Top Ten Replicated Findings from Behavioural Genetics
Plomin et al (2016) wrote a ground-breaking article about Behavioural Genetics – but it is a little difficult to read. This summary will help you identify recent findings relevant to an essay the topic of Genetics and Behaviour from the biological approach to understanding behaviour.
All of the findings briefly described have been successfully replicated many times, and some are now accepted as “laws” of behavioural genetics. Of course, as a famous behavioural geneticist, Plomin is bound to take this vie, but he is backed up by a lot of science, as you will see below.
Finding 1. All psychological traits show significant and substantial genetic influence
Studies have shown that not just IQ, schizophrenia and depression, but also autism, substance abuse, drug dependence, personality and many others have a significant genetic component. (References in original article linked above). Genome-wide complex trait analysis (GCTA) uses hundreds of thousands of DNA differences across the genome to estimate chance genetic similarity for each pair of individuals in a large sample of unrelated individuals and to relate this chance genetic similarity to phenotypic similarity.
Finding 2. No traits are 100% inheritable.
While some traits, such as individual differences in height, yield a heritability of about 90%, there is nothing which is 100% inheritable. There is always an environmental influence.
Finding 3. Heritability is caused by many genes of small effect.
Genome-wide association (GWA) has been used widely in attempts to identify specific DNA associations with traits and disorders. An association is a correlation between a trait or disorder and the frequency of one of the two alleles (forms) of a single nucleotide polymorphism (SNP). For example, the frequency of a particular allele of the gene that encodes apolipoprotein E is about 40% for individuals with Alzheimer’s disease and 15% for control individuals who do not have the disorder. (See Caspi et al, 2003, for research into a polymorphism on the HRRT serotonin transporter gene and depression).
So, it is a combination of many genes of small effect that result in the heritability of a trait.
Finding 4. Phenotypic correlations between psychological traits show significant and substantial genetic mediation
There is significant genetic overlap between anxiety and depression, and even between schizophrenia and bipolar disorder. Genetically, anxiety and depression are the same disorder. There is evidence for shared genetic risk between many disorders, and the genetic structure of mental disorders does not map neatly onto the DSM.
Finding 5. The heritability of intelligence increases throughout development
This is surprising, as if anything we would expect the environmental influences on intelligence to increase as we grew older. This could be due to new genetic influences, called innovation, as the brain structure changes throughout development.
Finding 6. Age-to-age stability is mainly due to genetics.
Phenotype stability from age to age is mainly due to genetics for personality, psychopathology and intelligence, for which most data is available.
This raises the question about the heritability of intelligence increasing throughout one’s life. It seems that genetic amplification might be responsible (rather than the innovation suggested above): genetic nudges early in development are amplified as children select, modify and create environments correlated with their genetic predispositions.
Finding 7: Most measures of the ‘environment’ show significant genetic influence.
Parenting, social support and life events show genetic influence, as humans select, modify and create environments correlated with their genetic predispositions regarding personality and psychopathology. How does this work? Well, parenting, for example, shows genetic influence that is driven by both child and parent inherited characteristics.
Finding 8. Most associations between environmental measures and psychological traits are significantly mediated genetically.
For example, there is a genetic influence on family socio-economic status (SES) and its association with children’s intelligence and educational performance. This is less surprising that it at first appears, as family SES correlates with parental intelligence. (This is a little worrying, as the risk is now that poverty will be seen as due to individual inheritance and therefore not needing social intervention.)
Finding 9. Most environmental effects are not shared by children growing up in the same family.
It is mainly genetics that accounts for similarity among siblings. It is not that the environment is unimportant, but that the relevant experiences are specific to each child in the family.
Finding 10. Abnormal is normal.
Common mental disorders are not qualitatively different from the normal range of behaviour; they are just extremes of the normal range. Genetic liability for disorders is distributed normally, and it is at the extremes of the same genetic influences that the common disorders occur. This has the possibility of opening up positive genetics for those in the positive area of the genetic liability (at very small risk) – looking at how these children and adults flourish and have resilience.
What are your thoughts? Are these findings too reductionist, deterministic and simplistic?
Could they be used to justify inequality of opportunities? This post was inspired by Dr Laura Swash