It is clear from multiple lines of evidence that all researched behavioural traits and  disorders  are influenced by  genes ; that is, they are  heritable . The single largest source of evidence comes from  twin studies , where it is routinely observed that monozygotic (identical)  twins  are more similar to one another than are same-sex dizygotic (fraternal) twins. [ 11 ] [ 12 ]


The conclusion that genetic influences are pervasive has also been observed in research designs that do not depend on the assumptions of the twin method.  Adoption studies  show that  adoptees  are routinely more similar to their biological relatives than their adoptive relatives for a wide variety of traits and disorders. [ 3 ]  In the  Minnesota Study of Twins Reared Apart , monozygotic twins separated shortly after birth were reunited in adulthood. [ 60 ]  These adopted, reared-apart twins were as similar to one another as were twins reared together on a wide range of measures including general  cognitive ability ,  personality ,  religious attitudes , and vocational interests, among others. [ 60 ]  Approaches using genome-wide  genotyping  have allowed researchers to measure genetic relatedness between individuals and estimate heritability based on millions of genetic variants. Methods exist to test whether the extent of genetic similarity (aka, relatedness) between nominally unrelated individuals (individuals who are not close or even distant relatives) is associated with phenotypic similarity. [ 48 ]  Such methods do not rely on the same assumptions as twin or adoption studies, and routinely find evidence for heritability of behavioural traits and disorders. [ 42 ] [ 44 ] [ 61 ]


Just as all researched human behavioural phenotypes are influenced by  genes  (i.e., are  heritable ), all such phenotypes are also influenced by the environment. [ 11 ] [ 59 ]  The basic fact that monozygotic  twins  are genetically identical but are never perfectly concordant for  psychiatric disorder  or perfectly  correlated  for behavioural  traits , indicates that the environment shapes human behaviour. [ 59 ]


The nature of this environmental influence, however, is such that it tends to make individuals in the same family more different from one another, not more similar to one another. [ 3 ]  That is, estimates of shared environmental effects (

 c

 2

 {\displaystyle c^{2}}

 ) in human studies are small, negligible, or zero for the vast majority of behavioural traits and psychiatric disorders, whereas estimates of non-shared environmental effects (

 e

 2

 {\displaystyle e^{2}}

 ) are moderate to large. [ 11 ]  From twin studies

 c

 2

 {\displaystyle c^{2}}

  is typically estimated at 0 because the correlation (

 r

 M
 Z

 {\displaystyle r_{MZ}}

 ) between monozygotic twins is at least twice the correlation (

 r

 D
 Z

 {\displaystyle r_{DZ}}

 ) for dizygotic twins. When using the  Falconer variance decomposition  (

 1.0
 =

 a

 2

 +

 c

 2

 +

 e

 2

 {\displaystyle 1.0=a^{2}+c^{2}+e^{2}}

 ) this difference between monozygotic and dizygotic twin similarity results in an estimated

 c

 2

 =
 0

 {\displaystyle c^{2}=0}

 . The Falconer decomposition is simplistic. [ 26 ]  It removes the possible influence of dominance and epistatic effects which, if present, will tend to make monozygotic twins more similar than dizygotic twins and mask the influence of shared environmental effects. [ 26 ]  This is a limitation of the twin design for estimating

 c

 2

 {\displaystyle c^{2}}

 . However, the general conclusion that shared environmental effects are negligible does not rest on twin studies alone.  Adoption research  also fails to find large (

 c

 2

 {\displaystyle c^{2}}

 ) components; that is, adoptive parents and their adopted children tend to show much less resemblance to one another than the adopted child and his or her non-rearing biological parent. [ 3 ]  In studies of adoptive families with at least one biological child and one adopted child, the sibling resemblance also tends to be nearly zero for most traits that have been studied. [ 11 ] [ 62 ]


The figure provides an example from  personality  research, where twin and adoption studies converge on the conclusion of zero to small influences of shared environment on broad personality traits measured by the  Multidimensional Personality Questionnaire  including positive emotionality, negative emotionality, and constraint. [ 63 ]


Given the conclusion that all researched behavioural traits and psychiatric disorders are heritable, biological siblings will always tend to be more similar to one another than will adopted siblings. However, for some traits, especially when measured during adolescence, adopted siblings do show some significant similarity (e.g., correlations of .20) to one another. Traits that have been demonstrated to have significant shared environmental influences include internalizing and  externalizing psychopathology , [ 64 ]  substance use [ 65 ]   [ non-primary source needed ]  and  dependence , [ 56 ] [ non-primary source needed ]  and  intelligence . [ 65 ]   [ non-primary source needed ]


Genetic effects on human behavioural outcomes can be described in multiple ways. [ 26 ]  One way to describe the effect is in terms of how much  variance  in the behaviour can be accounted for by  alleles  in the  genetic variant , otherwise known as the  coefficient of determination  or

 R

 2

 {\displaystyle R^{2}}

 . An intuitive way to think about

 R

 2

 {\displaystyle R^{2}}

  is that it describes the extent to which the genetic variant makes individuals, who harbour different alleles, different from one another on the behavioural  outcome . A complementary way to describe effects of individual genetic variants is in how much change one expects on the behavioural outcome given a change in the number of risk alleles an individual harbours, often denoted by the Greek letter

 β

 {\displaystyle \beta }

  (denoting the slope in a  regression  equation), or, in the case of binary disease outcomes by the  odds ratio

 O
 R

 {\displaystyle OR}

  of disease given allele status. Note the difference:

 R

 2

 {\displaystyle R^{2}}

  describes the population-level effect of alleles within a genetic variant;

 β

 {\displaystyle \beta }

  or

 O
 R

 {\displaystyle OR}

  describe the effect of having a risk allele on the individual who harbours it, relative to an individual who does not harbour a risk allele. [ 66 ]


When described on the

 R

 2

 {\displaystyle R^{2}}

  metric, the effects of individual genetic variants on  complex  human behavioural traits and disorders are vanishingly small, with each variant accounting for

 R

 2

 <
 0.3
 %

 {\displaystyle R^{2}<0.3\%}

  of variation in the phenotype. [ 3 ]  This fact has been discovered primarily through  genome-wide association studies  of complex behavioural phenotypes, including results on substance use, [ 67 ] [ 68 ]   personality , [ 69 ]   fertility , [ 70 ]   schizophrenia , [ 41 ]   depression , [ 69 ] [ 71 ]  and  endophenotypes  including brain structure [ 72 ]  and function. [ 73 ]  There are a small handful of  replicated and robustly  studied exceptions to this rule, including the effect of  APOE  on  Alzheimer's disease , [ 74 ]  and  CHRNA5  on  smoking  behaviour, [ 67 ]  and  ALDH2  (in individuals of  East Asian ancestry ) on  alcohol  use. [ 75 ]


On the other hand, when assessing effects according to the

 β

 {\displaystyle \beta }

  metric, there are a large number of genetic variants that have very large effects on complex behavioural phenotypes. The risk alleles within such variants are exceedingly rare, such that their large behavioural effects impact only a small number of individuals. Thus, when assessed at a population level using the

 R

 2

 {\displaystyle R^{2}}

  metric, they account for only a small amount of the differences in risk between individuals in the population. Examples include variants within  APP  that result in familial forms of severe early onset Alzheimer's disease but affect only relatively few individuals. Compare this to risk alleles within  APOE , which pose much smaller risk compared to  APP , but are far more common and therefore affect a much greater proportion of the population. [ 76 ]


Finally, there are classical behavioural disorders that are genetically simple in their etiology, such as  Huntington's  disease. Huntington's is caused by a single  autosomal   dominant  variant in the  HTT  gene, which is the only variant that accounts for any differences among individuals in their risk for developing the disease, assuming they live long enough. [ 77 ]  In the case of genetically simple and rare diseases such as Huntington's, the variant

 R

 2

 {\displaystyle R^{2}}

  and the

 O
 R

 {\displaystyle OR}

  are simultaneously large. [ 66 ]


In response to general concerns about the  replicability of psychological research , behavioural geneticists  Robert Plomin ,  John C. DeFries , Valerie Knopik, and  Jenae Neiderhiser  published a  review  of the ten most well-replicated findings from behavioural genetics research. [ 59 ]  The ten findings were:


Behavioural genetic research and findings have at times been controversial. Some of this controversy has arisen because behavioural genetic findings can challenge  societal beliefs  about the nature of human behaviour and abilities. Major areas of controversy have included genetic research on topics such as racial differences,  intelligence ,  violence , and  human sexuality . [ 78 ]  Other controversies have arisen due to misunderstandings of behavioural genetic research, whether by the  lay public  or the researchers themselves. [ 3 ]  For example, the notion of heritability is easily misunderstood to imply causality, or that some behaviour or condition is determined by one's genetic endowment. [ 79 ]  When behavioural genetics researchers say that a behaviour is X% heritable, that does not mean that genetics causes, determines, or fixes up to X% of the behaviour. Instead, heritability is a statement about genetic differences correlated with trait differences on the population level. [ citation needed ]


Historically, perhaps the most controversial subject has been on  race and genetics . [ 78 ]   Race  is not a scientifically exact term, and its interpretation can depend on one's culture and country of origin. [ 80 ]  Instead, geneticists use concepts such as  ancestry , which is more rigorously defined. [ 81 ]  For example, a so-called "Black" race may include all individuals of relatively recent  African  descent ("recent" because all humans are  descended from African ancestors ). However, there is more genetic diversity in Africa than the rest of the world combined, [ 82 ]  so speaking of a "Black" race is without a precise genetic meaning. [ 81 ]


Qualitative research  has fostered arguments that behavioural genetics is an ungovernable field without scientific  norms  or  consensus , which fosters  controversy . The argument continues that this state of affairs has led to controversies including race, intelligence, instances where variation within a single gene was found to very strongly influence a controversial phenotype (e.g., the " gay gene " controversy), and others. This argument further states that because of the persistence of controversy in behaviour genetics and the failure of disputes to be resolved, behaviour genetics does not conform to the standards of good science. [ 83 ]


The scientific assumptions on which parts of behavioural genetic research are based have also been criticized as flawed. [ 79 ]  Genome wide association studies are often implemented with simplifying statistical assumptions, such as  additivity , which may be statistically robust but unrealistic for some behaviours. Critics further contend that, in humans, behaviour genetics represents a misguided form of  genetic reductionism  based on inaccurate interpretations of statistical analyses. [ 84 ]  Studies comparing monozygotic (MZ) and dizygotic (DZ) twins assume that  environmental influences will be the same  in both types of twins, but this assumption may also be unrealistic. MZ twins may be treated more alike than DZ twins, [ 79 ]  which itself may be an example of evocative  gene–environment correlation , suggesting that one's genes influence their treatment by others. It is also not possible in twin studies to eliminate effects of the shared womb environment, although studies comparing twins who experience  monochorionic and dichorionic  environments in utero do exist, and indicate limited impact. [ 85 ]  Studies of twins separated in early life include children who were separated not at birth but part way through childhood. [ 79 ]  The effect of early rearing environment can therefore be evaluated to some extent in such a study, by comparing twin similarity for those twins separated early and those separated later. [ 60 ]


The  ACE model  is a  statistical model  commonly used to analyze the results of  twin  and  adoption studies . This classic  behaviour genetic  model aims to partition the  phenotypic   variance  into three categories:  additive genetic variance  (A), common (or shared) environmental factors (C), and specific (or nonshared) environmental factors plus  measurement error  (E). [ 1 ]  It is widely used in  genetic epidemiology  and  behavioural genetics . [ 2 ] [ 3 ]  The basic ACE model relies on several assumptions, including the absence of  assortative mating , [ 4 ]  that there is no  genetic dominance  or  epistasis , [ 5 ]  that all genetic effects are additive, and the absence of  gene-environment interactions . [ 3 ]  In order to address these limitations, several variants of the ACE model have been developed, including an ACE-β model, which emphasizes the identification of causal effects, [ 3 ]  and the ACDE model, which accounts for the effects of  genetic dominance . [ 6 ]


Adoption studies typically compare pairs of persons, e.g., adopted child and adoptive mother or adopted child and biological mother, to assess genetic and environmental influences on behavior. [ 1 ]  These studies are one of the classic research methods of  behavioral genetics . The method is used alongside  twin studies  to identify the roles of genetics and environmental variables that impact intelligence, and behavioral disorders. [ 2 ]


Adoption studies differ from  twin studies  in that adoption studies do not necessarily need to use twins; instead, they compare the traits of children to their parents, whether those are the adoptive parents or biological parents. [ 1 ]


There are two standard ways in which adoption studies are carried out; the adoptee's study method and the adoptee's family method. The adoptee's study method compares adoptee's similarity to their biological and adoptive parents. [ 3 ]  Similarity with the biological parent is expected to be due to genetics, while similarity with the adoptive parent is due to home-environment, which is referred as the shared environmental effect. The adoptee's family method compares non-biological siblings who are reared in the same household. [ 4 ]  Similarity to non-biological siblings raised in the same household is attributed to shared environmental effect, as the siblings are genetically unrelated but share the home environment.Variation that cannot be accounted for by either genetics or home-environment is typically described as a non-shared environment.


The first adoption study on  schizophrenia  published in 1966 by Leonard Heston demonstrated that the biological children of parents with schizophrenia were just as likely to develop schizophrenia whether they were reared by their parents or adopted [ 5 ]  and was essential in establishing schizophrenia as being largely genetic instead of being a result of child rearing methods. [ 6 ] [ 7 ]  Analogous studies that followed have shown that mental disorders such as alcoholism, antisocial behavior and depression have a large genetic component that can interact with environmental risk factors such as family conflict, poor coherence, and deviant communication. [ 4 ]


The most cited adoption projects that sought to estimate the  heritability of IQ  were those of Texas, [ 8 ]
Colorado [ 9 ]
and Minnesota [ 10 ]
that were started in the 1970s. These studies showed that while adoptive parents IQ does seem to have a correlation with adoptees IQ in early life, when the adoptees reach adolescence the correlation has faded and disappeared. The correlation with the biological parent seemed to explain most of the variation. In 2015 an adoption study that compared Swedish male-male full-sibships in which at least one member was reared by one or more biological parents and the other by adoptive parents was published. Parental education level was rated on a 5-point scale and each additional unit of rearing parental education was associated with 1.71 points higher IQ. The results were replicated with 2 341 male-male half-sibships, controlling for clustering within families, each additional unit of rearing parental education was associated with 1.94 IQ units. [ 11 ]  The study in Minnesota was conducted by Bouchard. It had an emphasis on identical twins that were separated and raised by different families. [ 12 ]


One of the most influential and widely cited adoption study on criminality was conducted by Sarnoff A. Mednick and Karl O. Christiansen in Denmark. They argued that relevant data demonstrated that criminality has a significant genetic component that interacts with environmental risk factors. [ 13 ]  Adoption studies that followed have had similar results. [ 4 ] "The Stockholm adoption study (2000 adoptees) found that criminality alone was not transmitted from biological parents to adoptees, but did find elevated rates of criminality in adopted-away offspring of biological parents with alcohol use disorders (AUD) alone, or with both AUD and criminality (Bohman, 1978)." [ 14 ]


In the mid-1970s, adoption studies were conducted to investigate the effects on children of having a biological parent with alcoholism. The study found that sons whose biological father has alcoholism were four times more likely to develop alcoholism within their lifetime, but were not more likely to have other mental disorders. The study, was unable to conclude what the impact was on daughters. [ 15 ] [ 16 ]  A more recent study was published in 2009 which compared the parental alcoholism of children in non-adoptive and adoptive families. This study found that the likelihood of children developing alcoholism later in life was associated more with genetic rather than environmental factors. [ 17 ]


Adoption studies have been used to study childhood obesity. This study showed a strong correlation for the environmental argument. Children were strongly influenced by adopted parents weight till mid childhood. During adolescence this dissipated. This study also showed that the biological parents and children had an even stronger correlation when it came to weight and BMI. This put more emphasis on genes than environment. [ 18 ]


In the early to mid-nineteen hundreds, we can find some evidence of adoption studies. These studies were thought to be very important as they wanted to match children with parents in every way possible. They thought they should be similar in looks, class, and mental capacities. They had methods of testing children to find out how smart they were. Mental tests were popularized by Goddard who used a version of the Binet scale. The Gesell Scale was made and became the most widely used by adoption agencies in the 1940s. This is a way of testing a baby's intelligence. This is determined through normal growth, development, and mental milestones. This raised some social and moral issues some children were deemed unfit for adoption because of their low mental test scores. The outcome of these selective adoption studies found that ultimately had no effect on the happiness or success of the children. It also had no effect on the satisfaction of the parents. [ 19 ]


Behavioral epigenetics  is the field of study examining the role of  epigenetics  in shaping  animal  and  human   behavior . [ 1 ]   It seeks to explain how nurture shapes nature, [ 2 ]  where nature refers to biological  heredity [ 3 ]  and nurture refers to virtually everything that occurs during the life-span (e.g., social-experience, diet and nutrition, and exposure to toxins). [ 4 ]   Behavioral epigenetics attempts to provide a framework for understanding how the expression of  genes  is influenced by experiences and the environment [ 5 ]  to produce individual differences in  behaviour , [ 6 ]   cognition , [ 2 ]   personality , [ 7 ]  and  mental health . [ 8 ] [ 9 ]


Epigenetic  gene regulation  involves changes other than to the  sequence  of  DNA  and includes changes to  histones  (proteins around which DNA is wrapped) and  DNA methylation . [ 10 ] [ 4 ] [ 11 ]   These epigenetic changes can influence the growth of  neurons  in the developing brain [ 12 ]  as well as modify the activity of neurons in the adult brain. [ 13 ] [ 14 ]   Together, these epigenetic changes in neuron structure and function are thought to have an influence on behavior. [ 1 ]


In  biology , and specifically  genetics , epigenetics is the study of  heritable  changes in  gene  activity which are  not  caused by changes in the  DNA  sequence; the term can also be used to describe the study of stable, long-term alterations in the transcriptional potential of a cell that are not necessarily heritable. [ 15 ] [ 16 ]  Genetic activity can be influenced by environmental factors, as well as parenting styles, diet and even social interactions. [ 17 ]


Examples of mechanisms that produce such changes are  DNA methylation [ 18 ]  and  histone modification , [ 19 ]  both alter how genes are expressed without changing the underlying  DNA sequence  and both are also essential for learning and memory. [ 20 ]  Gene expression can be controlled through the action of repressor proteins that attach to  silencer  regions of the DNA.


DNA methylation turns a gene "off" – it results in the inability of genetic information to be read from DNA; removing the methyl tag can turn the gene back "on". [ 21 ] [ 22 ]


Histone modification changes the way that DNA is packaged into chromosomes. These changes impact how genes are expressed. [ 23 ] {{


Epigenetic changes occur not only in the developing fetus, but also in individuals throughout the human life-span. [ 4 ] [ 24 ]


The first documented example of epigenetics affecting behavior was provided by  Michael Meaney  and  Moshe Szyf . [ 25 ]  While working at  McGill University  in  Montréal  in 2004, they discovered that the type and amount of nurturing a mother rat provides in the early weeks of the rat's  infancy  determines how that rat responds to  stress  later in life. [ 4 ]  This stress sensitivity was linked to a  down-regulation  in the expression of the  glucocorticoid receptor  in the brain.  In turn, this down-regulation was found to be a consequence of the extent of  methylation  in the  promoter  region of the glucocorticoid receptor  gene . [ 1 ]  Immediately after birth, Meaney and Szyf found that  methyl groups  repress the  glucocorticoid receptor  gene in all rat pups, making the gene unable to unwind from the histone in order to be transcribed, causing a decreased stress response. Nurturing behaviours from the mother rat were found to stimulate activation of stress signalling pathways that remove methyl groups from DNA. This releases the tightly wound gene, exposing it for transcription. The glucocorticoid gene is activated, resulting in lowered stress response. Rat pups that receive a less nurturing upbringing are more sensitive to stress throughout their life-span.


This pioneering work in rodents has been difficult to replicate in humans because of a general lack of availability of human brain tissue for measurement of epigenetic changes. [ 1 ]


A 2010 review discussed the role of DNA methylation in memory formation and storage, but the precise mechanisms involving neuronal function, memory, and methylation reversal remained unclear at the time. [ 26 ]


Further research investigated the molecular basis for  long-term memory .  By 2015 it had become clear that long-term memory requires gene transcription activation and de novo protein synthesis. [ 27 ]   Long-term memory formation depends on both the activation of memory promoting genes and the inhibition of memory suppressor genes, and  DNA methylation / DNA demethylation  was found to be a major mechanism for achieving this dual regulation. [ 28 ]


Rats with a new, strong long-term memory due to  contextual fear conditioning  have reduced expression of about 1,000 genes and increased expression of about 500 genes in the  hippocampus  of the  brain  24 hours after training, thus exhibiting modified expression of 9.17% of the rat hippocampal genome.  Reduced gene expressions were associated with methylations of those genes and hypomethylation was found for genes involved in synaptic transmission and neuronal differentiation. [ 29 ]


Further research into long-term memory has shed light on the molecular mechanisms by which methylation is created or removed, as reviewed in 2022. [ 30 ]   These mechanisms include, for instance, signal-responsive  TOP2B -induced double-strand breaks in  immediate early genes .  More than 100 DNA double-strand breaks occur, both in the hippocampus and in the medial prefrontal cortex (mPFC), in two peaks, at 10 minutes and at 30 minutes after contextual fear conditioning. [ 31 ]   This appears to be earlier than the DNA methylations and demethylations of neuron DNA in the hippocampus that were measured at one hour and 24 hours after contextual fear conditioning.


The double strand breaks occur at known memory-related  immediate early genes  (among other genes) in neurons after neuron activation. [ 32 ] [ 31 ]   These double-strand breaks allow the genes to be transcribed and then translated into active proteins.


One  immediate early gene  newly transcribed after a double-strand break is  EGR1 .  EGR1 is an important  transcription factor  in  memory  formation.  It has an essential role in  brain   neuron   epigenetic  reprogramming.  EGR1 recruits the  TET1  protein that initiates a pathway of  DNA demethylation .  Removing DNA methylation marks allows the activation of downstream genes (see  Regulation of gene expression#Regulation of transcription in learning and memory .  EGR1 brings TET1 to  promoter  sites of genes that need to be  demethylated  and activated (transcribed) during memory formation. [ 33 ]   EGR-1, together with TET1, is employed in programming the distribution of  DNA demethylation  sites on brain DNA during  memory formation  and in long-term  neuronal plasticity . [ 33 ]


DNMT3A2  is another immediate early gene whose expression in neurons can be induced by sustained synaptic activity. [ 34 ]   DNMTs bind to DNA and methylate cytosines at particular locations in the genome.  If this methylation is prevented by DNMT inhibitors, then memories do not form. [ 35 ]   If DNMT3A2 is over-expressed in the hippocampus of young adult mice it converts a weak learning experience into long-term memory and also enhances fear memory formation. [ 28 ]


In another mechanism reviewed in 2022, [ 30 ]  the  messenger RNAs  of many genes that had been subjected to methylation-controlled increases or decreases are transported by neural granules ( messenger RNPs ) to the  dendritic spines . At these locations the messenger RNAs can be  translated  into the proteins that control signaling at  neuronal   synapses .


Studies in rodents have found that the environment exerts an influence on epigenetic changes related to  cognition , in terms of learning and memory; [ 4 ]   environmental enrichment  correlated with increased  histone acetylation , and verification by administering  histone deacetylase inhibitors  induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories. [ 1 ] [ 36 ]   Research has also linked learning and long-term memory formation to reversible epigenetic changes in the hippocampus and cortex in animals with normal-functioning, non-damaged brains. [ 1 ] [ 37 ]   In human studies, post-mortem brains from patients with Alzheimer's dementia show high levels of histone de-acetylase. [ 38 ] [ 39 ]


Due to the stress that can be placed on individuals can increase levels of anxiety and the way the epigenetics are responding in relation to the individual. Epigenetics investigate how alterations upon environment and behavior can affect the way in which genes operate. [ 40 ]  Within research, it's know that majority of epigenetic modifications identified have been involved with anxiety-like phenotypes that involve genes that regulate the hypothalamic-pituitary adrenal axis which results  to the way our bodies respond to stress that we endure as people. [ 41 ]  Epigenetics is altered by many influences, whether it be genetic and or environmental. Within the prenatal times it is evident that through changes of DNA methylation, that maternal and pre-maternal distress have been connected to modifications in the fetal HPA axis. [ 42 ]  This demonstrates that the link between our development, stress and anxiety a mother can feel during this time creates a linkage in the response of how the epigenetic may be altered in the response of the HPA axis. Linkage of the impacts of childhood trauma in connection with epigenetic and anxiety, in that there is a change in DNA methylation process, increasing the chances of neuroendocrine damage to likely occur. In relation, the neuroendocrine damage induces the state of depression, making it mentally unstable for a person to possibly perform their daily activities. The Brain-derived neurotropic factor (BDNF) is known to change its state because of epigenetic mechanisms and contributes to the alters within the development process necessary for the brain of us individuals. [ 43 ]  Alterations within the epigenetic process can be treated using different types clinical procedures, by targeting specific changes and the treating them with the proper sort of care. [ 43 ]


Animal and human studies have found correlations between poor care during infancy and epigenetic changes that correlate with long-term impairments that result from neglect. [ 44 ] [ 45 ] [ 46 ]


Studies in rats have shown correlations between maternal care in terms of the parental licking of offspring and epigenetic changes. [ 44 ]  A high level of licking results in a long-term reduction in stress response as measured behaviorally and biochemically in elements of the  hypothalamic-pituitary-adrenal axis  (HPA).  Further, decreased DNA methylation of the  glucocorticoid receptor  gene were found in offspring that experienced a high level of licking; the glucorticoid receptor plays a key role in regulating the HPA. [ 44 ]   The opposite is found in offspring that experienced low levels of licking, and when pups are switched, the epigenetic changes are reversed. This research provides evidence for an underlying epigenetic mechanism. [ 44 ]   Further support comes from experiments with the same setup, using drugs that can increase or decrease methylation. [ 45 ]   Finally, epigenetic variations in parental care can be passed down from one generation to the next, from mother to female offspring. Female offspring who received increased parental care (i.e., high licking) became mothers who engaged in high licking and offspring who received less licking became mothers who engaged in less licking. [ 44 ]


In humans, a small clinical research study showed the relationship between prenatal exposure to maternal  mood  and genetic expression resulting in increased reactivity to stress in offspring. [ 4 ]  Three groups of infants were examined: those born to mothers medicated for  depression  with  serotonin reuptake inhibitors ; those born to depressed mothers not being treated for depression; and those born to non-depressed mothers. Prenatal exposure to depressed/anxious mood was associated with increased DNA methylation at the glucocorticoid receptor gene and to increased HPA axis stress reactivity. [ 44 ]   The findings were independent of whether the mothers were being pharmaceutically treated for depression. [ 44 ]


Environmental and epigenetic influences seem to work together to increase the risk of  addiction . [ 54 ]  For example, environmental stress has been shown to increase the risk of  substance abuse . [ 55 ]  In an attempt to cope with stress,  alcohol  and  drugs  can be used as an escape. [ 56 ]  Once substance abuse commences, however, epigenetic alterations may further exacerbate the biological and behavioural changes associated with addiction. [ 54 ]


Even short-term substance abuse can produce long-lasting epigenetic changes in the brain of rodents, [ 54 ]  via DNA methylation and histone modification. [ 19 ]  Epigenetic modifications have been observed in studies on rodents involving  ethanol ,  nicotine ,  cocaine ,  amphetamine ,  methamphetamine  and  opiates . [ 4 ]  Specifically, these epigenetic changes modify gene expression, which in turn increases the vulnerability of an individual to engage in repeated substance overdose in the future. In turn, increased substance abuse results in even greater epigenetic changes in various components of a rodent's  reward system [ 54 ]  (e.g., in the  nucleus accumbens [ 57 ] ). Hence, a cycle emerges whereby changes in areas of the  reward system  contribute to the long-lasting neural and behavioural changes associated with the increased likelihood of addiction, the maintenance of addiction and  relapse . [ 54 ]  In humans, alcohol consumption has been shown to produce epigenetic changes that contribute to the increased craving of alcohol. As such, epigenetic modifications may play a part in the progression from the controlled intake to the loss of control of alcohol consumption. [ 58 ]   These alterations may be long-term, as is evidenced in smokers who still possess nicotine-related epigenetic changes ten years after  cessation . [ 59 ]   Therefore, epigenetic modifications [ 54 ]  may account for some of the behavioural changes generally associated with addiction. These include: repetitive habits that increase the risk of disease, and personal and social problems; need for immediate  gratification ; high rates of relapse following treatment; and, the feeling of loss of control. [ 60 ]


Evidence for relevant epigenetic changes came from human studies involving alcohol, [ 61 ]  nicotine, and opiate abuse. Evidence for epigenetic changes stemming from amphetamine and cocaine abuse derives from animal studies. In animals, drug-related epigenetic changes in fathers have also been shown to negatively affect offspring in terms of poorer spatial  working memory , decreased  attention  and decreased  cerebral volume . [ 62 ]


Epigenetic changes may help to facilitate the development and maintenance of  eating disorders  via influences in the early environment and throughout the life-span. [ 24 ]   Pre-natal  epigenetic changes due to maternal stress, behaviour and diet may later predispose offspring to persistent, increased anxiety and  anxiety disorders . These anxiety issues can precipitate the onset of eating disorders and  obesity , and persist even after recovery from the eating disorders. [ 63 ]


Epigenetic differences accumulating over the life-span may account for the incongruent differences in eating disorders observed in monozygotic twins. At  puberty ,  sex hormones  may exert epigenetic changes (via DNA methylation) on gene expression, thus accounting for higher rates of eating disorders in men as compared to women  [ citation needed ] . Overall, epigenetics contribute to persistent, unregulated  self-control  behaviours related to the urge to  binge . [ 24 ]


Epigenetic changes including hypomethylation of glutamatergic genes (i.e., NMDA-receptor-subunit gene  NR3B  and the promoter of the AMPA-receptor-subunit gene  GRIA2 ) in the post-mortem brains of people with schizophrenia are associated with increased levels of the neurotransmitter  glutamate . [ 64 ]   Since glutamate is the most prevalent, fast, excitatory neurotransmitter, increased levels may result in the  psychotic episodes  related to  schizophrenia . Epigenetic changes affecting a greater number of genes have been detected in men with schizophrenia as compared to women with the illness. [ 65 ]


Population studies have established a strong association linking schizophrenia in children born to older fathers. [ 66 ] [ 67 ]  Specifically, children born to fathers over the age of 35 years are up to three times more likely to develop schizophrenia. [ 67 ]  Epigenetic dysfunction in human male  sperm cells , affecting numerous genes, have been shown to increase with age. This provides a possible explanation for increased rates of the disease in men. [ 65 ] [ 67 ] [ failed verification ]  To this end, toxins [ 65 ] [ 67 ]  (e.g.,  air pollutants ) have been shown to increase epigenetic differentiation. Animals exposed to ambient air from  steel mills  and  highways  show drastic epigenetic changes that persist after removal from the exposure. [ 68 ]  Therefore, similar epigenetic changes in older human fathers are likely. [ 67 ]  Schizophrenia studies provide evidence that the  nature versus nurture  debate in the field of  psychopathology  should be re-evaluated to accommodate the concept that genes and the environment work in tandem. As such, many other environmental factors (e.g.,  nutritional deficiencies  and  cannabis  use) have been proposed to increase the susceptibility of  psychotic disorders  like schizophrenia via epigenetics. [ 67 ]


Evidence for  epigenetic modifications for bipolar disorder  is unclear. [ 69 ]  One study found hypomethylation of a  gene promoter  of a  prefrontal lobe  enzyme (i.e., membrane-bound  catechol-O-methyl transferase , or COMT) in post-mortem brain samples from individuals with bipolar disorder. COMT is an enzyme that  metabolizes   dopamine  in the  synapse . These findings suggest that the hypomethylation of the  promoter  results in over-expression of the enzyme. In turn, this results in increased degradation of dopamine levels in the brain. These findings provide evidence that epigenetic modification in the prefrontal lobe is a risk factor for bipolar disorder. [ 70 ]  However, a second study found no epigenetic differences in post-mortem brains from bipolar individuals. [ 71 ]


The causes of  major depressive disorder  (MDD) are poorly understood from a  neuroscience  perspective. [ 72 ]   The epigenetic changes leading to changes in glucocorticoid receptor expression and its effect on the HPA stress system discussed above, have also been applied to attempts to understand MDD. [ 73 ]


Much of the work in animal models has focused on the indirect downregulation of  brain derived neurotrophic factor  (BDNF) by over-activation of the stress axis. [ 74 ] [ 75 ]   Studies in various rodent models of depression, often involving induction of stress, have found direct epigenetic modulation of BDNF as well. [ 76 ]


Epigenetics may be relevant to aspects of psychopathic behaviour through methylation and histone modification. [ 77 ]   These processes are heritable but can also be influenced by environmental factors such as smoking and abuse. [ 78 ]   Epigenetics may be one of the mechanisms through which the environment can impact the expression of the genome. [ 79 ]   Studies have also linked methylation of genes associated with nicotine and alcohol dependence in women, ADHD, and drug abuse. [ 80 ] [ 81 ] [ 82 ]  It is probable that epigenetic regulation as well as methylation profiling will play an increasingly important role in the study of the play between the environment and genetics of psychopaths. [ 83 ]


Several studies have indicated DNA cytosine methylation linked to the social behavior of insects, such as honeybees and ants. In honeybees, when nurse bee switched from her in-hive tasks to out foraging, cytosine methylation marks are changing. When a forager bee was reversed to do nurse duties, the cytosine methylation marks were also reversed. [ 84 ]  Knocking down the DNMT3 in the larvae changed the worker to queen-like phenotype. [ 85 ]  Queen and worker are two distinguish castes with different morphology, behavior, and physiology. Studies in DNMT3 silencing also indicated DNA methylation may regulate gene alternative splicing and pre-mRNA maturation. [ 86 ]


Many researchers contribute information to the  Human Epigenome Consortium . [ 87 ]  The aim of future research is to reprogram epigenetic changes to help with addiction, mental illness, age related changes, [ 2 ]  memory decline, and other issues. [ 1 ]  However, the sheer volume of consortium-based data makes analysis difficult. [ 2 ]  Most studies also focus on one gene. [ 88 ]   In actuality, many genes and interactions between them likely contribute to individual differences in personality, behaviour and health. [ 89 ]  As social scientists often work with many variables, determining the number of affected genes also poses methodological challenges. More collaboration between medical researchers, geneticists and social scientists has been advocated to increase knowledge in this field of study. [ 90 ]


Limited access to human brain tissue poses a challenge to conducting human research. [ 2 ]  Not yet knowing if epigenetic changes in the blood and (non-brain) tissues parallel modifications in the brain, places even greater reliance on brain research. [ 87 ]  Although some epigenetic studies have translated findings from animals to humans, [ 91 ]  a some researchers caution about the extrapolation of animal studies to humans. [ 1 ]  One view notes that when animal studies do not consider how the subcellular and cellular components, organs and the entire individual interact with the influences of the environment, results are too reductive to explain behaviour. [ 89 ]


Some researchers note that epigenetic perspectives will likely be incorporated into pharmacological treatments. [ 8 ]  Others caution that more research is necessary as drugs are known to modify the activity of multiple genes and may, therefore, cause serious side effects. [ 1 ]  However, the ultimate goal is to find patterns of epigenetic changes that can be targeted to treat mental illness, and reverse the effects of childhood stressors, for example. If such treatable patterns eventually become well-established, the inability to access brains in living humans to identify them poses an obstacle to pharmacological treatment. [ 87 ]  Future research may also focus on epigenetic changes that mediate the impact of psychotherapy on personality and behaviour. [ 44 ]


Most epigenetic research is correlational; it merely establishes associations. More experimental research is necessary to help establish causation. [ 92 ]  Lack of resources has also limited the number of intergenerational studies. [ 2 ]  Therefore, advancing longitudinal [ 90 ]  and multigenerational, experience-dependent studies will be critical to further understanding the role of epigenetics in psychology. [ 5 ]


Consumer behaviour  is the study of the motivations surrounding a purchase of a product or service. It has been linked to the field of  psychology , [ 1 ]   sociology [ 2 ]  and  economics [ 3 ]  in attempts to analyse when, why, where and how people purchase in the way that they do. However, little literature has considered the link between consumption behaviour and the basics of human  biology . Segmentation by biological-driven  demographics  such as  sex  and age are already popular and pervasive in marketing. As more knowledge and research is known,  targeting  based on consumers' biology is of growing interest and use to marketers.


As "human machines" [ 4 ]  being made up of cells controlled by a brain to influence aspects of behaviour, there must be some influence of biology on  consumer behaviour  and how purchase decisions are made as well. The  nature versus nurture  debate is at the core of how much biology influences these buying decisions, because it argues how much is can be explained through environmental and by biological factors.  Neuromarketing  is of interest to marketers in measuring the reaction of stimulus to marketing. [ 5 ] [ 6 ]


Lawson and Wooliscroft (2004) drew the link between  human nature  and the  marketing  concept, not explicitly biology, where they considered the contrasting views of  Hobbes  and  Rousseau  on mankind. Hobbes believed man had a self-serving nature whereas Rousseau was more forgiving towards the nature of man, suggesting them to be noble and dignified. Hobbes saw the need for a governing intermediary to control this selfish nature which provided a basis for the  exchange theory , and also links to Mcgregor's  Theory of X and Y , relevant to management literature. He also considered cooperation and competition, relevant to game theory as an explanation of man's motives and can be used for understanding the exercising of power in marketing channels. [ 7 ]  Pinker outlines why the nature debate has been suppressed by the nurture debate in his book  The Blank Slate . [ 8 ]


Cells  are the building blocks of all living organisms. Within these cells are coils of  DNA , genetic information instructing for how cells will develop and operate. A small segment of DNA is a  gene  which codes for the making of proteins and passing on  traits  to offspring in reproduction. The main goal of a gene is to reproduce and thrive in its environment in relative to competitors. [ 4 ]  Practical implications in  crime investigation , disorders and increasingly talent prediction and career  decision making [ 9 ]  have considered their association with genes and biology, but the idea of biology and marketing is a growing body of knowledge.  Neuromarketing  is a new phenomenon studying consumer's reactions to marketing stimuli. [ 5 ]


Richard Dawkins  outlines in  The Selfish Gene  (1976) [ 4 ]  that humans are machines made of genes, and genes are the grounding for everything people do. The  gene-centric view  outlines that  natural selection ,  evolution  and all behaviour must be traced back to the survival of competing genes as an extension of Darwin's theory being the survival of competing individuals. [ 4 ] [ 10 ]  The main goal of individuals, coming from genes, is to reproduce and thrive, where thriving involves protection, conquering competition and future growth. Therefore, everything that people do relates to thriving in their environment above competition, including the way people consume as a form of survival in their environment [ 11 ]  when simply purchasing the basic physiological needs of food, water and warmth. People also consume to thrive above others, for example in  conspicuous consumption  where a luxury car represents money and high social status [ 12 ]  and the application of makeup makes the person and their genes seem more attractive and worthy of passing to offspring. [ 4 ]


At least some behaviour must be influenced by genes because behaviour depends on the interaction of molecules and neurons in the brain. These interactions are a result of genes, however the influence on behaviour cannot go much further than this. Dawkins likened genes to a computer. They have been pre-programmed to build cells, develop cells and make them work together. Like a computer, the hardware is set in stone, but the software can change how they work, just like their environment. [ 4 ]  Genes indirectly influence behaviour as the  nervous system  and the brain is the intermediary in the transaction decision because it reasons and processes all of the gene instructions into one decision, movement or behaviour. [ 13 ] [ 14 ]  The way  neurons  connect is dependent on the environment, learning and experience. This introduces the nurture side of the nature nurture debate.


Epigenetics  is referred to as the ‘new genetics’ and phenomenon of importance to marketers because it studies how the environment can influence genes, and hence behaviour. The theory of  meiosis  is that exact replicas of parents' genes are passed to their offspring, with no variation influence from the environment. However genes have a protein wrapping the gene that can influence the  gene expression  and therefore  phenotypes  to the environment. [ 14 ]  How people act and consume now affects their  epigenome , and consequently their offspring's genome. [ 15 ]  This supports  Lamark's  theory, prior to Darwin, who initially proposed the theory of genes changing with behaviour and experience. [ 16 ]   A study from the University of Auckland warned pregnant women against dieting due to the increased likelihood in their child acquiring eating disorders such as obesity, [ 17 ]  hence the way people consume food.


The other side of the debate is the environment can shape attitudes, learning, sensation, thinking and behaviour  [ 18 ]


People who differ in  attitudes  toward education probably have different beliefs about the benefit of tertiary education, different feelings about having to go to class and different levels of commitment with respect to effort in assignments.


Attitude formation can be based on facts where a rational approach is taken, weighing up the pros and cons. A lot of the time, however, people acquire their attitudes from their parents, friends, and surrounding culture through a variety of learning mechanisms. [ 18 ] [ 19 ]  is a somewhat disturbing example of this. Marketers have long been aware of the influence of peers on attitudes and this is a particularly important concept for subcultures which are socially oriented and experienced based. Participants communicate via many means and move between geographic locations. [ 20 ]  An example of a  subculture  is  straight edge  and their consumption is therefore affected by the socially constructed attitudes of the subgroup. [ 21 ]


The  elaboration likelihood model  determines how easily attitudes can be changed. If the message goes through the peripheral route, people are far more likely to be influenced by how or whom or what surroundings the message is presented in. [ 22 ]  Therefore, advertising using a  celebrity endorser  such as  Justin Bieber for Proactive  may have a large impact on a person's attitude to skin care if the message is going through the latter route.


Habituation  is shared across species and is the simplest form of learning. Here a person's response to a stimulus weakens when it becomes familiar. [ 18 ]  For example, with drink driving advertising in New Zealand, a decade ago people saw cars smashing into each other as a scare tactic. The content of these adverts has become less and less shocking the more people have been exposed to them. People have now become so desensitised to them that a humour approach has to be taken and the latest example is the ‘Legend’ advert. [ 23 ]


Classical conditioning  is demonstrated in a real-world office setting. [ 24 ]


B. F. Skinner , [ 25 ]  theorist of  operant conditioning , shows how a pigeon has been taught to distinguish between two words and behaves appropriately depending on which one is being presented. It learned each response with a reward of food therefore its behaviour is being shaped by controlling its environment. An example of this conditioning in a  consumer behaviour  context is a cinema using a consumer incentive scheme. A consumer given a card which entitles the person to a free movie if the person brings a friend and free popcorn on Tuesdays with the purchase of a ticket  per se , they are more likely to go to a movie when perhaps they wouldn't have otherwise.


Shaping  is a learning technique and one of the most useful concepts for marketers assisting in the initial purchase of any new product. [ 26 ]


Empiricists  argue all knowledge comes from the senses, but if senses are only relevant to the proximal world, how do people know the distal world? They argue it is through learning and that prior experience plays a crucial role in shaping the perceptual world. Association is a key function which here refers to linking one sensory experience to another. [ 18 ]


Association is also relevant in enhancing generic memory. [ 18 ]  Many New Zealanders associate Phil Collins's song ‘In the air tonight’ and a gorilla playing on a drum set with a  Cadbury  Chocolate advertisement. [ 27 ]


Under normal conditions,  language  seems to develop in a similar way among all children but when children grow up in a radically different environment their language is significantly different. [ 18 ]  A number of examples including wild children show that certain elements of the early environment are essential for language learning. [ 28 ]   Amala and Kamala  and  Genie  never managed to fully progress to learning language. While these examples are extreme, they show that consumer's language is affected by their environment. [ 18 ]  This is especially true of marketing activities across geographical borders.


The environment has a profound effect on development.  Social deprivation  in infants and children leads to dramatic behavioural deficits  [ 18 ]  as evident in the behaviour of  Romanian orphans . [ 29 ]  In a consumer behaviour context,  vicarious learning  which involves changing behaviour by having an individual observe the actions of another and witness the consequences of that behaviour,  is used to develop new responses and inhibit undesired behaviours.  The former is done through educating consumers in product uses i.e. through product demonstrations and increasing attention to the message i.e. through celebrity endorsement. [ 30 ]


Matt Ridley suggests in Nature via Nurture (2003) [ 31 ]  the diversity of the  human species  is not hard-wired in the  genetic code , environments are critical. Nature is not at the expense of nurture, nor is nurture at the expense of nature, there is room for both; they work together.


Genes are cogs in the machine, not gods in the sky. They are switched on and off throughout life, by external as well as internal events, their job is to absorb information from the environment at least as often as to transmit it from the past. Genes do more than carry information; they respond to experience. [ 31 ]  Susan Mineka illustrated this concept exceedingly well with her idea of prepared learning in monkeys, [ 32 ]  where she found the predisposition of genes largely affected the acquisition of fear responses to certain stimuli. Lab-reared monkeys, through vicarious experience, were easily able to acquire a fear response to a snake, but not a flower. Nature provides the instinct, and elements of nurture depend on whether the instinct is expressed.


Genes predispose individuals to determine the extent to which an individual may engage or interact with certain environments. [ 31 ]  Ridley exemplified that having ‘athletic’ genes makes one want to practice a sport, and having ‘intellectual’ genes makes one seek out intellectual activities. "The genes are the agents of nurture and are more likely to be affecting appetite more than aptitude". Genes do not make the individual intelligent, the make them more likely to enjoy learning.  They encourage individuals to seek out environmental influences that will satisfy their appetites. "The environment acts as a multiplier of small genetic differences, pushing athletic children toward the sports that reward them, and pushing bright children to the books that reward them". [ 31 ]


Whether an individual develops certain  diseases  or  disorders  is also established, to a certain degree, on the basis of nature and nurture. Genes often predispose individuals to certain disorders or diseases, while environmental factors can trigger the onset. Susceptibility of  diabetes  is determined by inherited differences in DNA, but  environmental factors  such as diet, weight, age, and physical activity seem to be triggering the onset of the disease. Genetic make-up, in addition to the environment with which the genes are exposed to, is influencing the behaviour of consumers with regard to the food choices they make.  Addiction  to  substance abuse  is partially determined by genes, which predispose individuals to have addictive personalities; however the stimuli with which an addiction develops is dependent on the environment. Addiction is persistent and compulsive, and has a significant impact upon consumer behaviour. Individuals who experience substance abuse, for example, are prone to basing their consumption primarily around the purchasing of alcohol, even at the expense of other important aspects of well-being.


The link between biology and marketing is not a new phenomenon, especially through  segmentation  based on the biology of sex, age, and health condition. Certain products, for example, maternity products, are targeted at certain consumers based on their biology. Maternity clothes are purposely advertised to pregnant females looking to consume based on their changing biological processes and female predisposition.  The extent to which consumers are segmented and feel they are included or excluded in the segmentation in an ethical way makes this biological segmentation of growing interest for academics and marketers today. Various industries such as the insurance industry have been criticized to discriminate against consumers based on biology due to the use of genetic tests, where those with genetic diseases may have a higher premium. [ 33 ]  As scientists and marketers learn more about biology and gain greater access to consumer's biological information, ethical debates become increasingly apparent when engaging in marketing practices.


Measuring consumers' conscious and subconscious through studying their biological sensorimotor, cognitive and affective response to marketing stimuli, called  neuromarketing , is of increasing interest to marketers in order to gain insight into how they consume. [ 6 ] [ 34 ]  Dawkins (1989) explained that when people die they leave behind genes and  memes ; genes being the unit of genetic information, and memes the units of cultural information. Neuromarketing aims to examine the memory of these memes in order to manipulate them.


Through  fMRI ,  EEG ,  steady state topography  (SST) and  magnetoencephalography  (MEG) scans, [ 6 ]  marketers are able to study how consumers react, as a step towards understanding how they can influence consumption through marketing efforts. In conjunction with  qualitative research  methods, it can provide deep understanding into what, how and why people consume. Measuring eye tracking in e-service marketing is another example of quantitative biological methods measuring the way people consume. It analyses how consumers shop in an online environment by recording the number of mouse clicks and click maps based on eye movement. [ 35 ]


The famous Coke vs Pepsi study  [ 36 ]  used fMRI scans to show consumers sensory taste preference to  Pepsi  to  Coca-Cola . However, when participants were told they were drinking Coke, their brain activity also changed and they stated their preference for Coca-Cola. This shows that regardless of their biology and sensory reaction, people's consumption behaviour and preferences are influenced by the environment, in this case the perception of brands.


A number of studies have found that  human biology  can be linked with  political orientation . [ 1 ]  This means that an individual's biology may predispose them to a particular political orientation and  ideology  or, conversely, that subscription to certain ideologies may predispose them to measurable biological and  health outcomes .


Studies have found that subjects with  right-wing  (or  conservative  in the United States) political views have larger  amygdalae , [ 2 ]  report larger social networks and greater happiness than liberals, are more prone to express  disgust  to moral infringements and are more sensitive to perceived threats. [ 3 ] [ 4 ]  Those with  left-wing  (or  liberal  in the United States) political views are more likely to report greater relationship dissatisfaction and emotional distress than conservatives, to show more openness to experience as well as greater tolerance for uncertainty and disorder. [ 5 ] [ 6 ]


Genetic factors account for at least some of the variation of political views. [ 7 ] [ 8 ]  From the perspective of  evolutionary psychology , conflicts regarding  redistribution of wealth  may have been common in the ancestral environment and humans may have developed psychological mechanisms for judging their own chances of succeeding in such conflicts. These mechanisms may affect political views. However, many of the studies linking biology to politics remain controversial and unreplicated. [ 9 ] [ 10 ]


A 2011 study by cognitive neuroscientist Ryota Kanai at  University College London  found structural  brain  differences between subjects of different political orientation in a  convenience sample  of students at the same college. [ 2 ]  The researchers performed  MRI  scans on the brains of 90 volunteer students who had indicated their political orientation on a five-point scale ranging from "very  liberal " to "very  conservative ". [ 2 ] [ 11 ]


Students who reported more conservative political views were found to have larger  amygdala , [ 2 ]  a structure in the  temporal lobes  whose primary function is in the formation, consolidation and processing of  memory , as well as positive and negative conditioning (emotional learning). [ 12 ]  The amygdala is responsible for important roles in social interaction, such as the recognition of emotional cues in facial expressions and the monitoring of personal space, [ 13 ] [ 14 ]  with larger amygdalae correlating with larger and more complex social networks. [ 15 ] [ 16 ]  It is also postulated to play a role in threat detection, including modulation of  fear  and  aggression  to perceived threats. [ 17 ] [ 18 ] [ 19 ]  Conservative students were also found to have greater volume of gray matter in the left  insula  and the right  entorhinal cortex . [ 2 ]  There is evidence that conservatives are more sensitive to  disgust [ 3 ]  and one role of the insula is in the modulation of social emotions, such as the feeling of disgust to specific sights, smells and norm violations. [ 20 ] [ 21 ] [ 22 ]


Students who reported more liberal political views were found to have a larger volume of grey matter in the  anterior cingulate cortex , [ 2 ]  a structure of the brain associated with emotional awareness and the emotional processing of pain. [ 23 ] [ 24 ]  The anterior cingulate cortex becomes active in situations of uncertainty, [ 25 ]  and is postulated to play a role in  error  detection, such as the monitoring and processing of conflicting stimuli or information. [ 26 ]


The authors concluded, "Although our data do not determine whether these regions play a causal role in the formation of political attitudes, they converge with previous work to suggest a possible link between brain structure and psychological mechanisms that mediate political attitudes." [ 2 ]  In an interview with  LiveScience , Ryota Kanai said, "It's very unlikely that actual political orientation is directly encoded in these brain regions", and that "more work is needed to determine how these brain structures mediate the formation of political attitude." [ 1 ] [ 11 ] [ 27 ] [ 28 ]  Kanai and colleagues added that it is necessary to conduct a longitudinal study to determine whether the changes in brain structure that we observed lead to changes in political behavior or whether political attitudes and behavior instead result in changes of brain structure.


A 2024 study by Petalas et al achieved a partial replication of Kanai et al, using a larger sample size of 928 subjects, making it the largest preregistered replication study in political neuroscience to date. A positive relationship between the size of the amygdala and right-wing political views was found but at approximately a third of the effect size of the original study ( r  = 0.068 vs  r  = 0.23). The study also did not find a replication of the original finding of a positive relationship between a larger volume of grey matter in the anterior cingulate cortex and left-wing political view. [ 29 ]


Various studies suggest measurable differences in the psychological traits of  liberals  and  conservatives . Conservatives are more likely to report larger social networks, greater happiness and self-esteem than liberals, are more reactive to perceived threats and more likely to interpret ambiguous facial expressions as threatening. [ 30 ] [ 5 ] [ 4 ] [ 6 ]  Liberals are more likely to report greater emotional distress, relationship dissatisfaction and experiential hardship than conservatives, and show more openness to experience as well as greater tolerance for uncertainty and disorder. [ 5 ] [ 6 ] [ 30 ]


A study by David Amodio  et al.  at  New York University  and the  University of California, Los Angeles , found differences in how self-described liberal and conservative research participants responded to changes in patterns. [ 31 ]  Participants were asked to tap a keyboard when the letter "M" appeared on a computer monitor and to refrain from tapping when they saw a "W". The letter "M" appeared four times more frequently than "W", conditioning participants to press the keyboard when a letter appears. Liberal participants made fewer mistakes than conservatives during testing and their  electroencephalograph  readings showed more activity in the anterior cingulate cortex, the part of the brain that deals with conflicting information, during the experiment, suggesting that they were better able to detect conflicts in established patterns. Amodio warned against concluding that a particular political orientation is superior. He said: "The tendency of conservatives to block distracting information could be a good thing depending on the situation." [ 32 ] [ 33 ]


A 2017 study both replicated the original study and also found that conservatives performed better in a task in which choosing the simple strategy was the more optimal solution; while both liberals and conservatives started the task attempting the more complex but less effective strategy, conservatives switched to the simple strategy more quickly than liberals. [ 34 ]  Amodio's original study was also replicated by Weissflog  et al.  (2013) [ 35 ]  and Inzlicht  et al.  (2009). [ 36 ]  Conversely, Kremláček  et al.  (2019) [ 37 ]  and Wendell (2016) [ 38 ]  did not replicate Amodio's results. Both studies also argued that Weissflog and Inzlicht's results were not as concordant with the Amodio's findings as originally claimed.


A study of subjects' reported level of  disgust  linked to various scenarios showed that people who scored highly on the "disgust sensitivity" scale held more politically conservative views, [ 3 ]  which some researchers believe could be partially explained by personality traits. [ 39 ]  However, the findings of a 2019 study suggest that sensitivity to disgust among conservatives varies according to the elicitors used, and that using an elicitor-unspecific scale caused the differences in sensitivity to disappear between those of different political orientations. [ 40 ]


A 2018 study in the United States looking at levels of  cognitive reflection  (the tendency to favour analytic reasoning over instinctive or "gut" responses) found that those who voted for  Donald Trump  in the  2016 US presidential election  had lower levels of cognitive reflection than  Hillary Clinton  voters or third-party voters. However, this effect was mostly driven by Democrats who voted for Trump, while amongst Republicans, Clinton and Trump voters had more similar levels of cognitive reflection. Republicans who voted for third-party candidates or those who identified as libertarian had the highest levels of cognitive reflection. [ 41 ]


People with right-wing views had greater  skin conductance  response, indicating greater  sympathetic nervous system  response, to threatening images than those with left-wing views in one study. [ 42 ] [ 1 ]  There was no difference for positive or neutral images. Holding right-wing views was also associated with a stronger  startle reflex  as measured by strength of eyeblink in response to unexpected noise. Subsequent studies with substantially greater statistical power have failed to replicate these effects. [ 43 ] [ 44 ]


In an  fMRI  study published in  Social Neuroscience , three different patterns of brain activation were found to correlate with individualism, conservatism, and radicalism. [ 45 ]  In general, fMRI responses in several portions of the brain have been linked to viewing of the faces of well-known politicians. [ 46 ]  Others believe that determining political affiliation from fMRI data is overreaching. [ 47 ]


Heritability  compares differences in genetic factors in individuals to the total  variance  of observable characteristics (" phenotypes ") in a population, to determine the heritability coefficient. Factors including  genetics ,  environment  and random chance can all contribute to the variation in individuals' phenotypes. [ 48 ]


The use of  twin studies  assumes the elimination of non-genetic differences by finding the statistical differences between  monozygotic  (identical) twins, which have almost the same genes, and  dizygotic  (fraternal) twins. [ 49 ]  The similarity of the environment in which twins are reared has been questioned. [ 50 ] [ 51 ]


A twin study in 2005 by Alford  et al.  examined the attitudes regarding 28 different political issues such as capitalism, unions, X-rated movies, abortion, school prayer, divorce, property taxes, and the draft. Twins were asked if they agreed or disagreed or were uncertain about each issue. Genetic factors accounted for 53% of the variance of an overall score. However, self-identification as  Republican  and  Democrat  had a much lower heritability of 14%. It is worthwhile to note that identical twins correlated in opinion at a rate of 0.66 while fraternal twins correlated in opinion by 0.44. This likely occurs because identical twins share 100% of their DNA while fraternal twins share on average only 50% of their DNA. [ 52 ] [ 53 ]  However, Jonathan Kaplan argued that the role of individual genes is often extremely small due to many human physical traits being polygenic and may be overstated, [ 54 ]  observing that the study by Alford  et al.  made a case for the role of the  5-HTTLPR  region being involved in numerous psychological and personality traits, yet Border  et al.  (2019) found that multiple associations with 5-HTTLPR were spurious and underpowered. [ 55 ]


Jost  et al.  wrote in a 2011 review that "Many studies involving quite diverse samples and methods suggest that political and religious views reflect a reasonably strong genetic basis, but this does not mean that ideological proclivities are unaffected by personal experiences or environmental factors." [ 1 ]


In 2014, a study was performed on genomic data from 12,000 twin pairs from Australia, the USA, Denmark, Sweden and Hungary to examine genetic influences on political ideology. The study's  genome-wide association analysis  did not provide any definitive evidence of a specific genetic marker related to ideology. The authors remarked that, as with any complex trait, a single gene or small group of genes would not influence ideology directly but that there would likely be "thousands of genetic variants of very small effects and constellations of genes interacting with each other and the environment to influence behavior, indirectly". [ 56 ]


"A Genome-Wide Analysis of Liberal and Conservative Political Attitudes" by Peter K. Hatemi  et al.  traces DNA research involving 13,000 subjects. The study identifies several genes potentially [ qualify evidence ]  connected with political ideology. [ 57 ]


From an  evolutionary psychology  perspective, conflicts regarding  redistribution of wealth  may have been a recurrent issue in the ancestral environment. Humans may therefore have developed psychological mechanisms for judging their chance of succeeding in such conflicts which will affect their political views. For males, physical strength may have been an important factor in deciding the outcome of such conflicts. Therefore, a prediction is that males that have high physical strength and low  socioeconomic status  (SES) will support redistribution while males that have both high SES and high physical strength will oppose redistribution. Cross-cultural research found this to be the case; for females, their physical strength had no influence on their political views which was as expected since females rarely have physical strength above that of the average male. [ 58 ]  A study on political attitudes among  Hollywood  actors found that, while the actors were generally more left-leaning, male actors with great physical strength were more likely to support the Republican stance on foreign issues and foreign military interventions. [ 59 ]


An alternative evolutionary explanation for political diversity is that it is a  polymorphism , like those of gender and blood type, resulting from  frequency-dependent selection .  Tim Dean has suggested that we live in such a  moral ecosystem  whereby the advantage gained by having any one particular moral strategy diminishes as it becomes very common, causing evolution to produce individuals with a diversity of moral strategies. [ 60 ]  Alford  et al.  posit that political variation could offer groups different strategies of solving problems, thus variation is maintained by virtue of being adaptive at the group level. [ 61 ]


Studies linking genes and biology with political ideology have been criticised. Evan Charney publishing in  Perspectives on Politics  argues that Alford et al.'s research  is methodologically flawed, their data does not support their conclusions, and the creation of 'liberal' and 'conservative' ' phenotypes ' is untenable.  [ 62 ]  Furthermore, Doron Shultziner has also criticised the methodology and interpretation of  twin studies  used in the research supporting a connection between genetics and political ideology; arguing that identical twins are more likely to have similar political views is because they react to the environment in the same way. Shultziner further argues that the usage of the term "heritable" in the research has been questionable.  [ 63 ]


The relationship between  biology and sexual orientation  is a subject of on-going research. While scientists do not know the exact cause of  sexual orientation , they theorize that it is caused by a complex interplay of  genetic ,  hormonal , and  environmental influences . [ 1 ] [ 2 ] [ 3 ]  However, evidence is weak for hypotheses that the post-natal social environment impacts sexual orientation, especially for males. [ 3 ]


Biological theories for explaining the causes of sexual orientation are favored by scientists. [ 1 ]  These factors, which may be related to the development of a sexual orientation, include  genes , the early uterine environment (such as  prenatal hormones ), and  brain  structure. While the  evolutionary explanation  for  heterosexuality  in organisms that  reproduce sexually  is straightforwardly understood to be a  psychological adaptation  resulting from  greater reproductive success , [ 4 ]  evolutionary explanations for  homosexuality  rely upon other mechanisms of evolution such as  kin selection  and  inclusive fitness , or  antagonistic pleiotropy  that  favors heterozygotes  causing homosexuality among  homozygotes  as a  by-product .


The influence of hormones on the developing fetus has been the most influential causal hypothesis of the development of sexual orientation. [ 3 ] [ 5 ]  In simple terms, the developing fetal brain begins in a "female" state. Both  INAH3  (third interstitial nucleus of the anterior hypothalamus) area on the left side of the hypothalamus, which stores gender preference, and the center area of the bed stria terminalus (BSTc) area on the right side of the hypothalamus, which stores gender identity, are undeveloped and function as female. The action of the SRY gene in the Y-chromosome in the fetus prompts the development of testes, which release testosterone, the primary androgen receptor-activating hormone, to allow testosterone to enter the cells and masculinize the fetus and fetal brain. If a sufficient amount of testosterone is received by INAH3 at 12 weeks following conception, the testosterone stimulates the enlargement of INAH3, which is known to be involved in directing typical male sex behavior, such as attraction to females. If INAH3 does not receive enough testosterone to override the circulating estrogen, it may not grow to the size typically observed in males. Subsequently, INAH3 may function as female or partially female, potentially causing same-sex attraction to males. Although the  size  of INAH3 in homosexual men compared to heterosexual men may not be statistically different, homosexual men may have a greater cell  density  per unit volume than heterosexual men, though a similar total number of INAH3 neurons. [ 6 ]


Studies have shown that INAH3 in  gay men  has likely been exposed to lower levels of testosterone in the brain compared to straight men, or had different levels of receptivity to its masculinizing effects, or experienced hormone fluctuations at critical times during fetal development. In women, if INAH3 receives more testosterone than is normal for females, INAH3 may enlarge somewhat or even to the size that is normal for males, increasing the likelihood of same sex attraction. [ 3 ]  Supporting this are studies of the finger  digit ratio  of the right hand, which is a robust marker of prenatal testosterone exposure  [ disputed  –  discuss ] . Lesbians tend to have significantly more masculine digit ratios, a finding which has been replicated in numerous cross-cultural studies. [ 7 ]  Controlled experiments in animals, where scientists manipulate exposure to sex hormones during gestation, can also induce lifelong male-typical behavior and mounting in females, and female-typical behavior in males. [ 3 ] [ 7 ] [ 5 ] [ 8 ]


Maternal immune responses during fetal development are strongly demonstrated as causing male homosexuality and bisexuality. [ 9 ]  Research since the 1990s has demonstrated that as a woman has more sons, there is a higher chance of later born sons being gay. During pregnancy, male cells enter a mother's bloodstream, which provoke an immune response to neutralize them. These antibodies are then released on future male fetuses and may neutralize Y-linked antigens, which play a role in brain masculinization, leaving areas of the brain responsible for sexual attraction in the female-typical default position, i.e. expressing attraction to men. Each subsequent son will increase the levels of these antibodies, creating the observed  fraternal birth order effect . Biochemical evidence to support this effect was confirmed in a lab study in 2017, finding that mothers with a gay son, particularly those with older brothers, had heightened levels of antibodies to the NLGN4Y Y-protein than mothers with heterosexual sons. [ 9 ] [ 10 ]  This effect is estimated to account for between 15 and 29% of gay men, while other gay and bisexual men are thought to owe sexual orientation to genetic and hormonal interactions. [ 11 ] [ 9 ]


Socialization theories, which were dominant in the 1900s, favored the idea that children were born "undifferentiated" and were socialized into gender roles and sexual orientation. This led to medical experiments in which newborn and infant boys were surgically reassigned into girls after accidents such as botched circumcisions. These males were then reared and raised as females without telling them, but contrary to expectations, this did not make them feminine nor attracted to men. All published cases providing sexual orientation grew up to be strongly attracted to women. The failure of these experiments demonstrate that socialization effects do not induce feminine sexual behavior or psychology in males, and that the organizational effects of hormones on the fetal brain prior to birth have permanent effects. These indicate the primary role of nature, not post-birth nurture, in the development of male sexual orientation. [ 3 ]


In the brain, the sexually dimorphic nucleus of the preoptic area (SDN-POA) is a key region which differs between males and females in humans and a number of mammals (e.g., sheep/rams, mice, rats), and is caused by sex differences in hormone exposure. [ 3 ] [ 7 ]  Also, the  INAH-3  region is bigger in males than in females, and is known to be critical for sexual behavior. Dissection studies found that gay men had significantly smaller INAH-3 than heterosexual men, a shift in the female direction, as first demonstrated by neuroscientist  Simon LeVay , which has been replicated. [ 7 ]  Dissection studies are rare, however, due to lack of funding and brain samples. [ 3 ]


Long-term studies of  homosexual behavior in domesticated sheep  led by Charles Roselli have found that 6-8% of rams have a homosexual preference through their life. Dissection of ram brains also found a similar smaller (feminized) structure in homosexually oriented rams in the brain region equivalent to human SDN, the ovine sexually dimorphic nucleus (oSDN). [ 12 ] : 107–110   The size of the sheep oSDN has also been demonstrated to be formed in utero, rather than postnatally, underscoring the role of prenatal hormones in masculinization of the brain for sexual attraction. [ 8 ] [ 3 ]


Other studies in humans have relied on brain imaging technology, such as research led by  Ivanka Savic  which compared hemispheres of the brain. This research found that straight men had right hemispheres 2% larger than the left, described as modest but "highly significant difference" by LeVay. In heterosexual women, the two hemispheres were the same size. In gay men, the two hemispheres were also the same size, or sex atypical, while in lesbians, the right hemispheres were slightly larger than the left, indicating a small shift in the male direction. [ 12 ] : 112


A model proposed by evolutionary geneticist William R. Rice argues that a misexpressed epigenetic modifier of testosterone sensitivity or insensitivity that affected development of the brain can explain homosexuality, and can best explain twin discordance. [ 14 ]  Rice et al. propose that these epimarks normally canalize sexual development, preventing  intersex  conditions in most of the population, but sometimes failing to erase across generations and causing reversed sexual preference. [ 14 ]  On grounds of evolutionary plausibility, Gavrilets, Friberg and Rice argue that all mechanisms for exclusive homosexual orientations likely trace back to their epigenetic model. [ 15 ]  Testing this hypothesis is possible with current stem cell technology. [ 16 ]


Prenatal thyroid theory of same-sex attraction/gender dysphoria has been based on clinical and developmental observations of youngsters presenting to child psychiatry clinics in Istanbul/Turkey. The report of 12 cases with same-sex attraction/gender dysphoria born to mothers with thyroid diseases was first presented in EPA Congress, Vienna (2015) and published as an article in the same year. [ 17 ] [ 18 ]  The extremely significant relationship between the two conditions suggested an independent model, named as  Prenatal Thyroid Model of Homosexuality . According to Turkish child & adolescent psychiatrist Osman Sabuncuoglu, who generated the theory, maternal thyroid dysfunction may lead to abnormal deviations from gender-specific development in the offspring. Autoimmune destructive process as seen in Hashimoto thyroiditis, diminished supply of thyroid hormones and impacts on prenatal androgen system were all considered as contributing mechanisms. In a follow-up theoretical paper, [ 19 ]  previous research findings indicating higher rates of polycystic ovary syndrome (PCOS) in female-to-male transsexuals and lesbian women were conceived as an indication of  Prenatal Thyroid Model  since PCOS and autoimmune thyroiditis are frequently comorbid diseases. Likewise, increased rates of autism spectrum disorder in children born to mothers with thyroid dysfunction and overrepresentation of ASD individuals in gender dysphoria populations suggest such an association. A second group of young children with this pattern were presented in IACAPAP Congress, [ 20 ]  Prague (2018). Furthermore, 9 additional cases were reported in IACAPAP Congress, [1]  Rio de Janeiro (Sabuncuoglu, 2024).


The findings from previous research in LGBT populations had called for attention to be paid to thyroid system. [ 21 ] [ 22 ]  A commentary by Jeffrey Mullen, published shortly after the 2015 article, underlined the importance of  Prenatal Thyroid Model  and supported developments in this field. [ 23 ]  Afterwards, several authors have emphasized the role of thyroid system in sexuality while citing the  Prenatal Thyroid Model. [ 24 ] [ 25 ] [ 26 ] [ 27 ]  Among them, Carosa et al. concluded that thyroid hormones, affecting the human sexual function strongly, the thyroid gland must be considered, along with the genitals and the brain, a sexual organ. [ 24 ]  As a tertiary source, an authoritative book on the subject of interplay between endocrinology, brain and behavior has also cited the thyroid-homosexuality proposal article in the latest edition. [ 28 ]


Multiple genes have been found to play a role in sexual orientation. Scientists caution that many people misconstrue the meanings of  genetic  and  environmental . [ 3 ]   Environmental influence  does not automatically imply that the social environment influences or contributes to the development of sexual orientation. Hypotheses for the impact of the post-natal social environment on sexual orientation are weak, especially for males. [ 3 ]  There is, however, a vast non-social environment that is non-genetic, such as  prenatal development , which remains poorly understood. [ 3 ] : 76


Twin studies are one method of testing genetic and environmental influences, although they cannot reveal what kind of environmental influence this may include (social or non-social). [ 29 ]  Identical or monozygotic twins share their genes, while fraternal or dizygotic twins are only as genetically similar as any other sibling pair. When twins both share a trait, they are  concordant  for this trait; and when they differ they are  discordant . If identical twins have a higher rate of concordance for a trait than fraternal twins, it indicates that genes may contribute to the trait. [ 3 ] : 74–76


The 2016 Bailey et al. meta-analysis of all twin studies on sexual orientation found that the  median  concordance for homosexual or non-heterosexual orientation in twins in unbiased probability samples is 24% for monozygotic identical twins, and 15% for dizygotic twins. [ 3 ] : 74–76   According to Rice et al. the identical twin concordance for homosexuality is similar to identical twin concordance for two other traits influenced by prenatal androgens:  cryptorchidism  and  hypospadias  (feminized male gonads) which have an identical twin concordance around 25%, despite twins sharing genes and prenatal environments. [ 14 ] : 356


Twin studies have also found that among twins with differing sexual orientations, homosexual twins were significantly more  gender nonconforming  than their heterosexual co-twin, and that this was noticeable from a young age. [ 29 ]  Bailey states:


What kind of environmental factor can cause genetically identical twins reared in the same family from birth—often dressed alike and given the same toys—to differ in their sexual orientations? It is a fascinating question that we haven’t begun to answer well. One hint comes from the childhood behavior findings. When identical twins differed in their sexual orientation, the gay one tended to recall being much more feminine than the straight one. This means that the environmental factors that cause the twin differences are there early on, by childhood. Based on other things we know, such as studies of children with cloacal exstrophy, I suspect that these factors operate in the womb. [ 29 ]


Identical twins reared apart from birth are another method of studying the origin of psychological traits. Unfortunately, such twin pairs are rare. Three sets of male twin pairs exist in the literature. In the first pair found by Thomas Bouchard, both male twins reared apart from birth were homosexual. In a second pair found by Whitham, both males were also homosexual. In the third pair found by Bouchard, the male twins were neither definitively concordant nor discordant, as both had relations with males and females, thus this pair may be concordant for bisexuality. Among the female twin pairs; four female twin pairs were all discordant, although the small number of cases prevent any strong conclusions. [ 30 ]


According to William Rice and colleagues, the concordance of homosexuality among twins raises the possibility that homosexuality is not caused by genes nor atypical levels of hormones, but an epigenetic mechanism controlling how sensitive fetuses are to prenatal hormones. [ 14 ] [ 31 ] : 22


Sanders  et al.  2015


Sanders  et al.  2017


Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993,  Dean Hamer  and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families. [ 32 ]  Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of  Xq28 , which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed the " gay gene " in the media, causing significant controversy. In 1998, Sanders et al. [ citation needed ]  reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared with 6% on the paternal side. [ 33 ]


A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28. [ 34 ]  Two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men. [ 33 ]  One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results. [ 35 ]  Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation. [ 36 ]


Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects. In the full sample they did not find linkage to Xq28. [ 37 ]


Results from the first large, comprehensive multi-center genetic linkage study of male sexual orientation were reported by an independent group of researchers at the American Society of Human Genetics in 2012. [ 38 ]  The study population included 409 independent pairs of gay brothers, who were analyzed with over 300,000  single-nucleotide polymorphism  markers. The data strongly replicated Hamer's Xq28 findings as determined by both two-point and multipoint (MERLIN) LOD score mapping. Significant linkage was also detected in the pericentromeric region of chromosome 8, overlapping with one of the regions detected in the Hamer lab's previous genomewide study. The authors concluded that "our findings, taken in context with previous work, suggest that genetic variation in each of these regions contributes to development of the important psychological trait of male sexual orientation". Female sexual orientation does not seem to be linked to Xq28, [ 34 ] [ 39 ]  though it does appear moderately heritable. [ 38 ]


In addition to  sex chromosomal  contribution, a potential  autosomal  genetic contribution to the development of homosexual orientation has also been suggested. In a study population composed of more than 7000 participants, Ellis et al. (2008) found a statistically significant difference in the frequency of blood type A between homosexuals and heterosexuals. They also found that "unusually high" proportions of homosexual males and homosexual females were  Rh negative  in comparison to heterosexuals. As both blood type and Rh factor are genetically inherited traits controlled by  alleles  located on chromosome 9 and chromosome 1 respectively, the study indicates a potential link between genes on autosomes and homosexuality. [ 40 ] [ 41 ]


The biology of sexual orientation has been studied in detail in several animal model systems. In the common fruit fly  Drosophila melanogaster , the complete pathway of sexual differentiation of the brain and the behaviors it controls is well established in both males and females, providing a concise model of biologically controlled courtship. [ 42 ]  In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred female mice specifically lacking a particular gene related to sexual behavior. Without the gene, the mice exhibited masculine sexual behavior and attraction toward urine of other female mice. Those mice who retained the gene fucose mutarotase (FucM) were attracted to male mice. [ 43 ]


In interviews to the press, researchers have pointed that the evidence of genetic influences should not be equated with genetic determinism. According to Dean Hamer and Michael Bailey, genetic aspects are only one of the multiple causes of homosexuality. [ 44 ] [ 45 ]


In 2017,  Scientific Reports  published an article with a  genome wide association study  on male sexual orientation. The research consisted of 1,077 homosexual men and 1,231 heterosexual men. A gene named  SLITRK6  on  chromosome 13  was identified. [ 46 ]  The research supports another study which had been done by the neuroscientist  Simon LeVay . LeVay's research suggested that the  hypothalamus  of gay men is different from straight men. [ 47 ]  The SLITRK6 is active in the mid-brain where the hypothalamus is. The researchers found that the  thyroid stimulating hormone receptor  (TSHR) on chromosome 14 shows sequence differences between gay and straight men. [ 46 ]   Graves' disease  is associated with TSHR abnormalities, with previous research indicating that Graves' disease is more common in gay men than in straight men. [ 22 ]  Research indicated that gay people have lower body weight than straight people. It had been suggested that the overactive TSHR hormone lowered body weight in gay people, though this remains unproven. [ 48 ] [ 49 ]


In 2018, Ganna et al. performed another  genome-wide association study  on sexual orientation of men and women with data from 26,890 people who had at least one same-sex partner and 450,939 controls. The data in the study was meta-analyzed and obtained from the  UK Biobank  study and  23andMe . The researchers identified four variants more common in people who reported at least one same-sex experience on chromosomes 7, 11, 12, and 15. The variants on chromosomes 11 and 15 were specific to men, with the variant on chromosome 11 located in an olfactory gene and the variant on chromosome 15 having previously been linked to male-pattern baldness. The four variants were also correlated with mood and mental health disorders; major depressive disorder and schizophrenia in men and women, and bipolar disorder in women. However, none of the four variants could reliably predict sexual orientation. [ 50 ]


In August 2019, a genome-wide association study of 493,001 individuals concluded that hundreds or thousands of genetic variants underlie homosexual behavior in both sexes, with 5 variants in particular being significantly associated. Some of these variants had sex-specific effects, and two of these variants suggested links to biological pathways that involve  sex hormone  regulation and  olfaction . All the variants together captured between 8 and 25% of the variation in individual differences in homosexual behavior. These genes partly overlap with those for several other traits, including openness to experience and risk-taking behavior. Additional analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced by a similar set of genetic variants. They also found that the genetic effects that differentiate heterosexual from homosexual behavior are not the same as those that differ among nonheterosexuals with lower versus higher proportions of same-sex partners, which suggests that there is no single continuum from heterosexual to homosexual preference, as suggested by the  Kinsey scale . [ 51 ]


In October 2021, another research paper reported that genetic factors influence the development of same-sex sexual behavior. A two-stage genome-wide association study (GWAS) with a total sample of 1478 homosexual males and 3313 heterosexual males in  Han Chinese  populations identified two genetic loci (FMR1NB and ZNF536) showing consistent association with male sexual orientation. [ 52 ]


A study suggests linkage between a mother's genetic make-up and homosexuality of her sons. Women have two X chromosomes, one of which is "switched off". The inactivation of the X chromosome occurs randomly throughout the embryo, resulting in cells that are mosaic with respect to which chromosome is active. In some cases though, it appears that this switching off can occur in a non-random fashion. Bocklandt et al. (2006) reported that, in mothers of homosexual men, the number of women with extreme skewing of X chromosome inactivation is significantly higher than in mothers without gay sons. In a study of 94 participants, 13% of mothers with one gay son, and 23% of mothers with two gay sons, showed extreme skewing, compared to 4% of mothers without gay sons. [ 53 ]