A few days ago, geneticist Shai Carmi posted a new study on Twitter. And then he deleted his tweet and reposted a “I disavow” version. Well, what happened is that I quote tweeted it with the text “Rushton calling from the grave“. I managed to save the original tweet before it was completely deleted:
And the repost:
In fact, there weren’t a lot of racist replies to his tweet, but you can see why he realized his PR mistake. Here’s the study:
- Gui, A., Hollowell, A., Wigdor, E. M., Morgan, M. J., Hannigan, L. J., Corfield, E. C., … & Ronald, A. (2024). Genome-wide association meta-analysis of age at onset of walking. medRxiv, 2024-05.
Onset of walking is a developmental milestone with wide individual differences and high heritability in humans. In this genome-wide association study meta-analysis of age at onset of walking (N=70,560 European-ancestry infants), SNP-based heritability was 24.13% (SE=1.16%) with ∼11.9K variants accounting for about 90% of it, suggesting high polygenicity. We identified 11 independent genome-wide significant loci, including a “double hit” haplotype in which both decreased expression of RBL2 and a potentially deleterious missense variant in RBL2 are associated with delayed walking. Age at onset of walking (in months) was negatively genetically correlated with ADHD and BMI, and positively genetically correlated with intelligence, educational attainment, and adult brain gyrification. The polygenic score showed out-of-sample prediction of 3-5.6%, confirmed to be largely due to direct effects in sib-pair analyses, and was associated with volume of neonatal brain structures involved in motor control. This offers new biological insights of clinical relevance into neurodevelopment.
So what they did is that they trained a model (GWAS) to predict age at first walking based on people’s genetic data. The resulting genetic model shows genetic correlations with other traits of interest:
Age at onset of walking was negatively genetically correlated with childhood BMI48 (rg =-0.14, SE = 0.04, 95%CI [-0.22, -0.07]), adult BMI49 (rg = -0.10, SE = 0.02, 95%CI [-0.14, -0.06]) and ADHD50 (rg = -0.18, SE = 0.03, 95%CI [-0.24, -0.12]) and positively genetically correlated with educational attainment51 (rg = 0.12, SE = 0.02, 95%CI [0.08, 0.16]), IQ52 (rg = 0.09, SE = 0.03, 95%CI [0.04, 0.14]), and bipolar disorder53 (rg = 0.07, SE = 0.02, 95%CI [0.03, 0.12]).
In other words, children who learn to walk later are (eventually) less fat, less ADHD, higher in educational attainment, higher in intelligence, and apparently bipolar. The correlations are quite weak, this is not a strong genetic relationship. Nevertheless, this pattern of results mostly makes sense from a life history perspective where evolution can tune organisms to either develop well or develop fast. Those that take more time to develop reach a higher level of eventual performance. Phil Rushton famously compared many such phenotypes in his 3-way split of human races. His summary table (from Race, Evolution and Behavior):
One can point out many problems with this aggregation, e.g. most data are from within USA, not the races in their natural habitats or living under their own culture. Nevertheless, the thinking makes sense from a biological perspective. The association between developmental speed and intelligence holds between species in general (again, not always): longer lived, slower developing species are smarter (bigger brains, more complex behavior). Most life is very small and fast-paced and very low in intelligence. Bigger, slowly developing animals are much smarter than bacteria, insects, and so on. The association holds between primates species too, so it’s not just a primate thing. It holds in some ways between human subspecies (races), and now this new study has found that it holds in some aspect even within individuals of European ancestry.
The way forward from here would be to examine if the polygenic scores based on this model — trained exclusively on Europeans — can predict the variation we see between human races. In other words, can it get the population averages right? Will they correlate with the intelligence averages? If confirmed, this would provide the first direct evidence that these differences have a genetic origin between populations. It may or may not be possible with this particular model because it was trained on a relatively small sample of 70k people (the current model for educational attainment was trained on 3 million people). Because of this limited sample size, they only found 11 independent genetic variants (that is, not in the same location on the genome) with some provable association to age of first walking. Nevertheless, the polygenic scores predicted quite well when they were tested:
Between families, the correlation was about 0.20, and within families (between siblings) in the single dataset where this was possible, the correlation (the slope really) was about 0.16.
The authors looked at what kind of tissues the genetic variants they found were active by looking at the nearby genes and their tissue expression. They found it was all about the brain:
Significantly enriched cell type tissues were exclusively brain-based tissues, and moreover, strongest signals included tissues in the basal ganglia, cortex and cerebellum. In line with these findings, the polygenic score for age at onset of walking was associated with neonatal brain volume of the basal ganglia, thalami, medulla, pons and cerebellum. This is consistent with the known role of these brain areas in motor function6,62. Moreover, no non-brain tissue types showed significant enrichment.
This confirms the close link between age of first walking and brain design.
Finally, it should be said that the researchers of course did not mention Rushton. For good measure, they did also not mention life history theory, or r-K selection (an older framework). Or in general provide much speculation about why this might be very interesting from an evolutionary perspective. The word evolution does not appear in the article at all.
Added: William Shockley talks about maturation and intelligence in 1974