Heritability  is the proportion of variance caused by genetic factors of a specific trait in a population. [ 1 ]   Falconer's formula  is a mathematical  formula  that is used in  twin studies  to estimate the relative contribution of genetic vs. environmental factors to variation in a particular  trait  (that is, the heritability of the trait) based on the difference between  twin   correlations . [ 2 ]  Statistical models for heritability commonly include an error that will absorb phenotypic variation that cannot be described by genetics when analyzed. These are unique subject-specific influences on a trait. [ 1 ]  Falconer's formula was first proposed by the Scottish geneticist  Douglas Falconer . [ 3 ]


The formula is

 H

 b

 2

 =
 2
 (

 r

 m
 z

 −

 r

 d
 z

 )

 {\displaystyle {H_{b}}^{2}=2(r_{mz}-r_{dz})}

where

 H

 b

 2

 {\textstyle {H_{b}}^{2}}

  is the broad sense heritability,

 r

 m
 z

 {\displaystyle r_{mz}}

  is the (monozygotic, MZ)  identical twin  correlation, and

 r

 d
 z

 {\textstyle r_{dz}}

  is the (dizygotic, DZ)  fraternal twin  correlation. Falconer's formula assumes the equal contribution of environmental factors in MZ pairs and DZ pairs. Therefore, additional phenotypic correlation between the two pairs is due to genetic factors. Subtracting the correlation of the DZ pairs from MZ pairs yields the variance in phenotypes contributed by genetic factors. [ 4 ]  The correlation of same sex MZ twins is always higher than the DZ twin correlation with various sexes and thus all  gender differences  are evaluated as heritable. To avoid this error, only genetic studies comparing MZ twins with the same sex DZ twins are valid. Correlations between

 A
 =

 H

 b

 2

 {\textstyle A={H_{b}}^{2}}

  (additive genetics) and

 C

 {\displaystyle C}

  (common environment) must be included in the derivation shown below.


r

 m
 z

 =
 A
 +
 C
 +
 2
 ⋅

 Corr

 (
 A
 ,
 C
 )

 {\displaystyle r_{mz}=A+C+2\cdot {\text{Corr}}(A,C)}

 r

 d
 z

 =

 1
 2

 A
 +
 C
 +
 2
 ⋅

 Corr

 (

 1
 2

 A
 ,
 C
 )

 {\displaystyle r_{dz}={\frac {1}{2}}A+C+2\cdot {\text{Corr}}({\tfrac {1}{2}}A,C)}


The  Finno-Ugrian suicide hypothesis  proposes to link genetic ties originating among Finno-Ugric peoples to high rate of  suicide , claiming an  allele  common among them is responsible.


Mari  and  Udmurts  have been found to have a three times higher suicide rate than Finns and Hungarians. It has been thus theorized that such a possible allele may have arisen in those populations. [ citation needed ]


However, contrary to the hypothesis, available contemporary (1990–1994) suicide rates in the United States were uniformly negatively associated with the proportion of the population comprising people of self-reported Hungarian, Lithuanian, Polish, Russian, Slovakian, or Ukrainian descent. The findings of this first test outside Europe are therefore conflicting. A proposal based on the geographical study approach is offered to further the progress of investigations into the genetics of suicide. [ 2 ]


The  fruitless  gene  ( fru ) is a  Drosophila melanogaster   gene  that encodes several variants of a putative  transcription factor   protein . Normal  fruitless  function is required for proper development of several anatomical structures necessary for courtship, including  motor neurons  which innervate  muscles  needed for fly sexual behaviors. [ 1 ]  The gene does not have an obvious mammalian homolog, but appears to function in sex determination in species as distant as the mosquito  Anopheles gambiae . [ 2 ]


fruitless  serves as an example of how a gene or a group of genes may regulate the development and/or function of neurons involved in innate behavior.  Research on  fruitless  has received attention in the popular press, since it provokes discussion on  genetics of human sexual orientation , [ 3 ] [ 4 ]  and behaviors such as gender-specific  aggression . [ 5 ]


Male  flies with mutations in the  fruitless  gene display altered sexual behavior. Fruitfly courtship, which involves a complex male-initiated  ritual , may be disrupted in many ways by mutated  fru   alleles ;  fru  is necessary for every step in the ritual. Some alleles prevent courting entirely, while others disrupt individual components. Notably, some  loss-of-function  alleles change or remove  sexual preference . [ 1 ]


Although many genes are known to be involved in male courtship behavior, the  fruitless  gene has been considered noteworthy because it exhibits sex-specific  alternative splicing . When females produce the male-spliced gene product, they behave as males. Males that do not produce the male-specific product do not court females and are infertile. [ 1 ]  In the brain, a subset (ca. 2,000) of neurons express  fruitless [ 6 ]  and  fruitless  expression is sufficient to instruct sexually dimorphic connectivity.  [ 7 ] [ 8 ]


fruitless  has at least four  promoters , each encoding proteins containing both a BTB (Broad complex/tramtrack/bric-a-brac) domain and a  zinc finger   motif . Alternative splicing occurs at both the 5' and 3' ends, and there are several variants (other than the male- and female-specific splicing patterns). [ 1 ]   The fruitless gene locus also controls the expression of hundreds of other genes, [ 9 ]  any subset of which may actually regulate behavior.


Early work refers to the gene as  fruity , an apparent pun on both the common name of  D. melanogaster , the  fruit fly , as well as a  slang  word for  homosexual . As  social  attitudes towards homosexuality changed,  fruity  came to be regarded as offensive, or at best, not  politically correct . Thus, the gene was re-dubbed  fruitless , alluding to the lack of offspring produced by flies with the mutation. [ 10 ]   However, despite the original name and a continuing history of misleading inferences by the popular media, fruitless mutants primarily show defects in male-female courtship, though certain mutants cause male-male or female-female courtship. [ 11 ]


Gene–environment correlation  (or  genotype–environment correlation ) is said to occur when exposure to environmental conditions depends on an individual's  genotype .


Gene–environment correlations (or rGE) is  correlation  of two  traits , e.g. height and weight, which would mean that when one changes, so does the other. Gene–environment correlations can arise by both  causal and non-causal  mechanisms. [ 1 ]  Of principal interest are those causal mechanisms which indicate genetic control over environmental exposure. Genetic variants influence environmental exposure indirectly via behavior. Three causal mechanisms giving rise to gene–environment correlations have been described. [ 2 ]


Gene–environment correlation can also arise from non-causal mechanisms, including evolutionary processes and behavioral 'contamination' of the environmental measure. Evolutionary processes, such as  genetic drift  and  natural selection , can cause allele frequencies to differ between populations. For example, exposure to malaria-bearing mosquitoes over many generations may have caused the higher allele frequency among certain ethnic groups for the sickle  hemoglobin  (HbS) allele, a  recessive  mutation that causes  sickle-cell disease  but confers resistance against  malaria . [ 4 ]  In this way, HbS genotype has become associated with the malarial environment.


Twin and adoption studies  have provided much of the evidence for gene–environment correlations by demonstrating that putative environmental measures are  heritable . [ 5 ]  For example, studies of adult twins have shown that desirable and undesirable life events are moderately heritable as are specific life events and life circumstances, including divorce, the propensity to marry, marital quality and social support. Studies in which researchers have measured child-specific aspects of the environment have also shown that putative environmental factors, such as parental discipline or warmth, are moderately heritable. Television viewing, peer group orientations and social attitudes have all been shown to be moderately heritable. There is also a growing literature on the genetic factors influencing behaviors that constitute a risk to health, such as the consumption of alcohol, tobacco and illegal drugs, and risk-taking behaviors. Like parental discipline, these health related behaviors are genetically influenced, but are thought to have environmentally mediated effects on disease. To the extent that researchers have attempted to determine why genes and environments are correlated, most evidence has pointed to the intervening effects of personality and behavioral characteristics.


Environments are heritable because genotype influences the behaviours that evoke, select, and modify features of the environment. Thus, environments less amenable to behavioural modification tend to be less heritable. [ 1 ]  For example, negative life events that are beyond the control of the individual (e.g., the death of a loved one, losing one’s home in a natural disaster) have lower heritability than negative life events that may be dependent on an individual’s behaviour (e.g., getting a divorce, getting fired from a job). Similarly, personal life events (i.e., events that occur directly to an individual) are more highly heritable than network life events (i.e., events that occur to someone within an individual’s social network, thus affecting the individual indirectly).


Evidence for the existence of gene–environment correlations has recently started to accrue from  molecular genetic  investigations. The  Collaborative Studies on Genetics of Alcoholism  (COGA) group has reported that a  single-nucleotide polymorphism  in intron 7 of the gamma-aminobutyric acid A a2 receptor (rs279871; GABRA2) was associated with  alcohol dependence  and marital status. Individuals who had the high-risk GABRA2 variant (i.e., the variant associated with alcohol dependence) were less likely to be married, in part because they were at higher risk for  antisocial personality disorder  and were less likely to be motivated by a desire to please others. [ 6 ]  There is also molecular evidence for passive gene–environment correlation. A recent study found that children were almost 2.5 times more likely to be diagnosed with  attention-deficit hyperactivity disorder  (ADHD) if their mothers were divorced, separated, or never married. In this sample, however, mothers possessing the short allele of the  dopamine receptor  gene DRD2 were more likely to be divorced, separated, or never married. Moreover, their children were more likely to have ADHD. Therefore, part of the association between parental marital status and ADHD diagnosis among children in this sample is due to the  confounding variable  of maternal DRD2 genotype. [ 7 ]  Both of these studies also found evidence for  gene–environment interaction .


A  polygenic score  (PGS; also called a polygenic risk score), which is a number assigned to individuals based on variation in multiple genetic loci and their associated  regression  weights from  genome-wide association studies , can also be used to demonstrate gene–environment correlation. This effect, often referred to as "genetic nurture", is suggestive of passive gene–environment correlation when parental polygenic score independently predicts offspring outcome beyond the offspring's own PGS, and has been demonstrated for educational attainment in humans. [ 8 ] [ 9 ] [ 10 ]  Higher PGS for mental disorders such as  major depressive disorder ,  schizophrenia , and  ADHD  have also been found to be associated with higher reported exposures to stressful life events such in adults with depression. [ 11 ]


Doctors want to know whether exposure to environmental risk causes disease. The fact that environmental exposures are heritable means that the relationship between environmental exposure and disease may be  confounded  by genotype. That is, the relationship may be  spurious  (not causal), because the same genetic factors might be influencing both exposure to environmental risk and disease. In such cases, measures aimed at reducing environmental exposure will not reduce the risk for disease. On the other hand, heritability of exposure to environmental conditions itself does not mean environmental factors are not responsible for disease and so exposure reduction would benefit individuals with genetic predisposition to risk behavior.


For example, a study of children born to twin sisters investigated whether the relationship between parental divorce and offspring alcohol and  emotional  problems was causal or confounded by parental genotype. [ 12 ]  The study found that the offspring of twin sisters who were discordant for divorce had equally high levels of emotional problems, suggesting that genetic factors which made twin siblings divorce-prone also increased their children’s risk for depression and anxiety. This finding suggests that preventing the parents’ divorce would have had little impact on offspring risk for emotional problems (although the findings for alcohol problems in the children were consistent with a causal role for divorce).


The  Generalist Genes hypothesis  of learning abilities and disabilities was originally coined in an article by Plomin & Kovas (2005). [ 1 ]


The Generalist Genes hypothesis suggests that most  genes  associated with common  learning disabilities  and abilities are generalist in three ways.


The Generalist Genes hypothesis has important implications for education, cognitive sciences and molecular genetics. [ 2 ] [ 3 ] [ 4 ]


The  Genetic Studies of Genius ,  later known as the  Terman Study of the Gifted , [ 1 ]  is currently [update]  the oldest and longest-running  longitudinal study  in the field of psychology. It was begun by  Lewis Terman  at  Stanford University  in 1921 to examine the development and characteristics of  gifted  children into adulthood. [ 1 ] : xi  [ 2 ]


The results from the study have been published in five books, [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 1 ]  a  monograph , [ 7 ]  and dozens of articles. A related retrospective study of eminent men in history by  Catharine Cox , though not part of the longitudinal study, was published as part of the Genetic Studies of Genius. [ 8 ]  It further inspired the ongoing  Study of Mathematically Precocious Youth  longitudinal study.


Terman had previously performed studies in  intelligence , including his doctoral dissertation. [ 9 ]  In 1916, he adapted  Alfred Binet 's intelligence test for the  United States  and expanded its range. The result was the  Stanford–Binet Intelligence Scales , which are still in use today (in an updated form). After his service in developing the  Army Alpha  during  World War I , Terman returned to Stanford in order to start his study.


Terman had already found some bright children through his earlier research, and some of these were part of the sample in the Genetic Studies of Genius. [ 10 ]  He hired several assistants, including  Florence Goodenough  and Catharine Cox, to search the public schools of  California  for similarly gifted children. Terman initially hoped to find the 1,000 most intelligent children, [ 11 ]  but eventually found 1,444. [ 12 ]  However, Terman gradually added subjects to the study through 1928 until there were 1,528 (856 males and 672 females). [ 1 ] : 12   Not all subjects were discovered with the Stanford–Binet. Some were selected for the study with the National Intelligence Tests and the Army Alpha. The study subjects were born between 1900 and 1925, all lived in California, were 95–99% white, [ 13 ]  and the majority came from upper- or middle-class families. [ 1 ] : 11–14


Terman's goal was to disprove the then-current belief that gifted children were sickly, socially inept, and not well-rounded. Therefore, the first volume of the study reported data on the children's family, [ 14 ]  educational progress, [ 15 ]  special abilities, [ 16 ]  interests, [ 17 ]  play, [ 18 ]  and personality. [ 19 ]  He also examined the children's racial and ethnic heritage. [ 20 ]  Terman was a proponent of  eugenics , although not as radical as many of his contemporary  Social Darwinists , and believed that intelligence testing could be used as a positive tool to shape society. [ 2 ]


Based on data collected in 1921–22, Terman concluded that gifted children suffered no more health problems than normal for their age, save a little more  myopia  than average.  He also found that the children were usually social, were well-adjusted, did better in school, and were even taller than average. [ 21 ]  A follow-up performed in 1923–1924 found that the children had maintained their high  IQs  and were still above average overall. Data collected in the 1920s, also including a pioneering effort to implement above-level testing on a large scale, a practice that is widespread in  gifted education  today. [ 10 ]


Terman planned later follow-ups, and in his lifetime data would be collected in 1928, 1936, 1940, 1945, 1950, and 1955. At his death, the study was directed by Melita Oden, who collected additional data in 1960.  Robert Richardson Sears  later took charge of the study and collected data in 1972, 1977, 1982, and 1986. [ 1 ] : 18–24   Moreover, many study participants corresponded with Terman or visited Stanford University in order to keep him updated on their lives. [ 1 ] : 275–276


According to those who have access to the study archives, the files also include news articles, letters, and other documents related to the study participants. [ 22 ]  The later follow-ups asked questions about war service, college education, marital status and happiness, work, retirement, raising children, and other lifetime events and concerns. [ 23 ]


Well over half of men and women in Terman's study finished college, compared to 8% of the general population at the time. [ 24 ]  Some of Terman's subjects reached great prominence in their fields. Among them were head  I Love Lucy  writer  Jess Oppenheimer , [ 25 ]   American Psychological Association  president and educational psychologist  Lee Cronbach , [ 26 ]   Ancel Keys , [ 27 ]  and Robert Sears himself. [ 25 ]  Over fifty men became college and university faculty members. [ 28 ]  However, the majority of study participants' lives were more mundane. By the 4th volume of  Genetic Studies of Genius , Terman had noted that as adults, his subjects pursued common occupations "as humble as those of policeman, seaman, typist and filing clerk" [ 29 ]  and concluded:


At any rate, we have seen that intellect and achievement are far from perfectly correlated. [ 30 ]


The study has been criticized for not having a generalizable sample. [ 1 ] : 11  [ 31 ]  Moreover, Terman meddled in his subjects' lives, giving them letters of recommendation for jobs and college and pulling strings at Stanford to help them get admitted. [ 2 ] [ 22 ]  This makes the life outcomes of the sample biased and difficult to generalize. [ 2 ]


In his book  Fads and Foibles in Modern Sociology and Related Sciences  (p. 70–76), sociologist  Pitirim Sorokin  criticized the research, saying that Terman's selected group of children with high IQs did about as well as a random group of children selected from similar family backgrounds would have done. [ 32 ]


As in any longitudinal study, it is possible that the characteristics and behaviors of the sample are a partial result of the era in which they lived. Indeed, many members of the sample could not attend college, due to the  Great Depression  and World War II. [ 1 ] : 45   Almost half of women in the sample were  homemakers  for most of their lives. [ 1 ] : 87   Despite these shortcomings, the data from the sample is often used for studies because there is no other group of people who have been followed for so long.


As time has passed, the sample has dwindled. As of 2003, there were over 200 members of the sample still alive. [ 33 ]  The study is to continue until the final member of the sample either withdraws or dies. [ 2 ]  In the 21st century, researchers continue to publish articles based on the data collected in the Genetic Studies of Genius. For example, one article found that men who skipped a grade in childhood had higher incomes throughout adulthood. [ 34 ]


The field of  psychology  has been greatly influenced by the study of  genetics . [ 1 ]  Decades of research have demonstrated that both genetic and environmental factors play a role in a variety of behaviors in humans and animals (e.g. Grigorenko & Sternberg, 2003). The genetic basis of  aggression , however, remains poorly understood. Aggression is a multi-dimensional concept, but it can be generally defined as behavior that inflicts pain or harm on another. [ 2 ]


The genetic-developmental theory states that individual differences in a continuous  phenotype  result from the action of a large number of  genes , each exerting an effect that works with environmental factors to produce the trait. [ 3 ]  This type of trait is influenced by multiple factors making it more complex and difficult to study than a simple  Mendelian  trait (one  gene  for one  phenotype ). [ 3 ]


Past thoughts on genetic factors influencing aggression, specifically in regard to sex chromosomes, tended to seek answers from  chromosomal abnormalities . [ 4 ]  Four decades ago, the  XYY  genotype was (erroneously) believed by many to be correlated with aggression. In 1965 and 1966, researchers at the  MRC  Clinical & Population Cytogenetics Research Unit led by Dr. Court Brown at  Western General Hospital  in  Edinburgh  reported finding a much higher than expected nine XYY men (2.9%) averaging almost 6 ft. tall in a survey of 314 patients at the  State Hospital  for  Scotland ; seven of the nine XYY patients were mentally retarded. [ 5 ]  In their initial reports published before examining the XYY patients, the researchers suggested they might have been hospitalized because of aggressive behavior. When the XYY patients were examined, the researchers found their assumptions of aggressive behavior were incorrect. Unfortunately, many science and medicine textbooks quickly and uncritically incorporated the initial, incorrect assumptions about XYY and aggression—including psychology textbooks on aggression. [ 6 ]


The XYY genotype first gained wide notoriety in 1968 when it was raised as a part of a defense in two murder trials in  Australia  and  France . In the  United States , five attempts to use the XYY genotype as a defense were unsuccessful—in only one case in 1969 was it allowed to go to a jury—which rejected it. [ 7 ]


Results from several decades of long-term follow-up of scores of unselected XYY males identified in eight international newborn chromosome screening studies in the 1960s and 1970s have replaced pioneering but  biased  studies from the 1960s (that used only institutionalized XYY men), as the basis for current understanding of the XYY genotype and established that XYY males are characterized by increased height but are not characterized by aggressive behavior. [ 8 ] [ 9 ]  Though the link currently between genetics and aggression has turned to an aspect of genetics different from chromosomal abnormalities, it is important to understand where the research started and the direction it is moving in today.


As with other topics in  behavioral genetics , aggression is studied in three main experimental ways to help identify what role  genetics  plays in the  behavior :


These three main experimental types are used in  animal studies , studies testing heritability and  molecular genetics , and gene/environment interaction studies. Recently, important links between aggression and genetics have been studied and the results are allowing scientists to better understand the connections. [ 10 ]


The  heritability  of aggression has been observed in many animal strains after noting that some strains of birds, dogs, fish, and mice seem to be more  aggressive  than other strains.  Selective breeding  has demonstrated that it is possible to select for genes that lead to more aggressive behavior in animals. [ 10 ]  Selective breeding examples also allow researchers to understand the importance of  developmental  timing for genetic influences on aggressive behavior. A study done in 1983 (Cairns) produced both highly aggressive male and female strains of mice dependent on certain developmental periods to have this more aggressive behavior expressed. These mice were not observed to be more aggressive during the early and later stages of their lives, but during certain periods of time (in their middle-age period) were more violent and aggressive in their attacks on other mice. [ 11 ]  Selective breeding is a quick way to select for specific  traits  and see those selected traits within a few generations of  breeding . These characteristics make selective breeding an important tool in the study of genetics and aggressive behavior.


Mice  are often used as a model for human  genetic  behavior since mice and humans have  homologous   genes  coding for homologous  proteins  that are used for similar functions at some biological levels. [ 12 ]  Mice aggression studies have led to some interesting insight in human aggression. Using  reverse genetics , the  DNA  of genes for the receptors of many  neurotransmitters  have been  cloned  and  sequenced , and the role of neurotransmitters in rodent aggression has been investigated using  pharmacological  manipulations.  Serotonin  has been identified in the offensive attack by male mice against intruder male mice. Mutants were made by manipulating a receptor for serotonin by deleting a gene for the serotonin receptor. These mutant male mice with the knockout  alleles  exhibited normal behavior in everyday activities such as eating and exploration, but when prompted, attacked intruders with twice the intensity of normal male mice. In offense aggression in mice, males with the same or similar  genotypes  were more likely to fight than males that encountered males of other genotypes. Another interesting finding in mice dealt with mice reared alone. These mice showed a strong tendency to attack other male mice upon their first exposure to the other animals. The mice reared alone were not taught to be more aggressive; they simply exhibited the behavior. This implicates the natural tendency related to biological aggression in mice since the mice reared alone lacked a parent to model aggressive behavior. [ 13 ]


Oxidative stress  arises as a result of excess production of reactive oxygen species in relation to defense mechanisms, including the action of  antioxidants  such as superoxide dismutase 1 ( SOD1 ).  Knockout of the Sod1 gene was experimentally introduced in male mice leading to impaired  antioxidant  defense. [ 14 ]   These mice were designated ( Sod1-/- ).   The  Sod1-/-  male mice proved to be more aggressive than both  heterozygous  knockout males ( Sod1+/- ) that were 50% deficient in SOD1, and wild-type males ( Sod1+/+ ). [ 14 ]   The basis for the association of oxidative stress with increased aggression has not yet been determined.


Experiments designed to study biological mechanisms are utilized when exploring how  aggression  is influenced by  genetics .  Molecular genetics  studies allow many different types of behavioral traits to be examined by manipulating  genes  and studying the effect(s) of the manipulation. [ 15 ]


A number of  molecular genetics  studies have focused on manipulating candidate aggression  genes  in mice and other animals to induce effects that can be possibly applied to humans. Most studies have focused on  polymorphisms  of  serotonin  receptors,  dopamine  receptors, and  neurotransmitter  metabolizing  enzymes . [ 3 ]  Results of these studies have led to  linkage analysis  to map the serotonin-related genes and impulsive aggression, as well as dopamin-related genes and proactive aggression. In particular, the serotonin  5-HT  seems to be an influence in inter-male  aggression  either directly or through other molecules that use the 5-HT pathway. 5-HT normally dampens aggression in animals and humans. Mice missing specific genes for 5-HT were observed to be more aggressive than normal mice and were more rapid and violent in their attacks. [ 16 ]  Other studies have been focused on neurotransmitters. Studies of a  mutation  in the neurotransmitter metabolizing enzyme  monoamine oxidase A  (MAO-A) have been shown to cause a syndrome that includes violence and impulsivity in humans. [ 3 ]  Studies of the molecular genetics pathways are leading to the production of  pharmaceuticals  to fix the pathway problems and hopefully show an observed change in aggressive behavior. [ 16 ]


In determining if a  trait  is related to genetic factors or environmental factors,  twin studies  and adoption studies are used. These studies examine  correlations  based on similarity of a trait and a person's genetic or environmental factors that could influence the trait.  Aggression  has been examined via both twin studies and adoption studies. The human genetics related to aggression have been studied and the main genes have been identified. The  DAT1  and  DRD2  genes are heavily related to the genetics of aggression. [ 17 ] [ 18 ]  The DAT1 gene plays a role for its heavy relation to regulation of neurotransmission. The DRD2 Gene results in humans finding seemingly rewarding paths such as drug abuse. Through studies, DRD2 seems to be a risk factor in delinquency when children have related family trauma events. [ 19 ]


DAT1 is a gene that regulates dopamine levels in the brain. This study revealed that variations in the DAT1 gene were correlated with higher levels of aggression. Some people that have variations of the DAT1 gene exhibit more aggressive behaviors. DAT2 controls how the brain responds to dopamine. Certain combinations of DAT1 and DAT2 genes were linked to an increase or decrease in aggressive behaviors. While the relationship remains unclear, there is certainly a correlation between certain forms of DAT1 and DAT2 and varying combinations of each.  [ 20 ]  Changes in these genes can cause changes in neurotransmitter levels. When typical neurotransmitter levels change, other bodily behaviors are also affected. Examples of other functions that are impacted are intelligence, mood, and memory.  [ 21 ]


Twin studies  are studies typically conducted comparing  identical  and  fraternal  twins. They aim to reveal the importance of environmental and  genetic  influences for traits,  phenotypes , and disorders. Before the advancement of  molecular genetics , twin studies were almost the only mode of investigation of  genetic  influences on personality.  Heritability  was estimated as twice the difference between the  correlation  for identical, or monozygotic, twins and that for fraternal, or dizygotic, twins. Early studies indicated that personality was fifty percent genetic. Current thinking holds that each individual picks and chooses from a range of  stimuli  and events largely on the basis of their  genotype  creating a unique set of experiences; basically meaning that people create their own environments. [ 13 ]  It has been determined that there is a window in childhood that certain trauma events can trigger a lifetime of aggressive behavior. [ citation needed ]


Adoption studies  are a specific research designs that involve comparing traits between an adopted child and their biological and adoptive parents. These experiments aim to assess both biological and environmental factors that may be attributed to aggression. Adoption studies have shown stronger similarities between adopted children and their biological parents, indicating that there is a genetic component at play. However, children have also shown similarities with their adoptive parents, indicating that there are environmental factors as well. These studies further support the complex nature of aggression by proving that there are both biological and environmental factors involved. More research needs to be conducted to truly prove the causes of aggression.  [ 22 ]


Over time, studies pertaining to the genetics of aggression have improved, and become an interesting research topic for those looking for research opportunities. Experiments started in 1963 with the  Milgram's experiment . The results of this experiment proved that in certain situations, people can be coaxed into aggression and violence. The next big experiment pertaining to the genetics of aggression took place in 1973 as part of the  Stanford prison experiment . The conclusion drawn from this experiment was that in many cases, aggression is very unexpected at certain points. It was considered to be "elicited." This also revealed that aggression is often triggered in situations where someone feels an ideology that they hold a very powerful authority over someone else. It was concluded from both experiments that social aspects prove to be a big factor in the way people act aggressively. It was also concluded that every person has a potential to output aggressive behavior, but what is different between people is the extent of the point it takes to reach that output. [ citation needed ]


Aggression can manifest in different ways between biological males and females. A study evaluated these differences by using EEG and ECG to monitor neurobiological responses to aggravating stimuli. It was shown that anger and physical aggression was much greater in men than women. Men also scored higher on a scale regarding reactive aggression. The EEG test also supported the idea that women show weaker responses regarding aggression. It was also shown that men and women follow different pathways in the brain when aggression is invoked, although further studies are needed in order to solidify these findings.  [ 23 ]


Aggression can have many causes, including environmental factors. Environmental factors include any physical, chemical, and biological environmental factors that can influence aggression. Studies have shown that neighborhood greenspace can vastly reduce aggressive behaviors in children and adolescents. One proposed explanation for this finding is that greenspace has been proven to reduce stress and depression. HIgher stress and depression levels in parents have been shown to increase aggressive behaviors in children. By lowering stress and depression in parents, children are more likely to show a decrease in aggressive behaviors. In addition, greenspace promotes participation in physical activity and social involvement. Another study revealed that low-frequency, high-intensity, and continuous noises were associated with more aggressive behaviors.  [ 24 ]


Like many other medical conditions,  obesity  is the result of an interplay between environmental and genetic factors. [ 2 ] [ 3 ]   Studies have identified variants in several genes that may contribute to weight gain and body fat distribution, although only in a few cases are genes the primary cause of obesity. [ 4 ] [ 5 ]


Polymorphisms  in various  genes  controlling  appetite  and  metabolism  predispose to obesity under certain dietary conditions.  The percentage of obesity that can be attributed to genetics varies widely, depending on the population examined, from 6% to 85%, [ 6 ]  with the typical estimate at 50%. It is likely that in each person a number of genes contribute to the likelihood of developing obesity in small part, with each gene increasing or decreasing the odds marginally, and together determining how an individual responds to the environmental factors. [ 7 ]  As of 2006, more than 41 sites on the human genome have been linked to the development of obesity when a favorable environment is present. [ 8 ]  Some of these obesogenic (weight gain) or  leptogenic  (weight loss) genes may influence the obese individual's response to weight loss or weight management. [ 9 ]


Although genetic deficiencies are currently considered rare, variations in these genes may predispose to common obesity. [ 10 ] [ 11 ] [ 12 ]  Many candidate genes are highly expressed in the  central nervous system . [ 13 ]


Several additional loci have been identified. [ 14 ]  Also, several quantitative trait loci for  BMI  have been identified.


Confirmed and hypothesized associations include:


Some studies have focused upon inheritance patterns without focusing upon specific genes. One study found that 80% of the offspring of two obese parents were obese, in contrast to less than 10% of the offspring of two parents who were of normal weight. [ 30 ]


The  thrifty gene hypothesis  postulates that due to dietary scarcity during human evolution people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would more likely survive  famine . This tendency to store fat, however, would be maladaptive in societies with stable food supplies. [ 31 ]  This is the presumed reason that  Pima  Native Americans, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle. [ 32 ]


Numerous studies of laboratory rodents provide strong evidence that genetics play an important role in obesity. [ 33 ] [ 34 ]


The risk of obesity is determined by not only specific genotypes but also gene-gene interactions. However, there are still challenges associated with detecting gene-gene interactions for obesity. [ 35 ]


There are also genes that can be protective against obesity. For instance, in  GPR75  variants were identified as such alleles in ~640,000 sequenced  exomes  which may be relevant to e.g. therapeutic strategies against obesity. [ 36 ] [ 37 ]  Other candidate anti-obesity-related genes include  ALK , [ 38 ]   TBC1D1 , [ 39 ]  and  SRA1 . [ 40 ]


The term "non-syndromic obesity" is sometimes used to exclude these conditions. [ 41 ]  In people with early-onset severe obesity (defined by an onset before 10 years of age and  body mass index  over three  standard deviations  above normal), 7% harbor a single locus mutation. [ 42 ]


Related:


The  genetics of social behavior  is an area of research that attempts to address the question of the role that genes play in modulating the neural circuits in the brain which influence social behavior. Model genetic species, such as  D.melanogaster  (common fruit fly) and  Apis mellifera  (honey bee), have been rigorously studied and proven to be instrumental in developing the science of genetics. Many examples of genetic factors of social behavior have been derived from a bottom-up method of altering a gene and observing the change it produces in an organism. Sociogenomics is an integrated field that accounts for the complete cellular genetic complement of an organism from a top-down approach, accounting for all biotic influences  that effect behavior on a cellular level.


Sociogenomics , a subdiscipline of  genomics , is an integrative approach to behavioral biology that compares genomic data to behavioral  phenotype . Of particular interest are differential gene expression of mRNA ( transcriptomics ) and protein transcription ( proteomics ) that correspond to changes in behavior. Data of this sort is especially useful when comparing the genomic qualities of organisms with varying degrees of social organization. [ 1 ]


While sociogenomics integrates more fields of study and is more encompassing than classical genetics, the methodology is still considered  forward genetics . The goal is to determine genes or sets of genes and their artifacts that contribute to the expression of a phenotype.


Sociogenomic methodology has been applied to understanding the biology of eusociality include its cellular origin, caste determination in a  eusocial  hierarchy, and the mechanisms that mediate  division of labor . Efforts in genome sequencing have allowed researchers to examine eusocial insect behavior from a molecular perspective.


Notable progress in this field was made by the  Honey Bee Genome Sequencing Consortium , led by  Gene E. Robinson , which published and made public a completed honey bee ( Apis mellifera ) genome in October 2006. [ 2 ]  Completion of the honey bee genome and other model organism genomes has made further between-species sociogenomic comparisons possible.


To examine higher insect social order, researchers looked into the potential evolutionary history of a “foraging gene” in honey bees ( Apis mellifera ). Honey bees have a several week lifespan divided between two phases—one spent caring for the hive, the other spent foraging. The regulation of social foraging is important to maintain division of labor, requisite of eusocial organization. In order to discover how foraging in bees is genetically encoded, the honey bee genome was searched for genes that may be shared by other species. A molecular basis for feeding behavior has been determined in  Drosophila melanogaster , which shares a common insect ancestor. The “foraging gene” in  D. melanogaster  encodes a  cGMP  mediated  protein kinase  (PKG).  Naturally occurring allelic variation produces  behavioral syndromes  in  D. melanogaster , both “sitters” and “rovers”. The needs of a honey bee colony are communicated between bees by pheromones, chemical signals which trigger behavioral responses. Honey bees have a variant of the same foraging gene that controls the onset of foraging behavior. Elevated expression of this gene correlates with increased foraging activity; precocious foraging was induced in young workers by experimentally introducing PKG.


Further clues to the genetic origins of eusociality have been derived by comparing quality of genomic processes. Also applying to  A. mellifera ; by looking at the degree of  genetic linkage  and chromosomal recombination rates, light may be shed on the consequence of  group selection  on a eusocial insect colony. Within the Order  Hymenoptera , primitively and highly eusocial species tend to have greater gene linkage and significantly higher more DNA recombination events than non-social species.  This trend continues within groups of eusocial species, highly eusocial species have highly recombinant genomes. While contested, recombination activity might originate from the influence of group selection acting on developing eusocial organization in haplodiploids, where colonies that can best maintain a stable coefficient of relatedness are favored. [ 3 ]


An early study also determined the cellular basis of the discrete caste morphology of  A. mellifera . Queens arise when workers in a colony selectively feed chosen larvae  royal jelly . The caste differentiation occurs through an epigenetic process; non-heritable factors contributing to gene expression. Queen and worker morphological forms both come occur from the same genome, royal jelly nourishment is the non-genetic determiner. The pathway to queen morphs is through increased mRNA translation in the  cytosol . Biogenesis of organelles occurs at the same rate in both types of larvae, as evidenced by the ratio of mitochondrial DNA to nuclear DNA. Special feeding leads to an increase of metabolic rate for larval queen to facilitate the energy requirement to develop their larger body size. [ 4 ]


In songbirds,  egr1  is a transcription factor encoding gene that is active in the auditory forebrain when hearing a song from another songbird. The strength of the expression of  egr1  has much variability, dependent on the nature of the song. Songs previously unheard result in strong responses whereas familiar songs result in little or no response. Pure tones or white noise do not evoke any response. It is thought that the purpose of this genetic response to social stimuli is to update the brain's catalog of the changing natural environment. For example, it would be advantageous for a songbird to express more  egr1  in a situation where there is a new song heard (a potential intruder) compared to the familiar song of a known individual. In contrast, for the species of highly social  cichlid  fish  A. burtoni , the  egr1  gene plays an indirect role in reproduction. In this species, there is an established social dominance hierarchy and an individual's position determines their access to resources for reproduction. If the alpha male is removed from the group, a previous subordinate starts exhibiting dominant behavior and  egr1  is expressed in hypothalamus neurons that are responsible for producing a  neuropeptide  linked to sexual reproduction.
Overall, the role of transcription factor  egr1  in the context of social behavior clearly shows the link between genes and behavior. As a corollary to that described above, given an environmental cue  egr1  will induce or suppress the transcription of other genes.  Egr1  shows how social experience may trigger changes in the brain's gene networks. With higher capacity screening techniques, the expression of many genes simultaneously in response to social stimuli will provide a more complete picture. [ 5 ]


The neurobiology of drosophila mating behavior is an area of research that has studied in detail and has elucidated the genetic basis for behavior. The male courts a female based on  pheromones  from the female and previous experience courting other potential mates. The female accepts or rejects the male's courtship also based on pheromones, the acoustics of his courtship song, and her readiness to mate. The mating behavior of drosophila had been described almost a century ago, and the genetics of these behaviors have been studied for several decades. The current interest in neurobiology is trying to understand the neural circuits that provide the basis of action selection—how the brain maps sensory input, internal states, and individual experience to behavioral decisions.


The pathways that govern the mapping of pheromones to the brain of drosophila are beginning to be understood in detail. Pheromones are detected by  olfactory sensory neurons  (OSNs). A well-studied pheromone is cVA, which suppresses male courtship behavior when the male detects it from a female. cVA complexes with other proteins to form a  ligand , which binds to the  odorant receptor  Or67d present in OSNs, which is specific for cVA. In turn, the OSNs grow axons that will connect to the  glomerulus  DA1 in the  antennal lobe , which is analogous to the  olfactory bulb  in mammals. This glomerulus then connects to DA1  projection neurons  (PNs) which relay the pheromone signal further to higher brain centers in the protocerebrum (anterior part of an  arthropod brain ). It is noteworthy that there is significant neuronal convergence taking place between the OSNs and PNs—about 50 OSN inputs to 4 PNs.


Another pathway that has been studied is that involving another odorant receptor called Or47b, which is connected to the VA1v glomerulus. Its respective pathway conveys pheromones from odors in both sexes, and when the genetics of the involved neurons is changed, male courtship is delayed. As a simple model, one would view the integration of the Or67d/DA1 and Or47b/VA1v pathways as a way to describe the initiation of mating behavior in drosophila. The former will tend to inhibit male courtship, whereas the latter is thought to stimulate mating.


It is thought that the difference in the  fru  gene causes the bulk of the distinction in sexual differentiation in neural circuits. Although the sensory and motor circuits are nearly identical in both sexes, the  fru  gene fine tunes these according to the needs of either sex. There is learning taking place when a male engages in courtship behavior. A male learns by experience, after courtship rejection by females that have already mated he learns not to pursue other mated females. Similarly, courtship of receptive virgin females is learned after past mating successes. The  mushroom bodies  are a probable site for this experience-dependent modulation of pheromones, as disrupting  fru  in neurons in this area reduces short term courtship behavior. Long term courtship is suppressed by the presence of certain proteins in this region of the brain. [ 6 ]


For females, the decision whether to mate or not when courted by a male largely depends on the courtship song. Analogous to OSNs, the female's  Johnston's organ neurons  (JONs) distinguish the quality of the song, and a distinct mechanical stimuli projects signals to specific regions of the brain, which can lead to mating. The reluctance for a female to mate again after having mated before has a molecular basis. In the male  Drosophila  ejaculate, there is a sex peptide (SP) which binds to the sex peptide receptor (SRP) in the female's  fru  neurons, disrupting pathways that would compel the female to mate again.


Future research in this area hopes to further explain how the chemical and auditory signals are processed and mapped to behaviors in the fly's brain. Though the molecular mechanisms in the pathways vary between mammals and insects, it has been shown that the information is processed in similar ways. The relative simplicity of fly nervous systems could eventually hint at how neural circuits solve complex behavioral decision making.


In the past few decades, it has been discovered that  oxytocin  and  vasopressin  neuropeptides have key roles in the regulation of social cognition and behavior in mammals. Although homologs have been discovered which are pervasive across many taxa which have similar roles in social and reproductive behaviors, the specific influenced behaviors are quite diverse. For example, in snails the homolog for oxytocin/vasopressin conopressin modulates ejaculation in males and egg laying in females. On the other hand, for vertebrates there is  sexual dimorphism  in the neuropeptides—oxytocin induces maternal behavior in females and vasopressin induces territoriality, aggression and reproduction in males. In sheep, oxytocin has another effect on a female in addition to a generalized increase in maternal behavior—it induces mother-infant bond selectivity by priming the mother's  olfactory bulb , and the mother selectively learns the offspring's scent.


An insightful study of vasopressin is its role in the stimulation of monogamous behavior. The V1a  vasopressin receptor  gene is a mechanism most widely studied. Different species of  voles  were studied, prairie voles which are monogamous in nature and montane voles, which tend towards polygamy. Using  viral vector  mediated gene expression, which allows the cross-species transplanting of genes, when the V1a receptor expression was increased in the reward and reinforcement  neural circuitry  of montane voles, they acquired a more selective preference for their mate. Their behavior became more akin to that of prairie voles. Therefore, it is alteration of vasopressin receptor gene expression patterns is thought to affect social behavior, rather than the neuropeptide itself. A proposed mechanism for the difference in these patterns is the variation of  microsatellite DNA  length that is upstream of the V1a receptor gene—short microsatellite DNA in the  5'  flanking region of the gene has a different effect on prairie vole behavior than longer microsatellite DNA. Whether this is a mechanism that is replicable in the wild is uncertain. [ 7 ]


Genoeconomics  is an interdisciplinary field of  protoscience  that aims to combine  molecular genetics  and  economics . [ 1 ]


Genoeconomics is based on the idea that economic indicators have a genetic basis — that a person's  financial  behaviour can be traced to their  DNA  and that  genes  are related to  economic behaviour . As of 2023, the results have been inconclusive. Some minor correlations may have been identified between genetics and economic preferences. [ 2 ]


The word  genoeconomics  was coined in 2007. [ 3 ]


The field of economics and the economic indicators used by economists predate the  Empiricist Age . [ 4 ]  Genoeconomics adds biological foundations to these traditional economic indicators. [ 4 ]


Quantitative genetic data was not available to researchers until the year 2000, when the human genome was sequenced as part of the  Human Genome Project . [ 3 ]   Genetic milestones  of the late 20th and early 21st century, such as the sequencing of the human genome, has spurred interest in research combining economics and genetics. [ citation needed ]


Genoeconomics involves the study of  single-nucleotide polymorphisms  (SNPs). [ 3 ]  The field of genoeconomics uses genetic data to infer economic preferences such as  time preference ,  risk aversion , and educational attainment, [ 3 ]  as well as  macroeconomic  data such as per-capita income. [ 5 ]  For example, genoeconomic methodology was used in a 2012 study of  tobacco taxes in the United States , where such taxes vary across jurisdictions, to look at "the interaction of a single nicotinic receptor and state-level tobacco taxes to predict tobacco use". [ 3 ]  Additionally, genoeconomic research in 2013 found that two-fifths of the "variance of educational attainment is explained by genetic factors". [ 6 ]


Some genoeconomic researchers claim that the economic success of a country can be predicted by its  genetic diversity . [ 5 ]  The American economist  Enrico Spolaore  says that genoeconomic work could "reduce barriers to the flows of ideas and innovations across populations". [ 5 ]


Genoeconomic research is prone to the public misconception that genetically-influenced behaviours are separate from environmental factors. [ 7 ]  The authors of a 2012 paper said that their work "is not about a  nature or nurture  debate". [ 5 ]


Nature  published an online article written in 2012 about the various reactions on the subject. [ 8 ]  The field is criticized by biologists for lacking methodological rigour, [ 5 ]  drawing conclusions about causation based on  causal correlation , [ 3 ]  and working with small sample sizes. [ 5 ]  The political implications of the field are also a concern for some scientists; anticipating the publication of a genoeconomics article in the journal  American Economic Review , a group of scientists and social scientists wrote an open letter which said that "the suggestion that an ideal level of genetic variation could foster economic growth and could even be engineered has the potential to be misused with frightening consequences to justify indefensible practices such as ethnic cleansing or genocide". [ 5 ]


As with other  genetic-association research , [ 9 ]  the  reproducibility  of genoeconomic experiments is troublesome to the field. [ 10 ]  The small sample sizes used in genoeconomic research are also a problem. [ 11 ]  Commonly cited by scientists as a way to improve genoeconomic research is the use of more statistically  homogeneous  samples. [ 12 ]


In  behavioral genetics  and  epidemiology , the " Gloomy Prospect " refers to the notion that  non-shared environmental influences  are unsystematic, idiosyncratic, serendipitous events. It is generally used to describe the messy and individualized tiny and innumerable, but causal environmental effects. It can also be used as a label. [ 1 ]


The phrase, "gloomy prospect", was coined in a paper by  Plomin  and Daniels (1987), a review of biometric family studies, which intended to study why there existed such a large variation of traits of siblings despite being within the same family. They explain that, "One gloomy prospect is that the salient environment might be unsystematic, idiosyncratic, or serendipitous events such as accidents, illnesses, and other traumas, as biographies often attest... It is possible that nonshared environmental influences could be unsystematic in the sense of stochastic events that, when compounded over time, make children in the same family different in unpredictable ways" [ 2 ]


Turkheimer  and Waldron (2000) conducted a  meta-analysis  on the influx of new literature inspired by Plomin and Daniels (1987) regarding the systematic effects of environmental differences within families. The authors conclude in support of the gloomy prospect that their "quantitative review shows that measured nonshared environmental variables do not account for a substantial portion of the nonshared variability posited by biometric studies of behavior". [ 3 ] [ 4 ]  In  The Three Laws of Behavioral Genetics,  from Turkheimer (2000), it states that "The gloomy prospect is true. Non-shared environmental variability predominates not because of the systematic effects of environmental events that are not shared among siblings, but rather because of the unsystematic effects of all environmental events, compounded by the equally unsystematic processes that expose us to environmental events in the first place." [ 5 ]


Smith (2011) brings the gloomy prospect with  epidemiology  as an underlying mechanism of chance events. While he suggests that epidemiologists should embrace randomness in population health research and practice, he also noted that what seemed random at one level might be predictable at a different level. [ 6 ] [ 7 ]  However, the utility of embracing the gloomy prospect in epidemiology is not supported universally. [ 8 ]


The  God gene  hypothesis proposes that human  spirituality  is influenced by heredity and that a specific  gene , called  vesicular monoamine transporter 2  (VMAT2), predisposes humans towards  spiritual  or  mystic  experiences. [ 1 ]  The idea has been proposed by  geneticist   Dean Hamer  in the 2004 book called  The God Gene: How Faith is Hardwired into our Genes .


The God gene hypothesis is based on a combination of  behavioral genetic , neurobiological and psychological studies. [ 2 ]  The major arguments of the hypothesis are: (1) spirituality can be  quantified  by psychometric measurements; (2) the underlying tendency to spirituality is partially  heritable ; (3) part of this heritability can be attributed to the gene VMAT2; (4) this gene acts by altering  monoamine  levels; and (5) spirituality provides an evolutionary advantage by providing individuals with an innate sense of optimism.


According to the God Gene hypothesis, spirituality has a genetic component, of which ( VMAT2 ) comprises one component by contributing to sensations associated with   mystic  experiences, including the  presence of God  and feelings of connection to a larger universe.


The research uses the self-transcendence scale developed by psychologist  Robert Cloninger  to quantify spirituality using three sub-scales:  "self-forgetfulness" (as in the tendency to become totally absorbed in some activity, such as reading); "transpersonal identification" (a feeling of connectedness to a larger universe); and "mysticism" (an openness to believe things that remain unproven, such as  ESP ).   Cloninger suggests that taken together, these measurements are a reasonable way to  quantify  (make measurable) an individual's propensity to be  spiritual .


The self-transcendence measure was shown to be  heritable  by classical  twin studies  conducted by Lindon Eaves and Nicholas Martin. Their work demonstrated that approximately 40% of the variation in self-transcendence was due to genes.  By contrast, specific religious beliefs (such as belief in a particular deity) were found to have no genetic basis and are instead cultural units or  memes .  Similar conclusions were drawn from studies of identical twins reared apart.


In order to identify some of the specific genes involved in self-transcendence, Hamer analyzed DNA and personality score data from over 1,000 individuals and identified one particular locus, VMAT2, with a significant correlation.  VMAT2 codes for a vesicular monoamine transporter that plays a key role in regulating the levels of the brain chemicals  serotonin , dopamine and norepinephrine.  These monoamine transmitters are in turn postulated to play an important role in regulating the brain activities associated with mystic beliefs.


Hamer hypothesized that self-transcendence might provide an evolutionary advantage by providing human beings with an innate sense of optimism that gives people the will to keep on living and procreating, despite the inevitability of death, and promoting better health and recovery from diseases.


In the brain, VMAT2 proteins are located on  synaptic vesicles . VMAT2 transports  monoamine neurotransmitters  from the  cytosol  of monoamine  neurons  into vesicles. Developmental biologist and science blogger  PZ Myers  argues: "It's a pump. A teeny-tiny pump responsible for packaging a neurotransmitter for export during brain activity. Yes, it's important, and it may even be active and necessary during higher order processing, like religious thought. But one thing it isn't is a 'god gene.'" [ 3 ]


Popular science writer  Carl Zimmer  said that VMAT2 can be characterized as a gene that accounts for less than one percent of the variance of self-transcendence scores. These, Zimmer says, can signify anything from belonging to the Green Party to believing in  ESP .  Zimmer also points out that the God Gene theory is based on only one unpublished, unreplicated study. [ 4 ]


However, Hamer notes that the importance of the VMAT2 finding is not that it explains all spiritual or religious feelings, but rather that it points the way toward one neurobiological pathway that may be important. Currently, there are several VMAT2 inhibitors marketed as drugs including  deutetrabenazine ,  tetrabenazine , and  valbenazine . [ 5 ]   The question of the God Gene could be answered by experimental studies.


John Polkinghorne , a theoretical physicist and Anglican priest, member of the  Royal Society  and  Canon   Theologian  at  Liverpool Cathedral , was asked for a comment on Hamer's theory by the  British  national daily newspaper,  The Daily Telegraph . He replied: "The idea of a God gene goes against all my personal theological convictions. You can't cut faith down to the lowest common denominator of genetic survival. It shows the poverty of  reductionist  thinking." [ 6 ] [ 7 ]


Walter Houston, the  chaplain  of  Mansfield College, Oxford , and a fellow in  theology , told the  Telegraph : "Religious belief is not just related to a person's constitution; it's related to society, tradition, character—everything's involved. Having a gene that could do all that seems pretty unlikely to me."


Hamer responded that the existence of such a gene would not be incompatible with the existence of a personal God: "Religious believers can point to the existence of God genes as one more sign of the creator's ingenuity—a clever way to help humans acknowledge and embrace a divine presence." [ 7 ]  He repeatedly notes in his book that, "This book is about whether God genes exist, not about whether there is a God." [ 8 ]


Hereditary Genius: An Inquiry Into Its Laws and Consequences  is a book by  Francis Galton  about the  genetic inheritance  of  intelligence . It was first published in 1869 by  Macmillan Publishers . [ 1 ]  The first American edition was published by  D. Appleton & Company  in 1870. [ 2 ]  It was Galton's first major work written from a  hereditarian  perspective. [ 3 ]  It was later referred to as "the first serious study of the inheritance of intelligence" [ 4 ]  and as "the beginning of scientific interest in the topic of  genius ." [ 5 ]


In the book, Galton claimed that the sons of men whom he considered "eminent" in a given profession were more likely to achieve such eminence themselves than if they were not closely related to eminent individuals. He interpreted this pattern as evidence for genetic transmission of human intelligence, without considering the environment. [ 6 ]   Nicholas W. Gillham  stated "He (Galton) dismissed the obvious objection that an eminent father was more likely to find a suitable position for his son than one less fortunate. That is, environment might be important too." [ 6 ]


Galton’s controversial theories of intelligence have been influential, shaping the perspective of numerous researchers. [ 7 ]


Alfred Russel Wallace  wrote a favourable review of  Hereditary Genius  in  Nature , concluding that the book "...will take rank as an important and valuable addition to the science of  human nature ." [ 8 ]  In general, contemporary scientists in  Victorian England  reviewed the book favourably, but reception among non-scientific Victorian readers was more mixed: religious commentators were much more critical of the book than were those of neither a scientific nor a religious background. [ 9 ]  Writing in  the Journal of Anthropology , George Harris wrote, "We thank Mr. Galton for leading the way. We have canvassed his opinions freely; and, frequently as we differ from him, we must again assert our belief as to the value of his efforts, and the candid manner in which he has conducted his inquiries". [ 10 ]   Charles Darwin , a cousin of Galton, praised the book, writing in a letter to his cousin,


I have only read 50 pages of your book (to Judges), but I must exhale myself, else something will go wrong with my inside. I do not think I ever in all of my life read anything more interesting and original—and how well and clearly you put every point!" [ 6 ]


Research on the  heritability of IQ  inquires into the degree of variation in IQ within a  population  that is due to  genetic variation  between individuals in that population. There has been significant controversy in the academic community about the heritability of IQ since research on the issue began in the late nineteenth century. [ 1 ] [ 2 ]   Intelligence  in the normal range is a  polygenic trait , meaning that it is influenced by more than one gene, [ 3 ] [ 4 ]  and in the case of intelligence at least 500 genes. [ 5 ]  Further, explaining the similarity in IQ of closely related persons requires careful study because environmental factors may be correlated with genetic factors. Outside the normal range, certain single gene  genetic disorders , such as  phenylketonuria , can negatively affect intelligence. [ 6 ]


Early  twin studies  of adult individuals have found a heritability of IQ between 57% and 73%, [ 7 ]  with some recent studies showing heritability for IQ as high as 80%. [ 8 ]  IQ goes from being weakly correlated with genetics for children, to being strongly correlated with genetics for late teens and adults. The heritability of IQ increases with the child's age and reaches a plateau at 14–16 [ 9 ]  years old, continuing at that level well into adulthood. However, poor prenatal environment, malnutrition and disease are known to have lifelong deleterious effects. [ 10 ] [ 11 ]  Estimates in the academic research of the heritability of IQ have varied from below 0.5 [ 1 ]  to a high of 0.8 (where 1.0 indicates that monozygotic twins have no variance in IQ and 0 indicates that their IQs are completely uncorrelated). [ 12 ]  Eric Turkheimer and colleagues (2003) found that for children of low socioeconomic status heritability of IQ falls almost to zero. [ 13 ]  These results have been challenged by other researchers. IQ heritability increases during early childhood, but it is unclear whether it stabilizes thereafter. [ 14 ]  A 1996 statement by the  American Psychological Association  gave about 0.45 for children and about .75 during and after  adolescence . [ 15 ]  A 2004  meta-analysis  of reports in  Current Directions in Psychological Science  gave an overall estimate of around 0.85 for 18-year-olds and older. [ 16 ]  The general figure for heritability of IQ is about 0.5 across multiple studies in varying populations. [ 17 ]


Although IQ differences between individuals have been shown to have a large hereditary component, it does not follow that disparities in IQ between groups have a genetic basis. [ 18 ] [ 19 ] [ 20 ] [ 21 ]  The scientific consensus is that genetics does not explain  average differences in IQ test performance between racial groups. [ 22 ] [ 23 ] [ 24 ] [ 25 ] [ 26 ] [ 27 ]


Heritability is a  statistic  used in the fields of  breeding  and  genetics  that estimates the degree of  variation  in a  phenotypic trait  in a population that is due to genetic variation between individuals in that population. [ 28 ]  The concept of heritability can be expressed in the form of the following question: "What is the proportion of the variation in a given trait within a population that is  not  explained by the environment or random chance?" [ 29 ]


Estimates of heritability take values ranging from 0 to 1; a heritability estimate of 1 indicates that all variation in the trait in question is genetic in origin and a heritability estimate of 0 indicates that  none  of the variation is genetic. The determination of many traits can be considered primarily  genetic  under similar environmental backgrounds. For example, a 2006 study found that adult height has a heritability estimated at 0.80 when looking only at the height variation within families where the environment should be very similar. [ 30 ]  Other traits have lower heritability estimates, which indicate a relatively larger environmental influence. For example, a  twin study  on the heritability of depression in men estimated it as 0.29, while it was 0.42 for women in the same study. [ 31 ]


There are a number of points to consider when interpreting heritability:


Various studies have estimated the heritability of IQ to be between 0.7 and 0.8 in adults and 0.45 in childhood in the  United States . [ 15 ] [ 12 ] [ 39 ]  It has been found that estimates of heritability increase as individuals age. Heritability estimates in infancy are as low as 0.2, around 0.4 in middle childhood, and as high as 0.8 in adulthood. [ 8 ]  The brain undergoes morphological changes in development which suggests that age-related physical changes could contribute to this effect. [ 40 ]


A 1994 article in  Behavior Genetics  based on a study of Swedish monozygotic and dizygotic twins found the heritability of the sample to be as high as 0.80 in general cognitive ability; however, it also varies by trait, with 0.60 for verbal tests, 0.50 for spatial and speed-of-processing tests, and 0.40 for memory tests. In contrast, studies of other populations estimate an average heritability of 0.50 for general cognitive ability. [ 12 ]


In 2006,  David Kirp , writing in  The New York Times Magazine , summarized a century's worth of research as follows, "about three-quarters of I.Q. differences between individuals are attributable to heredity." [ 41 ]


There are some family effects on the IQ of children, accounting for up to a quarter of the variance. However, adoption studies show that by adulthood adoptive siblings aren't more similar in IQ than strangers, [ 42 ]  while adult full siblings show an IQ correlation of 0.24. However, some studies of twins reared apart (e.g. Bouchard, 1990) find a significant shared environmental influence, of at least 10% going into late adulthood. [ 39 ]   Judith Rich Harris  suggests that this might be due to biasing assumptions in the methodology of the classical twin and adoption studies. [ 43 ]


There are aspects of environments that family members have in common (for example, characteristics of the home). This shared family environment accounts for 0.25-0.35 of the variation in IQ in childhood. By late adolescence it is quite low (zero in some studies). There is a similar effect for several other psychological traits. These studies have not looked into the effects of extreme environments such as in abusive families. [ 15 ] [ 42 ] [ 44 ] [ 45 ]


The  American Psychological Association 's report " Intelligence: Knowns and Unknowns " (1996) asserts the necessity of a certain minimum level of responsible care for normal  child development . Environments that are severely deprived, neglectful, or abusive negatively affect various developmental aspects, including intellectual growth. Beyond this minimum threshold, the influence of family experience on child development is contentious. Variables such as home resources and parents' use of language are correlated with children's IQ scores; however, these correlations may be influenced by genetic as well as environmental factors. The extent to which variance in IQ results from differences between families, compared to the varying experiences of different children within the same family, is a subject of debate. Recent twin and adoption studies indicate that the effect of the shared family environment is significant in early childhood but diminishes substantially by late adolescence. These findings suggest that differences in family lifestyles, while potentially important for many aspects of children's lives, have little long-term impact on the skills measured by intelligence tests.


Although parents treat their children differently, such differential treatment explains only a small amount of non-shared environmental influence. One suggestion is that children react differently to the same environment due to different genes. More likely influences may be the impact of peers and other experiences outside the family. [ 15 ] [ 44 ]  For example, siblings grown up in the same household may have different friends and teachers and even contract different illnesses. This factor may be one of the reasons why IQ score correlations between siblings decreases as they get older. [ 46 ]


Certain single-gene  metabolic disorders  can severely affect intelligence.  Phenylketonuria  is an example, [ 6 ]  with publications documenting the capacity of treated phenylketonuria to produce a reduction of 10 IQ points on average. [ 47 ]  Meta-analyses have found that environmental factors, such as  iodine deficiency , can result in large reductions in average IQ; iodine deficiency has been shown to produce a reduction of 12.5 IQ points on average. [ 48 ]


The APA report "Intelligence: Knowns and Unknowns" (1996) also stated that:


"We should note, however, that  low-income  and non-white families are poorly represented in existing adoption studies as well as in most twin samples. Thus it is not yet clear whether these studies apply to the population as a whole. It remains possible that, across the full range of income and ethnicity, between-family differences have more lasting consequences for psychometric intelligence." [ 15 ]


A study (1999) by Capron and Duyme of  French  children adopted between the ages of four and six examined the influence of  socioeconomic status  (SES). The children's IQs initially averaged 77, putting them near retardation. Most were abused or neglected as infants, then shunted from one foster home or institution to the next. Nine years later after adoption, when they were on average 14 years old, they retook the IQ tests, and all of them did better. The amount they improved was directly related to the adopting family's socioeconomic status. "Children adopted by farmers and laborers had average IQ scores of 85.5; those placed with  middle-class  families had average scores of 92. The average IQ scores of youngsters placed in well-to-do homes climbed more than 20 points, to 98." [ 41 ] [ 49 ]


Stoolmiller  (1999) argued that the range of environments in previous adoption studies was restricted. Adopting families tend to be more similar on, for example, socio-economic status than the general population, which suggests a possible underestimation of the role of the shared family environment in previous studies. Corrections for range restriction to adoption studies indicated that socio-economic status could account for as much as 50% of the variance in IQ. [ 50 ]


On the other hand, the effect of this was examined by  Matt McGue  and colleagues (2007), who wrote that "restriction in range in parent disinhibitory psychopathology and family socio-economic status had no effect on adoptive-sibling correlations [in] IQ" [ 51 ]


Turkheimer  and colleagues (2003) argued that the proportions of IQ variance attributable to genes and environment vary with socioeconomic status. They found that in a study on seven-year-old twins, in impoverished families, 60% of the variance in early childhood IQ was accounted for by the shared family environment, and the contribution of genes is close to zero; in affluent families, the result is almost exactly the reverse. [ 13 ]


In contrast to Turkheimer (2003), a study by Nagoshi and Johnson (2005) concluded that the heritability of IQ did not vary as a function of parental socioeconomic status in the 949 families of Caucasian and 400 families of Japanese ancestry who took part in the Hawaii Family Study of Cognition. [ 52 ]


Asbury and colleagues (2005) studied the effect of environmental risk factors on verbal and non-verbal ability in a nationally representative sample of 4-year-old British twins. There was not any statistically significant interaction for non-verbal ability, but the heritability of verbal ability was found to be  higher  in low-SES and high-risk environments. [ 53 ]


Harden , Turkheimer, and  Loehlin  (2007) investigated adolescents, most 17 years old, and found that, among higher income families, genetic influences accounted for approximately 55% of the variance in cognitive aptitude and shared environmental influences about 35%. Among lower income families, the proportions were in the reverse direction, 39% genetic and 45% shared environment." [ 54 ]


In the course of a substantial review,  Rushton  and  Jensen  (2010) criticized the study of Capron and Duyme, arguing their choice of IQ test and selection of child and adolescent subjects were a poor choice because this gives a relatively less hereditable measure. [ 35 ]  The argument here rests on a strong form of  Spearman's hypothesis , that the hereditability of different kinds of IQ test can vary according to how closely they correlate to the  general intelligence factor  ( g ); both the empirical data and statistical methodology bearing on this question are matters of active controversy. [ 55 ] [ 56 ] [ 57 ]


A 2011 study by  Tucker-Drob  and colleagues reported that at age 2, genes accounted for approximately 50% of the variation in mental ability for children being raised in high socioeconomic status families, but genes accounted for negligible variation in mental ability for children being raised in low socioeconomic status families. This gene–environment interaction was not apparent at age 10 months, suggesting that the effect emerges over the course of early development. [ 58 ]


A 2012 study based on a representative sample of twins from the  United Kingdom , with longitudinal data on IQ from age two to age fourteen, did not find evidence for lower heritability in low-SES families. However, the study indicated that the effects of shared family environment on IQ were generally greater in low-SES families than in high-SES families, resulting in greater variance in IQ in low-SES families. The authors noted that previous research had produced inconsistent results on whether or not SES moderates the heritability of IQ. They suggested three explanations for the inconsistency. First, some studies may have lacked statistical power to detect interactions. Second, the age range investigated has varied between studies. Third, the effect of SES may vary in different demographics and different countries. [ 59 ]


A 2017 King's College London study suggests that genes account for nearly 50 per cent of the differences between whether children are socially mobile or not. [ 60 ]


A  meta-analysis  by Devlin and colleagues (1997) of 212 previous studies evaluated an alternative model for environmental influence and found that it fits the data better than the 'family-environments' model commonly used. The shared maternal ( fetal ) environment effects, often assumed to be negligible, account for 20% of covariance between twins and 5% between siblings, and the effects of genes are correspondingly reduced, with two measures of heritability being less than 50%. They argue that the shared maternal environment may explain the striking correlation between the IQs of twins, especially those of adult twins that were reared apart. [ 1 ]  IQ heritability increases during early childhood, but whether it stabilizes thereafter remains unclear. [ 1 ] [ needs update ]  These results have two implications: a new model may be required regarding the influence of genes and environment on cognitive function; and interventions aimed at improving the prenatal environment could lead to a significant boost in the population's IQ. [ 1 ]


Bouchard and McGue reviewed the literature in 2003, arguing that Devlin's conclusions about the magnitude of heritability is not substantially different from previous reports and that their conclusions regarding prenatal effects stands in contradiction to many previous reports. [ 7 ]  They write that:


Chipuer et al. and Loehlin conclude that the postnatal rather than the prenatal environment is most important. The Devlin et al. (1997a) conclusion that the prenatal environment contributes to twin IQ similarity is especially remarkable given the existence of an extensive empirical literature on prenatal effects. Price (1950), in a comprehensive review published over 50 years ago, argued that almost all MZ twin prenatal effects produced differences rather than similarities. As of 1950 the literature on the topic was so large that the entire bibliography was not published. It was finally published in 1978 with an additional 260 references. At that time Price reiterated his earlier conclusion (Price, 1978). Research subsequent to the 1978 review largely reinforces Price's hypothesis (Bryan, 1993; Macdonald et al., 1993; Hall and Lopez-Rangel, 1996; see also Martin et al., 1997, box 2; Machin, 1996). [ 7 ]


Dickens and Flynn (2001) argued that the "heritability" figure includes both a direct effect of the  genotype  on IQ and also indirect effects where the genotype changes the environment, in turn affecting IQ. That is, those with a higher IQ tend to seek out stimulating environments that further increase IQ. The direct effect can initially have been very small but  feedback  loops can create large differences in IQ. In their model an environmental stimulus can have a very large effect on IQ, even in adults, but this effect also decays over time unless the stimulus continues. [ 61 ]  This model could be adapted to include possible factors, like nutrition in early childhood, that may cause permanent effects.


The  Flynn effect  is the increase in average intelligence test scores by about 0.3% annually, resulting in the average person today scoring 15 points higher in IQ compared to the generation 50 years ago. [ 62 ]  This effect can be explained by a generally more stimulating environment for all people. The authors suggest that programs aiming to increase IQ would be most likely to produce long-term IQ gains if they taught children how to replicate outside the program the kinds of cognitively demanding experiences that produce IQ gains while they are in the program and motivate them to persist in that replication long after they have left the program. [ 61 ] [ 63 ]
Most of the improvements have allowed for better abstract reasoning, spatial relations, and comprehension. Some scientists have suggested that such enhancements are due to better nutrition, better parenting and schooling, as well as exclusion of the least intelligent people from reproduction. However, Flynn and a group of other scientists share the viewpoint that modern life implies solving many abstract problems which leads to a rise in their IQ scores. [ 62 ]


Recent research has illuminated genetic factors underlying IQ stability and change.  Genome-wide association studies  have demonstrated that the genes involved in intelligence remain fairly stable over time. [ 64 ]  Specifically, in terms of IQ stability, "genetic factors mediated phenotypic stability throughout this entire period [age 0 to 16], whereas most age-to-age instability appeared to be due to non-shared environmental influences". [ 65 ] [ 66 ]  These findings have been replicated extensively and observed in the United Kingdom, [ 67 ]  the United States, [ 68 ] [ 65 ]  and the Netherlands. [ 69 ] [ 70 ] [ 71 ] [ 72 ]  Additionally, researchers have shown that naturalistic changes in IQ occur in individuals at variable times. [ 73 ]


Kong [ 74 ]  reports that, "Nurture has a genetic component, i.e. alleles in the parents affect the parents' phenotypes and through that influence the outcomes of the child." These results were obtained through a meta-analysis of  educational attainment  and  polygenic  scores of non-transmitted alleles. Although the study deals with educational attainment and not IQ, these two are strongly linked. [ 75 ]


Spatial ability has been shown to be unifactorial (a single score accounts well for all spatial abilities), and is 69% heritable in a sample of 1,367 pairs of twins from the ages 19 through 21. [ 76 ]  Further only 8% of spatial ability can be accounted for by shared environmental factors like school and family. [ 76 ]  Of the genetically determined portion of spatial ability, 24% is shared with verbal ability (general intelligence) and 43% was specific to spatial ability alone. [ 76 ]


A 2009 review article identified over 50  genetic polymorphisms  that have been reported to be associated with cognitive ability in various studies, but noted that the discovery of small effect sizes and lack of replication have characterized this research so far. [ 77 ]  Another study attempted to replicate 12 reported associations between specific genetic variants and general cognitive ability in three large datasets, but found that only one of the genotypes was significantly associated with general intelligence in one of the samples, a result expected by chance alone. The authors concluded that most reported genetic associations with general intelligence are probably  false positives  brought about by inadequate sample sizes. [ 78 ]  Arguing that common genetic variants explain much of the variation in general intelligence, they suggested that the effects of individual variants are so small that very large samples are required to reliably detect them. [ 78 ]  Genetic diversity within individuals is heavily correlated with IQ. [ 79 ]


A novel molecular genetic method for estimating heritability calculates the overall genetic similarity (as indexed by the cumulative effects of all genotyped  single nucleotide polymorphisms ) between all pairs of individuals in a sample of unrelated individuals and then correlates this genetic similarity with phenotypic similarity across all the pairs. A study using this method estimated that the lower bounds for the narrow-sense heritability of crystallized and fluid intelligence are 40% and 51%, respectively. A replication study in an independent sample confirmed these results, reporting a heritability estimate of 47%. [ 4 ]  These findings are compatible with the view that a large number of genes, each with only a small effect, contribute to differences in intelligence. [ 78 ]


The relative influence of genetics and environment for a trait can be calculated by measuring how strongly traits  covary  in people of a given genetic (unrelated, siblings, fraternal twins, or identical twins) and environmental (reared in the same family or not) relationship. One method is to consider  identical twins  reared apart, with any similarities that exist between such twin pairs attributed to genotype. In terms of  correlation  statistics, this means that theoretically the correlation of tests scores between  monozygotic  twins would be 1.00 if genetics alone accounted for variation in IQ scores; likewise, siblings and  dizygotic  twins share on average half  alleles  and the correlation of their scores would be 0.50 if IQ were affected by genes alone (or greater if there is a positive correlation between the IQs of spouses in the parental generation). Practically, however, the  upper bound  of these correlations are given by the  reliability  of the test, which is 0.90 to 0.95 for typical IQ tests. [ 80 ]


If there is  biological inheritance  of IQ, then the relatives of a person with a high IQ should exhibit a comparably high IQ with a much higher probability than the general population. In 1982, Bouchard and McGue reviewed such correlations reported in 111 original studies in the United States. The mean correlation of IQ scores between monozygotic twins was 0.86, between siblings 0.47, between half-siblings 0.31, and between cousins 0.15. [ 81 ]


The 2006 edition of  Assessing adolescent and adult intelligence  by  Alan S. Kaufman  and Elizabeth O. Lichtenberger reports correlations of 0.86 for identical twins raised together compared to 0.76 for those raised apart and 0.47 for siblings. [ 82 ]  These numbers are not necessarily static. When comparing pre-1963 to late 1970s data, researchers DeFries and Plomin found that the IQ correlation between parent and child living together fell significantly, from 0.50 to 0.35. The opposite occurred for fraternal twins. [ 83 ]


Every one of these studies presented next contains estimates of only two of the three factors which are relevant. The three factors are G, E, and GxE. Since there is no possibility of studying equal environments in a manner comparable to using identical twins for equal genetics, the GxE factor can not be isolated. Thus the estimates are actually of G+GxE and E. Although this may seem like nonsense, it is justified by the unstated assumption that GxE=0. It is also the case that the values shown below are r correlations and not r(squared), proportions of variance. Numbers less than one are smaller when squared. The next to last number in the list below refers to less than 5% shared variance between a parent and child living apart.


Another summary:


In the US, individuals identifying themselves as Asian generally tend to score higher on IQ tests than Caucasians, who tend to score higher than Hispanics, who tend to score higher than African Americans. [ 87 ]  Yet, although IQ differences between individuals have been shown to have a large hereditary component, it does not follow that between-group differences in average IQ have a genetic basis. [ 19 ] [ 20 ] [ 26 ]  In fact, greater variation in IQ scores exists within each ethnic group than between them. [ 87 ]  The scientific consensus is that genetics does not explain average differences in IQ test performance between racial groups. [ 22 ] [ 24 ] [ 25 ] [ 26 ] [ 27 ]  Growing evidence indicates that environmental factors, not genetic ones, explain the racial IQ gap. [ 26 ] [ 27 ] [ 88 ]


Arguments in support of a genetic explanation of racial differences in average IQ are sometimes fallacious. For instance, some hereditarians have cited as evidence the failure of known environmental factors to account for such differences, or the high heritability of intelligence within races. [ 19 ]  Jensen and Rushton, in their formulation of Spearman's Hypothesis, argued that cognitive tasks that have the highest  g -load are the tasks in which the gap between black and white test takers is greatest, and that this supports their view that racial IQ gaps are in large part genetic. [ 89 ]  However, in separate reviews, Mackintosh, Nisbett  et al . and Flynn have all concluded that the slight correlation between  g -loading and the test score gap offers no clue to the cause of the gap. [ 90 ] [ 91 ] [ 92 ]  Further reviews of both  adoption studies  and racial admixture studies have also found no evidence for a genetic component behind group-level IQ differences. [ 93 ] [ 94 ] [ 95 ] [ 96 ]  Hereditarian arguments for racial differences in IQ have been criticized from a theoretical point of view as well. For example, the geneticist and neuroscientist Kevin Mitchell has argued that "systematic genetic differences in intelligence between large, ancient populations" are "inherently and deeply implausible" because the "constant churn of genetic variation works against any long-term rise or fall in intelligence." [ 21 ]  As he argues, "To end up with systematic genetic differences in intelligence between large, ancient populations, the selective forces driving those differences would need to have been enormous. What's more, those forces would have to have acted across entire continents, with wildly different environments, and have been persistent over tens of thousands of years of tremendous cultural change." [ 21 ]


In favor of an environmental explanation, on the other hand, numerous studies and reviews have shown promising results. Among these, some focus on the gradual closing of the black–white IQ gap over the last decades of the 20th century, as black test-takers increased their average scores relative to white test-takers. For instance, Vincent reported in 1991 that the black–white IQ gap was decreasing among children, but that it was remaining constant among adults. [ 97 ]  Similarly, a 2006 study by Dickens and Flynn estimated that the difference between mean scores of black people and white people closed by about 5 or 6 IQ points between 1972 and 2002, a reduction of about one-third. [ 98 ]  In the same period, the educational achievement disparity also diminished. [ 99 ]  Reviews by Flynn and Dickens, Mackintosh, and Nisbett  et al.  all accept the gradual closing of the gap as a fact. [ 98 ] [ 100 ] [ 101 ]  Other recent studies have focused on disparities in nutrition and prenatal care, as well as other health-related environmental disparities, and have found that these disparities may account for significant IQ gaps between population groups. [ 102 ] [ 103 ] [ 104 ] [ 105 ]  Still other studies have focused on educational disparities, and have found that intensive early childhood education and test preparation can diminish or eliminate the black–white IQ test gap. [ 106 ] [ 107 ] [ 108 ] [ 109 ]  In light of these and similar findings, a consensus has formed that genetics does not explain differences in average IQ test performance between racial groups. [ 22 ] [ 26 ]


Human behaviour genetics  is an interdisciplinary subfield of  behaviour genetics  that studies the role of  genetic  and environmental influences on  human   behaviour . Classically, human behavioural geneticists have studied the  inheritance  of behavioural traits. The field was originally focused on determining the importance of genetic influences on human behaviour (for e.g., do genes regulate human behavioural attributes). It has evolved to address more complex questions such as: how important are genetic and/or environmental influences on various human behavioural traits; to what extent do the same genetic and/or environmental influences impact the overlap between human behavioural traits; how do genetic and/or environmental influences on behaviour change across development; and what environmental factors moderate the importance of genetic effects on human behaviour ( gene-environment interaction ). [ 1 ]  The field is interdisciplinary, and draws from  genetics ,  psychology , and statistics. Most recently, the field has moved into the area of  statistical genetics , with many behavioural geneticists also involved in efforts to identify the specific genes involved in human behaviour, and to understand how the effects associated with these genes changes across time, and in conjunction with the environment. [ 2 ]


Traditionally, the human behavioural genetics were a psychology and phenotype based studies including intelligence, personality and grasping ability. During the years, the study developed beyond the classical traits of human behaviour and included more genetically associated traits like genetic disorders (such as  fragile X syndrome ,  Alzheimer's disease  and obesity). The traditional methods of behavioural-genetic analysis provide a quantitative evaluation of genetic and non-genetic influences on human behaviour. The family, twin and adoption studies marks the huge contribution for laying down the foundation for current molecular genetic studies to study human behaviour. [ 3 ]


In 1869,  Francis Galton  published the first empirical work in human behavioural genetics,  Hereditary Genius . Here, Galton intended to demonstrate that "a man's natural abilities are derived by inheritance, under exactly the same limitations as are the form and physical features of the whole organic world." Like most seminal work, he overstated his conclusions. His was a family study on the  inheritance of giftedness and talent . Galton was aware that resemblance among familial relatives can be a function of both shared inheritance and shared environments. Contemporary human behavioural quantitative genetics studies special populations such as  twins  and  adoptees .


The initial impetus behind this research was to demonstrate that there were indeed genetic influences on  human behaviour . In  psychology , this phase lasted for the first half of the 20th century largely because of the overwhelming influence of  behaviourism  in the field. Later behavioural genetic research focused on  quantitative methods .


In 1984, a research program named the Swedish Adoption/Twin Study of Aging (SATSA) was initiated in gerontological genetics. The research was executed on Twins Reared Apart (TRA) and Twins Reared Together (TRT). In this three-year interval study, the testing was carried out in two ways, Mail-Out Questionnaire and In-Person Testing (IPT). The IPT includes functional capacity, physical performance measurements, neurological state, general health, cardiovascular health, and cognitive abilities, all of which are particularly significant in ageing. The IPT had two major components for testing, Biomedical and Cognitive Assessment. The biomedical component was constructed to analyses the general health status like age changes, lungs function and capacity, physical strength. With this, the cognitive component was developed to represent and evaluate domains of crystallized and fluid intelligence and memory.


The data acquired from this study allowed researchers to assess genetic contributions to age changes and continuities throughout the length of the SATSA twins' later lives, which prolonged a decade and a half. [ 3 ]


Behavioural geneticists study both psychiatric and mental disorders, such as  schizophrenia ,  bipolar disorder , and  alcoholism , as well as behavioural and social characteristics, such as personality and social attitudes.