This is a summary of the 10 findings in the paper Top 10 Replicated Findings from Behavioral Genetics (Plomin et al 2016). I posted this as a comment a while back, but now I’m making it a full post so I can find it again more easily.
The authors show that all of these have large effect sizes and are well replicated, except where noted below. I notice that the authors cite themselves a lot as support for many of these claims. I am not an expert in any of this, so if they’re trying to pass off controversial ideas as widely accepted, I wouldn’t be able to see through it.
1. Significant genetic influence is ubiquitous in cognitive and psychological traits. Intelligence has about 50% heritability. Twin studies show intelligence correlation about 0.85 in identical twins vs 0.6 in fraternal twins.
2. Although basically all psychological traits have some heritability (typically 30-50%) none of them have close to 100% heritability. Contrast this with physical traits like height, which has about 90% heritability.
3. Heritability of complex traits is caused by many genes of small effect that add up. Example: tendency for open-field activity in mice shows a linear response to selection pressure over 30 generations, rather than a clear separation that would occur if it were controlled by just a few genes. “Genome-wide association studies” look at hundreds of thousands or millions of nucleotides covering most of the genome to detect population associations between a single-nucleotide polymorphism and a trait. It generally finds that even the most significant genetic changes by themselves have tiny effects (far less than 1% of variation).
4. Correlations between traits are usually caused largely by genetics. For example, the strong correlation between types of intelligence (R=0.76 between reading and math) is due more to genetics than environment (the reading/math correlation is about 64% genetic). Anxiety and depression are correlated entirely for genetic reasons (they are affected by all the same genes). The schizophrenia/bipolar connection is largely genetic too, as is neuroticism/depression. Another finding (not yet replicated) is that the correlation of 0.3 between exercise behavior and attitudes toward exercise is 70% genetic; I interpret this to mean that most of the genetic influence on exercise behavior is caused by the influence of those same genes on attitudes toward exercise.
5. Counterintuitively, heritability of intelligence increases linearly throughout development (from 41% at age 9 to 66% at age 17 in one twin study, and maybe as high as 80% in adulthood).
6. Stability of traits from age to age is largely due to genetics; changes that occur with age are largely environmental. So then how does the heritability of intelligence increase over time? The authors suggest “genetic amplification”: genetic nudges early in development get magnified as time goes by, perhaps due to genotype-environment correlation (kids choose or create environments that match their propensities). Some evidence supports this idea, but it may vary depending on the culture. The authors do not seem to consider genetic amplification one of the “replicated findings” noted in the title.
7. Most measures of the ‘environment’ show significant genetic influence. This is a generalization of the genotype-environment correlation mentioned above for intelligence. Parenting, social support, and some life events seem to be causally affected by a child’s genetics (not just correlated); this can be shown in twin studies. Same goes for school and work environments. Heritability averages 0.27. This again varies with culture; parenting is more affected by the child’s genetics in Japan than in Sweden. A child’s genetics have even been shown to have some effect on the family’s socioeconomic status.
8. Most associations between environmental measures and psychological traits are significantly mediated by genetics. Since genetic factors affect environmental measures as well as behavioral measures, we should not assume that correlations between parenting and children’s behavior are caused entirely by the environmental effect of parenting on children’s behavior. For instance, correlation between a child’s developmental index and measures of their home environment is stronger for genetically related families (0.44) than adopted families (0.29). So, much of what appears to be the effect of parenting on behavior is actually effect of the parents’ and child’s shared genetics on both the behavior and the environment. Disentangling genetic and environmental influences is important because it allows us to tailor interventions more effectively.
9. Most environmental effects are not shared by children growing up in the same family: salient experiences are specific to each child. Similarity among siblings is mainly due to shared genetics. Non-shared environment has a bigger effect on phenotypic variance than shared environment does. Shared environment between siblings (including going to the same schools) accounts for 10-15% of variance in academic achievement. Shared environment’s effect on intelligence decreases after adolescence. Specific non-shared environmental effects are hard to identify, and are likely due to additive effects of many seemingly inconsequential experiences.
10. Abnormal is normal: quantitative genetic methods suggest that common psychological disorders are the extremes of the same genetic factors responsible for heritability throughout the distribution. Reading disabilities, for instance, have been shown to have strong “group heritability,” indicating a genetic link between the disorder and normal variation in quantitative measures of reading ability. This is supported by the finding that many genes of small effect determine heritability of traits (finding 3); polygenic scores that sum these effects are normally distributed. An interesting exception involves severe intellectual disability (IQ < 70), which this type of analysis suggests is etiologically distinct from the normal distribution of intelligence (no significant group heritability).
The authors suggest that the above findings have replicated for reasons that are specific to the field of behavioral genetics, namely:
The controversy of the nature/nurture debate has motivated bigger and better studies;
Behavioral genetics has historically used better statistical methods than much of psychology, partly because studies often have to be observational rather than experimental;
Focusing on the net effects of genetics and environment is more reliable than studying specific genes (polygenic scores work better);
There are better incentives and opportunities (data) for replications;
Because genetic effect sizes are larger than other factors studied in psychology (e.g. sex differences generally account for less than 1% of variance on psychological traits).
Many of these advantages cannot easily transfer to other fields.
Link Summary: Top 10 Replicated Findings from Behavioral Genetics
This is a summary of the 10 findings in the paper Top 10 Replicated Findings from Behavioral Genetics (Plomin et al 2016). I posted this as a comment a while back, but now I’m making it a full post so I can find it again more easily.
The authors show that all of these have large effect sizes and are well replicated, except where noted below. I notice that the authors cite themselves a lot as support for many of these claims. I am not an expert in any of this, so if they’re trying to pass off controversial ideas as widely accepted, I wouldn’t be able to see through it.
1. Significant genetic influence is ubiquitous in cognitive and psychological traits. Intelligence has about 50% heritability. Twin studies show intelligence correlation about 0.85 in identical twins vs 0.6 in fraternal twins.
2. Although basically all psychological traits have some heritability (typically 30-50%) none of them have close to 100% heritability. Contrast this with physical traits like height, which has about 90% heritability.
3. Heritability of complex traits is caused by many genes of small effect that add up. Example: tendency for open-field activity in mice shows a linear response to selection pressure over 30 generations, rather than a clear separation that would occur if it were controlled by just a few genes. “Genome-wide association studies” look at hundreds of thousands or millions of nucleotides covering most of the genome to detect population associations between a single-nucleotide polymorphism and a trait. It generally finds that even the most significant genetic changes by themselves have tiny effects (far less than 1% of variation).
4. Correlations between traits are usually caused largely by genetics. For example, the strong correlation between types of intelligence (R=0.76 between reading and math) is due more to genetics than environment (the reading/math correlation is about 64% genetic). Anxiety and depression are correlated entirely for genetic reasons (they are affected by all the same genes). The schizophrenia/bipolar connection is largely genetic too, as is neuroticism/depression. Another finding (not yet replicated) is that the correlation of 0.3 between exercise behavior and attitudes toward exercise is 70% genetic; I interpret this to mean that most of the genetic influence on exercise behavior is caused by the influence of those same genes on attitudes toward exercise.
5. Counterintuitively, heritability of intelligence increases linearly throughout development (from 41% at age 9 to 66% at age 17 in one twin study, and maybe as high as 80% in adulthood).
6. Stability of traits from age to age is largely due to genetics; changes that occur with age are largely environmental. So then how does the heritability of intelligence increase over time? The authors suggest “genetic amplification”: genetic nudges early in development get magnified as time goes by, perhaps due to genotype-environment correlation (kids choose or create environments that match their propensities). Some evidence supports this idea, but it may vary depending on the culture. The authors do not seem to consider genetic amplification one of the “replicated findings” noted in the title.
7. Most measures of the ‘environment’ show significant genetic influence. This is a generalization of the genotype-environment correlation mentioned above for intelligence. Parenting, social support, and some life events seem to be causally affected by a child’s genetics (not just correlated); this can be shown in twin studies. Same goes for school and work environments. Heritability averages 0.27. This again varies with culture; parenting is more affected by the child’s genetics in Japan than in Sweden. A child’s genetics have even been shown to have some effect on the family’s socioeconomic status.
8. Most associations between environmental measures and psychological traits are significantly mediated by genetics. Since genetic factors affect environmental measures as well as behavioral measures, we should not assume that correlations between parenting and children’s behavior are caused entirely by the environmental effect of parenting on children’s behavior. For instance, correlation between a child’s developmental index and measures of their home environment is stronger for genetically related families (0.44) than adopted families (0.29). So, much of what appears to be the effect of parenting on behavior is actually effect of the parents’ and child’s shared genetics on both the behavior and the environment. Disentangling genetic and environmental influences is important because it allows us to tailor interventions more effectively.
9. Most environmental effects are not shared by children growing up in the same family: salient experiences are specific to each child. Similarity among siblings is mainly due to shared genetics. Non-shared environment has a bigger effect on phenotypic variance than shared environment does. Shared environment between siblings (including going to the same schools) accounts for 10-15% of variance in academic achievement. Shared environment’s effect on intelligence decreases after adolescence. Specific non-shared environmental effects are hard to identify, and are likely due to additive effects of many seemingly inconsequential experiences.
10. Abnormal is normal: quantitative genetic methods suggest that common psychological disorders are the extremes of the same genetic factors responsible for heritability throughout the distribution. Reading disabilities, for instance, have been shown to have strong “group heritability,” indicating a genetic link between the disorder and normal variation in quantitative measures of reading ability. This is supported by the finding that many genes of small effect determine heritability of traits (finding 3); polygenic scores that sum these effects are normally distributed. An interesting exception involves severe intellectual disability (IQ < 70), which this type of analysis suggests is etiologically distinct from the normal distribution of intelligence (no significant group heritability).
The authors suggest that the above findings have replicated for reasons that are specific to the field of behavioral genetics, namely:
The controversy of the nature/nurture debate has motivated bigger and better studies;
Behavioral genetics has historically used better statistical methods than much of psychology, partly because studies often have to be observational rather than experimental;
Focusing on the net effects of genetics and environment is more reliable than studying specific genes (polygenic scores work better);
There are better incentives and opportunities (data) for replications;
Because genetic effect sizes are larger than other factors studied in psychology (e.g. sex differences generally account for less than 1% of variance on psychological traits).
Many of these advantages cannot easily transfer to other fields.