"For genetics, a key question is whether the genetic causes of high intelligence are qualitatively or quantitatively different from the normal distribution of intelligence. We report results from a sibling and twin study of high intelligence and its links with the normal distribution. We identified 360,000 sibling pairs and 9000 twin pairs from 3 million 18-year-old males with cognitive assessments administered as part of conscription to military service in Sweden between 1968 and 2010. We found that high intelligence is familial, heritable, and caused by the same genetic and environmental factors responsible for the normal distribution of intelligence."
In conjunction with the earlier twin study, Rietveld 2013 & upcoming SSGAC hits, the silence of BGI, and "A genome-wide analysis of putative functional and exonic variation associated with extremely high intelligence" http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015108a.html , Spain et al, which finds no GWAS hits for high intelligence in their enriched sample but some evidence that avoiding bad alleles helps, it seems we can rule out the hypothesis that high intelligence is due in any important sense to interacting genes or complicated networks of effects (as some people, including some of my Google+ readers have argued in the past, based on rather poor grounds). It's additive genes of small effect the entire way.
This has several important implications:
- gene-hunters don't need to strain for enriched samples of high-IQ people; GWASes on normal people will work fine. If high-IQ people can be obtained cheaply, great, but if not, well, you're not missing anything important like large effect variants present only in the high-IQ
- Cochran's mutation load theory is not holding up well for intelligence, so engineering won't be as simple as 'creating the modal genome'
- but genetic engineering for high intelligence really is going to be as simple as selecting for or editing in as many additive variants as possible; additive increases will not simply 'break down' at IQ130 or some threshold like that.
- further, such engineering will yield healthy sane people: because all of these variants are present in the population, some at fairly high frequencies, we can be sure on evolutionary and GWAS grounds that they cannot be very harmful because they would have been selected against or detected in GWASes for diseases.
In conjunction with the earlier twin study, Rietveld 2013 & upcoming SSGAC hits, the silence of BGI, and "A genome-wide analysis of putative functional and exonic variation associated with extremely high intelligence" http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015108a.html , Spain et al, which finds no GWAS hits for high intelligence in their enriched sample but some evidence that avoiding bad alleles helps, it seems we can rule out the hypothesis that high intelligence is due in any important sense to interacting genes or complicated networks of effects (as some people, including some of my Google+ readers have argued in the past, based on rather poor grounds). It's additive genes of small effect the entire way.
This has several important implications:
- gene-hunters don't need to strain for enriched samples of high-IQ people; GWASes on normal people will work fine. If high-IQ people can be obtained cheaply, great, but if not, well, you're not missing anything important like large effect variants present only in the high-IQ
- Cochran's mutation load theory is not holding up well for intelligence, so engineering won't be as simple as 'creating the modal genome'
- but genetic engineering for high intelligence really is going to be as simple as selecting for or editing in as many additive variants as possible; additive increases will not simply 'break down' at IQ130 or some threshold like that.
- further, such engineering will yield healthy sane people: because all of these variants are present in the population, some at fairly high frequencies, we can be sure on evolutionary and GWAS grounds that they cannot be very harmful because they would have been selected against or detected in GWASes for diseases.
I get why this article supports the idea that high intelligence isn't due to a complex network of genes, but by itself, that doesn't show the effect is additive. Namely, there can be some complex negative interactions.
To put it another way, vow do you know variants which usually aren't present together won't interact negatively with one another?Oct 9, 2015
All of these variants are present at fairly high frequencies, so there's not much of a 'usually aren't present together'.Oct 10, 2015
How is this evidence against the modal hypothesis?49w
