Explain how far behaviour is inherited, what heritability means, how family, twin, adoption and molecular studies estimate genetic influence, how epigenetics works, and evaluate this research.
Each is in the Psychology glossary, with every other term in the subject.
A research design that compares adopted people with their biological relatives, who share their genes, and their adoptive relatives, who share their environment, to separate genetic from environmental influences.
One of the different versions of a gene; a person inherits one allele of each gene from each parent.
A research design that tests whether one gene, chosen in advance because of its biological role, is associated with a trait or disorder; many such findings have failed to replicate.
The percentage of pairs of twins or relatives in which both members show a trait or disorder, given that one of them has it.
Twins who develop from two eggs fertilised by two different sperm, so, like ordinary siblings, they share on average about 50% of the genes that vary between people.
An epigenetic process in which methyl groups attach to DNA, usually reducing the expression of a gene without changing its sequence.
The study of changes in gene expression that do not involve changes to the DNA sequence itself, including changes caused by the environment and experience.
The assumption in twin research that monozygotic and dizygotic twins experience equally similar environments, so that greater similarity in monozygotic twins can be attributed to genes.
Describe what genes are and how genetic inheritance passes traits from parents to children.
Explain what a heritability estimate measures and why it describes a population, not an individual.
Explain the logic of family, twin and adoption studies, including concordance rates and the equal environments assumption.
Describe how genome-wide association studies and polygenic scores study genetic influence at the level of DNA.
Explain how epigenetics allows the environment to change gene expression without changing the DNA sequence.
Explain why genes and environment interact and correlate, so that behaviour cannot be divided into “nature” and “nurture”.
Evaluate research into genetic inheritance with reference to measurement, causality, bias and responsibility.
Apply genetic inheritance to examples of behaviour in health, development, relationships and learning.
Genetic inheritance is the passing of traits from parents to their children through genes. Psychologists study it to find out how far differences between people in behaviour, such as intelligence, personality or the risk of a mental health disorder, are linked to differences in their genes, and how far they come from experience.
The question belongs to the biological approach, but it cannot be answered by biology alone. Every research design in this area has to separate the effects of genes from the effects of the environment, which raises problems of measurement and causality. Because claims about inherited differences between people have been misused in the past, the topic also raises questions of responsibility
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A section of DNA on a chromosome that carries the code for making a protein, and that is passed from parents to their children.
The tendency for people’s genes and environments to be related, because parents pass on both, because traits evoke reactions, and because people choose environments that suit them.
The transmission of traits from parents to their children through the genes they pass on.
A research method that scans hundreds of thousands of genetic variants across the genome in very large samples to find variants statistically associated with a trait or disorder.
The particular set of alleles that a person carries, either for one gene or across their whole genome.
The proportion of the variation in a trait within a population that is associated with genetic differences between its members; it does not apply to individuals and changes with the environment.
The gap between the heritability of a trait estimated from twin studies and the much smaller share of variation explained by genetic variants found in genome-wide association studies.
Twins who develop from a single fertilised egg that splits in two, so they share almost 100% of their genes; also called identical twins.
The debate about the relative contribution of inherited factors (nature) and environmental factors (nurture) to behaviour, now usually replaced by the study of how the two interact.
The observable or measurable characteristics of a person, such as height or anxiety level, which result from the interaction of their genotype and environment.
A single number that adds up the effects of many genetic variants a person carries, each weighted by its association with a trait in a genome-wide association study, to estimate genetic tendency towards that trait.
The practice of placing adopted children in families similar to their biological families, which makes genetic and environmental influences harder to separate in adoption studies.
A research design that compares the similarity of monozygotic twins with that of dizygotic twins on a trait, to estimate how far variation in the trait is associated with genetic differences.
Every cell in the body contains DNA, a long molecule that carries the instructions for building and running the body. DNA is packaged into 23 pairs of chromosomes: one chromosome of each pair comes from the mother and one from the father. A gene is a section of DNA that holds the code for making a particular protein, such as a receptor for a neurotransmitter or an enzyme that breaks one down.
Most genes come in slightly different versions, called alleles. Because a person inherits one copy of each gene from each parent, they can carry two identical alleles or two different ones. The full set of alleles a person carries is their genotype; the characteristics that can be observed or measured, such as height, eye colour or anxiety level, are their phenotype.
Some physical conditions follow from one gene. Huntington’s disease, for example, develops in almost everyone who inherits one faulty copy of a single gene. Psychological traits do not work like this. Intelligence, depression, schizophrenia and personality are each influenced by thousands of genetic variants, and each variant has a tiny effect on its own. Traits like these are called polygenic.
Genes also act at a distance from behaviour. A gene codes for a protein; the protein changes how neurons grow, connect or signal; those neural differences change how a person reacts to their experiences, and only then does behaviour change. At every step the environment can increase, reduce or redirect the effect. For this reason, psychologists talk about genes that influence or increase the risk of a behaviour, never about a “gene for” depression or intelligence.
People differ from one another on almost every psychological trait. Some of these differences are linked to differences in genes and some to differences in environment. Heritability is a statistic that estimates how much of the variation in a trait, within a particular population at a particular time, is associated with genetic variation between the people in it.
Researchers usually divide the remaining variation into two parts. The shared environment is everything that makes members of a family more alike, such as the family’s income, neighbourhood and parenting style. The non-shared environment is everything that makes them different, such as different friends, different illnesses or a different experience of the same event; it also includes measurement error.
A population, not a person. A heritability of 50% for a trait does not mean that half of each person’s trait comes from genes and half from the environment. Genes and experience work together inside every individual, so their contributions cannot be separated in one person, in the same way that the area of a rectangle cannot be divided into a part due to its length and a part due to its width.
Specific to an environment. If everyone in a population grew up in very similar environments, almost all remaining differences would be genetic and heritability would be high. If environments vary a lot, heritability falls. The same trait can therefore have different heritabilities in different countries, social classes or historical periods.
Not a measure of how changeable a trait is. Height is highly heritable, yet average height rose in many countries during the 20th century as nutrition improved. A high heritability says nothing about how effective a treatment, a school programme or a change in diet could be.
Polderman et al. (2015) combined almost every twin study published over 50 years: 2,748 publications covering 17,804 traits and over 14.5 million partly overlapping twin pairs. Across all traits, the average reported heritability was 49%. Heritability was found for almost every trait studied, but it was almost never close to 100%, so the environment also matters for virtually every human characteristic.
The first step in studying inheritance is to ask whether a trait is more common in the relatives of people who have it. In a family study, researchers identify people with a trait or disorder (called probands) and a comparison group without it, then measure the rate of the trait in their first-degree relatives (parents, siblings and children, who share about 50% of their varying genes with the proband).
Sullivan, Neale and Kendler (2000) combined five family studies of major depression and found that first-degree relatives of people with depression had about 2.8 times the odds of having depression themselves compared with relatives of people without it. This shows that depression runs in families.
Family studies cannot show why a trait runs in families. Relatives share genes, but they also share a home, a diet, a level of income, a way of talking about emotions and often the same stressful events. A child of a depressed parent may be at higher risk because of inherited genes, because of growing up with a parent who is unwell, or both. Family studies are therefore a starting point: they show familiality, and twin and adoption studies are needed to separate genes from shared environment.
Twin studies use a natural difference between two kinds of twins. Monozygotic twins (MZ, or identical twins) develop from one fertilised egg that splits in two, so they share almost 100% of their genes. Dizygotic twins (DZ, or non-identical twins) develop from two eggs fertilised by two sperm, so, like ordinary siblings, they share on average about 50% of the genes that vary between people.
Both kinds of twin are born at the same time into the same family, so they are assumed to share their environments to the same degree. If MZ twins are more similar than DZ twins on a trait, the extra similarity is attributed to their extra shared genes. If MZ and DZ twins are equally similar, the trait shows little genetic influence.
For a trait that a person either has or does not have, such as a diagnosis of schizophrenia, similarity is measured as a concordance rate: the percentage of twin pairs in which, when one twin has the trait, the other twin also has it. A higher concordance rate in MZ twins than in DZ twins suggests a genetic influence.
Hilker et al. (2018) linked two national registers in Denmark, the Danish Twin Register and the Danish Psychiatric Research Register, and identified 31,524 twin pairs born between 1951 and 2000. The concordance rate for schizophrenia was 33% in MZ twins and 7% in DZ twins, and the heritability of schizophrenia was estimated at 79%.
The chart shows both sides of the evidence. The large gap between MZ and DZ twins shows a strong genetic influence. However, MZ twins share almost all their genes, and in 67% of MZ pairs only one twin developed schizophrenia. Genes therefore increase vulnerability, but they do not decide the outcome on their own. This is the starting point of the diathesis-stress model, which explains why only some vulnerable people develop a disorder.
For a continuous trait, such as an IQ score or a score on a depression questionnaire, similarity is measured with a correlation between the scores of the two twins in each pair. A simple estimate of heritability (Falconer’s formula) doubles the difference between the MZ and DZ correlations, because MZ twins share about twice as many varying genes as DZ twins:
Modern studies use more complex statistical models, but the logic is the same: the greater the gap between MZ and DZ similarity, the higher the estimated heritability.
The twin method rests on the equal environments assumption: the assumption that MZ twins are treated no more alike than DZ twins in ways that matter for the trait. If MZ twins are treated more similarly (dressed alike, mistaken for each other, placed in the same class, closer friends with each other), some of their extra similarity could come from a more similar environment, and heritability would be overestimated.
Researchers have tested the assumption in several ways. One method uses twins whose parents were wrong about their zygosity, for example parents who believed their MZ twins were non-identical. If similar treatment caused similarity, these twins would be less alike than correctly labelled MZ twins. Such studies have generally found that actual zygosity matters more than what parents believe, so the assumption is reasonable for many traits, but MZ twins do share more similar experiences, so it remains a source of possible overestimation.
Adoption creates a second natural experiment. A child who is adopted soon after birth receives genes from the biological parents and an environment from the adoptive parents. If adopted children resemble their biological parents more than their adoptive parents on a trait, this points to genetic influence; if they resemble their adoptive parents more, it points to the shared environment.
In an early adoption study, Heston (1966) followed up children born to mothers with schizophrenia who had been separated from their mothers in infancy and raised in foster homes in the United States. As adults, these children were diagnosed with schizophrenia more often than a matched group of adoptees whose biological mothers had no psychiatric diagnosis. Since they had not been raised by their biological mothers, the higher rate could not be explained by being brought up by a parent with the disorder.
Selective placement. Adoption agencies often try to match adoptive families to the biological family (for example by social class or religion). The adoptive environment then resembles the one the biological parents would have provided, and genetic and environmental effects are mixed again.
The prenatal environment. The biological mother provides nine months of environment in the womb, including her diet, stress hormones and any drugs or alcohol. Similarity to the biological mother may partly reflect this environment, not genes.
Restricted range. Adoptive families are screened and tend to be stable and better off than average. If few adoptive homes are very poor, the effect of a poor environment cannot show up, and heritability is overestimated.
Small and unusual samples. Adoption has become less common in many countries, so samples are small, and adopted children may differ from other children in ways that limit generalisability.
Because family, twin and adoption designs each have different weaknesses, their results are most convincing when they agree. For most psychological traits all three designs point to a moderate genetic influence, with the non-shared environment explaining most of the rest. This agreement across methods is a form of triangulation.
YouTubeDesign | Who is compared | What it can show | Main limitation |
|---|---|---|---|
Family study | Relatives of people with and without a trait | Whether a trait runs in families (familiality) | Cannot separate shared genes from shared environment |
Twin study | MZ twins vs DZ twins | Heritability, from the extra similarity of MZ twins | Equal environments assumption may not hold |
Twins reared apart | MZ twins raised in different homes | Similarity with little shared family environment | Very rare; contact and selective placement |
Adoption study | Adoptees vs biological and adoptive relatives | Genetic influence separate from rearing environment | Selective placement, prenatal environment, restricted range |
Genome-wide association study | People with and without a trait, across their DNA | Which specific variants are associated with a trait | Each variant has a tiny effect; mostly European-ancestry samples |
Bouchard et al. (1990) aimed to estimate how far differences between people in intelligence, personality, interests and social attitudes are associated with genetic differences, using the rarest and most informative natural experiment in behaviour genetics: identical twins who were separated early in life and raised in different families.
From 1979, the Minnesota Study of Twins Reared Apart (MISTRA) at the University of Minnesota recruited monozygotic and dizygotic twins who had been separated in infancy and reared apart. By the time of the 1990 report, more than 100 sets of reared-apart twins or triplets had come to Minneapolis for about a week of intensive psychological and physiological assessment.
The twins completed several intelligence tests, personality and temperament questionnaires, measures of occupational and leisure interests and of social attitudes, plus medical examinations and life-history interviews. The design is a natural experiment in which the independent variable (genetic relatedness) cannot be manipulated, and similarity between twins was measured with intraclass correlations, then compared with published results for twins reared together.
The logic is that MZ twins reared apart (MZA) share all their genes but not their family environment. Their correlation on a trait is therefore a direct estimate of the share of variation linked to genes, provided their separate environments were not similar to each other.
Measure | Main finding |
|---|---|
Intelligence (IQ) | About 70% of the variance in IQ was associated with genetic variation |
Personality and temperament | MZ twins reared apart were about as similar as MZ twins reared together |
Occupational and leisure interests | MZ twins reared apart were about as similar as MZ twins reared together |
Social attitudes (e.g. religiousness) | MZ twins reared apart were about as similar as MZ twins reared together |
Sources: Bouchard, T. J., Lykken, D. T., McGue, M., Segal, N. L. and Tellegen, A. (1990). Sources of human psychological differences: the Minnesota Study of Twins Reared Apart. _Science, 250(4978), 223–228._
As well as the high estimate for IQ, the study found that being raised in the same home added little to the similarity of MZ twins on personality, interests and attitudes. Twins who had grown up hundreds of kilometres apart, in different families, were about as alike as twins who had grown up together.
Bouchard and colleagues concluded that genetic differences are associated with a large share of the variation in most psychological traits, and that the shared family environment explains surprisingly little. They suggested that genes may act largely indirectly: genetically influenced characteristics lead children to seek out, provoke and notice different experiences, so each child partly creates their own effective environment. They also stressed that strong heritability does not reduce the value of parenting, education or other interventions.
YouTubeThe estimate depends on MZA twins having uncorrelated environments. Critics have pointed out that many pairs were not separated at birth, that some were raised by relatives or in similar communities, and that many had met before testing, some several times. Adoption agencies also placed children in similar kinds of homes (selective placement). Each of these makes the twins’ environments more alike, so some of their similarity may be environmental, and heritability may be overestimated.
Twins were self-selected: many came forward after media reports, or because they had already found each other and noticed their similarities. Pairs who were strikingly alike may have been more likely to take part, a form of sampling bias. Famous cases, such as the “Jim twins”, who were reunited at 39 and found they had both married and divorced a woman named Linda, attracted attention but are not typical; Bouchard himself noted that most twins show more differences than this.
MISTRA received partial funding from the Pioneer Fund, a foundation that has supported research used to argue for innate group differences. This does not by itself make the findings wrong, but it raises questions about socially sensitive research: results on the heritability of intelligence can be misused to argue that differences between social or ethnic groups are genetic, a conclusion the study design cannot support because all heritability is measured within groups.
The twins were mainly from Western, industrialised countries and were raised in families that adoption agencies had approved, so the range of environments was narrower than in the world population. Turkheimer et al. (2003) found that heritability is much lower when environments include severe poverty, so the 70% figure cannot be generalised to all populations.
Twin and adoption studies estimate how much genes matter without measuring a single gene. Molecular genetics measures people’s DNA and looks for the specific variants associated with a trait. This research has gone through two stages.
In the 1990s and 2000s, researchers chose a gene that seemed biologically likely to matter (a candidate gene), such as the serotonin transporter gene for depression, and compared the frequency of its alleles in people with and without a disorder. The gene-environment interaction study by Caspi et al. (2003) is the best-known example, and is best understood as a test of the diathesis-stress model. Most candidate-gene findings did not replicate: Border et al. (2019) tested 18 of the most studied candidate genes for depression in samples of up to 443,264 people and found no clear evidence for any of them.
The problem was statistical power. Each variant turned out to have a far smaller effect than early studies assumed, so studies with a few hundred participants were too small to detect real effects reliably, and many of their significant results were false positives, a type I error.
A genome-wide association study (GWAS) does not start with a guess. It tests hundreds of thousands of genetic variants across the whole genome at once, in very large samples, and looks for variants that are more common in people with a trait. Because so many tests are carried out, a variant only counts as a finding if its p-value is extremely small (usually p < 0.00000005), which protects against false positives.
Lee et al. (2018) carried out a GWAS of educational attainment (years of schooling) in about 1.1 million people and identified 1,271 independent variants associated with it. Each variant had a tiny effect on its own. Many were in genes involved in brain development and communication between neurons.
GWAS of depression show the same pattern. The CONVERGE consortium (2015) sequenced the DNA of 5,303 Chinese women with recurrent major depression and 5,337 controls and found two variants on chromosome 10 associated with depression, one near a gene called SIRT1. No genetic variant for depression had been reliably replicated before, despite earlier analyses of more than 9,000 cases. The researchers attributed their success to selecting a group of severely and similarly affected patients, which reduced variation in how depression was measured.
Because each variant matters so little, researchers add up their effects. A polygenic score combines the thousands of variants a person carries, each weighted by its effect in a GWAS, into a single number that estimates their genetic tendency towards a trait.
In Lee et al. (2018), polygenic scores explained 11–13% of the variance in educational attainment and 7–10% of the variance in cognitive test performance in independent samples. This is much less than twin studies would predict, a gap known as the “missing heritability”. Possible reasons include rare variants that GWAS do not measure well, effects of genes that work together, and overestimation of heritability by twin studies.
Twin studies treat genes as fixed and the environment as separate from them. Research since the early 2000s shows that the two are more closely linked. Almost every cell contains the same DNA, yet a neuron and a skin cell look and work very differently because they use different genes. Whether a gene is used (expressed) or silenced is controlled by chemical marks attached to the DNA and to the proteins it is wrapped around, and some of these marks respond to experience. The study of these marks is called epigenetics.
The best-studied mark is DNA methylation. A small chemical group (a methyl group) attaches to the DNA at or near a gene and makes it harder for the cell’s machinery to read that gene. The more a gene is methylated, the less of its protein is usually made.
Weaver et al. (2004) showed in rats that pups licked and groomed more by their mothers had less methylation of a stress-hormone receptor gene in the hippocampus and calmer stress responses as adults, and that cross-fostering pups to a different kind of mother reversed the pattern. The finding showed that parental behaviour can change gene expression in the brain.
Heijmans et al. (2008) studied adults whose mothers had been pregnant during the Dutch Hunger Winter of 1944–45, a famine in the German-occupied Netherlands. Six decades later, people who had been exposed to famine around the time of conception had less methylation of a gene involved in growth (IGF2) than their same-sex brothers or sisters who had not been exposed. The comparison with siblings controls for family genes and upbringing, and the study gave the first human evidence that early-life conditions can cause epigenetic changes that last for life.
Epigenetics explains how the environment can change the biology of the body and brain, which supports an interactionist view of behaviour. It also explains why identical twins become more different as they age: their DNA is the same, but their methylation patterns diverge as their experiences differ.
The research also has clear limits. Most human studies measure methylation in blood or saliva, not in the brain, so it is unclear whether the same changes occur in neurons. Many findings are correlational: an experience and a methylation pattern occur together, but the methylation might be a result of illness or medication rather than a cause. Claims in popular media that trauma is passed on epigenetically to grandchildren go well beyond the human evidence, because most epigenetic marks are reset when eggs and sperm are formed.
The nature-nurture debate asked whether behaviour is caused by inheritance or by experience. Modern research shows that the question cannot be answered in that form, for three reasons: genes and environments interact, they are correlated, and heritability itself depends on the environment.
People do not receive their environments at random, a pattern called gene–environment correlation. A child’s genes and environment are often correlated, in three ways.
Passive: parents pass on both genes and a home. Parents who enjoy reading may pass on genes linked to verbal ability and also fill the house with books, so the child’s genes and environment point the same way.
Evocative: a child’s genetically influenced characteristics draw out reactions from others. A cheerful, sociable baby tends to receive more smiles and conversation than a withdrawn one.
Active: as children grow older, they choose environments that suit their dispositions. An adolescent with a tendency towards sensation-seeking may choose friends and activities that involve more risk.
Gene–environment correlation means that some effects that look environmental are partly genetic, and some effects that look genetic work through the environment. This is what Bouchard and colleagues meant when they suggested that genes act largely by shaping the effective environment.
Turkheimer et al. (2003) analysed IQ scores of 7-year-old twins from a large US study in which many families lived near or below the poverty line. In the poorest families, about 60% of the variation in IQ was associated with the shared environment and the genetic contribution was close to zero. In affluent families the result was almost exactly the reverse.
One explanation is that genetic potential can only show itself when the environment allows it: if all children lack books, good schools and adequate nutrition, differences in their genes make little difference to how they develop. A meta-analysis by Tucker-Drob and Bates (2016) found this pattern clearly in US studies but found zero or reversed effects in Western Europe and Australia, where social policies give more equal access to education and health care. The heritability of intelligence therefore depends on a country’s social and economic environment.
The same research designs are used across psychology. The table gives one example from each context and what the research shows.
Context | Example | What the research shows |
|---|---|---|
Health and well-being | Major depressive disorder: a meta-analysis by Sullivan, Neale and Kendler (2000) estimated its heritability at 37% | Genes explain a substantial minority of variation in depression risk; most of the rest comes from the non-shared environment |
Health and well-being | Schizophrenia: Hilker et al. (2018) found a heritability of 79% and an MZ concordance of 33% in Danish twins | High genetic influence, but most genetically identical co-twins stay well |
Human development | Intelligence: about 70% of variation was associated with genes in MISTRA, but Turkheimer et al. (2003) found near zero in poor US families | How strongly genes influence development depends on the environment |
Human relationships | Walum et al. (2008): in Swedish men, a variant of a vasopressin-receptor gene (AVPR1A) was associated with weaker partner bonding and more marital problems | A single variant shows a small association; it does not determine relationship behaviour |
Learning and cognition | Educational attainment: in Lee et al. (2018), polygenic scores explained 11–13% of variation | Many variants of tiny effect; most of the variation lies elsewhere |
Across the contexts, the pattern is consistent: genetic inheritance makes a real but partial contribution, many genes are involved, and the size of the genetic effect depends on the environment. Single-gene explanations are an example of biological reductionism.
Heritability is never observed directly: it is calculated from patterns of similarity using assumptions. Twin studies assume equal environments, adoption studies assume random placement, and both assume that MZ and DZ twins, or adoptees, are typical of the population. When these assumptions fail, estimates are biased, usually upwards. Molecular studies measure DNA directly but have so far explained much less variation than twin studies, and it is still debated whether this gap shows the limits of GWAS or an overestimation by twin studies.
Measurement of the trait matters too. A heritability estimate for “depression” depends on how depression is defined and measured: lifetime diagnosis by interview, current symptoms on a questionnaire or hospital records give different results. The CONVERGE study succeeded partly because it reduced this variation by recruiting only severe, recurrent cases.
A heritability estimate or a GWAS result shows an association between genetic variation and a trait. It does not show how the genes act, and it does not mean that the trait is fixed. Genes influence behaviour through long chains of biological and environmental events, and gene–environment correlation means that part of a “genetic” effect can travel through the environment a person chooses or evokes. Treating genetic influence as a fixed cause of behaviour is a form of determinism.
Most twin registers are in Scandinavia, the Netherlands, Australia, the United Kingdom and the United States, and most GWAS participants have European ancestry. Findings from these populations may not transfer to others, because both allele frequencies and environments differ. Polygenic scores built from European-ancestry samples predict much less well in people of African or Asian ancestry. Studies such as CONVERGE in China and the Colombo Twin and Singleton Study in Sri Lanka are attempts to correct this imbalance. The candidate-gene era also shows publication bias: small studies with significant results were published, and the many null results were not.
Claims about inherited differences were used in the early 20th century to justify eugenics programmes, including the forced sterilisation of people judged “unfit” in the United States, Scandinavia and, on the largest scale, Nazi Germany. Research on the heritability of intelligence and mental disorders is therefore socially sensitive: findings can be misread as showing that groups differ for genetic reasons, or used to stigmatise families with a history of mental illness.
Genetic research also raises questions about consent and the ownership of DNA. Members of the Havasupai Tribe in Arizona gave blood samples to Arizona State University for research on diabetes; the samples were later used without their consent for studies of schizophrenia, inbreeding and the tribe’s migration history, which contradicted the tribe’s own account of its origins. In 2010 the university agreed to pay US$700,000 in compensation and to return the samples. The case shows why Indigenous communities often ask for control over how their genetic data are used.
Genetic research gives a biological level of explanation. It cannot, on its own, explain why a person with a given genotype develops depression or does well at school; cognitive and sociocultural factors are always involved. Its most useful contribution is to show how much variation is linked to genes in a given population, and therefore how much remains to be explained by experience and culture.
Concept | How it applies to research on genetic inheritance |
|---|---|
Measurement | Heritability is inferred from similarity using assumptions (equal environments, random placement) that may not hold |
Causality | Associations between genes and traits do not show mechanisms; gene–environment correlation blurs cause and effect |
Bias | Mostly European-ancestry samples; publication bias in candidate-gene studies; volunteer twins |
Responsibility | History of eugenics, stigma, consent and data ownership (Havasupai case) |
Perspective | Genes are one level of explanation; biological reductionism ignores interaction with experience |
Change | A heritable trait can still change; heritability itself changes with the environment |
Paper 1 Section C does not ask about approach terms such as genetic inheritance directly, but genetic research is often the best evidence in an essay on biological explanations of a mental health disorder. Short evaluation questions on a single study practise the reasoning such essays need.
Genetic inheritance is the passing of traits from parents to children through genes; psychological traits are polygenic, influenced by thousands of variants of tiny effect.
Heritability estimates the share of variation in a trait within a population that is associated with genetic differences; it does not apply to individuals and changes with the environment.
Family studies show whether a trait runs in families but cannot separate genes from a shared environment.
Twin studies compare MZ and DZ twins; for schizophrenia, concordance is 33% in MZ and 7% in DZ twins, and heritability about 79%.
The equal environments assumption, selective placement and restricted range can bias twin and adoption estimates, usually upwards.
Bouchard et al. (1990) found that about 70% of IQ variance was associated with genes in twins reared apart, but the sample, contact between twins and funding are criticised.
GWAS and polygenic scores find many variants of tiny effect and explain less variation than twin studies (“missing heritability”).
Epigenetic marks such as DNA methylation let experience change gene expression without changing the DNA sequence.
Genes and environment correlate and interact; Turkheimer et al. (2003) found that the heritability of IQ was near zero in very poor US families.
Research on inheritance raises issues of measurement, determinism, European-ancestry bias, stigma and consent.
I can describe what genes are and how genetic inheritance works.
I can explain what heritability measures and give three of its limits.
I can explain the logic of family, twin and adoption studies, including concordance rates.
I can explain the equal environments assumption and how its failure would bias a heritability estimate.
I can describe the aim, method, results and evaluation of the Minnesota Study of Twins Reared Apart.
I can describe how GWAS and polygenic scores work and why they explain less variation than twin studies.
I can explain how DNA methylation allows experience to change gene expression.
I can evaluate genetic research with reference to measurement, causality, bias and responsibility.
I can apply genetic inheritance to a scenario in one of the contexts.