David Friedman says that while Leftists generally accept that evolution occurred they reject all implications evolution has for human nature.
People who say they are against teaching the theory of evolution are very likely to be Christian fundamentalists. But people who are against taking seriously the implications of evolution, strongly enough to want to attack those who disagree, including those who teach those implications, are quite likely to be on the left.
I think he is right on his basic points. The bulk of the (fairly unscientific) attacks on the idea of genetic causes of differences in intellectual performance come from the Left. The argument for the primacy of social environment as the biggest force determining our intelligence comes from the Left. Yet some genetic theorists find evidence that local selective pressures exerted even over several hundred years can cause big changes in cognitive function. Friedman starts out focusing on differences between the sexes in cognitive function.
Consider the most striking case, the question of whether there are differences between men and women with regard to the distribution of intellectual abilities or behavioral patterns. That no such differences exist, or if that if they exist they are insignificant, is a matter of faith for many on the left. The faith is so strongly held that when the president of Harvard, himself a prominent academic, merely raised the possibility that one reason why there were fewer women than men in certain fields might be such differences, he was ferociously attacked and eventually driven to resign.
Yet the claim that such differences must be insignificant is one that nobody who took the implications of evolution seriously could maintain. We are, after all, the product of selection for reproductive success. Males and females play quite different roles in reproduction. It would be a striking coincidence if the distribution of abilities and behavioral patterns that was optimal for one sex turned out to also be optimal for the other, rather like two entirely different math problems just happening to have the same answer.
Human male and female brains differ in fundamental ways. For example, women have a higher ration of white matter to gray matter than men. The scientific literature on male-female differences in cognition is now enormous. Yet a president of Harvard (Larry Summers) can still get forced from office in part because he took that scientific literature seriously.
Speaking as someone who thinks the evidence for the theory of evolution is overwhelming I am very disappointed at how evolution has been walled off from most discussions of human nature in the political sphere. Among most secularists (who like to fancy themselves as more scientific than the Christians) I see widespread embrace of a sort of modern Cartesian dualism where instead of placing the mind in a supernatural realm the genes that code for the mind are viewed as immune to evolutionary selective pressures. We are supposed to believe that humans have evolved so far that they've escaped the genes that code for their minds and that at birth the human mind is a Blank Slate (tabula rasa) almost totally molded by its environment.
I see the Left's Blank Slate as an even worse model for understand human nature than the fundamentalist Christian Original Sin view of human nature. The Original Sin model maps closer to what evolution produced: selfish desires that got selected for in order to cause behaviors that boost reproductive fitness. In the Original Sin model the idea that evil can be defeated in this world is laughable because the devil is whispering in everyone's ear and the battle between good and evil is constant. The temptations of sin are the desires and instincts placed in us by millions of years of natural selection. So the idea of Original Sin hits a lot closer to the truth than the view that we can perfect humans with smarter social policies. New Soviet Man is the antithesis of what a Darwinist ought to think is possible to achieve in human societies.
A June 2007 article from Plos Genetics, Localizing Recent Adaptive Evolution in the Human Genome, provides examples of localized evolution of cognitive function.
Several genes with functional roles in the development and function of the nervous system show very strong evidence (CLR p < 10−5) for a recent selective sweep. For example, SV2B, a gene encoding a synaptic vesicle protein with highest expression during brain development [36], exhibits strong evidence for a selective sweep in the African-American sample. Likewise, the protein encoded by DAB1 plays a developmental role in the layering of neurons in the cerebral cortex and cerebellum [37], and exhibits strong evidence for a selective sweep in the Asian sample. Other nervous system genes with strong evidence for a selective sweep include two candidate genes for Alzheimer disease (APPBP2 and APBA2) that bind the amyloid-beta precursor protein, two genes (SKP1A and PCDH15) with a role in sensory development, and several others with various roles in nervous system development and function (PHACTR1, ALG10, PREP, GPM6A, and DGKI).
A March 2007 article from Plos Biology, A Map of Recent Positive Selection in the Human Genome, finds plenty of signs up local cognitive evolution.
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 [46]. 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.
This all is unsurprising and I expect much more evidence to be uncovered of cognitive adaptations to local environments. For example, fishermen had different cognitive demands placed on them than farmers. With a boat one is in constant danger of death and one needs to be much more careful. The ideal personality for a crew member of a fishing boat is probably different than the ideal personality for a sheep herder and the ideal personality for a sheep herder is probably different than that for a tiller of soil. So an area with lots of coastlines and little farmable land probably have different average personality types than areas with lots of tillable soil.
While some will rush to dismiss these speculations evidence has already begun to emerge that genetic variations that affect cognitive function make people more adapted in some environments and less adapted in other environments. For example, a genetic variation that contributes to hyperactivity boosts success of nomadic tribesmen but makes them less successful when they move into urban environments. A lot of people with Attention Deficit Disorder (ADD) and Attention Deficit Hyperactivity Disorder (ADHD) probably have what we consider a disability in industrial society because their ancestors did better by having the genes that cause these cognitive states. Today ADHD causes people to be more violent and criminal.
While politically correct dogma would have us believe that humans are extremely similar excepting for appearances the latest genetic research shows that human groups are evolutionarily diverging from each other and in many ways. But these insights from research are entirely missing from political discussions.
As my regular readers know, I think we are on the verge of an enormous explosion of discoveries about human genetics and the roles genes play in causing differences in cognitive function, athletic performance, health, and other aspects of human function. People who anchor their political beliefs in either supernatural religious or secular religious belief systems are going to find the foundations of their beliefs blown away by this coming torrent of discoveries.
Too much fat causes lower eyelids to sag with age. This suggests mini-liposuction will work to reverse and prevent it.
Many theories have sought to explain what causes the baggy lower eyelids that come with aging, but UCLA researchers have now found that fat expansion in the eye socket is the primary culprit.
As a result, researchers say, fat excision should be a component of treatment for patients seeking to address this common complaint.
The study, published in the September issue of the peer-reviewed Journal of Plastic and Reconstructive Surgery, is the first to examine the anatomy of multiple subjects to determine what happens to the lower eyelid with age. It is also the first to measure what happens to the face with age using high-resolution magnetic resonance imaging (MRI).
"A common treatment performed in the past and present is surgical excision of fat to treat a 'herniation of fat' — meaning that the amount of fat in the eye socket does not change but the cover that holds the fat in place, the orbital septum, is weakened or broken and fat slips out," said lead author Dr. Sean Darcy, a research associate in the division of plastic and reconstructive surgery at the David Geffen School of Medicine at UCLA and a plastic surgery resident at the University of California, Irvine. "This orbital septum weakening or herniation-of-fat theory is what most plastic surgeons have been taught.
"However, our study showed there is actually an increase in fat with age, and it is more likely that the fat increase causes the baggy eyelids rather than a weakened ligament," Darcy said. "There have been no studies to show that the orbital septum weakens."
The study looked at MRIs of 40 subjects (17 males and 23 females) between the ages of 12 and 80. The findings showed that the lower eyelid tissue increased with age and that the largest contributor to this size increase was fat increase.
It is surprising to me that this explanation was only figured out in the year 2008.
How do vegetables and fruits reduce our risk of cancer? While this latest report doesn't show every step on the mechanism of effect part of the effect can be measured by looking at levels of gene expression. Black raspberries partially restore gene expression to normal levels in rats after exposure to a carcinogen (a cancer causing compound).
COLUMBUS, Ohio – New research strongly suggests that a mix of preventative agents, such as those found in concentrated black raspberries, may more effectively inhibit cancer development than single agents aimed at shutting down a particular gene.
Researchers at the Ohio State University Comprehensive Cancer Center examined the effect of freeze-dried black raspberries on genes altered by a chemical carcinogen in an animal model of esophageal cancer.
After exposure to a carcinogen blackberry powder restored less than a fifth of the affected genes to normal level.
The carcinogen affected the activity of some 2,200 genes in the animals’ esophagus in only one week, but 460 of those genes were restored to normal activity in animals that consumed freeze-dried black raspberry powder as part of their diet during the exposure.
Better not get exposed to carcinogens in the first place. But a lot of the mutations that lead to cancer happen even in the absence of environmental carcinogens. They just happen at a faster rate when carcinogens are present.
A study on humans with a genetic disorder confirms animal studies: low brain derived neurotrophic factor (BDNF) causes unusually strong appetites and obesity.
A brain chemical that plays a role in long term memory also appears to be involved in regulating how much people eat and their likelihood of becoming obese, according to a National Institutes of Health study of a rare genetic condition.
Brain derived neurotrophic factor (BDNF) is, as its name implies, produced in the brain. Studies of laboratory animals have suggested it also helps control appetite and weight. The NIH study, appearing in the August 28 New England Journal of Medicine, provides the first strong evidence that BDNF is important for body weight in human beings as well.
The NIH researchers studied children and adults with WAGR syndrome, a rare genetic condition. The researchers found that some of the people with this syndrome lack a gene for BDNF and have correspondingly low blood levels of the substance. The people in this subgroup also have unusually large appetites and a strong tendency towards obesity.
"This is a promising new lead in the search for biological pathways that contribute to obesity," said Duane Alexander, M.D., director of the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development. "This finding may eventually lead to the development of new drugs to regulate appetite in people who have not had success with other treatments."
Not all adults with WAGR syndome have the BDNF deletion. Those with WAGR without the deletion do not have a higher rate of obesity.
In the current study, the NIH researchers conducted analyses of chromosome 11 in 33 patients with WAGR syndrome. A total of 19 patients (58 percent) had deletions of all or a major proportion of one copy of the gene for BDNF. By age 10, all of the 19 were obese and were reported to have a strong tendency to overeat. Moreover, all of the 19 had blood levels of BDNF that were roughly 50 percent lower than those of patients who had two working copies of the BDNF gene. The patients who had two working copies of the BDNF gene were no more likely to develop childhood onset obesity than the general population, and did not report unusually high levels of overeating.
Leptin, a known appetite regulator, might work by controlling release of BDNF by the hypothalamus. Perhaps BDNF injections could suppress appetite in obese people.
Dr. Yanovski explained that BDNF is believed to work in combination with a variety of other substances that regulate appetite and body weight. Chief among these is leptin, a hormone found to be involved in signaling hunger. Dr. Yanovski added that release of BDNF in the hypothalamus, a part of the brain involved in controlling eating, is believed to be indirectly triggered by leptin. Studies of the relationship between the two, and of BDNF's action on tissues, may lead to the development of new drugs to treat obesity in some individuals.
If the BDNF release by the hypothalamus then reaches the rest of the brain by the bloodstream that opens up the possibility of injecting BDNF into the bloodstream as a treatment to reduce appetite. Injection has obvious downsides such as that you have to do it in the first place. Diabetics already carry this burden. Poking a needle into yourself one or more times a day is a painful and potentially dangerous chore and need to store the BDNF in a refrigerator are all downsides. Plus, the injection regime would tend to cause larger and less frequent bursts of blood BDNF than natural hypothalamus release. What we need: embeddable reservoirs that would gradually release the BDNF. Another possibility: Use gene therapy to convert some cells in the body into BDNF producers.
As the cost of genetic testing and other biological testing comes down the rate of discoveries such as this one will only go faster and faster until most of the biological mechanisms in the human body are understood. With these discoveries will come a big shrinkage of our perceived ability to act with free will. So many genes will be found to have variants that influence behavior that a growing portion of all that we do will be attributed at least partially to genetic causes.
Another in my continuing series on why we should develop rejuvenation therapies that will cure aging. Before you die of old age you will spend about the last 15 years of your life getting dumber.
ST. PAUL, Minn. – A new study shows that older people's mental skills start declining years before death, even if they don't have dementia. The study is published in the August 27, 2008, online issue of Neurology®, the medical journal of the American Academy of Neurology.
"These changes are different and separate from the changes in thinking skills that occur as people get older," said study author Valgeir Thorvaldsson, MSc, of Göteberg University in Sweden. "We found accelerated changes in people's mental skills that indicated a terminal decline phase years before death."
Your ability to compare figures will go before your spatial ability which in turn will go before your verbal ability. But it is all down, down, down until your whole body crashes.
The start of the decline is different for various cognitive abilities. Perceptual speed, which measures how quickly people can compare figures, begins declining nearly 15 years before death. Spatial ability starts declining nearly eight years before death. And verbal ability starts declining about six-and-a-half years before death.
The study involved 288 people with no dementia who were followed from age 70 to death, with an average age at death of 84. The participants' mental skills were measured up to 12 times over a period of 30 years, and they were evaluated to make sure they had not developed dementia.
A number of factors may explain this terminal decline in mental skills, Thorvaldsson said. "Cardiovascular conditions such as heart disease or dementia that is too early to be detected could be factors," he said. "Increased health problems and frailty in old age often lead to inactivity, and this lack of exercise and mental stimulation could accelerate mental decline."
Thorvaldsson noted that verbal abilities declined sharply in the terminal phase and did not decline significantly due to age only. "This indicates that people remain stable in their verbal abilities unless they are experiencing disease processes that also increase their mortality risk," he said. "A change in verbal ability might therefore be considered a critical marker for degeneration in health in older people."
I do not want to become dumber. Aging is a thief. It steals parts of your mind.
Halting and reversing brain aging is pretty much the most difficult rejuvenation therapy challenge in the human body. For other organs we will be able to grow younger replacements. Got a bad part? Replace it with a newer part. Medicine will become more like auto repair. But the brain needs to be rejuvenated in place. So will will need to focus on stem cells, gene therapy and nanodevices to repair the brain cells in place. That's a much tougher challenge than figuring out how to grow a new liver or kidney.
Are you easily startled? When DNA testing becomes very cheap you'll be able to find out if your COMT gene is to blame. If you can't stop from fixating on bad memories and fixate on bad scary things happening around you blame it on your COMT gene.
Inborn differences may help explain why trauma gives some people bad memories and others the nightmare of post-traumatic stress. Scientists in Germany and the United States have reported evidence linking genes to anxious behavior.
...
Researchers including Martin Reuter, PhD, of the University of Bonn, Germany, recruited 96 women averaging 22 years old from the Giessen Gene Brain Behavior Project, which investigates biomolecular causes of individual differences in behavior.
The researchers first determined which participants carried which variations (alleles) of the COMT gene, which encodes an enzyme that breaks down dopamine, weakening its signal. (COMT stands for a catabolic enzyme named catechol-O-methyltransferase.) Scientists call its two alleles Val158 and Met158. Depending on ethnicity, more or less half the population carries one copy of each. The rest of the population is roughly divided between carrying two copies of Val158 and two copies of Met158.
Using a well-validated psychophysiological measure, the researchers next measured the intensity of each participant's startle response by attaching electrodes to the eye muscles that, upon emotional arousal, contract and cause a blink. Participants then viewed pictures that were emotionally pleasant (such as animals or babies), neutral (such as a power outlet or hairdryer), or aversive (such as weapons or injured victims at a crime scene) -- 12 pictures of each type for six seconds each. A loud, 35-millisecond white noise, called a startle probe, sounded at random while they watched. When participants blinked, showing the startle response, a bioamplifier took readings from the electrodes and sent the information to a computer for analysis.
People carrying two copies of the Met158 allele of the COMT gene showed a significantly stronger startle reflex in the unpleasant-picture condition than did carriers of either two copies of Val158 allele or one copy of each. The two-Met carriers also disclosed greater anxiety on a standard personality test.
This finding confirms that specific variations in the gene that regulates dopamine signaling may play a role in negative emotionality. The authors speculated that the Met158 allele may raise levels of circulating dopamine in the brain's limbic system, a set of structures that support (among other things) memory, emotional arousal and attention. The researchers said that more dopamine in the prefrontal cortex could result in an "inflexible attentional focus" on unpleasant stimuli, meaning that Met158 carriers can't tear themselves away from something that's arousing -- even if it's bad.
Unpleasant stimuli are often undesirable conditions in one's environment. One can imagine why the tendency to focus on such things would be adaptive. Some of them would be problems that needed solving or threats that needed combating.
COMT is probably one of many genes that influence anxiety and the startle reflex. For some reason the Met158 allele of COMT is fairly new in human evolution. I wonder what the selective pressures were that led to its emergence.
The Met158 allele was created by a relatively recent mutation and only in the evolution of human beings. Other primate species such as chimpanzees carry only the Val/Val genotype. Co-author Christian Montag, Dipl. Psych., observes that for humans, wariness may have been adaptive. He points out, "It was an advantage to be more anxious in a dangerous environment."
Genetic variations in a protein that causes blood vessel growth, vascular endothelial growth factor (VEGF), appears to cause differences in brain size.
New Haven, Conn. — The size of a key area of the brain involved in memory and mood disorders is influenced by variation in a growth factor gene that influences blood vessel growth and has been widely studied in heart disease and cancer, Yale University researchers have found.
The magnetic resonance imaging brain scanning and genetics study, published online Tuesday in the journal Biological Psychiatry, is another piece of emerging evidence suggesting that vascular endothelial growth factor, or VEGF, may be crucial to mental health. And the variations in brain volume associated with the VEGF gene suggest a possible cause of cognitive symptoms reported by some patients using anti-VEGF therapies for cancer and other diseases.
We are on the cusp of a period of great discoveries in brain genetics. Hundreds (or perhaps thousands) of genetic variations that influence personality, behavior, and intellectual abilities will be discovered in the next decade. One use of this information will be to select between embryos for implantation when doing in vitro fertilization (IVF). In fact, the ability to use the genetic discoveries to select embryos will drive a surge in the use of IVF as people try to give their kids every possible competitive advantage.
Some of the genetic discoveries will be usable by those of us who already exist. For example, it will probably become possible to use gene therapy and cell therapy to change which genetic version of VEGF a person has as a way to boost blood vessel growth in the hippocampus. This might improve memory formation and reduce depression.
Now it appears that this growth factor may also be crucial for the development and repair of the hippocampus, an area of the brain where memory is consolidated and which has been implicated in mood disorders such as depression and in dementias such as Alzheimer’s disease.
When drugs, gene therapies, and cell therapies become available that will allow you to change your personality will you opt to do so? Most people in a recent study indicated they don't want to change cognitive traits that they think are fundamental to their identity. So which traits do you think are fundamental to your identity? Would you like to change any of them?
Healthy people are more willing to take drugs to enhance traits that are not fundamental to their identity.
According to a new study in the Journal of Consumer Research, people's willingness to take a pill or drug depends on whether the trait the drug promises to enhance is one they consider fundamental.
Authors Jason Riis (NYU, Harvard Business School), Joseph P. Simmons (Yale University), and Geoffrey P. Goodwin (Princeton University) examine the moral dilemmas that arise as technologies develop that not only cure disease but also enhance already-healthy people. As many young people without diagnosed disorders or deficits take Ritalin or Adderall to improve concentration or anti-depressants to lift their moods, this study examines what makes healthy people willing to take pills.
People do not see increasing their ability to concentrate as something that would alter their identity.
The researchers determined that people do not feel comfortable using a pill to enhance a trait they believe to be fundamental to their identity. But less-fundamental traits, including concentration, are more acceptable targets.
"We suggest that people's willingness to take psychological enhancements will largely depend on beliefs about whether those enhancements will alter characteristics considered fundamental to self-identity," the authors write.
During a series of studies, the researchers found that young people were less likely to agree to take a drug to increase their social comfort than one that increased their ability to concentrate. The most common reason participants said they wouldn't want to take a pill was because it would "fundamentally change who I am."
But with proper marketing it is possible to sell people on more kinds of changes to who they are.
Not surprisingly, the marketing message affected participants' responses. When the researchers tested different advertising taglines, they found that participants responded more positively to a drug promising to help them become "more than who you are," than one that would allow them to become "who you are."
"Together, this research converges to highlight the importance of identity expression and preservation in governing the choices and lives of consumers," write the authors.
Will introverts opt to become extroverts? I think it more likely introverts will decide to become extroverts than vice versa. What do you think?
Imagine you could make yourself more likely or less likely to become angry when you see something that you think is morally wrong. Would you tune your emotional response? If so, in which direction?
If public nudity makes you deeply embarrassed would you like to alter your brain so that you do not feel any embarrassment or shame when nude in front of others? Or would you like to suppress the embarrassment response in any other circumstances?
Would you be willing to use biotechnology such as neural stem cells to make you more relaxed or more confident or change something else about your mental state?
Here is one of the most fundamental traits: Do you find yourself having moral reactions that you intellectually disagree with on some level? Would you like to alter what you find morally wrong or morally acceptable?
Even New York isn't big enough to maintain all its direct destinations.
Starting next month, nonstop flights between New York and 25 domestic and international cities will disappear, and service to another 55 cities will be sharply curtailed, according to FareCompare.com, an airline-ticket research site that analyzed fall flight schedules at the request of Crain's.
Bangkok Thailand is among the cities losing direct service to the Big Apple. Ditto Bologna, Naples, and Palermo Italy. You'll probably have to go via Rome. Tucson Arizona will lose direct service too. A lot more people will be taking connecting flights and spending more time in intermediate airports.
A couple of months ago I came across a report that if (or, rather, when) oil prices go high enough direct flights across the United States and over similar distances on other continents will become rare. Instead people will travel in aircraft that go in hops. The problem with direct flights is that the fuel for the last part of the journey has to get carried the entire distance. Carrying fuel uses fuel to push that fuel along. So airplanes if airplanes carry less fuel and stop more often they become more fuel efficient. The elimination of direct flights from New York is probably partly a reflection of this fact.
Last year analysts estimated it cost around $60 a barrel to produce light oil from here. The most recent estimate from the Canadian Association of Petroleum Producers (CAPP) now puts that number at $75 to $90. Comparatively, Saudi Arabian crude is said to cost around $1 a barrel.
The oil tar sands in Alberta are not the only expensive place to produce oil. The deep water Gulf of Mexico oil has a similar cost.
Peter Robertson, vice chairman of Chevron, recently told lawmakers that the cost of new production in the deep water Gulf of Mexico could exceed $95 a barrel.
I would expect Tupi and other deep water fields off of Brazil to have similar or even higher costs.
One can find a similar trend across the fossil fuels extraction industries. Chesapeake Energy, a big natural gas outfit, reports more than a doubling in the cost of natural gas extraction from 2Q 2003 to 2Q 2008.
A deep recession could cause prices to fall below marginal costs. But prices will eventually rise up to or above marginal production costs. The age of cheap fossil fuels has ended. We can't enter a new era in cheap energy prices without breakthroughs in solar, nuclear, and biomass energy.
The US Food and Drug Administration (FDA) and similar agencies in other industrialized countries get politically punished more for approving drugs that turn out to have unexpected side effects. At the same time they few rewards for taking risks to approve drugs that might turn out to deliver large benefits. The willingness of politicians to criticize the FDA when drugs turn out to cause unexpected harm probably plays a role in a very large reduction in the rate at which the FDA approves drugs.
Why do terminally ill patients have to wait so long to get access to the only treatments that hold any promise of saving their lives? And why is it not their right to decide?
The problem has been magnified in recent years as the number of new drug approvals has fallen dramatically. The FDA approved just 16 new drugs last year, and is on pace to approve only 18 this year. That's down from a high of 53 in 1996 and 39 in 1997.
After a few high-profile drug scares, such as the 2004 withdrawal of Vioxx from the market, FDA officials have become gun-shy about approving new products. After all, the agency receives scathing criticism from Congress and the press when an approved drug turns out to be more risky than expected -- but rarely for keeping beneficial ones off the market.
This trend does not bode well for the development of rejuvenation therapies. The FDA will hold off approval of an anti-cancer drug for people who have a fatal disease. Never mind that people who have a fatal disease are going to die anyway. The FDA won't let people take a risk when they have little to lose. That makes no sense to me.
Rejuvenation therapies are going to treat that fatal disease called aging. Absent those therapies we are all going to die from complications of aging. Weakened immune systems will allow cancer cells to grow and spread. Weakened hearts and clogged arteries will lead to heart attacks and strokes. Aged brains and probably aged immune systems will allow junk to accumulate in our brains leading to neural cell death and eventual death from Alzheimer's or other brain diseases.
Faced with rising risks of death combined with increasing pain and disablement people should be given wider latitude to try new and unproven therapies. Once diagnosed with terminal illnesses people should be freed from government mandated restrictions on available therapies.
The outlook for concentrating solar electric power is sunny.
In fact, there’s a land rush at the federal Bureau of Land Management. As of July, the BLM reported more than 125 applications to build solar power on about 1 million acres of desert, up from just a handful of proposals a few years ago.
“We think there’s a good market there,” says Travis Bradford, an expert at the Prometheus Institute, a Boston-based solar-energy market research firm. His firm sees 12,000 megawatts (12 gigawatts) of solar thermal installed by 2020 and maybe 20 times that in coming decades.
That 12 gigawatts is probably equivalent to less than 6 gigawatts of solar. In fact, if it is based on peak power at noon then is average power even 4 gigawatts? That'd amount to less than 3 new nuclear power plants. This is the problem with solar power. The big scale-up doesn't become substantial for years to come.
Concentrated solar's estimated cost is similar to that of natural gas electric. But natural gas electric is available when you want it. So solar has to be cheaper in order to compete with natural gas without subsidy. Also, natural gas electric is more expensive than coal, wind, and nuclear electric. When solar falls down far enough to compete with the latter three sources that's when it becomes very interesting.
Concentrating solar technology produces electricity for about 17 cents per kilowatt hour (kWh), Mehos estimates. But subsidies remain critical to solar thermal development in both the US and Spain, two global hotbeds of CSP development. With the federal investment tax credit, or ITC, costs drop to about 15 cents per kWh – low enough to compete with natural gas.
A key feature of solar thermal is its potential to use heat-storage technology to generate power after the sun sets. Nevada Solar One is considering adding a molten-salt or similar system to allow it to supply power for several hours after sundown.
With such storage systems, solar thermal becomes even more attractive to utilities, experts say. Arizona Public Service is contracting with Abengoa to build a 280-megawatt solar thermal plant near Phoenix that will cost more than $1 billion and have molten-salt heat storage.
Storage means additional costs. But since concentrating solar produces heat before it produces electricity that heat creates the potential for storing the heat as a way to generate electricity after the sun goes down. That gives concentrating solar an advantage over photovoltaics (PV).
While concentrating solar is currently cheaper than photovoltaics I expect that will not always be the case. The company First Solar looks set to bring solar photovoltaics costs well below current concentrating solar electric costs.
But if you want the off-peak market, you’ll have to price your cells at about US $1 per watt. That price is called grid parity, and it’s the holy grail of the photovoltaic industry. At least 80 firms around the world, from Austin to Osaka, are in the chase.
Surprisingly, at the moment no company is closer to that grail than a little start-up called First Solar, which until very recently had been known only to specialists. It’s located in Tempe, Ariz., and analysts agree that it will very likely meet typical grid-parity prices in developed countries in just two to four years. It’s got a multibillion-dollar order book, it’s selling all the cells it can make, it’s adding production capacity as fast as it can, and its stock price has rocketed from $25 to more than $250 in just 18 months.
If First Solar alone can make 1 gigawatt of PV in 2010 and PV growth rates continue near 2008's level then then PV installations probably will leave concentrating solar in the dust.
Right now, First Solar depends mainly on a government-subsidized program in Germany, where it has contracts worth more than $6 billion through 2012. Other markets with the same type of subsidies (known as feed-in tariffs, which spread the cost of alternative energy among all customers) include France, Italy, Spain, South Korea, and Ontario, Canada. To fill these orders, the company is undergoing a massive expansion of its manufacturing facilities that should boost annual production capacity to just over 1 gigawatt by 2009. This capacity could supply one-sixth of that year’s estimated global solar-cell business, which is currently growing at 50 percent per year.
Maybe concentrating solar's big competitive long term advantage against PV is the ability to produce heat energy for storage. What do you think? Does concentrating solar have a big future?
Genetic engineering can make mice that are more or less addicted to cocaine than normal mice.
Using genetic engineering, researchers headed by Professor Dr. Günther Schütz at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have now been able to selectively switch off those protein components in dopamine-producing neurons that are integrated into the receptor complexes under the influence of cocaine. Jointly with the team of Professor Dr. Rainer Spanagel at the Central Institute of Mental Health (Zentralinstitut für Seelische Gesundheit, ZI) in Mannheim and the research group of Professor Dr. Christian Lüscher at Geneva University, the Heidelberg researchers studied the changes in physiology and behavior of the genetically modified animals.
The scientists performed standardized tests to measure addictive behavior in the animals. At first sight, both the genetically modified and the control animals displayed the usual behavior under the influence of cocaine. Forced to increase their agility, the lab animals covered significantly greater running distances and preferentially frequented those places where they had been conditioned to be regularly administered the drug.
If normal mice do not find drugs at the familiar places over a longer period of time, their addictive behavior and preference for the cocaine-associated places subside. However, this is not true for animals whose receptor subunit GluR1 has been switched off: These mice invariably frequent the places where they expect to find the drug, i.e., their addictive behavior persists.
Mice whose NR1 protein has been switched off have surprised scientists with a different conspicuous behavior. If control animals withdrawn from cocaine are readministered the drug after some time, addictive behavior and drug seeking are reactivated. In contrast, NR1 deficient animals proved to be resistant to relapsing into the addiction.
So find a drug that will suppress NR1 in humans and maybe kicking coke addictio would become a lot easier.
Blocking the gene NR1 and activating the gene GluR1 might extinguish cocaine addiction.
"It is fascinating to observe how individual proteins can determine addictive behavioral patterns," says Günther Schütz, and his colleague Rainer Spanagel adds: "In addition, our results open up whole new prospects for treating addiction. Thus, blocking the NR1 receptor might protect from relapsing into addiction. Selective activation of GluR1 would even contribute to 'extinguishing' the addiction."
Imagine a person genetically engineered with an assortment of genes that can be turned on and off to cause changes in behavior. Genetically engineered soldiers could be given a compound in their drinks that turn them alternatively docile in peace time or aggressive for training or war time. Or some really rich guy could pay surrogate parents to raise a genetically daughter who could be made to fall in love with and be totally loyal to whoever she was exposed to after eating a dinner with a special compound in it. The possibilities are endless.
Or how about this: an injectable gene therapy that will cause a person become more easily manipulated to switch loyalties. Spies could kidnap someone and turn them against their nation.
One of the hopes for rejuvenation therapies is to develop biotechnologies that can induce senescent (old and barely functioning) cells to commit suicide in order to make room for healthier cells to divide and take their place. But senescent cells serve useful functions.
Although post-reproductive life in humans is often associated with decline and a loss of powers, an analogous state in certain cells -- called senescence -- is proving to be one of ironic potency. Scientists at Cold Spring Harbor Laboratory (CSHL) today reported that a particular class of senescent liver cells orchestrates a sequence of events in living mice that can limit fibrosis, a natural response of the liver to acute damage.
The surprising finding follows on the heels of experiments conducted by the same CSHL team last year linking senescence in liver cells with the organ's ability to fight off liver cancer, also called hepatocellular carcinoma, or HCC.
The new findings are the first to establish a specific role for cellular senescence in a non-cancer pathology, and, the CSHL team notes, suggests a new therapeutic approach that could help human patients with precursors of serious liver diseases such as cirrhosis, which is the 12th most common cause of death in the United States.
Of course we need cures for cancer anyway. But these results might be the tip of the iceberg in terms of useful purposes served by senescent cells.
My fear on rejuvenation therapies is that it might be necessary to orchestrate many forms of repair at once in order to keep cells and metabolism in balance. If destroying senescent cells will increase the incidence of other forms of disease and malfunction then we will at least need to weigh the relative risks of treatment versus non-treatment.
" Fibrosis is a disease of many organs—lungs, kidneys, pancreas, prostate, skin," said Valery Krizhanovsky of Cold Spring Harbor Laboratory. "It's possible this mechanism in the liver is relevant to fibrotic situations in other tissues."
The state of cell-cycle arrest known as senescence was first described decades ago, but the phenomenon was thought to occur only in cultured cells in the laboratory, Krizhanovsky explained. More recent studies found that cellular senescence helps protect against the formation of tumors and aids in the response to certain anticancer agents.
Interestingly, the researchers said, senescent cells had also been observed in some aged or damaged tissues, including the cirrhotic livers of human patients. However, the functional contribution of cellular senescence to diseases other than cancer hadn't been examined.
Of course, just as better cancer treatments could eliminate concern that cancer could come as a complication of rejuvenation therapy a better treatment for fibrosis could eliminate the need for senescent cells to protect against fibrosis.
Update: Note that the need to leave senescent cells in place goes way down once we can replace whole organs. No need for senescent cells to suppress nearby cancer cells if all the cells in an organ are youthful and relatively undamaged. Grow new organs from a well tested stem cell line and then when, say, a new youthful liver replaces an old liver we get rid of the senescent cells and the precancerous cells at the same time.
If neuroendocrinologist Dr Zane Andrews has it right aging of appetite control neurons reduces appetite suppression in the brain and thereby causes excess eating.
A Monash University scientist has discovered key appetite control cells in the human brain degenerate over time, causing increased hunger and potentially weight-gain as we grow older.
The research by Dr Zane Andrews, a neuroendocrinologist with Monash University's Department of Physiology, has been published in Nature.
Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars.
Yet another vicious cycle. Your brain becomes damaged by the carbs. That makes you want more carbs. Hey, carbs are like cocaine. Insert my recurring comments about a lack of free will here.
"The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more," Dr Andrews said.
Dr Andrews said the attack on appetite suppressing cells creates a cellular imbalance between our need to eat and the message to the brain to stop eating.
"People in the age group of 25 to 50 are most at risk. The neurons that tell people in the crucial age range not to over-eat are being killed-off.
The proopiomelanocortin (POMC) neurons get hit by free radicals. We need neural stem cell therapy to replace POMC neurons to get our appetites under control. Imagine that. Stem cells for weight control.
"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMC's kick in.
"However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied," Dr Andrews said.
The free radicals also try to attack the hunger neurons, but these are protected by the uncoupling protein 2 (UCP2).
Oh what wretches we are. Dietary advice to replace fats with carbs might have sealed our fates and doomed us to early deaths. Even if we turn away from potatoes and buns today the damage has already been done.
Dr Andrews said the reduction in the appetite-suppressing cells could be one explanation for the complex condition of adult-onset obesity.
"A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration," Dr Andrews said.
Dr Andrews' next research project will focus on finding if a diet rich in carbohydrates and sugars has other impacts on the brain, such as the increased incidences of neurological conditions like Parkinson's disease.
We lack free will. It gets worse as we age. We need stem cell therapies to restore at least the illusion of free will - as well as make us skinnier and younger looking and feeling.
North America goes thru periodic droughts and cooling
ATHENS, Ohio (Aug. 19, 2008) – A stalagmite in a West Virginia cave has yielded the most detailed geological record to date on climate cycles in eastern North America over the past 7,000 years. The new study confirms that during periods when Earth received less solar radiation, the Atlantic Ocean cooled, icebergs increased and precipitation fell, creating a series of century-long droughts.
A research team led by Ohio University geologist Gregory Springer examined the trace metal strontium and carbon and oxygen isotopes in the stalagmite, which preserved climate conditions averaged over periods as brief as a few years. The scientists found evidence of at least seven major drought periods during the Holocene era, according to an article published online in the journal Geophysical Research Letters.
“This really nails down the idea of solar influence on continental drought,” said Springer, an assistant professor of geological sciences.
The sun is not a reliable supplier of light radiation. You can't trust the sun. It gets all bent out of shape by magnetic field fluctuations.
Geologist Gerald Bond suggested that every 1,500 years, weak solar activity caused by fluctuations in the sun’s magnetic fields cools the North Atlantic Ocean and creates more icebergs and ice rafting, or the movement of sediment to ocean floors. Other scientists have sought more evidence of these so-called “Bond events” and have studied their possible impact on droughts and precipitation. But studies to date have been hampered by incomplete, less detailed records, Springer said.
But we hopefully have hundreds of years to prepare for the next megadrought.
The climate record suggests that North America could face a major drought event again in 500 to 1,000 years, though Springer said that manmade global warming could offset the cycle.
If humans survive for the next 500 years and I'm still alive in a rejuvenated body I'm looking forward to the opportunity to do climate engineering to prevent a massive drought.
Here's a capability needed for Dr. McCoy's medical tricorder.
PHILADELPHIA, Aug. 20, 2008 — Chemists today described the first identification of a specific "odor profile" for skin cancer, a discovery that could form the basis of a rapid, non-invasive test for diagnosing the most common type of cancer in the United States. The findings may enable doctors in the future to diagnose skin cancer quickly and accurately by waving a handheld scanner or sensor above the skin, they reported today at the 236th national meeting of the American Chemical Society.
Note how they refer to doctors of the future using scanners to detect skin cancer. But once the technology becomes cheap enough it would make much more sense to embed cancer detection sensors in bathrooms, living rooms, and bed rooms. Scanning for cancer should become a daily practice in order to allow cancer to get detected at the earliest possible stage in development.
The researchers have found distinct patterns in the airborne chemicals that evaporate off of the surface of normal and cancerous skin cells. They expect nano-sensors to eventually allow the development of compact sensing equipment.
To examine whether skin odors change in people with skin cancer, Gallagher and colleagues used advanced chromatography techniques to sample and analyze the air above tumor sites in 11 patients diagnosed with basal cell carcinoma, the most common type of skin cancer with more than one million new cases every year. They compared the profile of chemicals detected above the tumor sites to profiles obtained from skin of 11 individuals without cancer.
"We found a different profile of chemicals above tumor sites relative to healthy skin," says Gallagher. "The same chemicals are present, but at skin cancer sites some chemicals are increased, while others are decreased compared to healthy individuals." She declined to give specific details about the chemicals found, noting that the researchers had applied for a patent on their technique.
The scientists eventually plan to identify a reliable "odor profile" of all three forms of skin cancer, including squamous cell cancer and melanoma, the deadliest form. If successful, the researchers hope to combine their method with emerging nano-sensor "electronic nose" technology designed to identify odorous chemicals. Gallagher envisions a wand-like "E-nose" that can be moved across the skin and will set off an alarm or beep when cancer is detected, similar to the fictional medical "tricorder" from Star Trek.
One can imagine beds, sinks, toilets, and other locations in a house will all some day have sensors embedded in them that detect a large assortment of diseases at very early stages. Early detection will reduce the total amount of accumulated damage and will make cures much easier for some diseases like cancer.
A report about a new imaging technology for osteoarthritis diagnosis mentions yet another example of why we should want to defeat and reverse the aging process. Half the people over the age of 65 have osteoarthritis.
PHILADELPHIA, Aug. 20, 2008 — A newly developed medical imaging technology may provide doctors with a long-awaited test for early diagnosis of osteoarthritis (OA), scientists from New York reported today at the 236th National Meeting of the American Chemical Society. By far the most common form of arthritis, OA is a bane of the Baby Boom generation, causing joint pain and disability for more than half of those over 65 – nearly 21 million people in the United States.
You stand a pretty good chance of spending a substantial part of your life in pain.
Magnetic resonance imaging can detect low levels of vital joint polymer glycosaminogycan (GAG) as an indication of osteoarthritis.
The new method uses a modified form of magnetic resonance imaging to determine the concentration of a polymer known as glycosaminogycan (GAG) that holds lots of water and gives cartilage its tough, elastic properties. GAG also is a recognized biomarker for both osteoarthritis and degenerative disc disease — a common cause of back pain. According to Jerschow, a low concentration of GAG is known to correlate with the onset of osteoarthritis and other cartilage disorders.
The diagnostic "tags" the hydrogen atoms attached to the GAGs in a way that makes them emit a signal that can be picked up by an MRI machine to determine the concentration of GAG and assess cartilage health.
Advanced OA is very easy to diagnose, Regatte points out. By then, however, joint replacement may be the only option. With early detection, physicians could prescribe dietary supplements, medication or other measures to ward off further cartilage damage.
Some day we'll have stem cell therapies and gene therapies to do joint rejuvenation. Before getting treated will we first get ourselves scanned for signs of deterioration? I'm thinking if joint stem cell therapies become available in 10 to 15 years for anyone over 40 treatment will make sense. Why even let the earliest stages of deterioration to happen before restoring joints to youthful condition?
On more than one occasion I've found myself defending drug addicts while arguing with someone who is obese. Basically I argued that their own inability to ignore their hunger is very similar to a drug addict's inabilty to ignore the craving for another dose. Each person who I made this argument to responded like I was insulting them. But the evidence strongly suggests common mechanisms involved in food and drug cravings. Now a new study finds that a drug under development against cocaine and meth causes weight loss in rats.
UPTON, NY -- Vigabatrin, a medication proposed as a potential treatment for drug addiction by scientists at the U.S. Department of Energy's (DOE) Brookhaven National Laboratory, also leads to rapid weight loss and reduced food intake according to a new animal study from the same research group. The study will be published online August 20, 2008, by the journal Synapse. Vigabatrin is currently undergoing U.S. Food and Drug Administration (FDA)-approved Phase II clinical trials against cocaine and methamphetamine addiction across the U.S.
In the current study, animals genetically bred to be obese experienced a loss of up to 19 percent of their total weight while non-obese animals lost 12 to 20 percent following short-term vigabatrin administration.
This might seem like good news for people who weigh too much. But it might also be bad news for coke and meth addicts. Will they eat enough while on this drug? Maybe so. Then again, if the drug works and they stop their drug addiction then that's a huge benefit.
"Our results appear to demonstrate that vigabatrin induced satiety in these animals," said Amy DeMarco, who led the study, working in the laboratory of Brookhaven Lab senior scientist Stephen Dewey. Dewey first identified vigabatrin as a potential addiction treatment and has conducted more than 20 years of preclinical research with this promising medication.
Earlier studies at Brookhaven Lab found a strong connection between obesity and addiction, including similar changes in the brains of the obese and those addicted to drugs like cocaine. Based on these connections, Dewey hypothesized that vigabatrin would quench food cravings in the lab rats.
This drug alters people's basic desires. If our desires can be altered so easily do we really have free will?
Getting to another lifetime seems unlikely even using the most advanced technologies.
The major problem is that propulsion -- shooting mass backwards to go forwards -- requires large amounts of both time and fuel. For instance, using the best rocket engines Earth currently has to offer, it would take 50,000 years to travel the 4.3 light years to Alpha Centauri, our solar system's nearest neighbor. Even the most theoretically efficient type of propulsion, an imaginary engine powered by antimatter, would still require decades to reach Alpha Centauri, according to Robert Frisbee, group leader in the Advanced Propulsion Technology Group within NASA's Jet Propulsion Laboratory.
Why go in the first place? Unless we could know in advance that travel to another solar system would provide us with a planet suitable for colonization what is the point in going? We have other types of planets to visit in this solar system. So we go to another solar system and it too has gas giants. For this I'm going to sit in a spacecraft for 50 years? I don't think so.
The development of rejuvenation therapies will eventually make it possible to travel to another solar system and live to see your spacecraft reach its destination. Though success will require design of spacecraft that are highly reliable for decades. Do not step on board until mean time between fatal failures is measured in the hundreds or thoiusands of years.
There's always the possibility that a discovery in physics will let us travel across the galaxy via another dimension. Hard to guess the odds of this happening.
You might be saying "but what about the opportunity to meet space aliens?". But there's a problem: either your microbes will kill them or their microbes will kill you. The odds of living on the same planet as creatures from another world seem pretty remote. Besides, they might be extremely xenophobic killers who enjoy hunting down and killing other intelligent species.
The purpose of this post is to provide you with health advice that you will enjoy following. Too many forms of health advice are joyless. Use cocoa powder without guilt.
McLEAN, VA (August 18, 2008) – Cocoa flavanols, the unique compounds found naturally in cocoa, may increase blood flow to the brain, according to new research published in the Neuropsychiatric Disease and Treatment journal. The researchers suggest that long-term improvements in brain blood flow could impact cognitive behavior, offering future potential for debilitating brain conditions including dementia and stroke.
In a scientific study of healthy, older adults ages 59 to 83, Harvard medical scientists found that study participants who regularly drank a cocoa flavanol-rich beverage made using the Mars, Incorporated Cocoapro® process had an eight percent increase in brain blood flow after one week, and 10 percent increase after two weeks.
In this first-of-its-kind study, the researchers found both short and long-term benefits of cocoa flavanols for brain blood flow, offering future potential for the one in seven older Americans currently living with dementia. When the flow of blood to the brain slows over time, the result may be structural damage and dementia. Scientists speculate that maintaining an increased blood flow to the brain could slow this cognitive decline.
I see from Googling that Mars sells this high flavanol chocolate under the CocoaVia brand. Some comments on the web say it is bitter. That is why flavanols get removed by most chocolate companies from chocolate during processing. But I'll put up with the bitter (more likely drown the bitter in honey) for the health benefits. Worth a try.
Somewhere around 6 months of age babies suddenly start paying much more attention to fearful faces.
Scientists working in the Academy-funded Research Programme on Neuroscience (NEURO) have discovered important changes in the way that infants react to another person’s face at age 5–7 months.
Infants aged 5 months react very differently to a fearful face than those aged 7 months. “At the age of 7 months babies will watch a fearful face for longer than a happy face, and their attentiveness level as measured by EEG is higher after seeing a fearful than a happy face. By contrast, infants aged 5 months watch both faces, when they are shown side by side, for just as long, and there is no difference in the intensity of attention in favour of the fearful face,” said Mikko Peltola, researcher at the University of Tampere, at the Academy’s Science Breakfast this week.
It seems that at age 6 months, important developmental changes take place in the way that infants process significant emotional expressions. A fearful face attracts intense attention by the age of 7 months. In addition, it takes longer for infants to shift their attention away from fearful than from happy and neutral faces.
I wonder how much variability there is in when this transition happens. Also, do babies with Asperger's Syndrome or autism go through this same transition in how they react to fearful faces and do they do this at the same point in time as normal children?
Also, is the intense attention to fearful faces a defense mechanism? Or is it a pointless reaction at age 6 months but a capability that needs to come sooner or later which just happens to occur at 6 months?
The rarer tree species are especially vulnerable to extinction.
Common tree species in the Amazon will survive even grim scenarios of deforestation and road-building, but rare trees could suffer extinction rates of up to 50 percent, predict Smithsonian scientists and colleagues in the Aug. 12 issue of the journal Proceedings of the National Academy of Science.
How resilient will natural systems prove to be as they weather the next several decades of severe, human-induced global change? The debate is on between proponents of models that maximize and minimize extinction rates.
The Amazon basin contains about 40 percent of the world's remaining rainforest. One of the fundamental characteristics of tropical forests is the presence of very rare tree species. Competing models of relative species abundance, one based on Fisher's alpha statistic and the other based on Preston's lognormal curve, yield different proportions of rare trees in the forest.
It isn't clear how much of the expected extinction they expect will come from climate change versus logging and conversion of forests to pasture and farm land.
A few thousand tree species might be lost.
In this offering, the authors use the neutral theory to predict the number of tree species and to test predictions of the Millenium Ecosystems Assessment that forecasts major tree extinctions in the Amazon over the next several decades. First, they estimate that the Brazilian Amazon has (or had) 11,210 large tree species, and, of these, 5,308 species are classified as rare.
Based on optimistic and non-optimistic scenarios for road construction in the Amazon published by the Smithsonian's William Laurance and colleagues in the journal Science in 2004, they predict that the rare species will suffer between 37 and 50 percent extinction, whereas the extinction rate for all trees could be from 20 to 33 percent overall.
How much rain forest will survive the growth in demand for trees, livestock grazing land, and farm land for food and biomass energy crops? Economic development, population growth, and depletion of oil and natural gas fields each create pressures to convert more and more wild lands into industrial uses. Jungles look to become rare.
Here's another report on our role as puppets with genes as the puppeteers. A group of researchers has published a paper in Nature Genetics offering evidence that genes involved in calcium ion flow across nerve membranes might contribute to bipolar depression.
The largest genetic analysis of its kind to date for bipolar disorder has implicated machinery involved in the balance of sodium and calcium in brain cells. Researchers supported in part by the National Institute of Mental Health, part of the National Institutes of Health, found an association between the disorder and variation in two genes that make components of channels that manage the flow of the elements into and out of cells, including neurons.
"A neuron's excitability – whether it will fire – hinges on this delicate equilibrium," explained Pamela Sklar, M.D., Ph.D., of Massachusetts General Hospital (MGH) and the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard, who led the research. "Finding statistically robust associations linked to two proteins that may be involved in regulating such ion channels – and that are also thought to be targets of drugs used to clinically to treat bipolar disorder – is astonishing."
People with bipolar disorder have my sympathy. Until researchers can come up with better treatments for it a lot of people have to go thru a lot of suffering. Nature is a sadistic bastard.
Since researchers think many genes contribute to bipolar it is hard to pick out the genes that contribute from all the background noise. But the genes they suspect are involved in key functions done by neurons and the researchers had a large sample of bipolar and non-bipolar study participants for which they did DNA tests.
To boost their odds, Sklar and colleagues pooled data from the latter two previously published and one new study of their own. They also added additional samples from the STEP-BD study and Scottish and Irish families, and controls from the NIMH Genetics Repository. After examining about 1.8 million sites of genetic variation in 10,596 people – including 4,387 with bipolar disorder – the researchers found the two genes showing the strongest association among 14 disorder-associated chromosomal regions.
Variation in a gene called Ankyrin 3 (ANK3) showed the strongest association with bipolar disorder. The ANK3 protein is strategically located in the first part of neuronal extensions called axons and is part of the cellular machinery that decides whether a neuron will fire. Co-authors of the paper had shown last year in mouse brain that lithium, the most common medication for preventing bipolar disorder episodes, reduces expression of ANK3.
Variation in a calcium channel gene found in the brain showed the second strongest association with bipolar disorder. This CACNA1C protein similarly regulates the influx and outflow of calcium and is the site of interaction for a hypertension medication that has also been used in the treatment of bipolar disorder.
The fact that a hypertension medication works against bipolar is interesting though not unprecedented. Lots of drugs are originally developed for one reason and found to have benefits for other disorders.
Note that they looked at 1.8 million sites of known genetic variation. Ongoing projects aimed at identifying all sites where we genetically differ make this sort of study possible where it wouldn't have been possible even 5 years ago. Faster and cheaper ways to do DNA testing are going to cause a massive torrent of brain gene discoveries over the next 5 years.
If you can't stand for some people to have more than others then you'll be miserable. Sure glad I'm tolerant of rich people.
To add some ammo to these explanations, Napier and Tost conducted a series of surveys on political attitudes of Americans and citizens of 8 Western countries, using previously collected data. Their results affirmed the "conservatives are happy, liberals are mad" findings of previous polls, but income, education, religion and other demographic variables couldn't explain the happiness gap.
However, when the authors instead grouped people by their "rationalisation of inequality," the differences between conservatives and liberals dissolved. Republican or Democrat, people not bothered by social or economic disparities tend to be happy.
This trend held for non-Americans, as well. Right-wingers in the Czech Republic, Germany, New Zealand, Norway, Slovakia, Spain, Sweden and Switzerland were all happier than liberals, on average.
My guess is that genetic differences account for a substantial fraction of the observed difference. Maybe the resistance to inequality was selected for because for most of human evolution having more stuff upped the odds that a person would create offspring who would create offspring. Nowadays the reproductive fitness advantage of having more stuff is much less or non-existent. Poorer people are creating more progeny than richer people. Yet this trait remains in some people.
My guess is that when we know far more about how our genetic differences cause cognitive differences we are going to discover that many of our political differences flow from our genetic differences. This could make disagreements stir up stronger passions because people will lose faith in an important (and incorrect) idea that helps legitimize the institutions of society: The idea that most policy disagreements can eventually be resolved by reaching consensus as a result of debate. If the opposing side holds their views because they are wired up by their genes to have ethical preferences that differ from one's own then one can always expect to disagree with one's opponents on key issues.
Even though people will know that certain of their preferences and beliefs come as a result of their genes my guess is that people will still cling strongly to those preferences and beliefs. Knowing that one can never convince the opposition of the rightness of one's viewpoint could make people less willing to argue and more willing to just try to seize more power to get one's genetic preferences turned into policy.
Update: My subject title is not meant to imply that rationalization was required to accept inequality while not being required to object to it. Whether oneneeds to do more rationalization to accept inequality than to object to it remains an open question. But even if one requires more cogitating to accept inequality that does not imply that inequality is bad. It could be that accepting inequality is wise (after all, the countries that tried to stamp it out impoverished themselves) but that seeing that as the correct choice requires creating a pretty sophisticated model of the world.
Though no comprehensive survey of the heat pump sector exists, Energy Department statistics on units shipped tell a striking story. In 2003, system manufacturers shipped 36,439 units. In 2006, the last year for which data is available, manufacturers shipped 63,683 units.
Bridgette Oliver, marketing and communications manager for ClimateMaster in Oklahoma City, the nation’s largest manufacturer of ground-source heat pump equipment, confirmed a rapid rise in sales. “Between 2005 and 2007, our revenue increased by 200 percent,” she said. “Our employees increased by 176 percent.”
Those are pretty small numbers when compared with the number of buildings constructed per year and even more so when we consider all existing housing stock.
One ground sink heat pump installer in Seattle claims a 5 year pay-back period.
There is a catch. A geothermal system costs more to install. Maloney believes that may be the reason why geothermal systems haven't become widely popular.
"Our costs are usually about 50 percent more than conventional equipment," said Maloney, comparing a geothermal system with a high-efficiency furnace, hot-water heater and air-conditioner installation. "That 50 percent you'll generally see back in about five years."
He estimates the cost of providing a conventional natural-gas system, including a furnace, air conditioner and water heater, might be $10,000. A ground-source geothermal system probably would cost $15,000 to $20,000, he said.
The payback period depends on what you are using now. If you are using oil the payback of a heat pump is a lot shorter than if you are using natural gas for example. Also, your weather matters as well. The capital costs pay back more rapidly if you have a lot of days where you need central heat or central cooling. Plus, you have to consider efficiency of each heat pump model. They aren't all the same in efficiency.
This comparative heating cost calculator will let you figure out how much you could save by switching to a lower cost way of heating.
A Texas company says that it has developed a cheaper and cleaner way to convert natural gas into gasoline and other liquid fuels, making it economical to tap natural-gas reserves that in the past have been too small or remote to develop.
The company behind the technology, Dallas-based Synfuels International, says that the process uses fewer steps and is far more efficient than more established techniques based on the Fischer-Tropsch process.
If this process works well it will drive up the price of natural gas as more natural gas gets used to produce liquid fuels for transportation. That will, in turn, reduce the desirability of natural gas for use in heating and electric power generation.
A better way to convert natural gas into liquid fuels using small chemical plants would allow many smaller and/or remote natural fields to be tapped. For example, the natural gas on the northern slope of Alaska hasn't been exploited yet because the costs of building a natural gas pipeline to bring it down to the lower 48 states is quite high. A couple of pipelines are in early development. But a way to convert the Alaska natural gas to liquid form would allow the existing Alaska oil pipeline to move the liquid south.
The article also mentions another start-up company, Gas Reaction Technologies, a spin-off from UC Santa Barbara, which claims its gas-to-liquid technology will work well for medium and small sized natural gas fields.
If either of these companies substantially lowers the cost of gas-to-liquid that will undermine the rationale for the T. Boone Pickens proposal to shift more toward natural gas as a vehicle fuel. Why use natural gas directly when it can be converted to a far more convenient liquid form? But since the conversion itself uses energy natural gas converted to liquid fuel represents a loss of energy that would not occur if natural gas was directly burned in cars.
I am skeptical that we'll ever see a big shift to natural gas for vehicle transportation. Liquid fuels are more convenient and use up less trunk space. Technological developments that cut costs for doing the natural gas-to-liquid conversion will provide a more convenient and therefore more valuable way to use natural gas.
People fighting the battle of the bulge need every advantage they can use. Here's an easy one: Cut out the spice monosodium glutamate. People in rural Chinese villages who put MSG on their food weigh more than those in the same villages who do not use MSG.
CHAPEL HILL – People who use monosodium glutamate, or MSG, as a flavor enhancer in their food are more likely than people who don't use it to be overweight or obese even though they have the same amount of physical activity and total calorie intake, according to a University of North Carolina at Chapel Hill School of Public Health study published this month in the journal Obesity.
Researchers at UNC and in China studied more than 750 Chinese men and women, aged between 40 and 59, in three rural villages in north and south China. The majority of study participants prepared their meals at home without commercially processed foods. About 82 percent of the participants used MSG in their food. Those users were divided into three groups, based on the amount of MSG they used. The third who used the most MSG were nearly three times more likely to be overweight than non-users.
"Animal studies have indicated for years that MSG might be associated with weight gain," said Ka He, M.D., assistant professor of nutrition and epidemiology at the UNC School of Public Health. "Ours is the first study to show a link between MSG use and weight in humans."
Because MSG is used as a flavor enhancer in many processed foods, studying its potential effect on humans has been difficult. He and his colleagues chose study participants living in rural Chinese villages because they used very little commercially processed food, but many regularly used MSG in food preparation.
"We found that prevalence of overweight was significantly higher in MSG users than in non-users," He said. "We saw this risk even when we controlled for physical activity, total calorie intake and other possible explanations for the difference in body mass. The positive associations between MSG intake and overweight were consistent with data from animal studies."
My guess is that those animal studies were controlled interventional studies. Anyone know?
Want some meat on part of the argument for why a Scripps researcher expects big ocean extinctions? Here's a pretty impressive indicator of bad trends in the oceans: the hypoxic (oxygen deficient) dead zones are growing in size.
A global study led by Professor Robert Diaz of the Virginia Institute of Marine Science, College of William and Mary, shows that the number of "dead zones"—areas of seafloor with too little oxygen for most marine life—has increased by a third between 1995 and 2007.
How much of that dead zone size growth is due to expanded use of nitrogen fertilizers? All of it? The only development I can see on the horizon that will change this trend is Peak Oil. Declining availability of fossil fuels will push up the cost of nitrogen fertilizer made using natural gas. But at some price of fertlizer the use of wind, solar, or nuclear electric power will become competitive for nitrogen fertilizer production. So I do not expect a permanent shift toward lower nitrogen fertilizer usage.
Diaz and collaborator Rutger Rosenberg of the University of Gothenburg in Sweden say that dead zones are now "the key stressor on marine ecosystems" and "rank with over-fishing, habitat loss, and harmful algal blooms as global environmental problems."
The study, which appears in the August 15 issue of the journal Science, tallies 405 dead zones in coastal waters worldwide, affecting an area of 95,000 square miles, about the size of New Zealand. The largest dead zone in the U.S., at the mouth of the Mississippi, covers more than 8,500 square miles, roughly the size of New Jersey.
Diaz began studying dead zones in the mid-1980s after seeing their effect on bottom life in a tributary of Chesapeake Bay near Baltimore. His first review of dead zones in 1995 counted 305 worldwide. That was up from his count of 162 in the 1980s, 87 in the 1970s, and 49 in the 1960s. He first found scientific reports of dead zones in the 1910s, when there were 4. Worldwide, the number of dead zones has approximately doubled each decade since the 1960s.
As China develops, the US population grows by 50%, and other areas grow in population and industry this these dead zones will grow much larger. Is it possible for farmers to maintain high levels of crop production without nitrogen fertilizer run-off so high that it causes dead zones at the mouths of rivers?
Diaz and VIMS colleague Linda Schaffner estimate that Chesapeake Bay now loses about 10,000 metric tons of carbon to hypoxia each year, 5% of the Bay's total production of food energy. The Baltic Sea has lost 30% of its food energy—a condition that has contributed to a significant decline in its fisheries yields.
From 1974 to 2000 world nitrogen fertilizer usage grew by about a factor of 2.5. The economic development of China, southeast Asia, and India creates the possibility of a far larger growth in nitrogen fertilizer demand in the next 25 years. How big will the dead zones become?
The outlook for fertilizer demand is up up up.
The FAO report estimates that world fertilizer supply (nitrogen, phosphate and potash nutrient) will increase by some 34 million tonnes representing an annual growth rate of 3 percent between 2007/08 and 2011/12, comfortably sufficient to cover demand growth of 1.9 percent annually.
Total production is expected to grow from 206.5 million tonnes in 2007/08 to 241 million tonnes in 2011/12. Fertilizer demand will increase from 197 million tonnes today to 216 million tonnes in 2011/12.
World nitrogen supply is forecast to rise by 23.1 million tonnes by 2011/12; world phosphate fertilizer supply will increase by 6.3 million tonnes and potash supply by 4.9 million tonnes.
The Daily Telegraph has a worldwide map of hypoxic areas.
Update: A Time article reports use of winter wheat crops could catch nitrogen released by spring thaws. But that costs money and the incentive isn't there to do this.
Emily Singer in Technology Review reports on more extensive uses to tests to detect banned treatments for athleti