Thinking positively: The genetics of high intelligence

This study tries to answer the question, "is the same true for high intelligence?" The two general theories are the Continuity Hypothesis and Discontinuity Hypothesis. As its name suggests, the Continuity Hypothesis predicts that the high end of the intelligence distribution is continuous; extremely intelligence individuals don't violate the intelligence distribution the way mentally challenged people do. The Discontinuity Hypothesis predicts the opposite.

By analyzing the genes of twins and other close family members, the researchers found strong evidence of the Continuity Hypothesis.

To actually try to explain the design here:

we think intelligence is caused by thousands of common genes, each of which slightly helps or hurts. When you have thousands of independent genes, then they add up to a normal distribution like the one we see when we measure a lot of people's intelligence. The exception is that there are too many retarded people; if the normal distribution was the whole story, then retarded people would be as rare as geniuses, but they are much more common than that. We explain there being too many retarded people by saying that they have one or a few very rare mutations, mutations which are very harmful. But another theory might be that the retarded have very few normal intelligence genes, or that intelligence genes don't simply add up but interact in complex ways, or that they have very harmful environments. How do we decide which theory is right? Well, we look at the retarded people vs their siblings; if their parents were lacking a lot of good genes, or they were being raised in a toxic waste dump, then we would expect the siblings to also be near-retarded themselves since they also inherited few good genes or are affected by the toxic waste. But they're not; they are almost average! This is more consistent with there being one bad mutation and the retarded sibling had bad luck than the other theories. This theory has since been confirmed by finding hundreds of unique and harmful mutations in retarded people. So we conclude that the effect of intelligence genes is indeed a normal distribution, with an occasional bad mutation overriding that and making someone retarded.

This immediately raises a question. If we admit that on the low end intelligence may be controlled by a single rare mutation, why not on the high end too? Maybe there are special genius genes floating around. This would be important because it means that you can't make much progress by just looking at the genes of regular people, and it also means that SNP studies will be extremely limited in what they can find. How can we check this? We can do the same thing as on the low end: if there is a special genius gene, then geniuses will have much higher IQ than their siblings do, who will be close to average; but if their parents have lots of good genes and there is no single special gene, then the siblings will also be well above average and similar to their genius sibling.

Using a very large set of siblings and twins, OP finds that very intelligent twins/teens are similar to their siblings. So this is the opposite of the retardation findings. There are rare genes for retardation, but there are not rare genes for genius.

Not necessarily. This is something you might expect if intelligence is a net fitness advantage and it is in a mutation load situation where rare variants need to be purged to keep things constant. But if intelligence is only worthwhile up to a certain point and it is controlled by frequency-dependent selection, or there is heterozygote advantage, or if intelligence is not necessarily reproductively fit at all, or other situations, then there could certainly be rare variants of large positive effect. (I would not have bet on their existence for many reasons, but not because it's impossible.)

To give an example, your claim would predict that there is no such thing as a single mutation which increases muscle mass a lot because it's a complex system affected by a lot of genes; yet nevertheless, there is a single mutation affecting myostatin which makes humans and pigs and dogs much more muscular, and it's even been edited into pigs with CRISPR this year and last year into sheep and cows. Presumably the reason that not all animals are ultra-strong thanks to the mutation is that it causes birthing difficulties and increases metabolic demands considerably, and so despite the obvious advantages of being ultra-strong, it's not actually fit.

To use your myostatin mutation example, the increase in muscle mass does not lead to significantly faster animals as the supporting structures are not there to utilise this increased muscle. Human intelligence is an emergent trait like speed determined by the co-ordination of many sub-systems.

These sort of emergent traits are almost never positively controlled by single large positive alleles. The one major exception are systems that are under different selection in males and females (e.g. height, plume color in birds, etc). In these examples two different systems have emerged controlled by the sex of the individual, but you don’t tend to find single genes that contribute massively in a positive way towards variation within each sex.

As an aside I remember reading a paper from long ago that suggested that high intelligence was the result of the relatively absence of mutant alleles at the various intelligence loci. When you look at the effect of null mutations at these loci the effect on intelligence is very low (less than a point for most). We all carry a large number of mutant alleles so the suggestion is that those with a high intelligence just happen by chance to have a lower frequency of negative mutant alleles. The interesting thing about this hypothesis is it would suggest that high intelligence is the default and low to normal intelligence is the result of mutational load. This is defiantly something that we can explore in the future as we get whole genome data from large numbers of people.

Some years ago, I read something that suggested otherwise. IIRC, it suggested that we had some idea of what alleles positively influenced intelligence based on the fact that Ashkenazi Jews were something like 2% of the population but had won something like 10% of Nobel Prizes and about 60% of the population had one or more alleles for serious genetic disorders known to impact neurology.

I remember this in part because, although I am not Jewish, I have one of the genetic disorders they tend to carry.

As far as I am aware there in no genetic disorder that only Ashkenazi’s suffer from that is not also present in the rest of the human population, the only difference is frequency.