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 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, but a larger effect of rearing environment on harder drug use. other behavioural genetic designs include discordant twin studies, children of twins designs, and mendelian randomization. general findings there are many broad conclusions to be drawn from behavioural genetic research about the nature and origins of behaviour. three major conclusions include: all behavioural traits and disorders are influenced by genes environmental influences tend to make members of the same family more different, rather than more similar the influence of genes tends to increase in relative importance as individuals age. genetic influences on behaviour are pervasive it is clear from multiple lines of evidence that all researched behavioural traits and disorders are influenced by genes; that is, they are heritable. the single largest source of evidence comes from twin studies, where it is routinely observed that monozygotic (identical) twins are more similar to one another than are same-sex dizygotic (fraternal) twins. the conclusion that genetic influences are pervasive has also been observed in research designs that do not depend on the assumptions of the twin method. adoption studies show that adoptees are routinely more similar to their biological relatives than their adoptive relatives for a wide variety of traits and disorders. in the minnesota study of twins reared apart, monozygotic twins separated shortly after birth were reunited in adulthood. these adopted, reared-apart twins were as similar to one another as were twins reared together on a wide range of measures including general cognitive ability, personality, religious attitudes, and vocational interests, among others. approaches using genome-wide genotyping have allowed researchers to measure genetic relatedness between individuals and estimate heritability based on millions of genetic variants. methods exist to test whether the extent of genetic similarity (aka, relatedness) between nominally unrelated individuals (individuals who are not close or even distant relatives) is associated with phenotypic similarity. such methods do not rely on the same assumptions as twin or adoption studies, and routinely find evidence for heritability of behavioural traits and disorders. nature of environmental influence just as all researched human behavioural phenotypes are influenced by genes (i.e., are heritable), all such phenotypes are also influenced by the environment. the basic fact that monozygotic twins are genetically identical but are never perfectly concordant for psychiatric disorder or perfectly correlated for behavioural traits, indicates that the environment shapes human behaviour. the nature of this environmental influence, however, is such that it tends to make individuals in the same family more different from one another, not more similar to one another. that is, estimates of shared environmental effects ( c 2 ) in human studies are small, negligible, or zero for the vast majority of behavioural traits and psychiatric disorders, whereas estimates of non-shared environmental effects ( e 2 ) are moderate to large. from twin studies c 2 is typically estimated at 0 because the correlation ( r m z ) between monozygotic twins is at least twice the correlation ( r d z ) for dizygotic twins. when using the falconer variance decomposition ( 1.0 = a 2 + c 2 + e 2 +c^+e^ ) this difference between monozygotic and dizygotic twin similarity results in an estimated c 2 = 0 =0} . it is important to note that the falconer decomposition is simplistic. it removes the possible influence of dominance and epistatic effects which, if present, will tend to make monozygotic twins more similar than dizygotic twins and mask the influence of shared environmental effects. this is a limitation of the twin design for estimating c 2 . however, the general conclusion that shared environmental effects are negligible does not rest on twin studies alone. adoption research also fails to find large ( c 2 ) components; that is, adoptive parents and their adopted children tend to show much less resemblance to one another than the adopted child and his or her non-rearing biological parent. in studies of adoptive families with at least one biological child and one adopted child, the sibling resemblance also tends to be nearly zero for most traits that have been studied. similarity in twins and adoptees indicates a small role for shared environment in personality. the figure provides an example from personality research, where twin and adoption studies converge on the conclusion of zero to small influences of shared environment on broad personality traits measured by the multidimensional personality questionnaire including positive emotionality, negative emotionality, and constraint. given the conclusion that all researched behavioural traits and psychiatric disorders are heritable, biological siblings will always tend to be more similar to one another than will adopted siblings. however, for some traits, especially when measured during adolescence, adopted siblings do show some significant similarity (e.g., correlations of .20) to one another. traits that have been demonstrated to have significant shared environmental influences include internalizing and externalizing psychopathology, substance use and dependence, and intelligence. nature of genetic influence genetic effects on human behavioural outcomes can be described in multiple ways. one way to describe the effect is in terms of how much variance in the behaviour can be accounted for by alleles in the genetic variant, otherwise known as the coefficient of determination or r 2 . an intuitive way to think about r 2 is that it describes the extent to which the genetic variant makes individuals, who harbour different alleles, different from one another on the behavioural outcome. a complementary way to describe effects of individual genetic variants is in how much change one expects on the behavioural outcome given a change in the number of risk alleles an individual harbours, often denoted by the greek letter β (denoting the slope in a regression equation), or, in the case of binary disease outcomes by the odds ratio o r of disease given allele status. note the difference: r 2 describes the population-level effect of alleles within a genetic variant; β or o r describe the effect of having a risk allele on the individual who harbours it, relative to an individual who does not harbour a risk allele. when described on the r 2 metric, the effects of individual genetic variants on complex human behavioural traits and disorders are vanishingly small, with each variant accounting for r 2 < 0.3 % <0.3\%} of variation in the phenotype. this fact has been discovered primarily through genome-wide association studies of complex behavioural phenotypes, including results on substance use, personality, fertility, schizophrenia, depression, and endophenotypes including brain structure and function. there are a small handful of replicated and robustly studied exceptions to this rule, including the effect of apoe on alzheimer's disease, and chrna5 on smoking behaviour, and aldh2 (in individuals of east asian ancestry) on alcohol use. on the other hand, when assessing effects according to the β metric, there are a large number of genetic variants that have very large effects on complex behavioural phenotypes. the risk alleles within such variants are exceedingly rare, such that their large behavioural effects impact only a small number of individuals. thus, when assessed at a population level using the r 2 metric, they account for only a small amount of the differences in risk between individuals in the population. examples include variants within app that result in familial forms of severe early onset alzheimer's disease but affect only relatively few individuals. compare this to risk alleles within apoe, which pose much smaller risk compared to app, but are far more common and therefore affect a much greater proportion of the population. finally, there are classical behavioural disorders that are genetically simple in their etiology, such as huntington's disease. huntington's is caused by a single autosomal dominant variant in the htt gene, which is the only variant that accounts for any differences among individuals in their risk for developing the disease, assuming they live long enough. in the case of genetically simple and rare diseases such as huntington's, the variant r 2 and the o r are simultaneously large. additional general findings in response to general concerns about the replicability of psychological research, behavioural geneticists robert plomin, john c. defries, valerie knopik, and jenae neiderhiser published a review of the ten most well-replicated findings from behavioural genetics research. the ten findings were: "all psychological traits show significant and substantial genetic influence." "no behavioral traits are 100% heritable." "heritability is caused by many genes of small effect." "phenotypic correlations between psychological traits show significant and substantial genetic mediation." "the heritability of intelligence increases throughout development." "age-to-age stability is mainly due to genetics." "most measures of the 'environment' show significant genetic influence." "most associations between environmental measures and psychological traits are significantly mediated genetically." "most environmental effects are not shared by children growing up in the same family." "abnormal is normal." criticisms and controversies