Study offers first genetic analysis of people with extremely high intelligence

August 5, 2015
Study offers first genetic analysis of people with extremely high intelligence

The first ever genetic analysis of people with extremely high intelligence has revealed small but important genetic differences between some of the brightest people in the United States and the general population.

Published today in Molecular Psychiatry, the King's College London study selected 1,400 high- individuals from the Duke University Talent Identification Program. Representing the top 0.03 per cent of the 'intelligence distribution', these individuals have an IQ of 170 or more - substantially higher than that of Nobel Prize winners, who have an average IQ of around 145.

Genetic research on intelligence consistently indicates that around half of the differences between people can be explained by genetic factors. This study's unique design, which focused on the positive end of the intelligence distribution and compared genotyping data against more than 3,000 people from the , greatly enhanced the study's power to detect genes responsible for the heritability of intelligence.

Researchers analysed (SNPs), which are DNA differences (polymorphisms) between individuals in the 3 billion nucleotide base pairs of DNA - steps in the spiral staircase of the double helix of DNA that make up the human genome. Each SNP represents a difference in a single nucleotide base pair, and these SNPs account for inherited differences between people, including intelligence. The study focused, for the first time, on rare, functional SNPs – rare because previous research had only considered common SNPs and functional because these are SNPs that are likely to cause differences in the creation of proteins.

The researchers did not find any individual protein-altering SNPs that met strict criteria for differences between the high-intelligence group and the control group. However, for SNPs that showed some difference between the groups, the rare allele was less frequently observed in the high . This observation is consistent with research indicating that rare functional alleles are more often detrimental than beneficial to intelligence.

Professor Robert Plomin from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King's College London, said: 'Rare functional alleles do not account for much on their own but in combination, their impact is significant.

'Our research shows that there are not genes for genius. However, to have super-high intelligence you need to have many of the positive alleles and importantly few of the negative rare effects, such as the rare functional alleles identified in our study.'

The researchers also analysed genome-wide similarity to explore the genetic architecture of intelligence.

Professor Plomin added: 'Previous research suggests that common SNPs in total account for around 25 per cent of the variance in intelligence. The question we asked, for the first time, was - how much will these functional variants account for? We found that the functional SNPs in our study explain around 17 per cent of the differences between people in intelligence.'

The authors acknowledge that environmental influences also have an impact, often interacting with genetic factors. Professor Plomin said: 'Clearly super-bright people such as those in our study are more likely to select environments conducive to their genetic propensity, so they might have grown up reading books that present intellectual problems or be more likely to attend a university.'

Professor Michael Simpson from the Division of Genetic and Molecular Medicine at King's College London, said: 'Our study demonstrates the challenges in identifying specific genetic variants that contribute to this complex trait, but provides potential insight into its genetic architecture that will inform future studies.'

Explore further: Same genes may influence GCSE results across range of subjects

More information: "A genome-wide analysis of putative functional and exonic variation associated with extremely high intelligence." Molecular Psychiatry advance online publication 4 August 2015; DOI: 10.1038/mp.2015.108

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JVK
1 / 5 (2) Aug 05, 2015
'Rare functional alleles do not account for much on their own but in combination, their impact is significant.


Doesn't that make the nutrient-dependent link from SNPs and RNA-mediated gene duplication to fixation of amino acid substitutions in the organized genomes of all individuals of all genera the most significant factor to consider in the context of how ecological variation leads to ecological adaptations that are perturbed by viruses and the accumulation of viral microRNAs that alter biophysically constrained protein folding chemistry?

Isn't that the concern Eugene Koonin expressed in his interview with Suzan Mazur?
http://www.huffin...216.html

Excerpt: "...the new understanding of evolution needs to integrate what we now know about viruses and virus-host interactions which, from my own perspective, has been absolutely one of the key factors of all evolution..."
JVK
1 / 5 (2) Aug 05, 2015
Journal article excerpt: "...the evidence for the contribution of protein-altering variants to the heritability of intelligence and the evidence that rare functional alleles are detrimental to intelligence provides a framework for defining the role of individual rare alleles."

What is the origin of the protein-altering variants? Could it be nutrient energy-dependent base pair changes that link RNA-mediated gene duplication and fixation of RNA-mediated amino acid substitutions via the physiology of reproduction to cell type differentiation in all cells of all individuals of all genera?

See for examples: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. http://www.ncbi.n...24693353
anonymous_9001
5 / 5 (1) Aug 05, 2015
Eugene Koonin:

"I certainly have never even thought about "rejecting" neo-Darwinism. All I said, in this interview and many previous publications, is that neo-Darwinsim Is a rather narrowly constrained theoretical framework that, for various reasons, leaves out many key evolutionary processes. One of the primary reasons for that is simply that at the time neo-Darwinism took its shape (1950s), the salient theory and especially observations were unavailable."
JVK
1 / 5 (2) Aug 05, 2015
A single nutrient-dependent base pair change and one amino acid substitution link morphological phenotypes in mice to morphological phenotypes in humans.

A single nutrient-dependent base pair change is linked to differences in human intelligence.

A single nutrient-dependent base pair change and one amino acid substitution link life history transitions in the behavior of adolescents and adult humans.

A universal trend of amino acid gain and loss in protein evolution http://www.nature...306.html does not link any base pair change or amino acid substitution to a last universal common ancestor.

In the context of neo-Darwinian theory, unless Koonin or someone else wants to offer his model, there is only one that has any explanatory power in the context of what is currently known to physicists, chemists, and biologists who understand how viruses are linked to mutations, not to evolution. That model is MY model.
anonymous_9001
5 / 5 (2) Aug 05, 2015
viruses are linked to mutations, not to evolution


Viral Mutagenesis as a Means for Generating Novel Proteins:

http://jvi.asm.or...abstract

unless Koonin or someone else wants to offer his model


The Biological Big Bang model for the major transitions in evolution:

http://www.biolog...t/2/1/21

If base pair changes are nutrient-dependent, then why did only one of Lenski's identical populations acquire the cit+ trait? Shouldn't they have all had an identical response since they were clones in identical environments?
JVK
1 / 5 (2) Aug 05, 2015
This situation is hopeless. I must turn to sarcasm in an attempt to communicate with an anonymous fool.

http://www.nature...638.html

Excerpt: "Nucleotides are essential for DNA synthesis and repair, and can be either obtained by de novo synthesis..."

Does anyone know how nucleotides automagically synthesize themselves?
If so, I might be able to link them to the de novo creation of the amino acid groups that are retained or displaced and explain the lower catalytic turnover observed in the context of RNA-mediated DNA repair and genome salvaging.

SARCASM ALERT: Arguably, I am only one step away from finding a cure for all pathologies. If I can find some automagically synthesizing nucleotides, I can place them into the context of Greg Bear's novel "Blood Music" and we can all evolve to our fullest potential when science fiction becomes fact.

But wait, did Greg Bear mention mutations or just viruses?

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