A better question is, how much education in biology and psychology is needed to appreciate these findings?
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.
High intelligence (general cognitive ability) is fundamental to the human capital that drives societies in the information age. Understanding the origins of this intellectual capital is important for government policy, for neuroscience, and for genetics. 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. High intelligence is a good candidate for “positive genetics” — going beyond the negative effects of DNA sequence variation on disease and disorders to consider the positive end of the distribution of genetic effects.
Take height as an example, most people tall or short have 'regular' genetics for their height. A bunch of different factors play together along with the environment to lead to the height they actually have. its basically like a 1000 different genes interacting that each may give you or take a way a fraction of an inch and all together they sum up to your actual height.
However sometimes you have people who are dwarfs, these arent just a combination of many genes, there is a overwhelming specific set of a few genes that totally overwhelm all the other height genes and give you greatly reduced height. Similarly on the other end of the spectrum you have some forms of giantism where a few genes overwhelm all the other height genes and give you greatly increased height.
This study is more or less saying high intelligence follows a model like regular tall height, many different genes interacting to sum up to above average height. Not a model like giantism or dwarfism where a very limited number of genes overwhelm the 'normal' genetics of intelligence.
> (1) we conclude that high intelligence is familial, heritable, (2) and caused by the same genetic factors responsible for the normal distribution of intelligence.
The 1st part is simple to understand, what is confusing everyone is the 2nd part... As the combination of both parts does not make sense (due to the type of "interpretation" presented).
Here is the clearer version -
(1) They found that intelligence was mostly hereditary (inherited via genes passed on by parents).
(2) They further found that the top scorers could also be divided into their own bell-curve. That the high-intelligence group had there own distribution that followed the same pattern (which gives the bell-curve even more validity).
To understand #2 just imagine a smart kid (in high-school) getting accepted into MIT, and once in, that smart kid finding out that he is now just "average" compared to some of the others.
These conclusions are very politically-incorrect, especially for a progressive country like Sweden where you are not supposed to even acknowledge that different dog breeds have different behaviors.
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.
Intelligence is selected for in humans. Therefore any individual gene that significantly boosts intelligence should be expected to have already spread through the population. As a result we should not expect to find any rare genes that make people super-smart. So super-smart people get there with a combination of different genes, each of which contributes very little.
The bottom end of the scale is the opposite story. Evolution says that individual genes that hurt intelligence should be selected against, and are therefore expected to be rare. (Mutation says that they should not be non-existent, but they should be rare.) Therefore there is no surprise in finding rare individual genes that significantly hurt intelligence.
This pattern is not unique to intelligence. It is predicted for any trait that has actively been selected for by evolution over a long period. The top of the range should look continuous. The bottom of the range tends to be dominated by deleterious point mutations.
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.
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.
Do you honestly see no possible connection between these two things?
That's a serious question, not intended as argumentative per se.
I don’t think anyone has shown that being a carrier for any of the common mutations found in the Ashkenazi population increases intelligence in a measurable way, but if anyone knows of such a study I would love to read it.
www.kuro5hin.org/story/2005/7/29/20293/9910
Edit: It contains the stats I was trying to reference above but was misremembering. They are 3% of the population and 27% of U.S. Nobel Prize winners.
The same can be said with drugs -- any chemical that your body could have reasonably produced on its own should be expected to reduce your reproductive fitness. So brain drugs should nearly all have side-effects.
It leads to significantly stronger animals. That's not useless, for either prey or predators.
> Human intelligence is an emergent trait like speed determined by the co-ordination of many sub-systems.
We don't know what human intelligence is on a neurological basis. Imaging studies are linking it to a number of things, but it's still preliminary and so it's premature to baldly assert that there's no possible single mutation which might help.
> 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.
Mutation load hasn't been found to be strongly correlated with intelligence in studies which have looked at it directly, and the GCTAs already upper bound any such effect: "The total burden of rare, non-synonymous exome genetic variants is not associated with childhood or late-life cognitive ability", Marioni et al 2014 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953855/ "A genome-wide analysis of putative functional and exonic variation associated with extremely high intelligence" http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201510... , Spain et al 2015