How the Green Movement Can Trigger the Great Human Dieoff

Powerful persons in the global green movement would like to see the human population of Earth reduced by at least 90%. For several decades, many of them believed that resource depletion, energy scarcity, mass starvation, or voluntary sterilisation might achieve their grand goal. But it is slowly dawning on them that if they are to slash the human population of the planet to a size that they consider manageable, they will have to be a bit more proactive.

Just in time for the great green engineered human dieoff, biological scientists have devised the perfect method of genocidal species extinction.

IN THE urban jungle of Juazeiro in Brazil, an army is being unleashed. It is an army like no other: the soldiers' mission is to copulate rather than fight. But they are harbingers of death, not love. Their children appear healthy at first but die just before they reach adulthood, struck down by the killer genes their fathers passed on to them.

These soldiers are the first of a new kind of creature - "autocidal" maniacs genetically modified to wipe out their own kind without harming other creatures....the approach should work with just about any animal - from invasive fish and frogs to rats and rabbits....it could transform the way we think about genetically engineered animals.

... the autocidal approach could not only be used to control invasive species such as cane toads, but that it is the only method that could work in many cases. "It's the only hope we have for the long-term control and eradication of these pests," he says. "Other efforts help, but in the end they are Band-Aids in the absence of a real solution."

Thresher has come up with a way to create fish that produce only male offspring. Releasing enough of these "daughterless" fish into the wild, with each passing on the daughterless habit, would turn a thriving invasive population into a bunch of reluctant bachelors destined for extinction.

...Models suggest that releasing enough daughterless carp to make up 5 per cent of the total population would effectively eradicate carp in the Murray-Darling basin by 2030. Thresher's models also suggest pests such as cane toads and rats could be tackled this way.

... One [approach] that has particular promise exploits chunks of "selfish" DNA that can spread themselves through the population and kill only when two copies are inherited. In theory a one-time release of just a few insects, rather than the continual release of millions, could wipe out a wild population (New Scientist, 22 March 2003).
_NewScientist

ArmageddonOnline.org
The last paragraph from the excerpt above describes the most subtle approach, and perhaps the easiest approach to genocide for greens to take. But they should be prepared to wait several generations to see the completion of their grand project. Such an approach should also allow environmentalists to create an antidote, so they they themselves and their associates could continue to live and procreate indefinitely. Think of it: a master race of environmentalists, sitting back and watching most of the rest of humanity fade away.

It is an approach without gas chambers, without germs, poisons, bullets, or bombs. A clean, test-tube approach that could propagate death and genocide far more broadly than any method previously devised.

Google Tech Talk: Steve Hsu -- Genetic Basis for Intelligence

This fascinating Google Tech Talk was given by Steve Hsu last week, and just put up at Google Tech Videos. Steve is a physics professor at the University of Oregon, with a special interest in human intelligence.

Slides for Steve Hsu's talk (PDF)

Hsu is involved in a study which seeks to find links between genes and high IQ. The study is looking for individuals with IQs that test higher than 3 standard deviations above the mean, in a clear effort to cut to the chase.

Hsu's talk is well worth watching for anyone interested in the genetics of cognitive ability. As high tech infrastructures grow more sophisticated and crucial to advanced societies' successes, their high IQ smart fractions take on an ever greater importance.

Smarter Near the Poles, and Nearing Clockwork Orange?

WiredHumans apparently evolved larger eyes and brains as they migrated closer to the poles. The larger eyes would allow for better adaptation to lower light levels in the wintertime. The larger brains would allow for better adaptation to the greater challenges of radically changing seasons.

Anthropologists at Oxford University collected 55 skulls, dating from the 1800s, that represented 12 different populations from around the globe. The researchers measured the eye socket and brain volumes and plotted them against the latitude of each individual’s country of origin.

The team, lead by the Institute of Cognitive and Evolutionary Anthropology’s Eiluned Pearce, found a significant positive correlation between the size of brain and the latitude of the country. People from the northern-European countries of Scandinavia had the biggest brains, while Micronesians, from just north of the equator, had the smallest. _Wired

While political correctness forces the authors to deny that the larger brains have anything to do with the demonstrated higher intelligences of peoples who migrated farther from the equator, such higher intelligence has been shown to correlate with higher latitude as well as brain size, time after time. HBD (human biodiversity) deniers argue this point out of ignorance, but with the coming of advanced brain imaging techniques which can determine the comparative sizes of some of the very smallest brain nuclei, such denial is becoming infantile at best.

Meanwhile, Cal Tech researchers are homing in on a part of the brain which controls human aggression and violence. We may well be approaching a "Clockwork Orange" scenario, where violence-prone people will be conditioned or modified to remove their violent tendencies.

Our story starts in the hypothalamus, an ancient region of the brain, conserved throughout mammalian evolution. In humans, it is about the size of an almond, housing a motley collection of neurons. These cells regulate distinct bodily functions such as temperature, circadian rhythms, sleep, hunger, thirst, sex, anger, aggression and response to stress. Earlier work showed that electrical stimulation of some of these sites provokes cats and rats to sudden bouts of rage and that the ventromedial hypothalamus (VMH) has some involvement in sexual behaviors. Yet the precise location of attack-promoting neurons, their mode of action, and the interplay between aggression and mating—normally two opposing forms of social interactions—had remained deeply mysterious.

Enter a team from the California Institute of Technology, under the leadership of neurobiologist David J. Anderson. In four steps, the seven scientists, spearheaded by postdoctoral fellow Dayu Lin (now at New York University), nailed down the critical role of aggression neurons in the VMH. The setting was the home cage of an individually housed, sexually experienced male mouse. When another mouse, either a male or a sexually receptive female, entered the cage, the resident male mouse usually attacked the former but mated with the latter. The scientists video recorded the behavior so that the detailed time course of interaction of every pair of animals—the cautious sniffing and retreating, the pushing, shoving and biting, the mounting and consummatory activities—in hundreds of encounters could be statistically analyzed and time-aligned using software developed by machine vision engineers Piotr Dollar and Pietro Perona.

...Stimulating the VMHvl [Editor: The VMHvl is the ventrolateral portion of the ventromedial hypothalamus] when the mouse was by itself did not do anything. Yet in the presence of another animal, the mouse initiated a concerted attack, often by biting the back of the intruder. Unusually for this species, the illuminated male indiscriminately attacked female, castrated male or anesthetized mice—and sometimes even a blown-up latex glove. Aggression ceased once the light stopped. The infection and light delivery had to be targeted to the VMHvl nucleus; stimulating nearby regions did not produce such an effect. It is a striking and immediate demonstration of the link between neurons and behavior. Exciting VMHvl neurons causes aggression.

Finally, Anderson and his team turned to the question of whether the VMHvl cells are necessary for aggression to occur. Using a different technique, they genetically “silenced” VMHvl cells, turning them effectively off for days at a time. This silencing significantly reduced the chances of an aggressive encounter and lengthened the time it took to initiate an attack. _SciAm

The researchers were able to temporarily "dim down" the tendency for the mouse to resort to violence. The techniques for achieving this level of control over the mouse VMHvl nucleus are quite tedious. Eventually the same level of control will be achieved with a nasal spray containing nano-scale capsules of precisely targeted gene modifiers.

Violence is endemic to large parts of Asia, South America, and Africa. And even within the troubled multicultural urban areas of Europe, Oceania, and North America, deadly violence can be a daily phenomenon. Will human authorities utilise the coming tools of behaviour modification, even if they interfere with "free will?" Or is it better to pack prisoners in cages like mammalian sardines, and allow them to do with each other as they wish? The intersection of sophisticated brain and genetic research with widespread sociopathology is likely to prove interesting.

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.

Is Mental Illness Preventable?

Of the 10 leading causes of disability in the world in 1990, five were mental disorders; specifically unipolar depression, alcohol use, manic depression, schizophrenia and obsessive-compulsive disorder (Murray and Lopez, 1996). It is clear that both the extent of mental health problems and the enormous associated personal, social and financial cost can not be addressed by treatment services alone. _Robinson et Pennebaker

Schizophrenia.com
Schizophrenia is one of the most debilitating and disabling of the mental illnesses. So if we could find a way to prevent schizophrenia -- even a substantial proportion of the disease -- we would be making impressive progress toward the goal of preventing mental illness.

Recent research findings from Duke and Johns Hopkins suggest that a proportion of schizophrenia with genetic causes could be prevented by early detection of susceptible persons in early childhood, with appropriate intervention before symptoms manifest themselves in late adolescence or early adulthood. Scientists have known for decades that brain structure in schizophrenia was not normal -- and even pointed toward an early developmental "lesion" as the cause of the structural abnormalities.

The critical network of signals which control early brain development is becoming better understood -- both in terms of general development and in terms of specific brain diseases when the signaling network goes awry. Here is more about the recent Duke et Johns Hopkins research:

Katsanis, who directs the Duke Center for Human Disease Modeling, and Akira Sawa, M.D., Ph.D., a Professor in the Department of Psychiatry at Johns Hopkins, were introduced to each other by a clinical colleague who thought that Bardet-Biedl syndrome (BBS) proteins that are involved in transport duties within cells might have a role in schizophrenia. Katsanis is an expert in using BBS genetic mutations and proteins to learn more about other diseases. BBS is a complex genetic disease with autism-like symptoms, cognitive defects and depression. Sawa is an expert on DISC1, the protein named Disrupted in Schizophrenia 1, known to be a major susceptibility factor for schizophrenia and related disorders.

Together, they discovered that these proteins are involved in a key switch for neurons that is necessary for brain development. When DISC1 gains a phosphate group at a specific site, it recruits BBS1. When BBS1 is missing in this system, the team could observe defective neuron migration, while a model with no DISC1 at all leads to defects in both cell proliferation and migration.

...Katsanis predicts that, for perhaps 10 percent of psychiatric illness, the illness is primarily driven by defects in this switch system. "So we now have ways to interpret variation in humans, in a context that is relevant to their particular cases, to their physiology -- that is where medicine will move next," Katsanis said.

...The study was published by Nature journal on April 6 in its advance online publication. _SD

The researchers were looking at brain signaling which controls early brain development -- the multiplying of brain neurons and subsequent placement in proper locations, orientiation, and connectivity to other parts of the brain. But there is another "brain growth spurt" which occurs just before adolescence, which could be just as critical to the subsequent development of schizophrenia and other types of mental illness which first manifest in adolescence or early adulthood. This neuronal growth spurt is no doubt also under the control of brain signaling proteins.

Prevention comes into the picture when scientists learn to correct abnormal signaling in early stages of development, or to compensate for abnormal brain development, later in childhood. Some genetic abnormalities can be treated now, and the opportunities to treat more genetic problems are growing rapidly.

That means that besides mental illness, many disadvantages which are widespread in the third world and in disadvantaged ethnic groups -- and which are at least partially genetically mediated (such as low intelligence and poor executive function) -- should be amenable to treatment in the not so distant future.

It is the denial of such genetically mediated disadvantages and disabilities which dooms sufferers to lifetimes of misery and underachievement. Such HBD deniers likewise doom entire societies and regions to generations of misery, poverty, widespread disease, and hopelessness.

Poor, Bare, Forked Animals Begin to Decipher Epigenome

NIH
The epigenome is the system of genome modifiers that guide gene expression. Epigenetics determines whether a cell will be a brain cell or a liver cell, even though both cells possess the same genome. Some preliminary results are beginning to come in from the US NIH's modENCODE program.

Sarah C.R. Elgin, PhD, the Viktor Hamburger Distinguished Professor in Arts & Sciences, who led the Washington University lab that is part of one of the modENCODE teams offers an explanation.

“We learned many things from the Human Genome Project,” Elgin says, “but of course it didn’t answer every question we had!

“Including one of the oldest: We all start life as a single cell. That cell divides into many cells, each of which carries the same DNA. So why are we poor, bare, forked creatures, as Shakespeare [Al Fin: Lear ActIII SceneIV] put it, instead of ever-expanding balls of identical cells?

“This work,” says Elgin, “will help us learn the answer to this question and to many others. It will help us to put meat on the bones of the DNA sequences.” _WUNewsroom

Wikipedia

The epigenetic code that determines whether genes are silenced or expressed consists of chemical modifications to the DNA, to “tails” that hang off the histones, or other packaging proteins.

“ENCODE and modENCODE are much more complicated projects than the Human Genome Project,” Elgin says, “because the DNA sequence is pretty much the same in every cell type, whereas the chromatin structure is different in every cell type. In fact we believe it is the chromatin structure that differentiates one cell type from another.

“That means we can’t just do one genome for the organism. We have to do every different cell type to get a complete picture of the organism, and that’s a daunting prospect.” _WU

The research relies upon the most advanced bio-research and computing technologies. The amount of data generated is staggering, and far beyond what an unaided human could organise and comprehend.

But this is the beginning of the true meat of genetics. Sure, they are looking at worms and fruit flies now. But humans and all human symbionts and parasites are on the list to be comprehensively studied. The knowledge to be gained will provide unimaginable benefits.

What Is Metabolic Engineering and Why Should We Care?

LBLNewsMetabolic Engineering is one of those bastard terms which is often spawned by science-savvy folks in academia who are functionally illiterate. For example, MIT has a lab department of Bioinformatics and Metabolic Engineering. Rice has studies in Biological Chemistry and Metabolic Engineering. Harvard teaches Systems Metabolic Engineering. Cornell has a lab for Biomolecular and Metabolic Engineering. At Berkeley, the subject falls under the Department of Chemical and Biomolecular Engineering... and so on. When will we be given entire departments of Respiratory Engineering, Mitochondrial Engineering, Liposome Engineering, or Cholesterol Membrane Engineering? There truly is no end to the number of departmental classifications that could be spawned by the postmodern twits of academia who have acquired a little bit of specialised scientific training.

Forgive me, I got a bit sidetracked. Chemical engineer Jay Keasling has published an article in Science discussing the "Future of Metabolic Engineering," in which he looks at the possibilities of creating designer molecules, cells, and micro-organisms.

In a paper published in the journal Science titled “Manufacturing molecules through metabolic engineering,” Keasling discusses the potential of metabolic engineering – one of the principal techniques of modern biotechnology – for the microbial production of many of the chemicals that are currently derived from non-renewable resources or limited natural resources. Examples include, among a great many other possibilities, the replacement of gasoline and other transportation fuels with clean, green and renewable biofuels.

“Continued development of the tools of metabolic engineering will be necessary to expand the range of products that can be produced using biological systems, Keasling says. “However, when more of these tools are available, metabolic engineering should be just as powerful as synthetic organic chemistry, and together the two disciplines can greatly expand the number of chemical products available from renewable resources.”

...Metabolic engineering is the practice of altering genes and metabolic pathways within a cell or microorganism to increase its production of a specific substance. Keasling led one of the most successful efforts to date in the application of metabolic engineering, when he combined it with synthetic organic chemistry techniques to develop a microbial-based means of producing artemisinin, the most potent of all anti-malaria drugs. He and his research group at JBEI are now applying that same combination to the synthesis of liquid transportation fuels from lignocellulosic biomass. In all cases, the goal is to engineer microbes to perform as much of the chemistry required to produce a desired final product as possible.

“To date, microbial production of natural chemical products has been achieved by transferring product-specific enzymes or entire metabolic pathways from rare or genetically intractable organisms to those that can be readily engineered,” Keasling says. “Production of non-natural specialty chemicals, bulk chemicals, and fuels has been enabled by combining enzymes or pathways from different hosts into a single microorganism, and by engineering enzymes to have new function.”

These efforts have utilized well-known, industrial microorganisms, but future efforts, he says, may include designer molecules and cells that are tailor-made for the desired chemical and production process. _LBLNews_via_BrianWang

Sound familiar, this metabolic engineering? Like a contrived illegitimate offspring of genetic engineering, synthetic biology, and metabolomics? It's bad enough to have a proliferation of -omics, such as genomics, proteinomics, metabolomics, glycomics, lipomics . . . It is almost enough to turn a person homicidalomic.

Psychiatry with its DSM is almost as insane. But these irrational and cumbersome systems of classification tend to evolve by the method of poorly punctuated disequilibrium, leaving those downstream to deal with the offalness of it all.

Does Keasling simply want to excel in a field that another researcher -- Craig Venter -- has already staked out -- synthetic biology? Venter has long since founded a company called Synthetic Genomics. Is it possible that Keasling is unwilling to share the same field with a person such as Venter, who is already hot on the trail of the very things that Keasling claims to be pursuing in the name of Metabolic Engineering? Fine. Do the same thing, but call it something different. No one will ever know.

Greater Human Genetic Diversity Than Previously Believed

ImgSource

As humans look more deeply into their genetic and epigenetic complement, they are discovering far greater genomic differences between humans than previously believed possible. The 1000 Genomes Project is reporting on results from its pilot phase:

Evan E. Eichler and coworkers of the University of Washington, Seattle, used data from the 1000 Genomes Project to analyze copy-number variations, which are differences in the number of times a particular gene sequence appears in the genome (Science 2010, 330, 641). About 1,000 genes "have been largely inaccessible to traditional genetic study as a result of their repetitive nature," Eichler said at the press briefing. Using newly developed sequence analysis algorithms and sequence tags, his team investigated copy-number variations in these genes, he said.

Eichler's team found that copy-number variations occur in fewer than 10% of human genes. Many of these genes map to regions that had been previously identified as highly repetitive and have been implicated in diseases such as schizophrenia and autism, the authors note.

Even at the pilot stage, the 1000 Genomes Project has already provided "a more complete catalog" of human genetic variation than was available previously, Durbin said. The project is already moving forward with its main phase, with the goal of sequencing 2,500 genomes. _ACSPubs

Whether 1000 genomes or 2500 genomes, the study is still quite preliminary, in terms of understanding the astounding magnitude of variation within the broad human genome and epigenome. As we begin to comprehend the vast numbers of differences in gene expression between even the closest of relatives, we may get a glimmer of understanding of how our molecular makeup generates the diverse worlds we inhabit.

Abstract of paper:

Copy number variants affect both disease and normal phenotypic variation, but those lying within heavily duplicated, highly identical sequence have been difficult to assay. By analyzing short-read mapping depth for 159 human genomes, we demonstrated accurate estimation of absolute copy number for duplications as small as 1.9 kilobase pairs, ranging from 0 to 48 copies. We identified 4.1 million "singly unique nucleotide" positions informative in distinguishing specific copies and used them to genotype the copy and content of specific paralogs within highly duplicated gene families. These data identify human-specific expansions in genes associated with brain development, reveal extensive population genetic diversity, and detect signatures consistent with gene conversion in the human species. Our approach makes ~1000 genes accessible to genetic studies of disease association.

Goat-Smelling Desert Dwellers Confused by Brasilian Interference

ImageSource

For many years, the All-Peninsular Goat-Smelling Mooch Award has been won by either Ahmed or Abdul. (It should be noted that the word "mooch" means something different in Arabic, being more linguistically akin to the Yiddish word "mensch".) Al Fin traveled to the peninsula to interview Abdul and Ahmed, the most highly skilled goat-smellers in peninsular history, to question them about Brasil's latest interference in the goat genome, and the implications this may have for their profession in the future.

Al Fin: Thank you very much, Abdul and Ahmed, for meeting with me today.

Ahmed and Abdul in unison: Salaam aleikum, Al.

AF: Wa aleikum salaam. I'll start with Abdul first. What do you think about Brasil's interference with goat genetics?

Abdul: It is a serious problem, Al. These interfered goats do not smell the same as a natural goat. It gives me a headache to think what these cursed Brasilian scientists are doing.

AF: I understand that some goat-smellers are worried that the Brasilians will insert some pig genes into their goats, and then release the pig-goats into peninsular herds to inter-breed with natural goats. Ahmed, what have you heard in that regard?

Ahmed: I was enraged when the imam announced this outrage at Friday noon prayer. We rushed into the streets with hands full of stones, looking for infidels and perverts. Fortunately we found a woman walking without a veil, with her head uncovered. It would have been a shame to waste the stones.

AF: I see. But can't you tell the difference in smell between natural goats and Brasil-interfered goats? Wouldn't such a thing lead to greater demand for goat-smellers, and higher profits for you?

Abdul: No, Al, you don't understand. Just to smell such a pig-goat would contaminate a goat smeller so that he could not go to mosque without enduring a prolonged purification ritual over a period of many days. Many of our best clients would be reluctant to hire us with such a taint over our heads.

AF: Hmmm. What do you intend to do, then?

Ahmed: We must declare jihad against the Brasilian scientists and destroy their laboratories before they can achieve their blasphemous goals.

AF: But what about all the good things that could come from the transgenic goat programs? Destroying the laboratories may prevent some important medical breakthroughs.

Abdul: Not our problem, Al. We must do what we must do.

AF: So. Thanks for meeting with me today Abdul and Ahmed.

A&A: As Salaamu Aleikum, Al.

Technology Review article about transgenic goat experiments in Brazil

Genes and IQ: The Connection is Real, But Complex

Robert Plomin, at King's College London, is reporting on a study of 4,000 British children which suggests that over 200 genes are responsible for superior reasoning ability and IQ. More:

SCIENTISTS have identified more than 200 genes potentially associated with academic performance in schoolchildren.

Those schoolchildren possessing the "right" combinations achieved significantly better results in numeracy, literacy and science.

The finding emerged from a study of more than 4000 British children to pinpoint the genes and genetic combinations that influence reasoning skills and general intelligence.

One of its main conclusions is that intelligence is controlled by a network of thousands of genes with each making just a small contribution to overall intelligence, rather than the handful of powerful genes that scientists once predicted.

The researchers believe their work could eventually lead to genetic tests to predict babies' academic potential.

"This kind of research could help us develop genetic tests to predict which kids are at risk of developing problems with their schooling, so that we could intervene to help them," said Robert Plomin, professor of behavioural genetics at the Institute of Psychiatry at King's College London, who will describe his work today at a meeting of the Royal Society.

_Australian

Scientists have known for years how important gene patterns are to the development of the brain. Specific gene variants can have a crucial effect on the wiring of the brain, and on the speed and efficiency of brain functioning. Individual genes have been identified, which are felt to have an influence on human intelligence, but it is the larger pattern of gene combinations which must be studied and understood.

Human intelligence and cognition are too complex to rely on any one gene. But the computational methods to make sense out of the massive interplay of the hundreds of genes which may affect intelligence have not always been available, or trustworthy.

But slowly, as scientists learn to study the interactions of hundreds of genes, the relationship between human intelligence and gene variants can become more clear. It is an important area of study. Only by thoroughly understanding how our genes make us what we are -- in partnership with our environment -- can we find the best ways to grow into the sort of humans who can boldly step into the hazardous future, and go where things are really scary. But in a good way.