Van den Heuvel’s team to build connectivity networks for each volunteer, and to measure the efficiency of each network. “It more or less reflects how many steps a [brain] region has to take to send information from one region to another,” he says.
This measure proved a decent predictor of each person’s IQ, explaining about 30 per cent of the differences between subjects, van den Heuvel says.
Intriguingly, the researchers found no link between the total number of connections in a subject’s brain network and their IQ. “We show that more intelligent people don’t have more connections, but they have more efficiently placed connections,” he says.”
If it’s genetic, genes work through biology and, once we understand the biology, we have lots of ways to manipulate biology,” says Richard Haier, a neuroscientist at the University of California, Irvine. “In my mind, one of the important directions of this kind of research should lead to ways to improve intelligence on a neurochemical basis.”
picking and choosing genetic copying of extreme humans – superhard bones
The late 1990s, a surprised radiologist in Connecticut came across a real-life version of Bruce Willis’s character in the movie Unbreakable. The patient came to the hospital after a motor vehicle accident. But rather than revealing broken bones, the x-rays revealed an extremely high bone density. (Bone-density testing later confirmed it to be the highest ever recorded. Eight times higher than the bone density for a man his age.) In 2002, Richard Lifton, a geneticist at Yale who specializes in genetic analysis of human outliers–people with extreme phenotypes–discovered that a mutation in a gene called LDL-related receptor protein 5 was responsible for the man’s high bone density, a condition shared by about half of his family. (While mutations in this gene can sometimes lead to health problems, Lifton says that this family’s only complaint was that they couldn’t float in water because their bones are so dense.)
Lifton’s team went on to study the molecular pathway affected by this mutation–and just seven years later, drugs targeting one of these molecules is in late-stage clinical testing for osteoporosis, a progressive disease of brittle bones that leads to fracture and a substantially increased risk of disability and death among the elderly.