Elston regression or restricted maximum likelihood to estimate the genetic variation that is "tagged" by, or predicted by, the SNPs. The proportion of phenotypic variation that is accounted for by the genetic relatedness has been called "SNP heritability". Intuitively, SNP heritability increases to the degree that phenotypic similarity is predicted by genetic similarity at measured SNPs, and is expected to be lower than the true narrow-sense heritability to the degree that measured SNPs fail to tag (typically rare) causal variants. The value of this method is that it is an independent way to estimate heritability that does not require the same assumptions as those in twin and family studies, and that it gives insight into the allelic frequency spectrum of the causal variants underlying trait variation.

Quasi-experimental designs[edit]
Some behavioural genetic designs are useful not to understand genetic influences on behaviour, but to control for genetic influences to test environmentally-mediated influences on behaviour. Such behavioural genetic designs may be considered a subset of natural experiments, quasi-experiments that attempt to take advantage of naturally occurring situations that mimic true experiments by providing some control over an independent variable. Natural experiments can be particularly useful when experiments are infeasible, due to practical or ethical limitations.

A general limitation of observational studies is that the relative influences of genes and environment are confounded. A simple demonstration of this fact is that measures of 'environmental' influence are heritable. Thus, observing a correlation between an environmental risk factor and a health outcome is not necessarily evidence for environmental influence on the health outcome. Similarly, in observational studies of parent-child behavioural transmission, for example, it is impossible to know if the transmission is due to genetic or environmental influences, due to the problem of passive gene-environment correlation. The simple observation that the children of parents who use drugs are more likely to use drugs as adults does not indicate why the children are more likely to use drugs when they grow up. It could be because the children are modelling their parents' behaviour. Equally plausible, it could be that the children inherited drug-use-predisposing genes from their parent, which put them at increased risk for drug use as adults regardless of their parents' behaviour. Adoption studies, which parse the relative effects of rearing environment and genetic inheritance, find a small to negligible effect of rearing environment on smoking, alcohol, and marijuana use in adopted children, [non-primary source needed] but a larger effect of rearing environment on harder drug use.[non-primary source needed]

Other behavioural genetic designs include discordant twin studies, children of twins designs, and Mendelian randomization.

General findings[edit]
There are many broad conclusions to be drawn from behavioural genetic research about the nature and origins of behaviour. Three major conclusions include:


 * 1) all behavioural traits and disorders are influenced by genes
 * 2) environmental influences tend to make members of the same family more different, rather than more similar