<Ul> <Li> 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 . </Li> <Li> 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). </Li> <Li> 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 . </Li> </Ul> <Li> 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 . </Li> <Li> 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). </Li> <Li> 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 . </Li>

What are some common approaches to studying how genetics relate to outcomes such as human behavior