Immune cells known as microglia, long thought to be activated in the brain only when fighting infection or injury, are constantly active and likely play a central role in one of the most basic, central phenomena in the brain – the creation and elimination of synapses. The findings, publishing next week in the online, open access journal PLoS Biology, catapult the humble microglia cell from its well-recognized duty of protecting the brain to direct involvement in creating the cellular networks at the core of brain behavior. Its apparent role as an architect of synapses – junctions between brain cells called neurons – comes as a surprise to researchers long accustomed to thinking of microglia as cells focused exclusively on keeping the brain safe from threats.
Pretty cool. While I did not expect this particular discovery I've been expecting to see lots of cell types to turn out to have more purposes than they were originally expected to serve. Here's why: It is economical to take a cell that is going to be there for one purpose and make it also do other tasks. Why not? It is there after all. It is getting fed. It is taking up room and resources. It has the full genome (complete genetic software program) of the organism. Get it to execute more pieces of genetic code. I see this as an example of the efficiency and economy of function that evolutionary processes running for hundreds of millions of years are able to produce.
Ron Guhname (not his real name), The Inductivist, used data from the General Social Survey to look at the question of whether the legalization of abortion in America caused a change in selective pressures for intelligence. Using the GSS Wordsum test as a rough measure of intelligence Ron finds that abortion did not appear to change the selective pressures for higher or lower intelligence. The selective pressures for lower intelligence continued unchanged.
The first year of the General Social Survey was 1972. I looked at white women ages 50 and over for all surveys conducted in the 70s. The mean number of kids for dull women (Wordsum 0-4) was 3.02. It was 2.22 for smart women (Wordsum 8-10). That's a ratio of 1.36. Looking at this decade, I calculated means for white women ages 45-59. For the unintelligent group, the mean number of kids is 2.38, and it's 1.76 for the bright group. That's a ratio of 1.35.
There is no difference between the two periods. The higher fertility of dull women seen prior to 1970 continues to the same degree today.
My guess is that women use the knowledge that they can get an abortion to become more lax about use of birth control and to enable more spontaneous beginnings of affairs. Abortion might still have caused changes in selective pressures because the women who are willing to go thru with an abortion might differ in some aspect of personality as compared to women who won't.
If you are curious about modern era selective pressures for intelligence see this report from an Australian twins study. For a book length treatment of selective pressures on humans see The 10,000 Year Explosion: How Civilization Accelerated Human Evolution by Gregory Cochran and Henry Harpending.
An area of the brain called the anterior supramarginal gyrus (aSMG) lights up with activity in humans when humans watch tool use. Rhesus monkeys do not show similar reactions in their brains when scanned with fMRI (functional magnetic resonance imaging).
Forty-seven people and five rhesus monkeys participated in the experiments. Two of the monkeys had been trained to obtain rewards beyond their reach by using either a rake or a pair of pliers.
Exactly the same areas of the brain became active in people and monkeys when they watched footage of hands simply grasping tools.
But when they watched videos of tools actually being used, the aSMG became active in the humans alone. It was silent even in the two trained monkeys'.
Do people who study mechanical engineering show more activity in the aSMG when they watch tool use? Do women show less aSMG activity while watching tool use? Are there genetic variations within human populations that increase and decrease aSMG activation when watching tool use?
Imagine a sort of aptitude test where one's brain gets scanned while one looks at and tries various forms of activity. Such a test might be able to reveal what one would most enjoy doing in the long run.
COLUMBIA, Mo. - For the past 2 million years, the size of the human brain has tripled, growing much faster than other mammals. Examining the reasons for human brain expansion, University of Missouri researchers studied three common hypotheses for brain growth: climate change, ecological demands and social competition. The team found that social competition is the major cause of increased cranial capacity.
To test the three hypotheses, MU researchers collected data from 153 hominid (humans and our ancestors) skulls from the past 2 million years. Examining the locations and global climate changes at the time the fossil was dated, the number of parasites in the region and estimated population density in the areas where the skulls were found, the researchers discovered that population density had the biggest effect on skull size and thus cranial capacity.
"Our findings suggest brain size increases the most in areas with larger populations and this almost certainly increased the intensity of social competition," said David Geary, Curator's Professor and Thomas Jefferson Professor of Psychosocial Sciences in the MU College of Arts and Science. "When humans had to compete for necessities and social status, which allowed better access to these necessities, bigger brains provided an advantage."
Was a better ability to deal with other humans or a better ability to deal with the rest of reality the primary driver of rising human intelligence for most the last couple of million years? Also, was there a shift in relative importance of various selective pressures over time? The the huge human evolution acceleration of the last 10,000 years suggests that either new selective pressures showed up or some existing selective pressures intensified.
Humans and other higher primates developed fancier circuitry in the brain to support more complex sequences of movement. This enabled more complex usage of tools.
PITTSBURGH, Jan. 12 – A new area of the cerebral cortex has evolved to enable man and higher primates to pick up small objects and deftly use tools, according to neuroscientists at the University of Pittsburgh School of Medicine and Pittsburgh's Veterans Affairs Medical Center.
The brain's primary motor cortex turns out to have neighboring "old" and "new" parts. In most animals, including cats, rats and some monkeys, the old primary motor cortex controls movement indirectly through the circuitry of the spinal cord, explained senior author Peter Strick, Ph.D., professor in the department of neurobiology at the School of Medicine and senior career scientist at the VA Medical Center.
But in man, the Great Apes and some monkeys, another area of the motor cortex developed and is now home to a special set of cortico-motoneuronal (CM) cells, he said. These cells directly control spinal cord motor neurons, which are the nerve cells responsible for causing contraction of shoulder, elbow and finger muscles. The direct control exerted by CM cells bypasses the limitations imposed by spinal cord circuitry and permits the development of highly complex patterns of movement, such as the independent finger action needed for playing an instrument or typing.
The development of greater ability to manipulate tools probably played synergistically with the development of more cognitive capacity in order to learn and remember what to use tools for. So this development probably created selective pressures for further evolution of the brain.
The old adage that we can only learn how to do something by trying it ourselves may have to be revised in the light of recent discoveries in neuroscience. It turns out that humans, primates, some birds, and possibly other higher animals have mirror neurons that fire in the same pattern whether performing or just observing a task. These mirror neurons clearly play an important role in learning motor tasks involving hand eye coordination, and possibly also acquisition of language skills, as well as being required for social skills, but the exact processes involved are only just being discovered. In particular the relationship between mirror neural networks and social cognitive tasks has been unclear, and greater knowledge of it could shed light on problems such as autism that may arise when this process goes wrong.
It could be that some on the autistic spectrum (high functioning autistics and Aspergers) are able to do more original mental work because they spend less of their mental resources activating neurons to mirror what others are feeling and doing.
Mirror neurons fire not only when watching someone else perform a task but also when watching someone else experience an emotion.
Just as the same mirror neurons fire when observing and doing certain tasks, so other mirror neurons may be triggered both when experiencing a particularly emotion and when observing someone else with that emotion. At the ESF conference it emerged that mirror neurons involved in emotion resided in both the insula and cingulate cortexes, two regions of the brain known to play roles in emotions and feelings. However until recently the mechanisms of interaction between these two had been largely unknown. "In the case of emotions, we can say that there is a good deal of overlap between areas from the insula and cingulate cortexes," said Viale. "These areas become active both when individuals feel an emotion (e.g. disgust) and also when they watch someone else feeling that emotion."
Mirror neurons were discovered in the 1980s by an Italian group led by Giacomo Rizzolatti, which placed electrodes in the inferior frontal cortex of macaque monkeys' brains to study neurons dedicated to control of hand movement. This led to the surprising observation that some of the neurons responded in the same way when monkeys saw a person pick up a piece of food as when they were doing it themselves. This introduced the principle of the mirror neuron as a neuron capable of being triggered by imitation, as a mechanism both for learning and empathising in social situations.
While mirror neutrons cannot be observed directly in humans because electrodes cannot be inserted into their brains, the action has been inferred by imaging of the whole brain using magnetic resonance imaging (MRI). This showed patterns of brain activity consistent with the firing of motor neurons.
More recently motor neurons have also been discovered in birds.
Modest proposal: Rate a movie by having people watch it and measure their emotional responses with fMRI scanners. A movie that activates a lot of mirror neurons might be successful. However, the feeling of being disgusted or angry with the movie needs to be separated from feelings of empathy for characters in the movie.
What I wonder: do any psychopaths have a diminished ability to feel emotions that mirror the emotions that others feel? Could one detect psychopaths by showing test subjects tragic and painful pictures and then see if their mirror neurons get activated?
Also, could intelligence agencies discover moles by showing them images of enemy countries and their own country and see if they more mirror neuron activation for happiness or friendliness from enemy country ideological images and less from their own?
Just punched someone? Blame it on natural selection. What to join the Marines and go into combat? Your genes are your puppeteer. Dream of shooting down enemies? Your genetic alleles for violence are expressing themselves in your brain. We want to beat up on other people because our genes tell us to. These results come from an unverified mathematical model. But surely natural selection has made men violent. Just the mechanism of exactly how needs to get filled in.
The mathematical analysis of the evolution war by Laurent Lehmann and Prof Marc Feldman of Stanford University focused on small-scale, pre-state societies, for instance hunter-gatherers societies.
In the Proceedings of the Royal Society, Biological Sciences, the study shows that the "selective pressure" on genes linked with belligerence and bravery can be substantial even in groups of large size, so that evolution has smiled on the most aggressive and audacious group.
What I want to know: Is belligerency getting selected for or against? Does the answer to the question differ between societies?
Some men who carry genetic variants that promote bravery might perish because of them, but the ones who survive may win more battles through their greater daring. The resulting opportunities for rape and pillage can create a net evolutionary benefit.
By having sex with their vanquished enemies’ wives and children, and by taking land on which their own womenfolk could grow or gather more food, particularly courageous and successful warriors would have more offspring who share their genes. “This has consequences for our understanding of the evolution of intertribal interactions, as hunter-gatherer societies are well known to have frequently raided neighbouring groups from whom they appropriated territory, goods and women,” the scientists said.
Really large scale societies that have been settled and centrally controlled for a long time (e.g. China) might have experienced long periods of selection against belligerency as the belligerent men ran afoul of central rule and got imprisoned or killed. So we might expect to find some groups to have lower frequencies of the genetic variants which cause male aggression.
Here is the abstract of the paper (PDF) and the full paper is at that link.
Tribal war occurs when a coalition of individuals use force to seize reproduction-enhancing resources, and it may have affected human evolution. Here, we develop a population-genetic model for the coevolution of costly male belligerence and bravery when war occurs between groups of individuals in a spatially subdivided population. Belligerence is assumed to increase an actor’s group probability of trying to conquer another group. An actor’s bravery is assumed to increase his group’s ability to conquer an attacked group.We show that the selective pressure on these two traits can be substantial even in groups of large size, and that they may be driven by two independent reproduction-enhancing resources: additional mates for males and additional territory (or material resources) for females. This has consequences for our understanding of the evolution of intertribal interactions, as hunter-gatherer societies are well known to have frequently raided neighbouring groups from whom they appropriated territory, goods and women.
Confirmation for genetic theorizing of this sort will not be long in coming. The costs of genetic testing have fallen by orders of magnitude in the last 10 years and the costs keep dropping. So the quantity of genetic testing is soaring. This enables large scale comparison of people for genetic and behavioral differences.
Once the genetic sources of violence become well characterized do you think the genetically most violence-prone people should be allowed to pass along their violence-causing genetic alleles to offspring?
The gap area where nerve cells connect to each other is called the synapse. Our higher intelligence comes not just from more synapses connecting between more nerves. The structure of each synapse is far more complex in creatures with higher intelligence.
Current thinking suggests that the protein components of nerve connections - called synapses - are similar in most animals from humble worms to humans and that it is increase in the number of synapses in larger animals that allows more sophisticated thought.
"Our simple view that 'more nerves' is sufficient to explain 'more brain power' is simply not supported by our study," explained Professor Seth Grant, Head of the Genes to Cognition Programme at the Wellcome Trust Sanger Institute and leader of the project. "Although many studies have looked at the number of neurons, none has looked at the molecular composition of neuron connections. We found dramatic differences in the numbers of proteins in the neuron connections between different species".
"We studied around 600 proteins that are found in mammalian synapses and were surprised to find that only 50 percent of these are also found in invertebrate synapses, and about 25 percent are in single-cell animals, which obviously don't have a brain."
It would be interesting to know for these 600 proteins whether there are differences in their genes between humans. The differences might account for some genetically caused differences in intelligence and personality.
Synapses used to be taught in neurobiology classes as pretty simple places where synaptic endings of axons release neurotransmitters that float across to bind to receptors on dendrites. Then that binding causes a wave of depolarization which propagates along a nerve. Well, the synapses probably function in much more complex ways.
Synapses are the junctions between nerves where electrical signals from one cell are transferred through a series of biochemical switches to the next. However, synapses are not simply soldered joints, but mini-processors that give the nervous systems the property of learning and memory.
Some day the ways in which memories get stored and information gets processed will be understood in enormous detail. Will that cause more people to abandon belief in a soul?
"The molecular evolution of the synapse is like the evolution of computer chips - the increasing complexity has given them more power and those animals with the most powerful chips can do the most," continues Professor Grant.
Simple invertebrate species have a set of simple forms of learning powered by molecularly simple synapses, and the complex mammalian species show a wider range of types of learning powered by molecularly very complex synapses.
"It is amazing how a process of Darwinian evolution by tinkering and improvement has generated, from a collection of sensory proteins in yeast, the complex synapse of mammals associated with learning and cognition," said Dr Richard Emes, Lecturer in Bioinformatics at Keele University, and joint first author on the paper.
What I want to know: Do other species have advances in their synaptic structure that humans do not have? In particular, some bird species are very smart for the size of their brains. Do they have very sophisticated synaptic structures that would allow them to be as smart or even smarter than us if only their brains were as large?
Why do kids have problems with attention deficit disorder and hyperactivity? I've long believed that surely these behaviors must have had evolutionary value or else they wouldn't exist. In other words, use of Ritalin and similar drugs to tame kids amounts to trying to put a damper on the genetic nature of hyperactive humans. Our problem is that we now live in technologically created environments which we did not encounter in our evolutionary past. Therefore in many cases we are not adaptive to our new environments. Well, finally some really detailed evidence to support my hunch: Kenyan nomads do better with an ADHD gene whereas those who have converted to settled living do worse with this same version of the DRD4 gene.
A propensity for attention deficit hyperactivity disorder (ADHD) might be beneficial to a group of Kenyan nomads, according to new research published in the open access journal BMC Evolutionary Biology. Scientists have shown that an ADHD-associated version of the gene DRD4 is associated with better health in nomadic tribesmen, and yet may cause malnourishment in their settled cousins.
Different versions of a receptor for the neurotransmitter dopamine make people more or less hyperactive.
A study led by Dan Eisenberg, an anthropology graduate student from Northwestern University in the US, analyzed the correlates of body mass index (BMI) and height with two genetic polymorphisms in dopamine receptor genes, in particular the 48 base pair (bp) repeat polymorphism in the dopamine receptor D4 (DRD4) gene.
The DRD4 gene codes for a receptor for dopamine, one of the chemical messengers used in the brain. According to Eisenberg "this gene is likely to be involved in impulsivity, reward anticipation and addiction". One version of the DRD4 gene, the '7R allele', is believed to be associated with food craving as well as ADHD. By studying adult men of the Ariaal of Kenya, some of whom still live as nomads while others have recently settled, the research team investigated whether this association would have the same implications in different environments.
While those with the DRD4/7R allele were better nourished in the nomadic population, they were less well-nourished in the settled population. Although the effects of different versions of dopamine genes have already been studied in industrialized countries, very little research has been carried out in non-industrial, subsistence environments like the areas where the Ariaal live, despite the fact that such environments may be more similar to the environments where much of human genetic evolution took place.
Eisenberg explains, "The DRD4/7R allele has been linked to greater food and drug cravings, novelty-seeking, and ADHD symptoms. It is possible that in the nomadic setting, a boy with this allele might be able to more effectively defend livestock against raiders or locate food and water sources, but that the same tendencies might not be as beneficial in settled pursuits such as focusing in school, farming or selling goods".
These findings suggest that behavior differences previously associated with the DRD4 gene, such as ADHD, are more or less effective depending on the environment. Research into how this might occur in Ariaal children is planned in the near future.
Think about a nomad guarding his herd. If he can focus in on one thing he might not notice predators or raiders approaching. If he can't sit still he is more likely to spend his time looking around and will notice more of his environment. If he's more distractable by movement he sees out of the corner of his eye he's more likely to notice livestock wandering off or a threat.
Or look at geeky guys who are smart at math and physics but not strong. The development of computers and other complex technologies have made them far more adaptive than they used to be. Highly coordinated muscular guys have become relatively less valuable in the job market as robots and hydraulic heavy duty equipment do increasing portions of the heavy lifting and manipulation. Women can do a larger fraction of all jobs because hard manual labor has dwindled as a portion of all work.
The continued rapid decline in costs for DNA sequencing and DNA testing will lead to a torrent of studies such as the one reported above. We will learn the identities of many more genetic variations that affect behavior, intellectual abilities, and physical abilities along with the distribution of these genetic variations around the world. Our picture of humanity is on the verge of radical change. These discoveries will finally demonstrate how evolution is the most powerful force shaping humanity.
Do humans really have unique modes of thought? Some of the ways which humans were believed to be unique in intellectual abilities have since been found present in other species. But a professor at Harvard believes other methods of thinking are uniquely human.
CAMBRIDGE, Mass. – Shedding new light on the great cognitive rift between humans and animals, a Harvard University scientist has synthesized four key differences in human and animal cognition into a hypothesis on what exactly differentiates human and animal thought.
In new work presented for the first time at the annual meeting of the American Association for the Advancement of Science, Marc Hauser, professor of psychology, biological anthropology, and organismic and evolutionary biology in Harvard’s Faculty of Arts and Sciences, presents his theory of “humaniqueness,” the factors that make human cognition special. He presents four evolved mechanisms of human thought that give us access to a wide range of information and the ability to find creative solutions to new problems based on access to this information.
“Animals share many of the building blocks that comprise human thought, but paradoxically, there is a great cognitive gap between humans and animals,” Hauser says. “By looking at key differences in cognitive abilities, we find the elements of human cognition that are uniquely human. The challenge is to identify which systems animals and human share, which are unique, and how these systems interact and interface with one another.”
Recently, scientists have found that some animals think in ways that were once considered unique to humans: For example, some animals have episodic memory, or non-linguistic mathematical ability, or the capacity to navigate using landmarks. However, despite these apparent similarities, a cognitive gulf remains between humans and animals.
Do these really seem like uniquely human intellectual abilities?
Hauser presents four distinguishing ingredients of human cognition, and shows how these capacities make human thought unique. These four novel components of human thought are the ability to combine and recombine different types of information and knowledge in order to gain new understanding; to apply the same “rule” or solution to one problem to a different and new situation; to create and easily understand symbolic representations of computation and sensory input; and to detach modes of thought from raw sensory and perceptual input.
Earlier scientists viewed the ability to use tools as a unique capacity of humans, but it has since been shown that many animals, such as chimpanzees, also use simple tools. Differences do arise, however, in how humans use tools as compared to other animals. While animal tools have one function, no other animals combine materials to create a tool with multiple functions. In fact, Hauser says, this ability to combine materials and thought processes is one of the key computations that distinguish human thought.
How certain can we be that no other animal creates tools with multiple functions?
The advantage that humans have with "floodlight" cognition seems one of degree.
According to Hauser, animals have “laser beam” intelligence, in which a specific solution is used to solve a specific problem. But these solutions cannot be applied to new situations or to solve different kinds of problem. In contrast, humans have “floodlight” cognition, allowing us to use thought processes in new ways and to apply the solution of one problem to another situation. While animals can transfer across systems, this is only done in a limited way.
“For human beings, these key cognitive abilities may have opened up other avenues of evolution that other animals have not exploited, and this evolution of the brain is the foundation upon which cultural evolution has been built,” says Hauser.
Apes bite and try to break a tube to retrieve the food inside while children follow the experimenter's example to get inside the tube to retrieve the prize, showing that even before preschool, toddlers are more sophisticated in their social learning skills than their closest primate relatives, according to a report published in the 7 September issue of the journal Science, published by AAAS, the nonprofit science society.
This innate proficiency allows them to excel in both physical and social skills as they begin school and progress through life.
"We compared three species to determine which abilities and skills are distinctly human," explained Esther Herrmann of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany and lead author of the research paper. Humans differ from their great ape relatives because human brains are about three times the size of the closest primate relatives and humans have language, symbolic math and scientific reasoning.
That extra gray matter makes its presence felt at a very young age.
The human kids were equally in ability to the primates in many areas but showed a clear advantage in understanding and communicating.
About 230 subjects – chimps, orangutans and 2.5 year-old children – were compared using a battery of tests and found all to be about equal in the physical cognitive skills of space, quantities and causality. In the social skills of communication, social learning and theory-of-mind skills, the children were correct in about 74 percent of the trials, while the two ape species were correct only about 33 percent of the time.
The researchers chose to study children at an age when they have about the same physical skill level of chimpanzees. Children at 2.5 years are old enough to handle these tasks and people have not taught them too much so they provide a good comparison, Herrmann said. The apes ranged in age from 3 to 21.
Some day (maybe 50 to 75 years from now) some evolutionary anthropologists will perform a similar set of experiments comparing genetically natural 2 and 3 year old humans to genetically engineered 2 and 3 year old transhumans. I predict the gap in intellectual abilities between the humans and transhumans will be larger than the gap measured here between humans and other primates.
An interesting article by Nicholas Wade in the New York Times surveys part of what is known about sexual orientation and other sexual differences in the brain. He discusses potential causes of homosexuality (while notably failing to mention Greg Cochran's germ theory) and quotes sexuality researcher Michael Bailey. All good stuff. But the most interesting part to me: the presence of genes on the X chromosome that get expressed in the brain may allow more rapid selection for favorable genetic variations which enhance cognitive function.
It so happens that an unusually large number of brain-related genes are situated on the X chromosome. The sudden emergence of the X and Y chromosomes in brain function has caught the attention of evolutionary biologists. Since men have only one X chromosome, natural selection can speedily promote any advantageous mutation that arises in one of the X’s genes. So if those picky women should be looking for smartness in prospective male partners, that might explain why so many brain-related genes ended up on the X.
The existence of only one X chromosome allows new genetic mutations to express their effects more drastically in men and therefore to get selected for more rapidly.
Several profound consequences follow from the fact that men have only one copy of the many X-related brain genes and women two. One is that many neurological diseases are more common in men because women are unlikely to suffer mutations in both copies of a gene.
Another is that men, as a group, “will have more variable brain phenotypes,” Dr. Arnold writes, because women’s second copy of every gene dampens the effects of mutations that arise in the other.
This probably at least partially explains why the standard deviation of IQ is higher in men than in women. That higher standard deviation means that compared to women there are more extremely brilliant men and also more very dim bulb men.
An interesting consequence of the higher male standard deviation for IQ is that women above average in IQ generally can find men who are as smart or smarter to pair up with. But in the below average territory the women are going to tend to be smarter than the males of their social class and neighborhoods.
What I've always wondered: When successful men divorce their middle aged wives and marry younger women are the second wives less bright on average than the first wives? In other words, do the men decide to be less choosy on IQ in order to get younger second wives? I'm not looking for anecdotes to the contrary. I want to know about averages. Also, are the children born to second marriages as smart on average as children born to first marriages?
Nobody knows what it does yet but a section of DNA that codes for DUF1220 has become heavily duplicated in humans as compared to other species.
The team compared the DNA sequences of humans, chimpanzees and monkeys, and looked for genes that were repeated more often in human DNA than in the other primate genomes. One gene that codes for a piece of protein called DUF1220 stood out. Humans carry 212 copies of DUF1220, whereas chimps have 37 copies, and monkeys have only 30 copies, the researchers found. Mice and rats each had a paltry single copy of the protein-coding region. When the team looked for the protein in the human body, they found it in many places, including in neurons in the brain.
It probably does stuff in the brain and we probably became smarter as a result of having many DUF1220 segments in the human genome.
Extreme gene duplication is a major source of evolutionary novelty. A genome-wide survey of gene copy number variation among human and great ape lineages revealed that the most striking human lineage–specific amplification was due to an unknown gene, MGC8902, which is predicted to encode multiple copies of a protein domain of unknown function (DUF1220). Sequences encoding these domains are virtually all primate-specific, show signs of positive selection, and are increasingly amplified generally as a function of a species' evolutionary proximity to humans, where the greatest number of copies (212) is found. DUF1220 domains are highly expressed in brain regions associated with higher cognitive function, and in brain show neuron-specific expression preferentially in cell bodies and dendrites.
Do humans differ in how many copies of MGC8902 and DUF1220 we have?
So there are two stories here. One is about the multiple duplication of MGC8902 on the human lineage. The draft human genome has 49 copies of it, chimpanzees have only 10.
A seperate story is about the proliferation of this DUF1220 domain, which occurs in many proteins. This domain increased in copy number on the human lineage compared to chimpanzees, the African ape lineage compared to orangutans, and primates compared to other mammals.
To me the DUF1220 story is the fascinating part. Not only one gene, but apparently many genes that contain this domain have been proliferating; additionally some genes apparently have acquired this domain during human evolution. In at least one gene, the DUF1220 domain shows evidence of positive selection, but the rest of the coding sequence doesn't.
In the next 10 years we will learn the identity of most of the genes that make us smarter than other specices. We will also learn which genetic variations make some humans smarter than others.
Using data from the International HapMap project (HapMap stands for Haplotype Map of genetic variations) researchers find evidence for recent changes in the frequencies of genes in different human populations.
By scanning the entire human genome in search of genetic variations that may signal recent evolution, University of Chicago researchers found more than 700 genetic variants that may be targets of recent natural positive selection during the past 10,000 years of human evolution.
In one of the first comprehensive genome scans for selection, the researchers found widespread evidence of evolution in all of the populations studied. Their results are published and freely available online in the open-access journal PLoS Biology.
The data analyzed here were collected by the International HapMap Project and consist of genetic data from 209 unrelated individuals who are grouped into three distinct populations: 89 East Asians, 60 Europeans and 60 Yorubans from Nigeria. The researchers found roughly the same number of signals of positive selection within each population. They also found that each population shares about one fifth of the signals with one or both of the other groups.
"This approach allows us to take a broad prospective to see what kinds of biological systems are undergoing adaptation," said Jonathan Pritchard, professor of human genetics and corresponding author of the paper. "There have been a lot of recent changes--the advent of agriculture, shifts in diet, new habitats, climatic conditions--over the past 10,000 years, and we're using these data to look for those signals of very recent adaptation."
Among the more than 700 signals the team found were previously known sites of recent adaptation, such as the salt-sensitive hypertension gene and the lactase gene--the strongest signal in the genome hunt. The lactase mutation, which enables the digestion of milk to continue into adulthood, appeared in approximately 90 percent of Europeans.
"Presumably," Pritchard said, "a few thousand years from now, if selection pressure remains the same, everyone will have [the selected mutation]."
Classifying all the genes by their biological functions, the researchers listed the top 16 categories that had the strongest signals, including olfaction (the sense of smell), reproduction-related processes and carbohydrate metabolism, which includes the lactase gene.
Other processes that show signals of selection include genes related to metabolism of foreign compounds, brain development and morphology. For example, the researchers found five genes involved in skin pigmentation that show evidence of positive selection in Europeans. "Only one of these five signals was known before," Pritchard said. The authors also found signals of reproductive selection and sexual competition in all three populations.
"Many of the signals, however, seem to be more specific to modern human adaptation," he said, "like skin pigmentation, which may respond to changes in habitat, or metabolism genes, like lactase, which may respond to changes in agriculture."
From the text of the journal article: They found several brain genes under selective pressure.
Recent articles have proposed that genes involved in brain development and function may have been important targets of selection in recent human evolution [8,9]. While we do not find evidence for selection in the two genes reported in those studies (MCPH1 and ASPM), we do find signals in two other microcephaly genes, namely, CDK5RAP2 in Yoruba, and CENPJ in Europeans and East Asians . Though there is not an overall enrichment for neurological genes in our gene ontology analysis, several other important brain genes also have signals of selection, including the primary inhibitory neurotransmitter GABRA4, an Alzheimer's susceptibility gene PSEN1, and SYT1 in Yoruba; the serotonin transporter SLC6A4 in Europeans and East Asians; and the dystrophin binding gene SNTG1 in all populations.
It is possible some genes with influence on brain function were missed in their analysis because the genes have as yet unidentified roles in influencing cognitive function. A couple of other factors suggest these results are far from comprehensive. First, they looked at only 800,000 single nucleotide polymorphisms (SNPs). Well, the human race has more than that. Also, and perhaps more importantly, they looked only at SNPs. Yet another type of genetic variation called large copy variations have fairly recently been found to create suprisingly large amounts of genetic variation between humans. So this latest result with such a small sample size of humans and a subset of all human genetic variations understates the extent of recent evolution in humans.
Regarding their lack of evidence for the recent evolution of MCPH1 and ASPM see my previous post Brain Gene Allele Frequences Show Brain Still Evolving. Also see my post PDYN Brain Gene Modified During Primate Evolution.
Human evolution did not stop tens of thousands of years ago. We are more different from each other due to genetic factors than left-liberal political ideologues would have you believe. We are still evolving and adapting to local environments. Starting some time in the next 20 or 30 years our rate of genetic change is going to accelerate by orders of magnitude and subpopulations of homo sapiens will diverge even more radically than human racial groups have diverged so far.
Logical organized minds with a knack for pattern recognition preferentially marrying each other in a process called "assortative mating" may be the cause of a rise in the incidence of autism.
Highly analytical couples, such as scientists, may be more likely to produce children with autism, an expert has argued.
Professor Simon Baron-Cohen, of the University of Cambridge, said the phenomenon might help explain the recent rise in diagnoses.
He believes the genes which make some analytical may also impair their social and communication skills.
Perhaps male scientists and computer programmers ought to marry literature professors, art professors, and lawyers? Organized and disorganized people should hook up? Systematic types should mate with chaotic types? Not sure what this would do the divorce rate. But it might lower the incidence of autism. Though it might come at the expense of lowering the frequency people born with the ability to be extremely talented scientists and engineers. Or maybe it would create managers better balanced between having technical and communications skills and therefore make industry more productive over all.
According to a survey of 1,000 members of the National Autistic Society, fathers and grandfathers of children with autistic spectrum conditions are twice as likely to work in a systemizing profession such as engineering.
Students in the natural sciences have a higher number of relatives with autism than do students in the humanities, and mathematicians have a higher rate of autistic spectrum conditions compared with the general population.
The theory that both parents of children with autism are strong systemizers is also evident from a study that shows both mothers and fathers score above average on a questionnaire that measures autistic traits.
The idea here is that people who hate to socialize who marry like minds are at risk of having kids who get even stronger doses of genes that push them in that direction with the extreme being autism.
Baron-Cohen is not the first person I've seen put forward this idea. Some argue that Silicon Valley has a disproportionate incidence of autism and that this is happening because male and female techies are hooking up there in workplaces and having babies.
IF this theory is correct (and it seems very plausible) then it adds further evidence to the argument that technology is causing big changes in selective pressures on genes which code for cognitive function. Evolution did not stop tens of thousands of years ago. Selective pressures can cause changes in mating practices that cause changes in distributions of genetic variations for brain genes and this can happen in a relatively short period of time.
The set of genes known to have been under selective pressure during primate evolution has gained another member: Prodynorphin. Regulatory regions for prodynorphin, an important brain gene, have been under natural selective pressure during evolution from lower primates to humans.
Durham, N.C. -- Researchers have discovered the first brain regulatory gene that shows clear evidence of evolution from lower primates to humans. They said the evolution of humans might well have depended in part on hyperactivation of the gene, called prodynorphin (PDYN), that plays critical roles in regulating perception, behavior and memory.
They reported that, compared to lower primates, humans possess a distinctive variant in a regulatory segment of the prodynorphin gene, which is a precursor molecule for a range of regulatory proteins called "neuropeptides." This variant increases the amount of prodynorphin produced in the brain.
While the researchers do not understand the physiological implications of the activated PDYN gene in humans, they said their finding offers an important and intriguing piece of a puzzle of the mechanism by which humans evolved from lower primates.
They also said that the discovery of this first evolutionarily selected gene is likely only the beginning of a new pathway of exploring how the pressure of natural selection influenced evolution of other genes.
They also said their finding demonstrates how evolution can act more efficiently to alter the regulatory segments, or "promoters," that determine genes' activity, rather than on the gene segment that determines the structure of the protein it produces. Such regulatory alteration, they said, can more readily generate variability than the hit-or-miss mutations that alter protein structure and function.
I think they are exaggerating to call PDYN "this first evolutionarily selected gene". See my discussion below of Microcephalin, ASPM, and the Ashkenazi Jewish genetic disease genes such as the sphingolipid pathway genes.
Prodynorphin is involved in many brain functions.
The researchers published their findings in an article in the December 2005 issue of the Public Library of Science. They were Gregory Wray and David Goldstein of Duke University; Matthew Rockman of Princeton University; Matthew Hahn of Indiana University; Nicole Soranzo of University College London; and Fritz Zimprich of the Medical University of Vienna in Austria. The research was sponsored by the National Science Foundation and NASA.
"We focused on the prodynorphin gene because it has been shown to play a central role in so many interesting processes in the brain," said Wray. "These include a person's sense of how well they feel about themselves, their memory and their perception of pain. And it's known that people who don't make enough of prodynorphin are vulnerable to drug addiction, schizophrenia, bipolar disorders and a form of epilepsy. So, we reasoned that humans might uniquely need to make more of this substance, perhaps because our brains are bigger, or because they function differently.
Note how the study of gene sequence variations from an evolutionary perspective allows scientists to find what areas most likely changed to make human minds different than the minds of other primates. The theory of evolution is not just an explanation of ancient events. Genetic models of evolution help in doing practical research in how the brain works.
"Also importantly, the part of the gene that produces the prodynorphin protein shows no variation within humans, or even between humans and any of the great apes," said Wray, who is a professor of biology. "So, if we found any variation in this gene due to evolution, it was likely to be in its regulation. And our premise is that the easiest way to generate evolutionary change is to alter regulation."
In their studies, the researchers analyzed the sequence structure of the PDYN promoter segment in humans and in seven species of non-human primates -- chimpanzees, bonobos, gorillas, orangutans, baboons, pig-tailed macaques and rhesus monkeys. They found significant mutational changes in the regulatory sequence leading to humans that indicated preservation due to positive evolutionary selection. They also found an "evolution-by-association," in which sequences near the regulatory segment showed greater mutational change -- as if they were "dragged along" with the evolving regulatory sequence.
The identification of areas of the genome which were under active selective pressure in evolution helps the search for genetic sequence variations which boost intelligence in the smarter folks among us. Areas of brain genes which are shown to be under recent selective pressure are the areas most likely to contain genetic variations that account for the huge range of intellectual ability found in the human population.
The report above about PDYN reminds me of previous reports about the brain gene ASPM. First Bruce Lahn of the University of Chicago found that ASPM underwent extended selective pressure and change in the primates. Then Lahn showed that ASPM and Microcephalin have been under strong selective pressure in recent human history and the genetic variations recently selected for were not selected for equally in all human populations. PDYN is basically at the research stage that ASPM was at before Lahn compared large numbers of humans for their ASPM variations. The next logical step with PDYN would be to compare regulatory regions for that gene in different human populations to see if they differ in their frequency of different genetic variations.
ASPM, PDYN, and Microcephalin make excellent candidates for genes whose variations cause differences in levels of intelligence. What we need is a massive study of people who would get IQ tested and also get genetically tested for which variations they have for these genes and for the regulatory regions for these genes. A number of other genes would also make good candidates for inclusion in such a study. as Greg Cochran, Henry Harpending, and Jason Hardy have recently demonstrated the genes which cause Jewish genetic diseases are also excellent candidates for comparisons of genetic sequences and IQ levels.
The Duke University researchers in the report at the top of this post have 250 more genes active in the brain they are going to look at for signs of natural selective pressures for brain evolution. My guess is that in the next 5 years the evolutionary approach to brain gene study is going to lead to the identification of many genetic variations that causes differences in intelligence. The work could go much faster if the genetic basis for IQ differences was not so taboo politically. But enough excellent work is getting done in this area that I'm hopeful about some major discoveries in spite of the taboo.
The discovery of genetic variations which boost IQ will lay the groundwork for attempts to boost human intelligence. People will use genetic tests to choose mates and choose egg and sperm donors to get smarter offspring. Also, the knowledge that up and down regulation of specific genes affectgs intelligence levels will lead to attempts to develop drugs which change the regulation of those genes in hopes of boosting intelligence. So the search for signs of selective pressures on brain genes will lead to IQ boosts that will eventually cause revolutionary changes in human societies.
Bruce Lahn and colleagues at the University of Chicago continue their ground-breaking research on the evolution of human intelligence with their finding that two genes involved in cognition have been under strong selective pressure since humans left Africa.
The gene Microcephalin (MCPH1) regulates brain size and has evolved under strong positive selection in the human evolutionary lineage. We show that one genetic variant of Microcephalin in modern humans, which arose ~37,000 years ago, increased in frequency too rapidly to be compatible with neutral drift. This indicates that it has spread under strong positive selection, although the exact nature of the selection is unknown. The finding that an important brain gene has continued to evolve adaptively in anatomically modern humans suggests the ongoing evolutionary plasticity of the human brain. It also makes Microcephalin an attractive candidate locus for studying the genetics of human variation in brain-related phenotypes.
A popular myth holds that evolution takes hundreds of thousands or millions of years to produce significant differences in a species. But even 1000 years is enough time in human evolution to produce large changes in allele frequencies. Heck, just look at the different rates of growth of various human population in the 20th century. At the beginning of the century white Europeans were about 25% of the world's population and last I read they were at 10% (or was it even lower?) and dropping. That caused big changes in the frequencies of a large number of alleles (places where DNA sequences differ between people).
Think about the times when these alleles started increasing in frequency in Lahn's reports. One he estimates started sweeping approximately 37,000 years ago. Another started sweeping approximately 5,800 years ago. Note they might both be much older. But those dates appear to be the dates when they really started spreading. They have both spread far in some human populations and yet not in others. This has big implications. Many other alleles for other traits (e.g. the ability to make lactase while an adult or red hair) obviously have spread in some populations on time scales in the thousands of years. But some people didn't want to believe that this could or did happen for brain gene alleles. Well, yes, it did.
I've coined a term to describe people who argue that the brain hasn't changed much since humans left Africa: Neo-Cartesian Dualists. Why that term? Well, Cartesian Dualism was the idea that the mind somehow existed independent of the brain. The modern Neo-Cartesian Dualism basically holds (not that I think its believers all really understand this implication of their myth) that the genes for coding the brain exist independent of any Darwinian selective force. The brain genes exist in a sort of magical realm where either natural selection can't reach or natural selection magically operates equally on all humans. But this could only be the case if a supernatural entity intervened to make it so. Reality does not work that way.
Howard Hughes Medical Institute researchers who have analyzed sequence variations in two genes that regulate brain size in human populations have found evidence that the human brain is still evolving.
They speculate that if the human species continues to survive, the human brain may continue to evolve, driven by the pressures of natural selection. Their data suggest that major variants in these genes arose at roughly the same times as the origin of culture in human populations as well as the advent of agriculture and written language.
The research team, which was led by Bruce T. Lahn, a Howard Hughes Medical Institute investigator at the University of Chicago, published its findings in two articles in the September 9, 2005, issue of the journal Science.
Their analyses focused on detecting sequence changes in two genes - Microcephalin and “abnormal spindle-like microcephaly associated” (ASPM) - across different human populations. In humans, mutations in either of these genes can render the gene nonfunctional and cause microcephaly - a clinical syndrome in which the brain develops to a much smaller size than normal.
In earlier studies of non-human primates and humans, Lahn and his colleagues determined that both Microcephalin and ASPM showed significant changes under the pressure of natural selection during the making of the human species. “Our earlier studies showed that Microcephalin showed evidence of accelerated evolution along the entire primate lineage leading to humans, for the entire thirty to thirty-five million years that we sampled,” he said. “However, it seemed to have evolved slightly slower later on. By contrast, ASPM has evolved most rapidly in the last six million years of hominid evolution, after the divergence of humans and chimpanzees.”
Here is the most important part:
The researchers first sequenced the two genes in an ethnically diverse selection of about 90 individuals. The researchers also sequenced the genes in the chimpanzee, to determine the “ancestral” state of polymorphisms in the genes and to assess the extent of human-chimpanzee divergence.
In each gene, the researchers found distinctive sets of polymorphisms, which are sequence differences between different individuals. Blocks of linked polymorphisms are called haplotypes, whereby each haplotype is, in essence, a distinct genetic variant of the gene. They found that they could further break the haplotypes down into related variants called haplogroups. Their analysis indicated that for each of the two genes, one haplogroup occurs at a frequency far higher than that expected by chance, indicating that natural selection has driven up the frequency of the haplogroup. They referred to the high-frequency haplogroup as haplogroup D.
When the researchers compared the ethnic groups in their sample for haplogroup D of ASPM, they found that it occurs more frequently in European and related populations, including Iberians, Basques, Russians, North Africans, Middle Easterners and South Asians. That haplogroup was found at a lower incidence in East Asians, sub-Saharan Africans and New World Indians. For Microcephalin, the researchers found that haplogroup D is more abundant in populations outside of Africa than in populations from sub-Saharan Africa.
Selective pressures on brain genes continued after humans migrated from Africa. The size of those selective pressures was not the same in populations that moved to various different parts of the world. Natural selection did not stop operating on brain genes once humanity developed into distinct races. The implications of this result are profound.
The ASPM haplogroup D spread started perhaps about 5,800 years ago (and that is an estimate around some range) and its emergence coincided with the spread of agriculture and the emergence of culturally modern humans!
To produce more informative statistical data on the frequency of haplotype D among population groups, the researchers applied their methods to a larger population sample of more than one thousand people. That analysis also showed the same distribution of haplogroups.
Their statistical analysis indicated that the Microcephalin haplogroup D appeared about 37,000 years ago, and the ASPM haplogroup D appeared about 5,800 years ago - both well after the emergence of modern humans about 200,000 years ago. “In the case of Microcephalin, the origin of the new variant coincides with the emergence of culturally modern humans,” said Lahn. “And the ASPM new variant originated at a time that coincides with the spread of agriculture, settled cities, and the first record of written language. So, a major question is whether the coincidence between the genetic evolution that we see and the cultural evolution of humans was causative, or did they synergize with each other?”Lahn said that the geographic origin and circumstances surrounding the spread of the haplogroups can only be surmised at this point. “One can make guesses, but our study doesn't reveal how these positively selected variants arrived," he said. "They may have arisen in Europe or the Middle East and spread more readily east and west due to human migrations, as opposed to south to Africa because of geographic barriers. Or, they could have arisen in Africa, and increased in frequency once early humans migrated out of Africa.” While the roles of Microcephalin and ASPM in regulating brain size suggest that the selective pressure on the new variants may relate to cognition, Lahn emphasized that this possibility remains speculative. “What we can say is that our findings provide evidence that the human brain, the most important organ that distinguishes our species, is evolutionarily plastic,” he said. Finding evidence of selection in two such genes is mutually reinforcing, he pointed out. “Finding this effect in one gene could be anecdotal, but finding it in two genes would make it a trend. Here we have two microcephaly genes that show evidence of selection in the evolutionary history of the human species and that also show evidence of ongoing selection in humans.”
I've been expecting the left-liberal inequality taboo to die by 2015. But declines in the cost of DNA sequencing combined with research results such as that reported above make me more optimistic. The taboo might have only about 5 more years to run.
Also see my previous posts "Many Genes Changed To Make Human Ancestors Progressively Smarter", "Researchers Find Key Gene For Evolution Of Human Intelligence", "Human Brain Size Regulating Gene To Be Inserted Into Mice", and "Genetic Causes Of Infidelity Found In Twins Study".
Update: Nicholas Wade of the New York Times provides more details on the frequency of each allele in different human populations.
They report that with microcephalin, a new allele arose about 37,000 years ago, although it could have appeared as early as 60,000 or as late as 14,000 years ago. Some 70 percent or more of people in most European and East Asian populations carry this allele of the gene, as do 100 percent of those in three South American Indian populations, but the allele is much rarer in most sub-Saharan Africans.
With the other gene, ASPM, a new allele emerged some time between 14,100 and 500 years ago, the researchers favoring a mid-way date of 5,800 years. The allele has attained a frequency of about 50 percent in populations of the Middle East and Europe, is less common in East Asia, and found at low frequency in some sub-Saharan Africa peoples.
The handwriting is on the wall. The evidence about human genetic differences in cognition found in psychometric research increasingly is getting buttressed by results from biological research. The discovery of more alleles that affect cognitive ability combined with DNA sequence comparisons will, within a few years time, lead to the collapse of the most damaging myth of our era.
Standing still when a threat is detected is a defensive, protective reaction. This ancestral and automatic behavior allows the prey to stay unnoticed by a potential predator. A new study published in Psychophysiology finds that humans, like many other complex animals, freeze when encountering a threat. The mere picture of an injured or mutilated human induces this reaction. When viewing these unpleasant images, the study’s participants froze as their heart rate decelerated and amount of their body sway reduced. The authors found that this abrupt reaction, so critical for the survival of some animals, has stayed with humans.
Forty-eight male volunteers stood barefoot on a stabilometric platform, to measure balance and body sway, and viewed twenty-four pictures from three different categories. They were: pleasant (sports), neutral (objects), and unpleasant (injured or mutilated humans). Posturographic and electrocardiographic recordings were collected. The author found a significant reduction in body sway along with increased muscle stiffness following the unpleasant/mutilation block of pictures compared to the neutral pictures. The number of heartbeats per minute was also lower after viewing the mutilation pictures than after looking at the others. “This pattern resembles the ‘freezing’ and ‘fear bradycardia’ seen in many species when confronted with threatening stimuli, mediated by neural circuits that promote defensive survival,” author Eliane Volchan explains.
This suggests the threat of predators - whether human or animal - was a significant selective force even in later human evolution. Else the behavior likely would have been lost by now.
Ashkenazi Jews pose two mysteries for biological science. First, why do they have so many genetic diseases that fall into just a few categories of metabolic function such as the sphingolipid storage diseases Tay-Sachs, Gaucher, Niemann-Pick, and mucolipidosis type IV? The rates of such diseases are so high that their incidence must be the result of either a recent genetic bottleneck where the Ashkenazi population was very small or natural selective pressures aimed at some other phenotype(s) selected for these genotypes due to advantages that those genotypes offer for other functionality. The second mystery is why are Jews so smart? Granted, a lot of Jews want to argue that they are just studious due to their culture. Also, lots of ideologues - particularly on the political Left - stand ready to attack anyone who argues that ethnic and racial groups differ in average intelligence. But the higher average level of Ashkenazi Jewish intelligence is so glaringly obvious that I figure anyone who tries to argue otherwise is either engaged in intellectual con artistry or is ignorant or foolish. So again, why are Jews so smart?
Well, three researchers at the University of Utah, anthropologist Henry Harpending, Gregory Cochran (a Ph.D. physicist turned genetic theorist), and Jason Hardy put forth a hypothesis that seeks to explain both mysteries simultaneously. Nicholas Wade of the New York Times has written one of the two news stories about it to date. The proposed hypothesis holds that Jews developed their genetic diseases as a side effect of strong selective pressures for higher intelligence during the Middle Ages as they were forced to work mainly in occupations that required greater cognitive ability. (same article here)
A team of scientists at the University of Utah has proposed that the unusual pattern of genetic diseases seen among Jews of central or northern European origin, or Ashkenazim, is the result of natural selection for enhanced intellectual ability.
The selective force was the restriction of Ashkenazim in medieval Europe to occupations that required more than usual mental agility, the researchers say in a paper that has been accepted by the Journal of Biosocial Science, published by Cambridge University Press in England.
The Economist has the other article about this research paper. The distribution of the Jewish genetic diseases is clustered too much into a few areas of genetic functionality This concentration of mutations argues for selective pressures as the logical explanation for rate of occurrence of these mutations in Ashkenazi Jews.
What can, however, be shown from the historical records is that European Jews at the top of their professions in the Middle Ages raised more children to adulthood than those at the bottom. Of course, that was true of successful gentiles as well. But in the Middle Ages, success in Christian society tended to be violently aristocratic (warfare and land), rather than peacefully meritocratic (banking and trade).
Put these two things together—a correlation of intelligence and success, and a correlation of success and fecundity—and you have circumstances that favour the spread of genes that enhance intelligence. The questions are, do such genes exist, and what are they if they do? Dr Cochran thinks they do exist, and that they are exactly the genes that cause the inherited diseases which afflict Ashkenazi society.
That small, reproductively isolated groups of people are susceptible to genetic disease is well known. Constant mating with even distant relatives reduces genetic diversity, and some disease genes will thus, randomly, become more common. But the very randomness of this process means there should be no discernible pattern about which disease genes increase in frequency. In the case of Ashkenazim, Dr Cochran argues, this is not the case. Most of the dozen or so disease genes that are common in them belong to one of two types: they are involved either in the storage in nerve cells of special fats called sphingolipids, which form part of the insulating outer sheaths that allow nerve cells to transmit electrical signals, or in DNA repair. The former genes cause neurological diseases, such as Tay-Sachs, Gaucher's and Niemann-Pick. The latter cause cancer.
That does not look random. And what is even less random is that in several cases the genes for particular diseases come in different varieties, each the result of an independent original mutation. This really does suggest the mutated genes are being preserved by natural selection. But it does not answer the question of how evolution can favour genetic diseases. However, in certain circumstances, evolution can.
Greg has referred to this hypothesis as "overclocking". The analogy is to overclocking computer processors (computer processing units or CPUs). Some hobbyists turn up the clocks on their desktop PCs to them run faster than they were designed to run. This can cause system instability and other problems. In the case of the Ashkenazis in Europe the hypothesis proposes that selective pressures for higher Ashkenazi intelligence were so high that it caused the propagation of mutations that pushed their intelligence up so quickly (evolutionarily speaking) that the selective pressure overrode the reduction in reproductive fitness caused by the deleterious side effects on some of those who received those mutations. The problem with overclocking is that "Sometimes you get away with it, sometimes you don't."
But I'll hazard a guess: the change accelerates some brain system tied to cognitive functioning - nearly redlines it, leaves it vulnerable to common insults in a way that can cause spectacular trouble. You might compare to overclocking a chip. Sometimes you get away with it, sometimes you don't.
More generally, if this is what I think it is, all these Ashkenazi neurological diseases are hints of ways in which one could supercharge intelligence. One, by increasing dendrite growth: two, by fooling with myelin: three, something else, whatever is happening in torsion dystonia. In some cases the difference is probably an aspect of development, not something you can turn on and off. In other cases, the effect might exist when the chemical influence is acting and disappear when the influence does. In either case, it seems likely that we could - if we wanted to - developed pharmaceutical agents that had similar effects. The first kind, those affecting development, would be something that might have to be administered early in life, maybe before birth. while the second kind would be 'smart pills' that one could pop as desired or as needed. Of course, we have to hope that we can find ways of improving safety. Would you take a pill that increased your IQ by 10 or 15 points that also had a 10% chance of putting you in a wheel chair?
Looked at from this perspective many Jews have paid and continue to pay a high price from the effects of mutations that "overclock" their brains.
This hypothesis cries out to be tested because if it is proven then, as Greg points out, these mutations point in directions for research aimed at raising human intelligence. Drugs or gene therapies that raise intelligence would have enormous economic value and one can even put a price tag on the value of higher intelligence. However, such calculations understate the economic value of higher intelligence because most of the value of scientific and technological knowledge produced by high IQ people flows to lower IQ people.
The paper is downloadable as a 40 page PDF (on big PDFs I get better results downloading to a file and then opening rather than running Acrobat Reader from within a browser).
This paper elaborates the hypothesis that the unique demography and sociology of Ashkenazim in medieval Europe selected for intelligence. Ashkenazi literacy, economic specialization, and closure to inward gene flow led to a social environment in which there was high fitness payoff to intelligence, specifically verbal and mathematical intelligence but not spatial ability. As with any regime of strong directional selection on a quantitative trait, genetic variants that were otherwise fitness reducing rose in frequency. In particular we propose that the well-known clusters of Ashkenazi genetic diseases, the sphingolipid cluster and the DNA repair cluster in particular, increase intelligence in heterozygotes. Other Ashkenazi disorders are known to increase intelligence. Although these disorders have been attributed to a bottleneck in Ashkenazi history and consequent genetic drift, there is no evidence of any bottleneck. Gene frequencies at a large number of autosomal loci show that if there was a bottleneck then subsequent gene flow from Europeans must have been very large, obliterating the effects of any bottleneck. The clustering of the disorders in only a few pathways and the presence at elevated frequency of more than one deleterious allele at many of them could not have been produced by drift. Instead these are signatures of strong and recent natural selection.
Their argument against a population bottleneck is key to their larger argument. Dismissal of the bottleneck argument leads inevitably to the argument that the frequency of these mutations that cause genetic diseases must be the result of selective pressure. If they are the result of selective pressure then the next obvious question is what was being selected for? Cochran, Harpending, and Hardy claim higher intelligence increased reproductive fitness for Jews in medieval Europe who were legally prevented from performing in occupations that had lower need for intelligence. Simultaneously Jews were allowed to work in more cognitively demanding occupations involving money handling even as the Catholic Church banned Christians from many of those same occupations.
They take their argument all the way down to the molecular level and argue that the sphingolipid mutations in some of the Jewish genetic diseases boost glucosylceramide which in turn boosts neural axon growth.
The sphingolipid storage mutations were probably favored and became common because of natural selection, yet we don’t see them in adjacent populations. We suggest that this is because the social niche favoring intelligence was key, rather than geographic location. It is unlikely that these mutations led to disease resistance in heterozygotes for two reasons. First, there is no real evidence for any disease resistance in heterozygotes (claims of TB resistance are unsupported) and most of the candidate serious diseases (smallpox, TB, bubonic plague, diarrheal diseases) affected the neighboring populations, that is people living literally across the street, as well as the Ashkenazim. Second and most important, the sphingolipid mutations look like IQ boosters. The key datum is the effect of increased levels of the storage compounds. Glucosylceramide, the Gaucher storage compound, promotes axonal growth and branching (Schwartz et al., 1995). In vitro, decreased glucosylceramide results in stunted neurons with short axons while an increase over normal levels (caused by chemically inhibiting glucocerebrosidase) increases axon length and branching. There is a similar effect in Tay-Sachs (Walkley et al., 2000; Walkley, 2003): decreased levels of GM2 ganglioside inhibit dendrite growth, while an increase over normal levels causes a marked increase in dendritogenesis. This increased dendritogenesis also occurs in Niemann-Pick type A cells, and in animal models of Tay- Sachs and Niemann-Pick.
Figure 1, from Schwartz et al. (1995) shows the effect of glucosylceramide, the sphingolipid that accumulates in Gaucher disease. These camera lucida drawings of cultured rat hippocampal neurons show the effect of fumonisin, which inhibits glucosylceramide synthesis, and of conduritol B-epoxide (CBE) which inhibits lysosomal glycocerebrosidase and leads to the accumulation of glucosylceramide, thus mimicking Gaucher disease. Decreased levels of glucosylceramide stunt neural growth, while increased levels caused increased axonal growth and branching.
Dendritogenesis appears to be a necessary step in learning. Associative learning in mice significantly increases hippocampal dendritic spine density (Leuner et al., 2003), while enriched environments are also known to increase dendrite density (Holloway, 1966). It is likely that a tendency to increased dendritogenesis (in Tay-Sachs and Niemann-Pick heterozygotes) or to increased axonal growth and branching (in Gaucher heterozygotes) facilitates learning.
Heterozygotes have half the normal amount of the lysosomal hydrolases and should show modest elevations of the sphingolipid storage compounds. A prediction is that Gaucher, Tay-Sachs, and Niemann-Pick heterozygotes will have higher tested IQ than control groups, probably on the order of 5 points.
We do have strong but indirect evidence that one of these, Gaucher disease, does indeed increase IQ. Professor Ari Zimran, who heads the Gaucher Clinic at the Shaare Zedek Medical Centre in Jerusalem, furnished us a list of occupations of 302 Gaucher patients. Because of the Israeli medical care system, these are essentially all the Gaucher patients in the country. Of the 255 patients who are not retired and not students, 81 are in occupations that ordinarily average IQ’s greater than 120. There are 13 academics, 23 engineers, 14 scientists, and 31 in other high IQ occupations like accountants, physicians, or lawyers. The government of Israel states that 1.35% of Israeli’s working age population are engineers or scientists, while in the Gaucher patient sample 37/255 or 15% are engineers or scientists. Since Ashkenazim make up 60% of the workforce in Israel, a conservative base rate for engineers and scientists among Ashkenazim is 2.25% assuming that all engineers and scientists are Ashkenazim. With this rate, we expect 6 in our sample and we observe 37. The probability of 37 or more scientists and engineers in oursample, given a base rate of 2.25%, is approximately 4 x 10-19 . There are 5 physicists in the sample, while there is an equal number, 5, of unskilled workers. In the United States the fraction of people with undergraduate or higher degrees in physics is about one in one thousand. If this fraction applies even approximately to Israel the expected number of physicists in our sample is 0.25 while we observe 5. Gaucher patients are clearly a very high IQ subsample of the general population.
Are there Ashkenazi mutations other than these sphingolipid storage disorders that likely became common because of strong selection for IQ? There are several candidates.
Ever since torsion dystonia among the Ashkenazim was first recognized, observers have commented on the unusual intelligence of patients. Flatau and Sterling (Eldridge, 1976) describe their first patient as showing “an intellectual development far exceeding his age”, and their second patient as showing “extraordinary mental development for his age.” At least ten other reports in the literature have made similar comments. Eldridge (1970, 1976) studied 14 Jewish torison dystonia patients: he found that their average IQ before the onset of symptoms was 121, compared to an averge score of 111 in a control group of 14 unrelated Jewish children matched for age, sex, and school district. Riklan and colleagues found that 15 Jewish patients with no family history of dystonia (typical of DYT1 dystonia) had an average verbal IQ of 117 (Eldridge, 1979; Riklan et al., 1976).
If this hypothesis is correct (and I believe it is) then it is problematic for efforts to raise human intelligence. How many of the intelligence raising genetic variants bring undesirable side effects? Some scientists speculate that assortive mating of high IQ people is contributing to a rising incidence of autism and Asperger's Syndrome. As smart people become more likely to breed with other smart people the odds increase that pairs of autosomal recessives or other problematic combinations of intelligence boosting genes will be inherited by offspring.
Has human intelligence been selected for so rapidly in the last couple of thousand years that a large portion of all intelligence boosting mutations have undesirable side effects? When a selective pressure is strong early adaptations will have side effects. Henry Harpending explained in the gnxp.com thread on this subject:
Re mechanism: The argument (well known to breeders where there is no argument) goes like this:
In a drastic new environment there is big fitness payoff to IQ. In this new environment there is a payoff to "turning down" BRCA1 to free up early CNS development but at the cost of higher cancer rates later in life. Eventually, especially in a big population, a BRCA1 variant with the optimum activity will show up. Meanwhile carriers of one normal and one broken BRCA1 gene have a big fitness advantage because they have, say, 90% of normal suppression of early CNS development. So the broken BRCA1 allele is favored by selection even though homozygotes for it die. After a long time it would be replaced by the optimum allele but it takes a long time for that optimum allele to show up.
Exactly this argument applies to myostatin in several European breeds of beef cattle: it causes muscle hypertrophy and obstetric difficulties. The muscle hypertrophy is good but the obstetric difficulties require veterinarians and in the wild would have been lethal.
Re the implications of our model for eugenics, yes, big time, eugenics is IMHO a route to disaster. Well understood engineered gene introductions could be fine but eugenics would be almost certain to bring all kinds of nightmares.
But keep in mind that the human race already has many genetic variations to choose from that contribute to determining cognitive ability. A massive comparison of DNA sequence information between hundreds of thousands of people combined with IQ testing and collection of a lot of life history and medical history information could demonstrate many of the positive and negative effects of each genetic variation which affects cognitive function. Likely some will be better optimized to provide a cognitive boost without much downside.
Advances in biotechnology will provide ways to avoid some of the harmful side effects of these "overclocking" mutations. One way to accomplish this would be to discover regulatory regions in the genome that could be harnessed to selectively turn on the mutated genes only in the nervous system and turn on normal versions of these genes only in cells outside of the nervous system.
I've got to state the obvious because the obvious is politically incorrect: If smart people have more babies than dumb people the average IQ will rise. If dumb people have more babies than smart people then the average IQ will drop. I'm guessing the latter is currently happening. Bummer dudes.
Proof of this hypothesis would point scientists in the direction of genes to look at for intelligence enhancement. For example, if the mutation for Gaucher's disease causes an IQ boost then drugs that increase the level of glucosylceramide in neurons might accelerate learning by increasing the rate of axon growth to connect neurons to each other.
The hypothesis could be tested fairly rapidly. Recruit some thousands of Ashkenazi Jews to take IQ tests and to have a few dozen genes tested for assorted genetic variations. Compare the IQ test results to the genetic tests and see if all the known genetic variations in sphingolipid storage metabolism, DNA repair, and several other categories account for a large proportion of Ashkenazi Jewish genetic variations.
We also need to find out whether these various potential intelligence boosting mutations have differing effects from each other on other aspects of cognition. Anyone recruited into testing the hypothesis should also have information collected on their mental health, personality, preferences, values, educational history, occupation, income, criminal record, and anything else that might provide clues as the effects of these mutations on cognitive function. For example, do some IQ-boosting mutations favor a career in law whereas others favor a career in medicine or science or math?
Jewish efforts to avoid passing along genes that have harmful effects might be lowering average Jewish intelligence. Some of the genetic variants (e.g. the genes underlying Tay-Sachs, Gaucher, and Niemann-Pick diseases) are autosomal recessive and therefore cause diseases only when a person has two copies of them. If having single copies of these genetic variations boosts intelligence but Jewish couples engage in practices that reduce the number of copies they pass along in general (e.g. by using pre-implantation genetic diagnosis to choose an embryo that has 0 copies of a mutation) then that will reduce the number of Jewish babies born with single copies and therefore if the hypothesis is correct then the resulting babies will be less bright than the average Ashkenazi Jew.
Should the hypothesis be proven then Jewish breeding practices could be adjusted to maximize the benefit of intelligence boosting genetic variations while avoiding the harmful effects. Ideally each child should get one and only one copy of each genetic variation that is autosomal recessive for diseases. Get the intelligence boosting benefit of a single copy while avoiding the diseases that come from having two copies. To execute this strategy a Jewish person would need to get genetically tested and then look for a mate who has complementary mutations for higher intelligence.
If each member of a couple has one copy of an autosomal recessive mutation then, on average, 2 out of 4 pregnancies they start will have the exact 1 desired recessive mutation. But 1 of the other 4 pregnancies will have 2 copies and hence would result in genetic disease. The other 1 of the 4 pregnancies would not have the IQ boosting genetic mutation and hence would not be as smart. If the couple each have the same 3 different autosomal recessives mutations that each boost IQ then the odds of getting a baby that has exactly 1 copy of each of the 3 mutations is only 1 in 8.
The low odds of getting all the desired mutations with the optimal number of copies of each mutation poses a big problem to aspiring eugenicists whether Jewish or non-Jewish. One biotechnological approach to solving this problem would use microfluidics devices to separate and identify each chromosome from a cell to get just exactly the set of chromosomes from each parent chosen for an optimal trade-off of cognitive ability and other qualities. Then somehow insert all those chromosomes back into a cell and kick it into an embryonic state. But we are probably 10 or 20 years away from having such a capability.
Every time a man or woman chooses someone to mate with they are making choices based on the appearances, status, demonstrated intelligence, and other qualities of that person. Women attracted to rock stars, movie stars, and sports stars are driven by genetically caused eugenic desires.
Use of genetic tests to choose a mate is already done to avoid passing on harmful mutations to offspring. This practice will become much more widespread as the significance of more genetic variations becomes known. The negative connotations associated with the term eugenics are already wearing off. As more people can derive benefits from the use of genetic information to guide reproductive decisions eugenic practices will become very widespread. When that happens the term eugenics may be replaced by a different term that effectively means the same thing. But regardless of what it gets called eugenics will become widely accepted and practiced.
Step back and look at Jewish and European history from the context of this hypothesis. A few things come to mind. First off, Middle Ages bans on Christian money lending created an environmental niche in which high IQ was selected for in Jews. This led to a few important historical consequences. First off, it led to financial and reproductive success of urban Jews and hence resentment against them by both elites and masses in Europe. This resentment of course led to pogroms and Hitler's "Final Solution". There's an old Japanese saying that comes to mind: "The nail that sticks up gets hammered down". Well, smart Jews stood out and the response of jealousy and resentment against the more successful "other" is a recurring theme in human history.
But here's the twist: Catholic usury restrictions, by creating an environmental niche that selected for higher Ashkenazi IQs, therefore made possible the eventual return of Jews to Israel. An ethnic group of much lower intelligence never would have been able to pull off the creation and defense of a state in that location against such hostile neighbors.
The persecutions of Jews can also be seen in the context of successful minorities around the world. Yale law professor Amy Chua wrote a book about persecution of economically successful minorities entitled World on Fire: How Exporting Free Market Democracy Breeds Ethnic Hatred and Global Instability where she describes attacks in a number of countries (e.g. Indonesia) against Chinese and other groups that are minorities that are economically more successful than the majorities in countries where they live.
Suppose the successful minorities who are persecuted are successful as a result of genetically caused higher intelligence or perhaps due to other genetically controlled cognitive qualities. When this becomes proven scientifically and becomes widely known will the knowledge lead to more or less persecution of cognitively more able and more successful ethnic groups? For example, will Malaysians or Indonesians resent Chinese people even more if genetically caused higher intelligence in Chinese becomes the accepted explanation for greater Chinese economic success in Malaysia and Indonesia? Or will lower class people become more willing to accept their lots in life if group average differences in genetic endowments for cognitive ability are shown to be responsible for the bulk of inter-group differences in incomes, wealth, achievement, and status?
If you are interested in the evolution of human intelligence, the methods by which evolution has changed the human brain to make it smarter, or how changes in human societies can cause changes in natural selective pressure on human evolution then read this paper. If you are interested in the prospects for future intelligence enhancement then, again, read it. If you are interested in the causes interracial conflict or if you are interested in how religious and cultural practices can exert selective pressures on human populations then read it. If you want to dispute the hypothesis then read the full paper and examine their evidence before trying to disagree.
The savage persecutions suffered by Jews suggest that high intelligence can generate resentment among the masses. No doubt there will be some who will suggest that the Cochran-Harpending paper should have been suppressed to prevent awareness of the secret of Ashkenazi intelligence from seeping out.
But you have to be a true-blue intellectual to assume that the only way anybody would ever notice anything as obvious as Jewish brainpower is if it gets mentioned in the New York Times. Political correctness doesn't keep facts from being talked about—just from being written about in an intelligent, constructive manner.
Yes, everyone thinks Jews are smarter, even many people who publically deny they believe this. Persecutions of smart minorities happen already. An honest accurate discussion of the causes of resentment smarter and more successful groups would, in my view, make it easier to ameliorate the causes of resentment between ethnic groups. I think people would be less prone to ascribe Jewish successes to conspiracies if Jews were accepted as being smarter for genetic reasons. High IQ genes cause higher intelligence. Higher intelligence increases productivity when learning and working. Hence greater wealth. That's a lot less reason for resentment than the idea that some group is no more productive but engages in conspiracies to take from others.
Steve thinks the Parsis have managed to achieve great success while generating less resentment from other groups.
On the other hand, the happier experience of another ethnic minority that may also have evolved stronger intellectual capacities under similar urban conditions—the prosperous Parsis of Bombay—may offer clues to mitigating envy.
I wonder if the Parsis were able to do this simply because India was broken up into so many castes that the Parsis had a hard time being noticed by the average Indian.
In any case, the Cochran-Harpending paper offers a fairly new but crucial perspective on the old nature and nurture question. The researchers have demonstrated that it's quite possible for nurture to change nature. Culture can drive heredity. Economics and social customs alter gene frequencies.
This is an incredibly important point. Currently genetic variations for higher intelligence are being selected against in industrialised societies. We've probably changed selective pressures in other ways. But at this point I can only guess as to those chances. Are introverts or extroverts more or less likely to reproduce relative to each other than in the past? I don't know. Are genes for height being selected for? My guess is yes. The genes for obesity might be getting selected for in modern societies. I would have expected heavier weight people to have a harder time finding mates and hence be less likely to reproduce. But perhaps obese people are willing to settle for less desirable mates due to their own perceived lower attractiveness and hence they spend less time searching for for the ideal mate and hence start reproducing sooner and in greater numbers.
Humanity has not escaped from natural selection. The genes that code for the brain are not immune to the pressures of natural selection. Anyone remember the tune "Elvis is everywhere"? Well, "Darwin is everywhere".
Given that modern genetic technology will soon make it easy to ensure that a child has exactly one copy of such a gene, it seems like this sort of thing is a “low-hanging fruit” for genetic engineering. If such a gene is common, then having one copy is probably an evolutionary advantage - otherwise it would be (mildly) selected against. The main disadvantage is the chance that your kids might end up with two copies of the recessive, so if technology can prevent that, now you just have upside. I wouldn’t be suprised if it soon becomes common to give your offspring many such genes - which would have the side effect of making it impossible for them to reproduce with similarly endowed partners without using genetic engineering.
The problem is if you have a lot of recessives boost intelligence when you have a single copy and your mate has them too then the odds would be very low that your offspring would not get two copies of at least one of the genes. Given that these genes cause diseases when you get two copies that would make natural reproduction very risky for offspring.
The obvious solution to this problem is to adjust these genes with additional regulatory mechanisms to make them no longer cause diseases when two copies are present. But development of such regulatory mechanisms requires additional and difficult genetic engineering work.
March 2009 Update: This work has since become part of the basis of an excellent book by Cochran and Harpending entitled The 10,000 Year Explosion: How Civilization Accelerated Human Evolution.
The genes that regulate brain development and function evolved much more rapidly in humans than in nonhuman primates and other mammals because of natural selection processes unique to the human lineage. Researchers reported their findings in the cover article of the Dec. 29, 2004, issue of the journal Cell.
"Humans evolved their cognitive abilities not due to a few accidental mutations, but rather, from an enormous number of mutations acquired though exceptionally intense selection favoring more complex cognitive abilities," said lead scientist Bruce Lahn, an assistant professor of human genetics at the University of Chicago and an investigator at the Howard Hughes Medical Institute.
"We tend to think of our own species as categorically different – being on the top of the food chain," Lahn said. "There is some justification for that."
From a genetic point of view, some scientists thought that human evolution might be a recapitulation of the typical molecular evolutionary process, he said. For example, the evolution of the larger brain might be due to the same processes that led to the evolution of a larger antler or a longer tusk. It's just a particular feature that is exaggerated in the human species.
"We've proven that there is a big distinction. Human evolution is, in fact, a privileged process because it involves a large number of mutations in a large number of genes," Lahn said. "To accomplish so much in so little evolutionary time – a few tens of millions of years – requires a selective process that is perhaps categorically different from the typical processes of acquiring new biological traits."
Generally speaking, the higher up the evolutionary tree, the bigger and more complex the brain becomes (after scaling to body size). But this moderate trend became a huge leap during human evolution. The human brain is exceptionally larger and more complex than the brains of nonhuman primates, including man's closest relative, the chimpanzee.
One way to study evolution at the molecular level is to examine changes of when and where proteins are expressed in the body. "But there are many challenges to study the evolution of protein expression. Instead, we chose to track structural changes in proteins," said graduate student Eric Vallender, lead author of the article along with former graduate student Steve Dorus, both of Lahn's laboratory.
Researchers examined the DNA of 214 genes involved in brain development and function in four species: humans, macaques (an Old World monkey), rats and mice. (Primates split from rodents about 80 million years ago; humans split from macaques 20 million to 25 million years ago; and rats split from mice 16 million to 23 million years ago.)
For each of these brain-related genes, they identified changes that altered the structure of the resulting protein, as well as those that did not affect protein structure. Only those genetic changes that alter protein structure are likely to be subject to evolutionary selection, Lahn said. Changes in the gene that do not alter the protein indicate the overall mutation rate – the background of random mutations from which evolutionary changes arise, known as the gene's molecular clock. The ratio of the two types of changes gives a measure of the pressure of natural selection driving the evolution of the gene.
Researchers found that brain-related genes evolved much faster in humans and macaques than in rats and mice. Additionally, the human lineage has a higher rate of protein changes than the macaque lineage. Similarly, the human lineage has a higher rate than the chimpanzee lineage.
"For brain-related genes, the amount of evolution in the lineage leading to humans is far greater than the other species we have examined," Lahn said. "This is based on an extensive set of genes."
They argue that a significant fraction of genes in the human genome were impacted by this selective process. The researchers estimate there may have been thousands of mutations in thousands of genes that contributed to the evolution of the human brain. This "staggering" number of mutations suggests that the human lineage was driven by intense selection process.
The study also revealed two dozen "outliers" – those genes with the fastest evolutionary rates in the human lineage. Of these, 17 are involved in controlling brain size and behavior, arguing that genes that affect brain size and behavior are preferential targets of selection during human evolution. Lahn and his colleagues now are focusing on these outlier genes, which may reveal more about how the human brain became bigger and better.
For two of these outliers, ASPM and Microcephalin, previous work from Lahn's group already has implicated them in the evolutionary enlargement of the human brain. Loss-of-function mutations in either ASPM or Microcephalin cause microcephaly in humans – a severe reduction in the size of the cerebral cortex, the part of the brain responsible for planning, abstract reasoning and other higher cognitive function.
One of the study's major surprises is the relatively large number of genes that have contributed to human brain evolution. "For a long time, people have debated about the genetic underpinning of human brain evolution," said Lahn. "Is it a few mutations in a few genes, a lot of mutations in a few genes, or a lot of mutations in a lot of genes? The answer appears to be a lot of mutations in a lot of genes. We've done a rough calculation that the evolution of the human brain probably involves hundreds if not thousands of mutations in perhaps hundreds or thousands of genes -- and even that is a conservative estimate."
It is nothing short of spectacular that so many mutations in so many genes were acquired during the mere 20-25 million years of time in the evolutionary lineage leading to humans, according to Lahn. This means that selection has worked "extra-hard" during human evolution to create the powerful brain that exists in humans.
Lahn further speculated that the strong selection for better brains may still be ongoing in the present-day human populations. Why the human lineage experienced such intensified selection for better brains but not other species is an open question. Lahn believes that answers to this important question will come not just from the biological sciences but from the social sciences as well. It is perhaps the complex social structures and cultural behaviors unique in human ancestors that fueled the rapid evolution of the brain. "This paper is going to open up lots of discussion," Lahn said. "We have to start thinking about how social structures and cultural behaviors in the lineage leading to humans differed from that in other lineages, and how such differences have powered human evolution in a unique manner. To me, that is the most exciting part of this paper."
Though I am skeptical that better brains are being selected for today. In industrial countries smarter people have fewer kids. So how are better brains still being selected for? I don't see it.
His research and speculations put Lahn into politically incorrect territory. The idea that human brains are still under selective pressure (which is extremely obvious in my view) opens up the possibility that different human environments have been and still are selecting for cognitively different humans. If humans are being selected for to be better suited for each enviromental niche that humans have occupied and currently occupy then humans have less in common with each other than radical egalitarians would like us to believe.
These brain genes that Lahn found to have undergone so many changes leading to humans are excellent candidates for genes that cause changes in intelligence between humans. My guess is that within 10 years DNA sequencing costs will be so low that large scale comparisons of Lahn's genes of interest will be possible using humans with different measured levels of IQ. Then we will find out which genetic variations cause higher levels of intelligence and also different patterns and styles of thinking. For example, I fully expect genetic variations that cause conservative and left-liberal and other categories of political attitudes will be found.
Also see my previous posts on Bruce Lahn's research on human brain genetics and brain evolution: Researchers Find Key Gene For Evolution Of Human Intelligence and Human Brain Size Regulating Gene To Be Inserted Into Mice and Genetic Causes Of Infidelity Found In Twins Study.
Update: Godless Capitalist has more coverage of this story.
David Stephens, a biologist at the University of Minnesota thinks some people hobbled by excessive impulsiveness because their ancestors benefitted from the behavior.
The new experiments were modeled on how animals encounter and exploit food clumps. The jays encountered one clump at a time and obtained some food from it. Then they had to decide whether to wait for a bit more from the same clump or leave and search for another clump. Not surprisingly, the birds still acted impulsively, preferring items they could get quickly. They considered only the size and wait time for their next reward--never a reward beyond that, even though it may have been bigger.
What did surprise Stephens was that the birds that went for the immediate reward were able to "earn" as much or more food in the long run as birds that were forced to wait for the larger reward or to follow a mixed strategy. The reason, he said, was that in the wild, animals aren't faced with an either-or choice of "small reward now or big reward later." What happens is that when they find a small bit of food, they don't wait; they just go back to foraging, and they may find lots of little rewards that add up to more than what they would get if they had to hang around waiting for bigger and better.
"Animals, I think, come with a hardwired rule that says, 'Don't look too far in the future,'" Stephens said. "Being impulsive works really well because after grabbing the food, they can forget it and go back to their original foraging behavior. That behavior can achieve high long-term gains even if it's impulsive."
The work may apply to humans, he said, because taking rewards without hesitation may have paid off for our foraging ancestors, as it does for blue jays and other foragers. Modern society forces us to make either-or decisions about delayed benefits such as education, investment and marriage; the impulsive rules that work well for foragers do more harm than good when applied in these situations.
"Impulsiveness is considered a big behavior problem for humans," said Stephens. "Some humans do better at binary decisions like 'a little now or a lot later' than others. When psychologists study kids who are good at waiting for a reward, they find those kids generallly do better in life. It looks as though this is a key to success in the modern world, so why is it so hard for us to accept delays? The answer may be because we evolved as foragers who encountered no penalties for taking resources impulsively.
We are no longer in the environments our ancestors evolved in. We have changed and continue to change our environments. Since natural selection takes many generations to adjust a species to environmental changes humans just are not adapted to the environments we are creating with technology. So Stephens' argument strikes me as very plausible.
Humans are going to have to adapt themselves and their offspring to modern environments. Successful adaptation will require the development of drugs, gene therapies, and stem cell therapies to adjust brains to be more adaptive and compatible with modern environments.