Adopt a Chimpanzee, Send it to the Best Schools, And Discover How Genes Affect IQ

The story of what made us human is probably not going to focus on changes in our protein building blocks but rather on how evolution assembled these blocks in new ways by changing when and where in the body different genes turn on and off. Experimental and computational studies now under way in thousands of labs around the world promise to elucidate what is going on in the 98.5 percent of our genome that does not code for proteins. It is looking less and less like junk every day. _SciAm

The truth is, anyone with the least scientific judgment accepts that the genes affect IQ (and EF, executive function). Different breeding populations of primates have evolved differently -- from the inside out. "As within, so without", as they say. But then, you already knew that.

So we know that humans and chimps are different -- genetically, morphologically, and behaviourally. What is the "difference that makes the difference" between chimps and humans?

The human brain is well known to differ considerably from the chimpanzee brain in terms of size, organization and complexity, among other traits. Yet the developmental and evolutionary mechanisms underlying the characteristics that set the human brain apart are poorly understood. HAR1 had the potential to illuminate this most mysterious aspect of human biology.

..... until humans came along, HAR1 evolved extremely slowly. In chickens and chimps—whose lineages diverged some 300 million years ago—only two of the 118 bases differ, compared with 18 differences between humans and chimps, whose lineages diverged far more recently. The fact that HAR1 was essentially frozen in time through hundreds of millions of years indicates that it does something very important; that it then underwent abrupt revision in humans suggests that this function was significantly modified in our lineage.

.....HAR1 is active in a type of neuron that plays a key role in the pattern and layout of the developing cerebral cortex, the wrinkled outermost brain layer. When things go wrong in these neurons, the result may be a severe, often deadly, congenital disorder known as lissencephaly (“smooth brain”), in which the cortex lacks its characteristic folds and exhibits a markedly reduced surface area. Malfunctions in these same neurons are also linked to the onset of schizophrenia in adulthood. HAR1 is thus active at the right time and place to be instrumental in the formation of a healthy cortex....

Beyond having a remarkable evolutionary history, HAR1 is special because it does not encode a protein. For decades, molecular biology research focused almost exclusively on genes that specify proteins, the basic building blocks of cells. But thanks to the Human Genome Project, which sequenced our own genome, scientists now know that protein-coding genes make up just 1.5 percent of our DNA. The other 98.5 percent—sometimes referred to as junk DNA—contains regulatory sequences that tell other genes when to turn on and off and genes encoding RNA that does not get translated into a protein, as well as a lot of DNA having purposes scientists are only beginning to understand.

.....It might seem surprising that no one paid attention to these amazing 118 bases of the human genome earlier. But in the absence of technology for readily comparing whole genomes, researchers had no way of knowing that HAR1 was more than just another piece of junk DNA.

Language Clues
Whole-genome comparisons in other species have also provided another crucial insight into why humans and chimps can be so different despite being much alike in their genomes. In recent years the genomes of thousands of species (mostly microbes) have been sequenced. It turns out that where DNA substitutions occur in the genome—rather than how many changes arise overall—can matter a great deal. In other words, you do not need to change very much of the genome to make a new species. The way to evolve a human from a chimp-human ancestor is not to speed the ticking of the molecular clock as a whole. Rather the secret is to have rapid change occur in sites where those changes make an important difference in an organism’s functioning.

HAR1 is certainly such a place. So, too, is the FOXP2 gene, which contains another of the fast-changing sequences I identified and is known to be involved in speech. _SciAm

Of course, none of the sub-species of humans -- the semi-isolated breeding populations -- are as different from the other human populations as all chimpanzees are different from all humans. At the same time, no one truly understands human gene expression well enough to say which differences between human populations are potentially important, and which are not. Likewise, a significant amount of interbreeding between formerly isolated breeding populations takes place in modern societies such as those in the US, the UK, Canada, and Australia. These "natural experiments" in inter-mixing between formerly isolated populations should provide an unbiased science with a number of "natural experiments", perhaps revealing a "dose-response" gradient to genetic effects.

The best approach to the science of genetic influences on behaviour and intelligence would be to pursue the topic as seriously as the Manhattan Project was pursued in WWII. The goal is the discovery of methods that allow humans to become more intelligent. It is a far more important goal than life extension. Who wants to live forever in the middle of an Idiocracy? Not I. Of course, once we are more intelligent, life extension becomes a more important goal, and more achievable.

The popular leftist denial of important genetic behavioural and intelligence differences between populations is the equavalent of shooting oneself in the head to relieve a headache. In the name of a faux "equality" that never existed, leftist zomboids in academy, government, and the media prevent the type of understanding that is required to eventually allow anyone who wishes to become more intelligent. A better example of idiocracy is hard to find.