You're So Special!

In the past few years the two of us and our colleagues have come on especially intriguing suspects that seem to operate more in the brain than in other tissues: jumping genes. Such genes, which have been found in virtually all species, including humans, can paste copies of themselves into other parts of the genome (the full set of DNA in the nucleus) and alter the functioning of the affected cell, making it behave differently from an otherwise identical cell right next to it. Many such insertions in many different cells would be expected to yield subtle or not so subtle differences in cognitive abilities, personality traits and susceptibility to neurological problems. _SciAm

This animation by Muotri and Marchetto shows the higher rate of activity of the jumping genes in the Rett-afflicted cells (more green dots) than in the WT (wild type) ones. (The olfactory bulb is shown in red, the striatum in magenta and the cerebellum in cyan.) _SciAm

Jumping gene transposons are capable of inserting significant differences in the gene expression of identical twins. When these differences are inserted into brain cell DNA, they can cause identical twins to behave and perform differently from one another. Scientists have barely begun to understand how important this mechanism is to both long term evolution and rapid short term variation.

Nature to scientists: "Everything you think you know, just ain't so!"

Retrotransposons make up as much as half of the nucleotides, or DNA building blocks, in the human genome. In contrast, the approximately 25,000 protein-coding genes we possess make up less than 2 percent of mammalian DNA. The jumping genes are descendants of the first primitive molecular replication systems that invaded the genomes of eukaryotes (organisms having cells that contain a nucleus) long ago. A group led by Haig H. Kazazian, Jr., at the University of Pennsylvania showed in 1988 that retrotransposons, which were once thought of as nonfunctional junk DNA, were active in human tissues.

...Retrotransposition often fails to run its course, which produces truncated, nonfunctional copies of the original L1 DNA. Sometimes these snippets (or the whole L1 copy) have no effect on a protein-coding gene. Other times, though, they can have any of several consequences, both good and bad, for a cell’s fate. They may, for instance, drop into and thus alter the protein-coding region of a gene. This maneuver can lead to creation of a new variant of the protein that helps or harms an organism. Or this positioning may stop a given protein from being made. In other instances, the newly pasted DNA may fall outside of a coding region but act as a promoter (a switch that can turn on nearby genes) and alter the level of gene expression—the amount of protein made from the gene—with, once again, good or bad results for the cell and the organism. When LI retrotransposons end up in many places in neurons or in many cells of the brain, or both, the brain will be very different from the one that would have formed without their influence. It stands to reason that such genetic mosaicism could affect behavior, cognition and disease risk and could also help explain why one identical twin may remain disease-free when a sibling is diagnosed with schizophrenia, for example.

...The continuing research into jumping genes in the brain could potentially challenge an entire academic discipline. Behavioral geneticists often follow groups of identical twins over long periods to control for the effects of genes and determine the environmental contributions to such disorders as schizophrenia. The new findings showing that jumping genes actively revise genomes after an embryo forms question the assumption that “identical” twins are genetically alike. Indeed, the new discoveries will make it ever harder to disentangle the relative effects of nature and nurture on our psyches.

The question remains: Why has evolution not destroyed these vestiges of ancient viruses from within our cells, given that jumping genes have a high chance of introducing potentially fatal genetic flaws? To answer the question, we should acknowledge that humans have always been under attack by viral parasites and other invaders that expand the size of our genomes with jumping DNA. The bodies of humans and our evolutionary forebears may not have been able to fully eliminate the interlopers, but they have adapted to at least coexist with the invaders by silencing them through a variety of clever mechanisms that mutate and disable them. It also appears that, in some cases, our genomes have commandeered the genetic machinery of L1 retroelements to enhance our own survival, which is one reason that cells may sometimes allow, or even encourage, L1s to jump around the genome under carefully controlled conditions. _SciAm

Evolution has always been something of a crap shoot. The wider the range of variation that can be generated, the more likely to find suitable fits for various environmental niches.

What does this mean for the genetics of behaviour and intelligence differences? It means quite the opposite of what the authors above suggest. In the past, behavioural differences in identical twins have been attributed largely to differences in non-shared environment. Now we know better. Rather than detracting from the importance of the genes in influencing behaviours and aptitudes, this research intensifies the importance of genes and gene regulation.

Humans, Apes, Addicts, and Microbes: Their Common Thread

The common thread that links life on Earth is the thin thread of DNA that coils, circles, and works its way through the generations, through the species, changing the face of the planet as it evolves.

Economist
Our brains are formed by our genes, working through the environment. Some genes control an entire platoon of other genes. The genes that determine how our brains grow and function are still evolving. If these "commander" genes evolve, remarkable changes can occur over a fairly short time span. The human species appears to be changing on a more rapid time scale than most scientists are willing to accept.

...human beings have suites of genes that probably cause their brains to be “plastic” and thus receptive to change far longer (to the age of about five) than is true for chimps or monkeys (whose brains are plastic for less than a year after birth). Moreover, Dr Khaitovich was able to work out how the expression of these modules of genes was co-ordinated, by looking at the switches, known as transcription factors, that turn them on and off.

Indeed, by comparing modern genomes with their discoveries about Neanderthals Dr Paabo’s group has found that the regulatory process for one of the modules came into existence after the modern human and Neanderthal lines separated from one another, about 300,000 years ago. _Economist

Of course, it does no good to have brains that are more plastic, if the caregivers of young children do not take advantage of that period of plasticity to give the children skills, competencies, wisdom, and knowledge that will serve them well throughout their lives.

Some people may be born at a tremendous disadvantage, genetically speaking. Addictive and criminal behaviour appear to be at least partially heritable. Societies deal with these problems in different ways. There is always room for improvement -- beginning with the acknowledgement of the genetic component.

Humans have turned a corner in understanding their own genetics. They can now re-program the genes of living humans, and are on the verge of re-programming the genes of embryos and zygotes. Artificial evolution, in other words.

Humans are also making progress toward understanding the complex genetics of their environments -- the microbial world in which they are immersed. We live in microbial soup, which is quite difficult to sort out with the old genetic tools that required culturing organisms before their genomes could be sequenced.

Now, scientists can extract individual genomes out of the common slurry, and sequence these mystery guests.

To extract individual genomes, Armbrust’s PhD student Vaughn Iverson exploited skills that had he gained as a computer scientist designing video compression technology at Intel in Portland, Oregon. He developed a computational method to break the stitched metagenome into chunks that could be separated into different types of organisms. He was then able to assemble the complete genome of Euryarchaeota, even though it was rare within the sample. He plans to release the software over the next six months.

It’s a different tack from that taken by early marine metagenomics efforts, which began in earnest with Craig Venter’s Global Ocean Sampling effort in 20032. “Our survey offered a broad-stroke picture of microbial diversity and the dominant players in the world’s oceans,” says Kenneth Nealson, director of the microbial and environmental genomics group at the J. Craig Venter Institute in San Diego, California. “This clever approach demonstrates that they can pull out the sequence of uncultured organisms — information we need to get a clue as to how microbes share limiting resources in the ocean.” _Nature

We finally understand that it is necessary to understand the full complement and range of genomics, genetics, and epigenetics in which we live -- and how we interact with this milieu in order to work out our lives.

Genetics and evolution have been underrated and ignored by most human intellectuals. But no one -- including these neglectful intellectuals -- is ignored by the genetic universe we inhabit. Not one living thing.

Cross-posted from Al Fin, the Next Level

Human Intelligence Comes from the Genes

LAMC3 Gene and Effect on Brain Convolutions
The difference between the brain on the left above and the brain on the right, comes from a single gene -- LAMC3 -- which influences the formation of convolutions in the cerebral cortex. Brain convolutions allow for much greater volume of cerebral cortex, which is associated with the higher intelligence seen in apes, cetaceans, and humans (one of the apes). An alteration of the nucleic acid sequence in the LAMC3 gene in humans can apparently lead to the loss of convolutions in the cortex in affected individuals, as seen in the image above.

The folding of the brain is seen only in mammals with larger brains, such as dolphins and apes, and is most pronounced in humans. These fissures expand the surface area of the cerebral cortex and allow for complex thought and reasoning without taking up more space in the skull. Such foldings aren't seen in mammals such as rodents or other animals. Despite the importance of these foldings, no one has been able to explain how the brain manages to create them. The LAMC3 gene – involved in cell adhesion that plays a key role in embryonic development – may be crucial to the process.

An analysis of the gene shows that it is expressed during the embryonic period that is vital to the formation of dendrites, which form synapses or connections between brain cells. "Although the same gene is present in lower organisms with smooth brains such as mice, somehow over time, it has evolved to gain novel functions that are fundamental for human occipital cortex formation and its mutation leads to the loss of surface convolutions, a hallmark of the human brain," Gunel said. _Medicalxpress

Thousands of genes take part in the intricate developmental dance of forming the central nervous system in all its complexity. But specific genes play more dominant roles in differentiating human brains from brains of "lower" animals.

Genes control the size of particular systems and components of the brain which are instrumental in providing for more rapid mental processing and more complex processing. Some brains can hold more ideas in the mind simultaneously, while performing transformative operations on those ideas. "Human calculators" capable of computing solutions to complex arithmetical and mathematical problems in their heads, are one obvious example. But the mental machinations of scientific theorists, elite diagnosticians, and top level novelists, illustrate the same type of differentiation of mental ability -- largely originating at the genetic level.

James Watson -- one of the discoverers of the modern genetic theory of DNA inheritance -- received almost universal condemnation for expressing a few elementary facts of human genetic biodiversity. Here is some background information concerning that shameful episode of modern human culture and its prejudices:

GNXP: James Watson tells the Inconvenient Truth

Slate: Created Equal [AF Note: After being threatened with a similar fate as that of Watson, the much beaten-down Saletan (author of the slate piece above) published a "mea culpa" and submitted to the PC inquisition]

Useful PDF article from Robert Plomin discussing Genes and Intelligence

It is critical to understand how many genes are involved in weaving the fabric of higher intelligence. It is not a question of finding THE GENE for intelligence. Rather it is a question of understanding how all the many genes which create the potential for intelligence, work together.

And it is important to become a bit more sophisticated about how a crucial variability in gene expression can occur -- even when conventional genetic analyses fail to distinguish between two genomes.

Humans are not all the same. In fact, no two humans are exactly the same -- even identical twins. This is true for reasons of gene expression, in all its many levels of complexity -- both known and unknown. These differences can also originate from differences in experience and culture, as in when identical twins are separated at birth and raised in entirely different environments. But even then, the powerful impact of genes on the life outcome of the separated twins is all to obvious.

IQ is not everything. Executive Function (EF) is also crucial to life success. But EF is perhaps even more heritable than IQ. That is why it is so crucial to take advantage of a child's critical developmental windows for boosting the components of competent thinking, acting, and planning when one can. After that time period passes, it is mostly too late for those at the greatest genetic disadvantage.

"Flynn Effect" Contradicts Heritability of Intelligence?

One of the quickest paths to career suicide for an academic or any public figure, is to assert that human intelligence is genetically bounded, and roughly 50 - 80% heritable. The preponderance of scientific evidence points toward a genetic limiting of the "g factor", commonly associated with intelligence, with substantiating research coming from China. And yet the existence of the "Flynn Effect" -- the apparent rise in IQ test scores across several national populations over the past century -- has led many people to suggest that the IQ measure is too changeable to be a true indication of genetically "determined" intelligence.

Average IQ scores in many nations have apparently risen by between 5 points and 25 points per generation, over much of the past century. The increase has come largely in the measure of "fluid intelligence," which is one measure of problem-solving capacity.

Explanations for this general, but uneven, trend include better nutrition, better education and familiarity with testing, a more stimulating childhood environment, better control of childhood infectious disease, and an increase in hybrid vigour from less inbreeding of populations. Changes in variance for the different sample distributions can also introduce problems in interpreting such a trend.

The issues of general human intelligence, and the genetics of intelligence, are complex and multi-factorial. Many genetic and epigenetic factors are involved in the "biological bounding" of human intelligence, as well as other biological and environmental factors which bear on gene expression.

It is never a question of "either genetics or environment," but is always both. Thus it is not a question of genetic "determination" of intelligence, but rather a genetic bounding of intelligence. It can be easier to understand that measures such as height potential or "tallness" are "genetically bound" (in the absence of hGH and other exogenously administered growth factors). Similarly, intelligence potential is genetically bound in the absence of NZT or other hypothetical efficacious brain boosters.

So are people really getting smarter? The Flynn effect does not seem to be particularly relevant to the high IQ end of the distribution. So the smarter people do not seem to be getting smarter. But part of the lower end of the distribution seems to have moved toward the middle, and parts of the middle may have moved toward the higher end, on IQ test scores.

"Flynn Effect" improvements in scores seem to have slowed consiberably in advanced nations over the past 20 years. Whatever the cause of the trend, it may have largely played itself out in those nations. But if better nutrition, higher levels of stimulation, and lower infectious disease load are at least partially responsible for the trend of rising IQ scores, we should expect improvements in scores across the more impoverished areas of the third world which are able to move out of poverty.

How much of an improvement? One possible answer would be to look at the children of affluent persons in third world nations, as a "preview of coming scores." Rich people's children are generally provided with the best medical care, education, and generally more intellectually stimulating environments. Look at the top end of performance for the most advantaged children in these countries. What do you find?

You will find the "gifted" and "advantaged" in countries across Subsaharan Africa topping out at 1 standard deviation below average populations of the advanced world and about 2 standard deviations below gifted children in the advanced world. In most of tribal Asia, gifted and advantaged groups top out at roughly 1 standard deviation below their counterparts in advanced countries -- higher than Africans but significantly lower on average than East Asians and Europeans.

Similarly, you can look at the segment of African American children in the US which is most advantaged and gifted, and find persistent IQ score gaps between this group and far less advantaged European and East Asian children -- who nonetheless score higher on IQ and aptitude tests than their more advantaged black cohorts.

It is wrong to assume that the Flynn Effect will raise the overall average human IQ score of Earth, and it is wrong to assume that it will equalise IQ scores between population groups which have maintained stable and long-lasting differences in IQ scores over time.

Whenever nutrition, education, medical care, and intellectual stimulation are roughly equal, the genetic component in bounding intelligence comes to the forefront. Of course there is always room to improve on all those counts -- and on other determinants of intelligence which have not yet been discovered or delineated. But underneath it all, is the genetic component which will never be equalised, but which may well be compensated for with clever science and technology, in the future.

Al Fin cognitive scientists and psychometricians feel that the nutritional and infectious disease components were of limited relevance to the Flynn Effect in the advanced world since the 1940s -- except among truly impoverished populations, which are rare in the western developed world. Other explanations for the increase in scores which are more likely include increased early childhood stimulation and a greater familiarity with test taking.

The "critical window of development" theory is likely to be quite pertinent to the Flynn Effect in western populations over the past century. If a child is exposed to language, music, math, executive function training, and certain types of abstract thinking within the critical developmental timeframe, it is more likely that he will emerge from that period with better developed skills.

IQ gains in childhood that come from a highly stimulatory intellectual environment may not be permanent, however. And not all children will tolerate such external manipulations well. But the more cognitive and behavioural competencies the child is given at an early age (within reason), the more likely he will be to retain at least some of them. Each child is an individual and should be treated as such.

In conclusion, the Flynn Effect is a variable and limited trend in the rise of IQ scores across many nations. It should be yet another reminder of the remarkable complexity of human intelligence and behaviour, all of which derive ultimately from the human genome.

Megafoundation links and views on intelligence

Clear Genetic Links to Poor Impulse Control, Drug Dependency

University of Michigan medical researchers have identified genetic links to aberrant brain function leading to alcohol and drug dependencies.

The results, published online April 12 in Molecular Psychiatry, suggest that variations in the GABRA2 gene contribute to the risk of alcoholism by influencing impulsive behaviors, at least in part through a portion of the cerebral cortex known as the insula, says study senior author Margit Burmeister, Ph.D., research professor at U-M's Molecular and Behavioral Neuroscience Institute.

...Individuals under distress who also have the risky genetic variant tend to act impulsively, a behavior that may lead to the development of alcohol problems, says lead author Sandra Villafuerte, Ph.D., a research investigator at U-M's Molecular and Behavioral Neuroscience Institute and Department of Psychiatry.

"Developing deeper understandings of the various genetic and environmental factors involved in risky behaviors may guide prevention and treatment efforts in the future," Villafuerte says.

The study included 449 people, who came from 173 families – 129 of whom had at least one member diagnosed with alcohol dependence or abuse. Those with certain variations in the GABRA2 gene were more likely to have alcohol dependence symptoms and higher measures of impulsiveness in response to distress, the study found. Stronger associations were found in women than in men.

...Researchers also used functional magnetic resonance imaging (fMRI) to observe changes of blood flow in the brains of 44 young adults from these families as they performed a task in which they anticipated winning or losing money.

"The neuroimaging allowed us to see for the first time how these genetic variants create differences in how the brain responds in certain situations," says Mary M. Heitzeg, Ph.D., a research assistant professor in U-M's Department of Psychiatry and U-M's Addiction Research Center.

They found that individuals with one form of the GABRA2 gene associated with alcoholism showed significantly higher activation in the insula when anticipating rewards and losses than those with other combinations. This higher activation was also related to a greater level of impulsiveness in response to distress.

..."We believe these results suggest GABRA2 exerts an influence on an underlying neural system that impacts early risk factors and, later, alcohol dependency," says Burmeister, also a professor of psychiatry and human genetics at the U-M Medical School. "In the future, we hope to further examine the effects of family environment and other behavioral and environmental factors." _PO

Genetic influences on behaviours are too numerous to count, yet are extremely difficult to pin down with specificity. That is because multiple causes at several different levels are influencing the events which we observe. It will take many years to sort the many levels of causation -- many of them circular (incorporating feedbacks) in nature.

Persons who are indoctrinated into the religion of political correctness tend to eschew all discussion of genetic influences on behaviour. Funding for research can be difficult to obtain if highly indoctrinated "ethicists" feel that the valid findings of the research may be misconstrued in a way as to contradict politically correct dogma.

But such a PC approach only dooms persons who suffer from genetic disadvantages of behaviour to lifetimes of suffering. Much better to learn everything we can about these phenomena, so as to be able to compensate for these genetically based behavioural and cognitive disadvantages on as many levels as possible.

One approach to compensating for genetic defects in brain functioning is to run a low level dc current through the skull into the brain.

Better Genes, Better Brains

Better brains tend to run in families. The crucial brain determinants of life success -- IQ and Executive funtion -- are between 60% and 80% heritable. Exciting new tools for studying the genomics of the brain, such as the Allen Human Brain Map (read more here), are being used in conjunction with imaging tools such as diffusion tensor imaging, to study the individual nature of how human brains manifest underlying genomes.

A recent study from Australia looks at how genetics influences the efficiency of how human brains are wired -- and how well they work.

“Some brains are wired better than others, and 60% of the differences can be explained by genetic factors,” said lead author Alex Fornito from the Melbourne Neuropsychiatry Centre at the University of Melbourne. “The novelty is that we now have new methods to identify different aspects of brain network organisation. Previously it was very difficult to try and map these connections.”

...“We found some of the strongest effects in the prefrontal cortex, where up to 80% of the differences between people were attributable to genes. The prefrontal cortex plays a vital role in planning, strategic thinking, decision-making and memory.”

Previous work has shown that people with more efficient brain connections score higher on tests of intelligence, and that brain network cost-efficiency is reduced in people with schizophrenia, particularly in the prefrontal cortex. _Cosmos

Finding the links between genes and intelligence, or between genes and impulse control, requires extensive research and great deal of time. At the US NIMH, the Functional Neurogenomics Program is dedicated to teasing out the numerous connections between the genome and all aspects of brain function. Likewise, in research centers around the world, scientists are hard at work discovering how differences in our genes create differences in our brains, which create differences in the worlds which each of us experiences.

This is not merely an academic problem. The endeavour holds keys to unlocking many of the most vexing problems of human societies worldwide.

NYTimes Discovers, Denies Racial IQ Differences

Update 30 November 2010: I am adding a more rigorous graphic portraying SAT score by race by SES. The source of the image is sociologist La Griffe du Lion.   SAT math scores are a fair proxy for IQ scores, and this graphic illustrates the clear and sustained gap between white and black scores, all the way across the SES spectrum.  More observant readers would have already noticed the contradiction in the graphic further down (2nd image down), showing IQ scores and IQ gap by SES.  Despite the IQ gap remaining at about 1 SD (15 points) all the way up the SES spectrum, the PC graphics designers chose to narrow the IQ gap as the SES rose.   Such gratuitous editorials-in-graphics form give social science a bad name.   I left the IQ gap graphic in despite a number of problems, to see if any reader would point out the most obvious one -- the erroneous narrowing of the gap.  Please try harder next time.  ;-)

In tony suburban Shaker Heights, Ohio, funding is generous, support programs aimed at black students (about half of the student population, not an alienated minority) abound, there is no ability tracking (students track themselves), and such racism as can be found is too intermittent to destroy the academic curiosity of a human being of normal resilience. Yet blacks there cluster at the very bottom of the school _McWhorter

We know that blacks -- particularly black males -- lag in academic and professional achievement worldwide, whenever pitted against members of any race except Australian aboriginals. There is no limit to the number of excuses given for why blacks cannot compete -- poverty, a sick culture, racial discrimination, legacies of slavery, a history of tropical diseases, lack of role models... A new report described in the NYTimes takes another look at the "achievement gap." The report finds that poverty cannot be used as a credible excuse -- the achievement gap starts at the earliest stages of life, even among wealthy blacks.

“There’s accumulating evidence that there are racial differences in what kids experience before the first day of kindergarten,” said Ronald Ferguson, director of the Achievement Gap Initiative at Harvard. “They have to do with a lot of sociological and historical forces. In order to address those, we have to be able to have conversations that people are unwilling to have.” _NYT_via_IHE

The achievement gap only widens as children grow older, as can be seen by comparing testing results for all age groups. There is a good argument to be made that only 4% of American Blacks are qualified for a rigorous 4 year college degree -- regardless of their socioeconomic class or preparatory training.

The denial of human biodiversity (HBD) goes deep in American academia and general culture. Genetics is a relatively new science compared to political and economic philosophy, and will require time to be integrated into the general psyche -- particularly when it is fighting against embedded prejudice.

The sheer persistence of the racial achievement gap across time and geographic space argues for a more rigorous examination of its causes -- no holds barred, no topic off the table for research and publication. That is the only way to achieve as level a playing field as we will ever get, and it will require the deepest understanding of genetics possible.

This map shows IQs of indigenous people for various continents and nations. European and East Asian people evolved to average population IQs of roughly 100 or slightly higher. Most of the rest of the world's population IQ average is somewhere between 80 and 95. Only among African and Australian aboriginals does one find average population IQs which are so low as to allow one to foresee a worldwide stratification in achievement whenever these low-IQ groups might be paired against higher-IQ groups in an academic or professional achievement race.

This is basic information that has been known since the early 1900s when reliable psychometric testing first became available. How ironic that it is those claiming to be most educated and sophisticated who are the slowest to comprehend the obvious -- and to use that information in order to help those who lag. For it is the persistent denial of basic facts which holds those who lag down, without any genuine hope.

Emory's Smart New Mice are Cognitive Knockouts

Image Source

The hippocampus plays a key role in our ability to remember what happens to us, and in navigating our way through the world around us. There is a great deal about the hippocampus which remains unknown. Consider the hippocampal area CA2, pictured above. Recent research from the medical school at Emory University has found that in mice, knocking out a gene (RGS14) radically changes the activity of hippocampal CA2 -- leading to mice with markedly enhanced spatial learning and object recognition abilities, when compared with their littermate controls.

Here is more:

Mice with a disabled RGS14 gene are able to remember objects they'd explored and learn to navigate mazes better than regular mice, suggesting that RGS14's presence limits some forms of learning and memory.
The results were published online in the Early Edition of the Proceedings of the National Academy of Sciences.
Since RGS14 appears to hold mice back mentally, John Hepler, PhD, professor of pharmacology at Emory University School of Medicine, says he and his colleagues have been jokingly calling it the "Homer Simpson gene."
RGS14 is primarily turned on in one particular part -- called CA2 -- of the hippocampus, a region of the brain known for decades to be involved in consolidating new learning and forming new memories. However, the CA2 region lies off the beaten path scientifically and it's not clear what its functions are, Hepler says.
RGS14, which is also found in humans, was identified more than a decade ago. Hepler and his colleagues have previously shown that the RGS14 protein can regulate several molecules involved in processing different types of signals in the brain that are known to be important for learning and memory. They believe RGS14 is a key control protein for these signals. _SD

Although the researchers have not identified any problems in the RGS14 knockout mice in terms of development or behaviour, it is too early to know whether such a simple gene knockout procedure in humans would be safe or effective -- for purposes of cognitive enhancement.

The finding is intriguing in the sense that the deletion of a single gene can have such a profound effect on the cognitive prospects of a mouse. A mutation in the right place could have the same result, in terms of improved learning. How many similar transformational surprises are waiting in the human genome?

We should not expect that any environmental intervention could come close to achieving a similar transformation of these specific cognitive skills as the genetic deletion achieved. Considering the somewhat conservative nature of evolution since the last great extinction event, it is unlikely that we have evolved in a way to take the greatest advantage of the potentials of our brains. In other words, our brains are likely to have many such genetic tweaks that are waiting to be discovered, to give us a leg up on our present and future challenges.

At this time it is still possible to envision a "next level" of human development. But such a hypothetical plane of development can only be reached by genetic means. How radical must such a transformation be? That depends upon where one starts. If humans continue on the present descent into Idiocracy, there will come a time when it will be too late to reverse the trend.

The easiest choice is to go back to sleep. Because, if you choose to be awake, the things you are forced to experience may be more than you can bear.

H/T Brian Wang

More on the "molecular conspiracy against plasticity" occurring in CA2

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Long Memories and Obsessive Behaviours FKBP

Reducing the activity of a gene called FKBP12 in the brains of mice affected neuron-to-neuron communication (synapse) and increased both fearful memory and obsessive behavior, indicating the gene could provide a target for drugs to treat diseases such as autism spectrum disorder, obsessive-compulsive disease and others, said researchers from Baylor College of Medicine in Houston _SD

We are what our brains make us, but our brains are what our genes + environment makes us. People with lower expression of FKBP 12 protein may have longer memories, but at the expense of more fear, anxiety, and compulsion. At least, Baylor University studies in mice suggest such an effect of genetic biodiversity in rodents.

The protein FKBP12 regulates several important cell signaling pathways, and decreasing its activity enhances long-term potentiation in the hippocampus, said Dr. Susan Hamilton, chair of molecular physiology and biophysics at BCM and a senior author of the report. (Long-term potentiation means the enhancement of the synapse or communication between neurons.)

It accomplishes this by fine-tuning a particular pathway called mTOR signaling (mammalian target of rapamycin). The mice in whose brains the activity of the gene was reduced had longer memories and were more likely to exhibit repetitive behaviors than normal mice. _SD

The effect of FKBP12 protein may be mediated at least in part via mitochondrial efficiency.

Gene expression exerts a powerful affect on humans and other animals from the very earliest stages of development. Scientists at Hebrew University-Hadassah have elaborated the effect of gene G9a on specialisation of early pluripotent cells into differentiated cell types. More on basic action of G9a in gene expression.

It is futile to attempt to completely separate the impact of an organisms environment from gene expression. But it is just as futile to attempt to separate gene expression from an organism's (and human's) behaviour. Ideological adherents of the "Blank Slate" hypothesis are being forced into a very tight logical corner. And because such Blank Slatists control large areas of government, universities, and the media across North America and Europe, expect some extremely erratic and dysfunctional behaviour from them as their cause falls into greater disrepute.

I Just Always Thought It Was PMS

Anyone who has raised more than one child from birth understands that children are born with distinct behavioural predispositions and tendencies. Now a study of women of European descent suggests that women, at least, can be genetically predisposed to anger.

University of Pittsburgh researchers have found that behaviors such as anger, hostility and aggression may be genetic, rooted in variations in a serotonin receptor gene. Indrani Halder, Ph.D., of the Cardiovascular Behavioral Medicine Program at the University of Pittsburgh, will present the findings today at the American Psychosomatic Society's Annual Meeting, held in Budapest, Hungary.

Previous studies have associated the hormone serotonin with anger and aggression in both humans and animals and have shown that increased serotonin activity is related to a decrease in angry and aggressive behaviors. In the study being presented today, researchers sought to determine if this relationship was genetically determined. The study is the first to look at the relationship between variations in the serotonin receptor 2C gene and anger and hostility.

Completed at the University of Pittsburgh's Behavioral Physiology Laboratory, the study looked at 550 unrelated women of European descent. In order to find normal variations in genes and behavior, the women were not prescreened for behavioral type. Researchers found that those who had one or both of two alterations in the promoter region of the serotonin receptor 2C gene were more likely to score lower on two common tests for anger, hostility and aggression.

Source.

Now it is only a matter of extending the research to include women of other ethnic groups, and men. I wonder why they selected women particularly for this study? Further speculation on that point has been prematurely curtailed by our sponsor.

Beyond Smart Drugs: Getting Smarter

Aubrey de Grey's SENS approach to gerontology may very well help us to live longer, perhaps much longer. Then what? Humans really do need to become smarter. Present levels of human intelligence are just about good enough to get us all killed. To go beyond what was discussed in the posting Smart Drugs, I would like to look toward longer term prospects for boosting intelligence--permanently.

Returning briefly to neuroscientist Michael Gazzaniga in his Oct 2005 SCIAM articleSmarter On Drugs, we see the real essence of the problem. Smart drugs temporarily augment the brains we have, but they do not make them better. To do that, we have to go further:

We have isolated one gene involved in intelligence, and others will follow. We know which parts of the brain are influenced by particular genes and which parts correlate with high IQ. We also know some of the neurochemicals involved in learning and memory. With such knowledge, we will gain understanding of what needs to be manipulated to increase intelligence in people who were not blessed with brilliance in their genomes or further increase the intelligence of those who were. Gene therapy could insert, delete, turn on or turn off genes that we find to be associated with intelligence.

We know about the Human Genome Project, and we understand that it is the foundation for much bigger things. We have heard about the International Hapmap Project, and we may have a vague idea of the possibilities that will be generated because of it. Diseases and other human attributes possess significant genetic components. We need to know what they are.

But we must think more broadly than mere genes. Genes are only part of the story. The better understanding of proteins, or proteomics, holds many of the keys we are looking for. In addition, non-coding RNA is a critical piece of the puzzle. The entire control structure of each cell is a highly complex internetwork of feedback systems. If you add the feedback systems of neighboring cells and tissues, then take into account signals coming to the cell from the blood, lymph, nerve terminals, and other meta-control systems--and you begin to see the problem.

We were talking about how to become more intelligent, using the genes. But now we understand that it can never be just the genes. It has to include the entire biological environment of the nervous system, and the entire organism.

But, wait. The organism is not hermetically sealed. The organism has inputs from the outside, and outputs to the outside. We know that growing organisms have to be given adequate nutrition, physical exercise, and mental stimuli to develop normally. They also need emotional nurturing. From Intelligence Testing Blog, we learn from Kevin that even video games may contribute to cognitive enhancement in young children. But what about the mature, developed organism--human? Assuming he is getting optimal nutrition, exercise, mental challenge, and emotional support? What else can be done?

OK, I talked about ampakines, donezepil, and modafinil here. If you are living on the edge of your mental capacity, it might be worth it to you, to try to get your hands on some donezepil. Modafinil should be treated gently, since everyone needs ample sleep, and with modafinil the temptation is to skimp on sleep to get more done, potentially abusing the body in the process. Ampakines are not available yet, but will be relatively soon. These are temporary approaches.

While we are waiting for researchers to understand the genetics, proteomics, and epigenetics of intelligence, there may be more permanent actions we can take to augment our mental capacity.

Assuming your nutrition is indeed optimal, your physical activity regular, your mental stimulation productive, and your emotional supports satisfying--what else can you do?

Neurofeedback is a technology that has been largely ignored by the public and news media, but is an approach that holds enormous potential for mental growth, even for mature and normal human mind/brains. It is still experimental in terms of stimulating mental growth for normal brains, but it is safe and non-invasive.

People with phobias, such as math phobia, are preventing themselves from progressing in the direction of their phobia. Such persons can certainly be helped by neurofeedback and other behavioural approaches.

There are many commercial programs, such as this one, that tries to capitalise on the human desire to improve oneself. This is another group that seems to be taking an even more advanced approach to developing mind improving technology. And while Daniel Amen may be rightly criticised by his peers for jumping too quickly into imaging technology to diagnose common everyday conditions, there is no doubt that Amen is at the leading edge of the curve, and may have the last laugh after all.

Taking nutritional supplements may not be a bad idea, either. In addition to the multivitamins, the extra vitamin C and E, and the minerals, taking curcumin, lipoic acid, and precursors for neurotransmitters might be helpful for many, particulary those with depression, fatigue, or ADD. This is not medical advice, but merely a suggestion for something that might be looked into.

Long life and increased intelligence are not the final goal. To reach the final goal, you must also include enlightenment, and wisdom. Using both sides of the brain to the fullest extent. Mysticism and holism are only part of wisdom. Wisdom also includes the ability to look at the details with exquisite clarity, and being able to place them into dynamic context.

We have some distance yet to travel, many things to learn. There is no reason not to use the footstools, ladders, and knotted ropes dangling above us.