The remarkable “powers” of evolution are now shown to degrade (aka “mutate”) the human genes essential to intelligence.
Remarkably, they found that some of the same genes that influence human intelligence in healthy people were also the same genes that cause impaired cognitive ability and epilepsy when mutated, networks which they called M1 and M3.
On discovering those who are not so impaired:
up to 65 per cent of the difference in pupil’s GCSE grades was down to genetics, after analysing genetic data fro, 12,500 twins. . . .In contrast shared environmental factors such as home and school environment contributed between 14 and 21 per cent. The rest was made up by individual external influences such as diseases or friends.
Instead of the politically correct “I’m OK You’re OK”,
Professor Robert Plomin believes that children should be genetically screened at the age of four so that an individualised curriculum could be tailored to their needs.
Science is indeed now quantifying the “descent of man” – with mutations degrading intelligent humans downward.
See: Intelligence genes discovered by scientists
“Imperial College London has found that two networks of genes determine whether people are intelligent or not so bright.”
Alix Warburton, Fabio Miyajima, Kanvel Shazadi, Joanne Crossley, Michael R. Johnson, Anthony G. Marson, Gus A. Baker, John P. Quinn, Graeme J. Sills, NRSF and BDNF polymorphisms as biomarkers of cognitive dysfunction in adults with newly diagnosed epilepsy, Epilepsy & Behavior, Volume 54, January 2016, Pages 117–127
Cognitive dysfunction is a common comorbidity in people with epilepsy, but its causes remain unclear. It may be related to the etiology of the disorder, the consequences of seizures, or the effects of antiepileptic drug treatment. Genetics may also play a contributory role. We investigated the influence of variants in the genes encoding neuron-restrictive silencer factor (NRSF) and brain-derived neurotrophic factor (BDNF), proteins previously associated with cognition and epilepsy, on cognitive function in people with newly diagnosed epilepsy. A total of 82 patients who had previously undergone detailed neuropsychological assessment were genotyped for single nucleotide polymorphisms (SNPs) across the NRSF and BDNF genes. Putatively functional SNPs were included in a genetic association analysis with specific cognitive domains, including memory, psychomotor speed, and information processing. Cross-sectional and longitudinal designs were used to explore genetic influences on baseline cognition at diagnosis and change from baseline over the first year since diagnosis, respectively. We found a statistically significant association between genotypic variation and memory function at both baseline (NRSF: rs1105434, rs2227902 and BDNF: rs1491850, rs2030324, rs11030094) and in our longitudinal analysis (NRSF: rs2227902 and BDNF: rs12273363). Psychomotor speed was also associated with genotype (NRSF rs3796529) in the longitudinal assessment. In line with our previous work on general cognitive function in the healthy aging population, we observed an additive interaction between risk alleles for the NRSF rs2227902 (G) and BDNF rs6265 (A) polymorphisms which was again consistent with a significantly greater decline in delayed recall over the first year since diagnosis. These findings support a role for the NRSF–BDNF pathway in the modulation of cognitive function in patients with newly diagnosed epilepsy.
I wonder when scientists will have the courage to publicly recognize that mutations are probably >>99.99999999% harmful?