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 ratio 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 , 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 , 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 . 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?
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.
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 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?
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 addiction 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 engineered 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.
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.
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.
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?
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.
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?
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 one needs 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 seeing acceptance of inequality as the correct choice requires creating a pretty sophisticated mental 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.
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 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 of tests to detect banned treatments for athletic enhancement.
In an attempt to catch those athletes out, the Olympic antidoping lab has dramatically stepped up testing compared with previous games, conducting 1,000 more tests than in Athens in 2004 and double the number at the Sydney games in 2000. That increase comes largely from greater numbers of tests per sample, rather than from an increase in the number of samples collected.
Note the greater number of tests per sample. That probably reflects the use of gene chips and other miniaturization of biological testing devices. That miniaturization results in a level of automation, precision, and cost reduction that enables such a large number of tests on a single sample. So this is not so much a report on increased vigilance as increased ability to be vigilant.
The sports organizations are trying to stay ahead of the development of performance enhancement drugs.
The IOC and the World Anti-Doping Agency (WADA) are also developing new testing techniques, although they won't give details about any new tests that they plan to run at this year's Olympics. "We need the elements of secrecy to try to be ahead of the game," says Catlin. This secrecy won WADA a dramatic victory at the Tour de France last month. Its drug-testing lab caught several cyclists using a longer-lasting form of EPO called CERA. Soon after the athletes were caught, it was revealed that the agency had been working with Swiss drugmaker Roche to develop a test to detect CERA while the drug was still being tested by the U.S. pharmaceutical company Amgen.
I expect some future performance enhancement treatments will be harder to detect. As we learn how exercise causes the body to grow bigger muscles, more vasculature, and other changes that enhance performance we will also learn many more ways to intervene. Some of these ways will so closely mimic what exercise normally does to the body that it will be hard to tell them apart from exercise. Already recent advances have identified two compounds that mimic the effects of exercise. Many more will be found.
Attempts to regulate enhancement of athletes will run up against even tougher obstacles in the future. First off, genetic engineering to enhance offspring will put the earliest intervention point for athletic enhancement to before birth. Will some people be banned from athletic competition because they were genetically engineered? Some of them will be hard to detect unless their genetic sequences are compared against that of both parents.
Genetic enhancement after birth will become common as well. Parents will seek to remedy health and other deficiencies in their children by getting them gene therapies and stem cell therapies as advances make more forms of enhancement possible. Genetic "Wild type" humans will some day be the exception.
The identification of all the genetic variants that enhance athletic performance will show that Olympic athletes are, for the most part, lucky winners in a sort of genetic lottery. While their training helped them get to the Olympics their fortunate genetic endowments will show that most people do not have the genetic profiles needed to compete at the Olympic level. Some will find this unfair and will argue that everyone should be allowed to get the same genetic advances added to their bodies after birth so that they too can compete at the highest level. How will this debate turn? I expect the proponents of enhancement will eventually win the debate and sports competitions between enhanced humans will become more common than competitions between wild type humans.
Human activities are cumulatively driving the health of the world's oceans down a rapid spiral, and only prompt and wholesale changes will slow or perhaps ultimately reverse the catastrophic problems they are facing.
Such is the prognosis of Jeremy Jackson, a professor of oceanography at Scripps Institution of Oceanography at UC San Diego, in a bold new assessment of the oceans and their ecological health. Publishing his study in the online early edition of the Proceedings of the National Academy of Sciences (PNAS), Jackson believes that human impacts are laying the groundwork for mass extinctions in the oceans on par with vast ecological upheavals of the past.
Many forms of environmental damage are acting synergistically to cause a greater impact.
He cites the synergistic effects of habitat destruction, overfishing, ocean warming, increased acidification and massive nutrient runoff as culprits in a grand transformation of once complex ocean ecosystems. Areas that had featured intricate marine food webs with large animals are being converted into simplistic ecosystems dominated by microbes, toxic algal blooms, jellyfish and disease.
Jackson, director of the Scripps Center for Marine Biodiversity and Conservation, has tagged the ongoing transformation as "the rise of slime." The new paper, "Ecological extinction and evolution in the brave new ocean," is a result of Jackson's presentation last December at a biodiversity and extinction colloquium convened by the National Academy of Sciences.
The nutrient run-off from farms will get worse as more farms automate in response to high world food prices and growing demand from industrializing countries. The same will happen with overfishing. More countries need to impose more severe restrictions on fishing.
Jackson sees 3 main drivers of this coming ecological disaster.
To stop the degradation of the oceans, Jackson identifies overexploitation, pollution and climate change as the three main "drivers" that must be addressed.
"The challenges of bringing these threats under control are enormously complex and will require fundamental changes in fisheries, agricultural practices and the ways we obtain energy for everything we do," he writes.
If we slowed, stopped, and reversed human population growth that would greatly reduce the strain on the oceans. But even a shrinking population that is rapidly industrializing (e.g. China) will put a growing strain on the environment. We also need for developing countries to put a greater priority on controlling pollution. But they are far more interested in raising their living standards.
The world faces a big problem with China's industrialization in particular. The US industrialized with a much smaller population than it has now. So it went through its dirtiest stage with perhaps an eighth or tenth of China's current population. To have a country as big as China industrialize and go through its most polluting stage with so many people means a massive scale of pollution. Add in India, south east Asia, and other industrializing areas and the quantities of pollutants going into the atmosphere and oceans exceeds the pollution from European and American industrialization and comes up top of the remaining quantities of pollutants still emitted in the West.
I expect world pollution to get much worse before it gets better.
(BRONX, NY) — As people age, their cells become less efficient at getting rid of damaged protein — resulting in a buildup of toxic material that is especially pronounced in Alzheimer's, Parkinson's disease, and other neurodegenerative disorders.
Now, for the first time, scientists at the Albert Einstein College of Medicine of Yeshiva University have prevented this age-related decline in an entire organ — the liver — and shown that, as a result, the livers of older animals functioned as well as they did when the animals were much younger. Published in the online edition of Nature Medicine, these findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompany old age. The study's senior author was Dr. Ana Maria Cuervo, associate professor in the departments of developmental & molecular biology, medicine and anatomy & structural biology at Einstein.
A declining ability to take out intracellular trash is one of the causes of aging. Though apparently some scientists are not convinced yet.
The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. Many studies have documented that these processes become less efficient with age, allowing protein to gradually accumulate inside cells. But aging researchers continue debating whether this protein buildup actually contributes to the functional losses of aging or instead is merely associated with those losses. The Einstein study was aimed at resolving the controversy.
The chaperone system of intracellular removal of damaged proteins declines with age and Dr. Cuervo targeted it for genetic enhancement to keep it going stronger as mice age.
One of these surveillance systems — responsible for handling 30 percent or more of damaged cellular protein — uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell's many lysosomes — membrane-bound sacs filled with enzymes. When the chaperone and its cargo "dock" on a receptor molecule on the lysosome's surface, the damaged protein is drawn into the lysosome and rapidly digested by its enzymes.
In previous work, Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal's lifespan and, perhaps, maintain the function of the animal's cells and organs as well?
To find out, Dr. Cuervo created a transgenic mouse model equipped with an extra gene — one that codes for the receptor that normally declines in number with increasing age. Another genetic manipulation allowed Dr. Cuervo to turn on this extra gene only in the liver and at a time of her choosing, merely by changing the animals' diet.
To keep the level of the receptor constant throughout life, Dr. Cuervo waited until mice were six months old (the age that the chaperone system's efficiency begins to decline) before turning on the added receptor gene. When the mice were examined at 22 to 26 months of age (equivalent to approximately 80 years old in humans), the liver cells of transgenic mice digested and recycled protein far more efficiently than in their normal counterparts of the same age — and, in fact, just as efficiently as in normal six-month old mice.
But will this bit of genetic engineering extend the lives of mice? Consider that if all it took to make livers last longer was to add a copy of a gene that evolution probably would have caused that change to happen already. Mutations that just create an extra copy of a gene have happened many times and we have lots of genes in us with multiple extra copies. So if this really helps why don't mice already have this mutation?
Among the 7,000 men and women aged 45 from across England, Scotland and Wales that they studied, those who were smokers, non-drinkers, the overweight and the underweight all reported higher rates of chronic pain.
Among the women, vitamin D levels also appeared to be important.
This finding was not explained by gender differences in lifestyle or social factors, such as levels of physical activity and time spent outdoors, say the authors.
Women with vitamin D levels between 75 and 99 mmol/litre - a level deemed necessary for bone health - had the lowest rates of this type of pain, at just over 8%.
Women with levels of less than 25 mmol/litre had the highest rates, at 14.4%.
Hey, vitamin D is good for you and there's a decent chance you do not have enough of it. Your odds of not getting enough go way up in winter.
Scientists in a laboratory at Georgia Tech have developed a way to grow tendons that merge into bone. Previous lab-grown tendons lacked the ability to attach to bone.
Tissue engineering can produce tendons, cartilage, and even bladders. But only now have researchers managed to make different tissues blend into one another, as they do naturally in the body.
Such gradients are necessary for some structures and organs to function properly, says bioengineer Andrés García, who with colleagues at the Georgia Institute of Technology demonstrated a way to grow tendons that gradually "fade" to bone at one end.
We need the ability to grow replacement parts as our parts wear out from age. Given the ability to grow replacement parts we can replace old parts of our body with more youthful parts and make ourselves young again.
Men who have immune system genes dissimilar to women have odors which are more attractive to women. This is probably an evolutionary consequence of the advantage of giving one's children genetically diverse immune systems. But the hormones in the contraceptive pill alter sense of smell of women so they are more attracted to men who are immunologically more similar.
The contraceptive pill may disrupt women's natural ability to choose a partner genetically dissimilar to themselves, research at the University of Liverpool has found.
The Pill leads a woman's attraction machinery astray.
Disturbing a woman's instinctive attraction to genetically different men could result in difficulties when trying to conceive, an increased risk of miscarriage and long intervals between pregnancies. Passing on a lack of diverse genes to a child could also weaken their immune system.
So the Pill causes a mismatch in mate selection.
Humans choose partners through their body odour and tend to be attracted to those with a dissimilar genetic make-up to themselves, maintaining genetic diversity. Genes in the Major Histocompatibility Complex (MHC), which helps build the proteins involved in the body's immune response, also play a prominent role in odour through interaction with skin bacteria. In this way these genes also help determine which individuals find us attractive.
The research team analysed how the contraceptive pill affects odour preferences. One hundred women were asked to indicate their preferences on six male body odour samples, drawn from 97 volunteer samples, before and after initiating contraceptive pill use.
Craig Roberts, a Lecturer in Evolutionary Psychology who carried out the work in collaboration with the University of Newcastle, said: "The results showed that the preferences of women who began using the contraceptive pill shifted towards men with genetically similar odours.
There's an even bigger problem: If a woman on the Pill meets a guy, finds him pheromonally attractive, gets married, and then stops using the Pill she can suddenly find her husband's smell very much not to her liking.
"Not only could MHC-similarity in couples lead to fertility problems but it could ultimately lead to the breakdown of relationships when women stop using the contraceptive pill, as odour perception plays a significant role in maintaining attraction to partners."
How many marriages and relationships has the Pill brought together which fell apart when the woman stopped taking the Pill?
What could be done about it: Once genetic testing becomes cheap and widely available online dating services could match men and women by comparing Major Histocompatibility Complex (MHC) genes. Avoid dating someone who might seem attractive because you are on the Pill.
But doesn't the MHC attraction mechanism work for men as well? They won't be on the Pill. Are men finding that funny-smelling women who are on the Pill are hitting on them? Someone should do a study on this.
The discovery reported in this post is yet another example of how we are genetically programmed to do and feel as we do.
If you have the less common rs16969968 form of the CHRNA5 gene and you smoke a cigarette you are more likely to get hooked. Yet another reduction in the possible scope for free will.
In a paper published in the September issue of the journal Addiction, , a multi-university collaborative team of researchers specializing in statistical genetics, gene analysis, and trait analysis reports an association between a variant in the CHRNA5 nicotine receptor gene, initial smoking experiences, and current smoking patterns.
The genetic and smoking data come from 435 volunteers. Those who never smoked had tried at least one cigarette but no more than 100 cigarettes in their lives, and never formed a smoking habit. The regular smokers had smoked at least five cigarettes a day for at least the past five years.
The regular smokers in the study were far more likely than the never-smokers to have the less common rs16969968 form of the CHRNA5 gene, in which just one base-pair in the gene sequence was different from the more common form. This kind of genetic variation is called a single nucleotide polymorphism or SNP.
Smokers were also eight times as likely to report that their first cigarettes gave them a pleasurable buzz.
"It appears that for people who have a certain genetic makeup, the initial physical reaction to smoking can play a significant role in determining what happens next," says senior author and project leader, Ovide Pomerleau, a professor of psychiatry at the University of Michigan Medical School and founder of the U-M Nicotine Research Laboratory.
"If cigarette smoking is sustained, nicotine addiction can occur in a few days to a few months," he adds. "The finding of a genetic association with pleasurable early smoking experiences may help explain how people get addicted — and, of course, once addicted, many will keep smoking for the rest of their lives."
Among those who ever try smoking this gene explains only part of the difference between those who become addicted and those who do not. Expect more discoveries of genes that contribute to the odds of getting addicted.
We are witnessing an acceleration of the rate of discovery of genetic factors that influence behavior. This acceleration in the rate of discovery will accelerate as DNA testing costs continue to drop. So expect to see many more reports of genes that influence behavior.
Time for another in my continuing saga of why you need to get a lot of vitamin D. While previous studies have found evidence that higher vitamin D concentrations reduce the risk of death Johns Hopkins researchers think their new study is a big and sufficiently well controlled study to finally feel confident that vitamin D cuts death rates.
Researchers at Johns Hopkins are reporting what is believed to be the most conclusive evidence to date that inadequate levels of vitamin D, obtained from milk, fortified cereals and exposure to sunlight, lead to substantially increased risk of death.
In a study set to appear in the Archives of Internal Medicine online Aug. 11, the Johns Hopkins team analyzed a diverse sample of 13,000 initially healthy men and women participating in an ongoing national health survey and compared the risk of death between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 17.8 nanograms per milliliter or lower.
Of the 1,800 study participants known to have died by Dec. 31, 2000, nearly 700 died from some form of heart disease, with 400 of these being deficient in vitamin D. This translates overall to an estimated 26 percent increased risk of any death, though the number of deaths from heart disease alone was not large enough to meet scientific criteria to resolve that it was due to low vitamin D levels.
Yet, researchers say it does highlight a trend, with other studies linking shortages of vitamin D to increased rates of breast cancer and depression in the elderly. And earlier published findings by the team, from the same national study, have established a possible tie-in, showing an 80 percent increased risk of peripheral artery disease from vitamin D deficits.
Breast cancer, depression, and peripheral artery disease should be on everyone's list of things to avoid.
Hey, they did a big study and have clearer results than other studies. So they are bragging. But they deserve to brag. So why not?
Researchers note that other studies in the last year or so in animals and humans have identified a connection between low levels of vitamin D and heart disease. But these studies, they say, were weakened by small sample numbers, lack of diversity in the population studied and other factors that limited scientists' ability to generalize the findings to the public at large.
"Our results make it much more clear that all men and women concerned about their overall health should more closely monitor their blood levels of vitamin D, and make sure they have enough," says study co-lead investigator Erin Michos, M.D., M.H.S.
Small amounts of sunlight can make the difference. Though in winter better think about taking a vitamin D pill. Your benefit probably tops out at 2000 IU per day. Though only a blood test would tell you whether you are at the 50 nanograms per milliliter concentration at which benefit is maximized.
Aware of the cancer risks linked to too much time spent in the sun, she says as little as 10 to 15 minutes of daily exposure to the sun can produce sufficient amounts of vitamin D to sustain health. The hormone-like nutrient controls blood levels of calcium and phosphorus, essential chemicals in the body.
If vitamin supplements are used, Michos says there is no evidence that more than 2,000 international units per day do any good. Study results show that heart disease death rates flattened out in participants with the highest vitamin D levels (above 50 nanograms per milliliter of blood), signaling a possible loss of the vitamin's protective effects at too-high doses.
The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units (or blood levels nearing 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.
Are you still not taking vitamin D? If not, what's your problem? Secret death wish? A feeling of futility? Or maybe you are one of those rare people who like having doctors fuss all over you? In that case it is safer to use fake symptoms. So take the vitamin D anyhow.
Natural selection never came up with a way for Douglas fir trees to grow higher than 350 to 400 feet. So will humans ever use genetic engineering to lift that limit?
CORVALLIS, Ore. – The Douglas-fir, state tree of Oregon, towering king of old-growth forests and one of the tallest tree species on Earth, finally stops growing taller because it just can't pull water any higher, a new study concludes.
This limit on height is somewhere above 350 feet, or taller than a 35-story building, and is a physiological tradeoff between two factors in the tree's wood - a balance between efficiency and safety in transporting water to the uppermost leaves.
The findings are being published this week in Proceedings of the National Academy of Sciences, by a team of scientists from Oregon State University and the U.S.D.A. Forest Service. The research was funded by grants from the U.S. Department of Agriculture and the Forest Service.
The article briefly describes the limitations on tree growth caused by the mechanism by which water is lifted up through the tree. Well, okay. But can bioengineering produce a better way for a tree to grow much taller? Will humans (or, more likely, transhumans) some day conduct competitions to genetically engineer trees and other species to lift them far beyond their existing limits? I see every discovery of why plants and animals are limited as constituting a challenge to figure out how to make biological organisms that can exceed their documented limits. Human sports limits will be one focus of competition. But I expect trees, plants, animals to inspire other competitions to lift biological performance.
Before you say this is far fetched, biogerontologist Aubrey de Grey and entrepreneur David Gobel co-founded the Methuselah Mouse Prize which basically incentivizes scientists to genetically engineer mice to make them live longer. If the promoters of this prize succeed in their goal of speeding up the development rejuvenation therapies for humans then you might live long enough to both enter contests to create higher growing trees and to live hundreds of more years to see which tree designs reach new heights.
In 2001, Breiter collaborated with Daniel Kahneman, PhD, of Princeton University and Peter Shizgal, PhD, Concordia University, Montreal, to show how the brain's reward/aversion circuitry followed the principles of what is called prospect theory when responding to the anticipation and receipt of a financial reward, helping to lay the groundwork for the field now called neuroeconomics. Kahnemann was a co-recipient of the 2002 Nobel Prize in economics for his earlier development of prospect theory, which describes the different ways people evaluate positive and negative outcomes in uncertain situations.
The current report connects molecular genetics with earlier studies of choice and preference and with investigations of the brain's reward circuitry. The researchers focused on a gene called CREB1 that has been implicated in animal studies of the brain's reward/aversion function. Study lead author Roy Perlis, MD, medical director of the MGH Bipolar Program, and colleagues previously found that depressed men with a particular variation near the gene coding for CREB report greater difficulty suppressing anger. Another study of theirs associated the same variation with a threefold greater risk of suicidal thinking in major depressive disorder patients soon after beginning antidepressant therapy. The 28 participants in the current study had no evidence of any psychiatric disorder or physical disorder that might influence brain activity.
Willingness to view expressions of different emotions seems influenced by which version of CREB1 you have.
In addition to analyzing each participant's version of the CREB1 gene, the researchers conducted a set of experiments. As the participants viewed facial expressions reflecting different emotional states – happy, neutral, sad, fearful and angry – fMRI scans were taken to examine the activity of brain structures associated with processing pleasant or unpleasant experiences. In another test, participants viewed the same pictures and could change how long they viewed an image by the way they pressed keys on a keyboard. Many earlier studies have established the keypress experiment as a quantitative measure of preference. In the version used in this study, keypress responses reflected participants' judgment and decisions about how much or how little they preferred the facial expressions.
The fMRI study showed that, during the viewing of angry faces, the activity of a structure called the insula, involved in the response to unpleasant situations, depended on which version of the CREB1 gene a participant inherited. In the keypress experiment, responses indicating a preference against the angry expression paralleled the CREB1-affected fMRI activity seen in the insula in the first experiment and also differed depending on the CREB1 variant that had been inherited.
This one gene accounts for 20% of the differences seen in how people chose options in response to the facial expressions.
"We were surprised to see that variation in the CREB1 gene would account for more than 20 percent of the difference in how healthy participants weighed different options and expressed specific preferences," says Perlis. "Our previous studies and the work of other groups suggested that variation in this gene could be important for judgment and decision-making by the brain, but we needed to connect this to a measurable decision-making effect in both behavior and brain activity."
If more genes exist which influence how people react then future discoveries will leave even less room for free will. This process of discovery will repeat for more genes and more aspects of human behavior. These researchers are already looking into other genes which might influence thought and behavior.
Breiter adds, "This study connects quantitative measurements across three levels of observation – brain activity, genomic variation and the expression of preference. We now are investigating the potential role of other genes and will go on to assess how this relationship across three levels of observation may be affected by conditions such as depression and addiction."
Update: The more our personalities are found to be determined by genes the more human nature will change once selection of genes for offspring (basically offspring genetic engineering) becomes possible. People are bound to make some decisions for offspring genes that are different than what the offspring would get naturally. If people become empowered to make decisions that change a large variety of cognitive characteristics then they will make those decisions. What decisions will they make? That is one of the biggest questions we face about the future of humanity.
If you could get into a time machine and pop out 100 years in the future would you find the personalities you meet congenial? Enjoyable to be around? Cut-throat? Amoral? Extremely pushy and aggressive? Will something resembling civil society still exist? Will humans live in enormous tension with each other? The genetic variations exist to make all these outcomes possible. Which outcomes occur (and the answer may differ by country, religion, social class, etc) will be determined by the genetic choices people make for their offspring.
We hear a lot about the bright prospects for cellulosic ethanol. But a group at UC Davis thinks they've found a cheap way to turn cellulose into furan-based organic liquids.
Mark Mascal and Edward B. Nikitin at the University of California, Davis (USA) have now developed an interesting new method for the direct conversion of cellulose into furan-based biofuels. As they report in the journal Angewandte Chemie, their simple, inexpensive process delivers furanic compounds in yields never achieved before.
Atmospheric carbon dioxide is viewed as the ultimate carbon source of the future. It is most efficiently "harvested" by plants via photosynthesis. Currently, biofuel producers primarily use starch, which is broken down to form sugars that are then fermented to give ethanol. Cellulose is however the most common form of photosynthetically fixed carbon. The problem is that the degradation of cellulose into its individual sugar components, which could then be fermented, is a slow and expensive process. "Another problem is that the carbon economy of glucose fermentation is poor," explains Mascal, "for every 10 g of ethanol produced, you also release 9.6 g CO2."
Could we avoid the breakdown of cellulose and fermentation? Mascal and Nikitin demonstrate that we can indeed. They have developed a simple process for the conversion of cellulose directly into "furanics", which are furan-based organic liquids. Furans are molecules whose basic unit is an aromatic ring made of one oxygen and four carbon atoms. The main product the researchers obtain under the conditions they have been developing is 5-chloromethylfurfural (CMF).
One of the compounds produced by this process might work in diesel fuel blends.
CMF and ethanol can be combined to give ethoxymethylfufural (EMF), and CMF reacts with hydrogen to give 5-methylfurfural. Both of these compounds are suitable as fuels. EMF has previously been investigated and found to be of interest in mixtures with diesel by Avantium Technologies, a spin-off of Shell.
"Our method appears to be the most efficient conversion of cellulose into simple, hydrophobic, organic compounds described to date," says Mascal. "It also surpasses the carbon yields of glucose and sucrose fermentation. Furanics could be established as both the automotive energy source and chemical starting material of the future."
If this works then it could shift the biomass advantage against ethanol. That would make government ethanol fuel mandates in the United States even dumber than they already are.
Put a monkey in front of a keyboard, and he might come up with something like this: Biblis A, Neckar-Westheim 1, Brunsbüttel, Biblis B, Isar 1, Unterweser, Philippsburg 1. The names, though, are far from meaningless. All of them are nuclear power plants in Germany -- seven of the 17 still in operation in the country. And all seven of them are scheduled to be shut down between 2010 and 2012 and taken off the electricity grid.
If Germany phases out its nuclear power plants (which currently supply over a quarter of Germany electric power) it will face electric power shortages.
The reason for the planned shut downs is clear -- they are part of the country's legislated shift away from atomic energy. But just what that means for Germany's energy supply only becomes apparent after looking at a small graphic that Stephan Kohler, chief executive of the Germany Energy Agency, keeps in a plastic folder in his office. The graphic estimates trends in both consumption and production of electricity in Germany's near future. Whereas the consumption line gently and consistently falls, the production line climbs slightly for the next couple of years -- and then it plunges. The edge of the cliff depicted in the diagram coincides with 2010, just when the 126,036 gigawatt hours of electricity produced by Biblis, Neckar-Westheim and Brunsbüttel disappear.
Germany has 17 out of Europe's 130 nuclear power plants. Britain has 19 and France has 59. If Germany goes through with its nuclear power phase-out it will inevitably buy more electric power from French nuclear plants and also build more coal fired electric power generating plants. Germany's plan to phase out nuclear power is not doing either Germany or the world any favors. But the government of Chancellor Angela Merkel is showing signs of backpedaling on the nuclear power phase-out.
"The chancellor has noticed that the discussion about the use of atomic energy has been re-energized" said Merkel spokesman Thomas Steg recently. Her party is willing to go even further. "For the foreseeable future," party leadership recently wrote in a policy paper on global warming, "the contribution of nuclear energy to the production of electricity in Germany is irreplaceable."
The world has 439 nuclear power plants in operation, 36 under construction, and 81 planned. While Russia, India, and China each have 6 nuclear power plants under construction Russia's 6 make a much higher ratio of power plants under construction to people and so Russia's commitment to nuclear power is much bigger.
German electric power providers plan to build 26 new coal fired electric power plants. Germany has 3 choices: A) Raise prices to cut back on demand; or B) Build more coal plants, or C) reverse the decision to phase out the nuclear power plants. While the majority of Germans still favor the nuclear phase out the majority has shrunk considerably in just 8 months. The plans for coal plants suggest that there's no stomach left for raising already high electric power costs. Germany already has electric power costs more than double the US costs.
In absolute values, household electricity prices were highest in January 2006 in Denmark (23.62 euro per 100 kWh), followed by Italy (21.08), the Netherlands (20.87) and Germany (18.32). The lowest prices were observed in Greece (7.01), Lithuania (7.18), Estonia (7.31) and Latvia (8.29).
At the time of this writing the exchange rate is about 1.5 Euro per US dollar. Even if it reached parity of 1 to 1 the cost for electricity would be $0.1832 per kwh which is almost double the 2008 US average rate of $0.1031 per kwh. Shutting down the nuclear power plants will drive it higher still. My guess is that the German government will eventually reverse their decision to phase out nuclear power in Germany.
Our cells contain organelles called mitochondria which break down sugar to provide energy. Those organelles have their own small genome separate from the very large genome found in almost every cell nucleus (excepting red blood cells). A scientific team in Germany has now successfully sequenced the mitochondrial DNA of Neanderthals. Using that information these scientists have calculated that Neandertals and humans went their separate ways about 660,000 years ago.
A study reported in the August 8th issue of the journal Cell, a Cell Press publication, reveals the complete mitochondrial genome of a 38,000-year-old Neandertal. The findings open a window into the Neandertals' past and helps answer lingering questions about our relationship to them.
" For the first time, we've built a sequence from ancient DNA that is essentially without error," said Richard Green of Max-Planck Institute for Evolutionary Anthropology in Germany.
The mitochondrial DNA is only about 15,000 letters (a little less). So by itself it doesn't tell us much about the vast bulk of ways that humans and Neandertals differ. But that amount of information is enough to estimate how far the two species formed separate from each other.
Analysis of the new sequence confirms that the mitochondria of Neandertal's falls outside the variation found in humans today, offering no evidence of admixture between the two lineages although it remains a possibility. It also shows that the last common ancestor of Neandertals and humans lived about 660,000 years ago, give or take 140,000 years.
Here's the really interesting part: We might some day have a complete Neanderthal genome sequence.
Scientists eventually hope to sequence a full Neanderthal genome.
That information would open up the possibility of eventually bringing Neanderthals back to life. What do you think of doing this?
Suppose some billionaire bankrolled the cloning of a Neanderthal. On what basis should we decide whether to grant it human rights? Suppose it has an IQ in the lower range for humans (say 80). But suppose it was totally hostile to us and dangerous. Should it be granted full rights? Or a subset of rights?
The ability to create creatures that are closer to humans than existing primates will force us to come up with far more precise criteria for what should be granted rights. We already grant subsets of rights to children and even to some adults. People imprisoned or committed to mental hospitals do not have all rights. But a Neanderthal or perhaps a dog or pig or lion genetically engineered to have low human IQs would pose much more complicated questions about why we grant rights. Imagine a 100 IQ creature who we could know will try to kill us. Imagine a 90 IQ creature that will not try to kill us or try to rob or otherwise harm us. Do we grant full rights to the latter while keeping the smarter but more dangerous creature in a sort of zoo?
Some people marvel at the supposed miracle of childbirth. Others claim that our bodies are evidence of intelligent design. Some arguments against the theory of evolution point to the eye as a supposedly amazing piece of engineering (even though a look at the cell layers that light has to pass thru to reach the rods and cones seem like poor engineering to me - to say nothing about widespread problems with sight and focus). Another example of poor human body engineering comes from a new report from the Medical College of Georgia that after giving birth to babies many women suffer from post partum depression as a result of an after effect of chemical signals that the fetus sent to ensure an adequate blood supply.
That crosstalk allows the mother's blood to flow out of the uterine artery and get just a single cell layer away from the fetus' blood, says Dr. Puttur D. Prasad, biochemist in the Medical College of Georgia School of Medicine.
That controlled exchange between the blood of mother and fetus is courtesy of the placenta regulating levels of serotonin, a neurotransmitter commonly associated with depression. But platelets that enable blood clotting also secrete serotonin which prompts platelets to aggregate and the placenta to want to get rid of it.
The same serotonic transporter mechanism that works in neurons gets used to control placental blood flow. This dual use of a component causes huge amounts of mental pain among new mothers.
"If there were no proper control here, blood leaving the mother's blood vessel would trigger release of serotonin, platelets would aggregate, vessels constrict and the fetus wouldn't get what it needs," says Dr. Prasad. An MCG research team led by Dr. Vadivel Ganapathy first reported evidence of serotonin transporter gene expression in the placenta back in 1989 in the Journal of Biological Chemistry. Now they know the gene plays an important role in the crosstalk that forestalls clotting until after birth.
If you were going to intelligently design an organism would you reuse the same transporter mechanism both for brain functioning and for feeding a developing fetus? The interleukin-1 beta that is used to stimulate serotonin transporters in the uterus also travels to the brain and as a side effect causes neurons all over the brain to make too many serotonin transporters.
When the fetus and placenta are gone, blood continues flowing from the mother's uterine artery until platelets move in to stop it, Dr. Prasad explains. Serotonin levels begin to rise and interact with receptors on the smooth muscle of the uterus. This stimulates production of interleukin-1 beta which the MCG researchers found regulates expression of serotonin-hoarding transporters. Interleukin-1 beta gets in the mother's bloodstream, crosses the blood brain barrier and creates more serotonin transporters on the neurons when they are not needed.
This lousy design is a product of evolution. The alternative is that the design is the product of an intelligent designer who isn't intelligent enough to make a really good design. It worked well enough to propagate the species and so the genetic sequences that code for this mechanism survived.
Until interleukin-1 beta levels normalize, there's too little communication between serotonergic neurons and moms get the blues, says Dr. Prassad. "We believe that 80 percent of women experience postpartum blues because of this effect of interleukin-1 beta. If our hypothesis holds true, lowering interleukin-1 beta levels may be a better treatment option." He notes that while serotonin reuptake inhibitors, commonly used for depression, work well in these women, transferring the drug to the baby during nursing can be problematic.
A woman pines to have a baby for many years. She finally finds Mr. Right, they work hard and save up enough money, get a decent house, they try to start a pregnancy, out comes the baby, and then due to poor genetic design of regulatory systems she spends weeks or even months suffering depression. Natural selection also brings us many genetic diseases too. Nature is cruel.
Oil prices have declined on demand destruction. The CEO of BP observes a big decline in oil demand in developed countries.
Tony Hayward, chief executive of BP, said last week that the oil company had detected a drop in demand of up to 10 per cent in countries that are members of the Organisation of Economic Cooperation and Development (OECD).
US fuel demand averaged 20.2 million barrels a day during the past four weeks, down 2.4% from a year earlier, the Energy Department said July 30.
Consumption of petroleum products, which account for about half of the island's energy supply, fell 4.1 percent from a year earlier to the equivalent of 4.5 million kiloliters of oil, the bureau said. Demand for diesel declined 21 percent, while that for gasoline dropped 8.7 percent. Power consumption climbed 8.2 percent to 20.9 billion kilowatt-hours in June, with demand by industrial and energy companies 12 percent higher than a year earlier.
Oil consumption in the United States and OECD nations is weakening but China and India have yet to show signs of falling demand, making it unclear if the price fall below $120 is a turning point, the IEA's chief said. "We don't know if this is a turning point. We'd like to know but we don't have an answer yet," Nobuo Tanaka, executive director of the International Energy Agency (IEA), the adviser to 27 industrialised countries, told Reuters on Tuesday.
NEW DELHI : India’s oil imports from the Middle East increased to 89.73 million tones in 2007-08, up by 11 percent, compared to 80.81 million tones in 2006-07, according to Petroleum Ministry.
The Western countries will continue to cut back while Asian demand continues to grow. Eventually Western demand destruction won't be able to balance Asian demand growth. Then things will get ugly.
Jerome Groopman has a good article in The New Yorker surveying the growing threat of antibiotic-resistant bacteria.
Of the so-called superbugs—those bacteria that have developed immunity to a wide number of antibiotics—the methicillin-resistant Staphylococcus aureus, or MRSA, is the most well known. Dr. Robert Moellering, a professor at Harvard Medical School, a past president of the Infectious Diseases Society of America, and a leading expert on antibiotic resistance, pointed out that MRSA, like Klebsiella, originally occurred in I.C.U.s, especially among patients who had undergone major surgery. “Until about ten years ago,” Moellering told me, “virtually all cases of MRSA were either in hospitals or nursing homes. In the hospital setting, they cause wound infections after surgery, pneumonias, and bloodstream infections from indwelling catheters. But they can cause a variety of other infections, all the way to bacterial meningitis.” The first deaths from MRSA in community settings, reported at the end of the nineteen-nineties, were among children in North Dakota and Minnesota. “And then it started showing up in men who have sex with men,” Moellering said. “Soon, it began to be spread in prisons among the prisoners. Now we see it in a whole bunch of other populations.” An outbreak among the St. Louis Rams football team, passed on through shared equipment, particularly affected the team’s linemen; artificial turf, which causes skin abrasions that are prone to infection, exacerbated the problem. Other outbreaks were reported among insular religious groups in rural New York; Hurricane Katrina evacuees; and illegal tattoo recipients. “And now it’s basically everybody,” Moellering said. The deadly toxin produced by the strain of MRSA found in U.S. communities, Panton-Valentine leukocidin, is thought to destroy the membranes of white blood cells, damaging the body’s primary defense against the microbe. In 2006, the Centers for Disease Control and Prevention recorded some nineteen thousand deaths and a hundred and five thousand infections from MRSA.
But while MRSA is still a problem right now help is on the way with new drugs in the pipeline to treat staph infections. The more problematic threat comes from gram negative bacteria for which development of new antibiotics is more difficult.
Unlike resistant forms of Klebsiella and other gram-negative bacteria, however, MRSA can be treated. “There are about a dozen new antibiotics coming on the market in the next couple of years,” Moellering noted. “But there are no good drugs coming along for these gram-negatives.” Klebsiella and similarly classified bacteria, including Acinetobacter, Enterobacter, and Pseudomonas, have an extra cellular envelope that MRSA lacks, and that hampers the entry of large molecules like antibiotic drugs. “The Klebsiella that caused particular trouble in New York are spreading out,” Moellering told me. “They have very high mortality rates. They are sort of the doomsday-scenario bugs.”
The article points to the widespread use of antibiotics in livestock feed as contributing to the development of drug-resistant bacterial strains.
You might think this doesn't have anything to do with you. But you are one car accident away from being in a hospital. Also, the drug resistance mutations found in bacteria in hospitals will likely swap genetic material with other species of bacteria that are found more widely outside of hospitals. So more common bacteria might develop antibiotic resistance.
Medical and scientific experts now agree that bacteria, not influenza viruses, were the greatest cause of death during the 1918 flu pandemic.
Government efforts to gird for the next influenza pandemic – bird flu or otherwise – ought to take notice and stock up on antibiotics, says John Brundage, a medical microbiologist at the Armed Forces Health Surveillance Center in Silver Spring, Maryland.
Brundage's team culled first-hand accounts, medical records and infection patterns from 1918 and 1919. Although a nasty strain of flu virus swept around the world, bacterial pneumonia that came on the heels of mostly mild cases of flu killed the majority of the 20 to 100 million victims of the so-called Spanish flu, they conclude.
If the H5N1 avian influenza or some other flu strain mutates into a form that cause cause a severe pandemic then a big store of antibiotics could help. If you are into personal survival and don't trust your government then you could try to talk a doctor into giving you some antibiotic prescriptions and then store the drugs in a cool dry place. Anyone know about shelf life for various antibiotics? Which ones last the longest?
The most important thing to do in a pandemic is to avoid getting exposed to the virus in the first place. While facial masks can help simply staying away from other people is the best way to avoid a bug.
Animal migration surely ranks as one of nature's most visible and widespread phenomena. Every minute of every day, somewhere, some place, animals are on the move. The migrants span the animal kingdom, from whales and warblers to dragonflies and salamanders. But is migration an endangered phenomenon? Around the world, many of the most spectacular migrations have either disappeared due to human activities or are in steep decline. Those of us living in eastern North America can no longer experience the flocks of millions of passenger pigeons that temporarily obscured the sun as they migrated to and from their breeding grounds. Nor can residents of the Great Plains climb to the top of a hill and gaze down up hundreds of thousands of bison trekking across the prairies, as was possible less than two centuries ago.
I view this as a loss. I realize some of my readers see the expansion of humanity as some sort of Manifest Destiny which is a value that trumps all other values (really). But I do not see why the expansion of the human race up to 7, 8, 9+ billion people enriches my life. Seems quite the opposite is the case.
I think migrating geese honking at high altitudes are really cool. If I could go back in a time machine I would go back and (among other things) watch the massive carrier pigeon migration before hunters wiped them out entirely Non-migratory species aren't shrinking as much as migratory species.
Even the less iconic migrations show signs of trouble. Birdwatchers in North America and Europe, for example, complain that fewer songbirds are returning each spring from their winter quarters in Latin America and Africa, respectively. Indeed, a recent continent-wide analysis of European breeding birds concluded that long-distance migrants (i.e., those species that breed in Europe but winter in sub-Saharan Africa) have suffered sustained and often severe population declines, more so than related nonmigratory species . In central Asia, the number of saiga, a peculiar migratory antelope of the dry steppe grasslands and semi-desert, has dropped by over 95% in the past two decades, from over one million to fewer than 50,000 .
The causes of all these declines vary depending on the species and the locale, but in general, the threats to migrants fall into four nonexclusive categories: habitat destruction, the creation of obstacles and barriers such as dams and fences, overexploitation, and climate change. Most of the migrants are in little immediate danger of extinction; rather, they are becoming less and less common. Thus, birdwatchers can still see all of the species of migratory songbirds they seek each spring; they simply have to work harder to do so. Bison still roam national parks and private ranches in the American West, but today's herds number in the hundreds or low thousands, rather than the hundreds of thousands or millions. And there are still lots of salmon to catch off the coast of Norway or British Columbia—just not as many as there used to be.
Migrant species that are not in immediate danger of extinction will come under greater pressure as more billions of humans populate the Earth and each human uses a larger ecological footprint. Do you care?
Salmon are a dim shadow of their former numbers.
Prior to European settlement, 160–226 million kilograms of salmon migrated each year up the rivers of Washington, Idaho, Oregon, and California. Today, after decades of dam construction, overfishing, water withdrawals for irrigation, logging, and streamside grazing by livestock, salmon populations have plummeted. The total biomass of spawning salmon in the Pacific Northwest is now estimated to be only 12–14 million kilograms. Gresh et al.  have calculated that the rivers of the Northwest receive just 6%–7% of the marine-derived nitrogen and phosphorus they once received from the abundant salmon population. How this shortfall may be affecting the ecology of the region's rivers or adjacent farmlands is largely unknown.
Migratory bird numbers might undergo a big shrinking. Wetlands destruction probably will contribute to that. Biomass energy crops will reduce available habitats as well.
We can imagine an analogous situation developing with respect to migratory birds. Each spring, more than 30,000 tons of migratory songbirds migrate from their wintering grounds in Latin America and the Caribbean to their breeding grounds in the United States and Canada. (This biomass value is derived by combining breeding population totals from the North American Landbird Conservation Plan with species-specific weights from various sources.) If we assume these birds consume 10%–35% of their body weight per day in insects (roughly matching the requirements of a 100-gram bird and a 10-gram bird, respectively), then they are eating anywhere from 3,000–10,500 tons of insects per day. (During the breeding season, when the birds are feeding offspring, these figures would be much higher.) Several studies have shown that birds reduce insect populations in temperate forests, thus raising the question of whether ongoing declines in migratory birds pose a threat to the health of our forests and farmlands.
Similarly, one wonders how the ecology of the Serengeti would change if its migratory population of wildebeest (exceeding 1 million individuals) were to collapse, given the major role these animals surely play in terms of consuming herbaceous vegetation and redistributing nutrients via their urine and dung (Figure 1).
Humans are diverting a rising fraction of all biomass for their own purposes. The politically sponsored push for biomass energy just accelerates that trend. Population growth and industrialization also lead to more habitat destruction. One result: half the world's primate species are threatened with extinction.
Edinburgh, Scotland – Mankind’s closest relatives – the world’s monkeys, apes and other primates – are disappearing from the face of the Earth, with some literally being eaten into extinction.
The first comprehensive review in five years of the world’s 634 kinds of primates found that almost 50 percent are in danger of going extinct, according to the criteria of the IUCN Red List of Threatened Species.
Issued at the 22nd International Primatological Society Congress in Edinburgh, Scotland, the report by the world’s foremost primate authorities presented a chilling indictment on the state of primates everywhere. In Asia, more than 70 percent of primates are classified on the IUCN Red List as Vulnerable, Endangered or Critically Endangered – meaning they could disappear forever in the near future.
This problem is going to get far worse as the human population hits 7, 8, 9 billion and as rising Asian buying power surpasses Western buying power to cause more tearing down of rain forests for food, crop land, and grazing land. Expanding cities also convert land from farming and necessitate the conversion of more forests and savannahs into agricultural uses.
Southeast Asia is especially hard hit.
With the input of hundreds of experts worldwide, the primate review provides scientific data to show the severe threats facing animals that share virtually all DNA with humans. In both Vietnam and Cambodia, approximately 90 percent of primate species are considered at risk of extinction. Populations of gibbons, leaf monkeys, langurs and other species have dwindled due to rampant habitat loss exacerbated by hunting for food and to supply the wildlife trade in traditional Chinese medicine and pets.
“What is happening in Southeast Asia is terrifying,” said Jean-Christophe Vié, Deputy Head of the IUCN Species Program. “To have a group of animals under such a high level of threat is, quite frankly, unlike anything we have recorded among any other group of species to date.”
Elsewhere, species from tiny mouse lemurs to massive mountain gorillas face challenges to survive. In Africa, 11 of the 13 kinds of red colobus monkeys assessed were listed as Critically Endangered or Endangered. Two may already be extinct: Bouvier’s red colobus (Procolobus pennantii bouvieri) has not been seen in 25 years, and no living Miss Waldron’s red colobus (Procolobus badius waldroni) has been seen by a primatologist since 1978, despite occasional reports that some still survive.
“Among the African species, the great apes such as gorillas and bonobos have always tended to grab the limelight, and even though they are deeply threatened, it is smaller primates such as the red colobus that could die out first," said IPS President Richard Wrangham.
Market solutions will not prevent this disaster. Ecotourism can save only a small fraction of the threatened land because far more people will buy food, biomass energy, and wood products than will pay to visit wilderness areas. The buying power (both mass market and political market) is lined up against habitat preservation.
Here's another research result that will some day guide prospective parents who want to select and modify embryos to guarantee the success of their kids. Our brains are wired up to find certain facial shapes as more trustworthy.
A pair of Princeton psychology researchers has developed a computer program that allows scientists to analyze better than ever before what it is about certain human faces that makes them look either trustworthy or fearsome. In doing so, they have also found that the program allows them to construct computer-generated faces that display the most trustworthy or dominant faces possible.
Such work could have implications for those who care what effect their faces may have upon a beholder, from salespeople to criminal defendants, the researchers said.
In a paper appearing in the online edition this week of the Proceedings of the National Academy of Sciences, Alexander Todorov, an assistant professor of psychology and public affairs at Princeton, and Nikolaas Oosterhof, a research specialist, continue an inquiry into the myriad messages conveyed by the human face. In 2005, Todorov's lab garnered international headlines with a study published in Science demonstrating that quick facial judgments can accurately predict real-world election results.
This opens up the possibility that Hollywood casting agents could use software to go through large numbers of photos to discover, for example, faces that would make for fearsome dictators or slashers or evil spies.
A U-shaped mouth and an almost surprised look to the eyes maximize feelings of trustworthiness. Eyebrows close to the eyes project a dominant look.
From there, using a commercial software program that generates composites of human faces (based on laser scans of real subjects), the scientists asked another group of test subjects to look at 300 faces and rate them for trustworthiness, dominance and threat. Common features of both trustworthiness and dominance emerged. A trustworthy face, at its most extreme, has a U-shaped mouth and eyes that form an almost surprised look. An untrustworthy face, at its most extreme, is an angry one with the edges of the mouth curled down and eyebrows pointing down at the center. The least dominant face possible is one resembling a baby's with a larger distance between the eyes and the eyebrows than other faces. A threatening face can be obtained by averaging an untrustworthy and a dominant face.
With the ability to predict reactions to faces comes the ability to design faces to maximize desired reactions. Want to design a dominant and highly trusted face for a future leader?
Using the program and the ratings from subjects, the scientists could actually construct models of how faces vary on these social dimensions. Once those models were established, the scientists could exaggerate faces along these dimensions, show them to other test subjects to confirm that they were eliciting the predicted emotional response, and find out what facial features are critical for different social judgments.
Within 20 years if not sooner offspring genetic engineering will be used to choose appearances of offspring. Imagine the possibilities. Ambitious parents who want their kids to become CEOs and high elected officials will select embryos that will grow up to to become adults with facial appearances and body shapes that maximize their potential to dominate and control others.
Are faces that elicit feelings of trust really more trustworthy? Why would our genes that cause that reaction have been selected for unless that reaction was justified?
By bypassing regulatory systems that control internal vitamin C levels scientists were able boost vitamin C concentrations so high that it killed cancer cells.
High-dose injections of vitamin C, also known as ascorbate or ascorbic acid, reduced tumor weight and growth rate by about 50 percent in mouse models of brain, ovarian, and pancreatic cancers, researchers from the National Institutes of Health (NIH) report in the August 5, 2008, issue of the Proceedings of the National Academy of Sciences. The researchers traced ascorbate's anti-cancer effect to the formation of hydrogen peroxide in the extracellular fluid surrounding the tumors. Normal cells were unaffected.
Natural physiologic controls precisely regulate the amount of ascorbate absorbed by the body when it is taken orally. "When you eat foods containing more than 200 milligrams of vitamin C a day--for example, 2 oranges and a serving of broccoli--your body prevents blood levels of ascorbate from exceeding a narrow range," says Mark Levine, M.D., the study's lead author and chief of the Molecular and Clinical Nutrition Section of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the NIH. To bypass these normal controls, NIH scientists injected ascorbate into the veins or abdominal cavities of rodents with aggressive brain, ovarian, and pancreatic tumors. By doing so, they were able to deliver high doses of ascorbate, up to 4 grams per kilogram of body weight daily. "At these high injected doses, we hoped to see drug-like activity that might be useful in cancer treatment," said Levine.
Keep in mind that cutting tumor size by 50% does not cure cancer. The remaining cells can bounce back and still kill you. But maybe combined with other treatments vitamin C can help fight cancer.
EEStor claims that its system, called an electrical energy storage unit (EESU), will have more than three times the energy density of the top lithium-ion batteries today. The company also says that the solid-state device will be safer and longer lasting, and will have the ability to recharge in less than five minutes. Toronto-based ZENN Motor, an EEStor investor and customer, says that it's developing an EESU-powered car with a top speed of 80 miles per hour and a 250-mile range. It hopes to launch the vehicle, which the company says will be inexpensive, in the fall of 2009.
But skepticism in the research community is high. At the EESU's core is a ceramic material consisting of a barium titanate powder that is coated with aluminum oxide and a type of glass material. At a materials-research conference earlier this year in San Francisco, it was asked whether such an energy-storage device was possible. "The response was not very positive," said one engineering professor who attended the conference.
Click through to read the details on what they claim and why some academics are skeptical. If they succeed and can hit low enough price points then electric cars become quite viable. Plus, wind and solar will become more viable as baseload power sources. We are in a race between the depletion of oil fields and the development of substitute technologies. Battery technologies play a very important part in that race.
ST. PAUL, Minn. – Eating tuna and other types of fish may help lower the risk of cognitive decline and stroke in healthy older adults, according to a study published in the August 5, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology.
For the study, 3,660 people age 65 and older underwent brain scans to detect silent brain infarcts, or small lesions in the brain that can cause loss of thinking skills, stroke or dementia. Scans were performed again five years later on 2,313 of the participants. The people involved in the study were also given questionnaires about fish in their diets.
The study found that people who ate broiled or baked tuna and other fish high in omega-3 fatty acids (called DHA and EPA) three times or more per week had a nearly 26 percent lower risk of having the silent brain lesions that can cause dementia and stroke compared to people who did not eat fish regularly. Eating just one serving of this type of fish per week led to a 13 percent lower risk. The study also found people who regularly ate these types of fish had fewer changes in the white matter in their brains.
The only 26% reduction in lesions from eating fish is to be expected. With diet and lifestyle changes we can slow the rate of brain aging. But we can't stop it. To do better than that we need to develop stem cell therapies, gene therapies, and nanobots to do repairs.
"While eating tuna and other types of fish seems to help protect against memory loss and stroke, these results were not found in people who regularly ate fried fish," said Jyrki Virtanen, PhD, RD, with the University of Kuopio in Finland. "More research is needed as to why these types of fish may have protective effects, but the omega-3 fatty acids EPA and DHA would seem to have a major role."
Types of fish that contain high levels of DHA and EPA nutrients include salmon, mackerel, herring, sardines, and anchovies.
"Previous findings have shown that fish and fish oil can help prevent stroke, but this is one of the only studies that looks at fish's effect on silent brain infarcts in healthy, older people," said Virtanen. Research shows that silent brain infarcts, which are only detected by brain scans, are found in about 20 percent of otherwise healthy elderly people.
By the time you reach 60 you will have a one in five chance of having brain microbleed microlesions. The longer you live the more these pockets of neuronal cell death will accumulate. We need to develop rejuvenating treatments that will prevent this accumulating brain damage. Adult stem cells to rejuvenate blood vessels would probably help.
My fear with biomass energy is that we will find plants that can convert sunlight to usable energy so efficiently that biomass energy can compete on cost but not efficiently enough to limit use of land for energy to a very small area. Well, miscanthus looks like it will help make the nightmare scenario cost effective. Miscanthus beats corn and switchgrass for biomass production.
CHAMPAIGN, Ill. — In the largest field trial of its kind in the United States, researchers have determined that the giant perennial grass Miscanthus x giganteus outperforms current biofuels sources – by a lot. Using Miscanthus as a feedstock for ethanol production in the U.S. could significantly reduce the acreage dedicated to biofuels while meeting government biofuels production goals, the researchers report.
The new findings, from researchers at the University of Illinois, appear this month in the journal Global Change Biology.
If these researchers are correct then half of US agricultural acreage could supply all current US liquid fuels needs.
Using corn or switchgrass to produce enough ethanol to offset 20 percent of gasoline use – a current White House goal – would take 25 percent of current U.S. cropland out of food production, the researchers report. Getting the same amount of ethanol from Miscanthus would require only 9.3 percent of current agricultural acreage. (View a narrated slideshow about Miscanthus research.)
That is bad news. Why? Because there is the rest of the world with Asian demand on a course that will send it far past current US liquid fuel demand. A way to make cost competitive liquid fuel from agriculture will pull much more land around the world into biomass energy production. That cuts into land available for all the other species of critters on this planet.
Miscanthus might displace corn for use in ethanol production.
“What we’ve found with Miscanthus is that the amount of biomass generated each year would allow us to produce about 2 1/2 times the amount of ethanol we can produce per acre of corn,” said crop sciences professor Stephen P. Long, who led the study. Long is the deputy director of the BP-sponsored Energy Biosciences Institute, a multi-year, multi-institutional initiative aimed at finding low-carbon or carbon-neutral alternatives to petroleum-based fuels. Long is an affiliate of the U. of I.’s Institute for Genomic Biology. He also is the editor of Global Change Biology.
In trials across Illinois, switchgrass, a perennial grass which, like Miscanthus, requires fewer chemical and mechanical inputs than corn, produced only about as much ethanol feedstock per acre as corn, Long said.
“It wasn’t that we didn’t know how to grow switchgrass because the yields we obtained were actually equal to the best yields that had been obtained elsewhere with switchgrass,” he said. Corn yields in Illinois are also among the best in the nation.
Advances in agricultural biotechnology will boost yields. But dwindling supplies of oil and natural gas will drive up input costs. Also, population growth will reduce land available for farming as more land gets converted into residential and commercial building usage. A big global push for population control would help reduce the severity of this problem.
The history of weight loss research has generally been that few weight losers keep the weight off. Well, in one group of overweight and obese women adding an additonal 5 hours per week of exercise and sustaining this kept off the lost weight.
In addition to limiting calories, overweight and obese women may need to exercise 55 minutes a day for five days per week to sustain a weight loss of 10 percent over two years, according to a report in the July 28 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
More than 65 percent of U.S. adults are overweight, a public health concern, according to background information in the article. "Among obese adults, long-term weight loss and prevention of weight regain have been less than desired," the authors write. "Therefore, there is a need for more effective interventions." Current recommendations prescribe 30 minutes of moderate physical activity on most days of the week, for a total of 150 minutes per week. However, a growing consensus suggests that more exercise may be needed to enhance long-term weight loss.
To calculate the amount of exercise needed, John M. Jakicic, Ph.D., of the University of Pittsburgh, and colleagues enrolled 201 overweight and obese women in a weight loss intervention between 1999 and 2003. All the women were told to eat between 1,200 and 1,500 calories per day. They were then assigned to one of four groups based on physical activity amount (burning 1,000 calories vs. 2,000 calories per week) and intensity (moderate vs. vigorous). Group meetings focusing on strategies for modifying eating and exercise habits, as well telephone calls with the intervention team, also were conducted over the two-year period.
The only women who kept off all the lost weight burned more calories per week doing exercise. But they also continued to better follow weight loss diet advice.
After six months, women in all four groups had lost an average of 8 percent to 10 percent of their initial body weight. However, most were not able to sustain this weight loss. After two years the women's weight was an average of 5 percent lower than their initial weight, with no difference between groups.
The 24.6 percent of individuals who did maintain a loss of 10 percent or more over two years reported performing more physical activity (an average of 1,835 calories per week, or 275 minutes per week over the baseline level of activity) than those who lost less weight. They also completed more telephone calls with the intervention team, engaged in more eating behaviors recommended for weight control and had a lower intake of dietary fat.
I wonder if the problem of obesity is due to our appetites being evolutionarily tuned to eat for a higher average level of activity.
If we take pills that emulate exercise will this keep off the fat? More muscle would mean more calories burned per day since muscle just sitting there uses energy. So boosting our muscle mass would probably help keep the weight off. Exercise with more muscle mass would burn more calories per unit time.
I do not expect obesity to last as a problem for much longer than perhaps 15 years. Even if anti-obesity drugs take 10 years to develop we should know enough within 5 years what sorts of drugs to develop to boost muscle mass, reduce appetite, and increase breakdown of fat. The recent report about compounds that emulate the effects of exercise are an example of how fast our understanding of metabolism is advancing.
When Alexis Gorman, 26, wanted to tell a man she had been dating that the courtship was over, she felt sending a Dear John text message was too impersonal. But she worried that if she called the man, she would face an awkward conversation or a confrontation.
Alexis, did you really want to achieve your first real fame in life by getting described in the New York Times as someone who used Slydial to ditch some guy? Also, did you do this as a way to make him hear it twice?
If you get bad news from a romantic interest in email, well, they didn't want to tell you directly.
So she found a middle ground. She broke it off in a voice mail message, using new technology that allowed her to jump directly to the suitor’s voice mail, without ever having to talk to the man — or risk his actually answering the phone.
The technology, called Slydial, lets callers dial a mobile phone but avoid an unwanted conversation — or unwanted intimacy — on the other end. The incoming call goes undetected by the recipient, who simply receives the traditional blinking light or ping that indicates that a voice mail message has been received.
That is what I like: Technological ways to avoid undesired intimacies.
More ways to avoid intimacy might make people more willing to engage in it in the first place. If you can back out of a relationship more easily it is less risky to start one in the first place. Perhaps Ms. Gorman sees voice mails as a more humane way that text messaging to stop after a couple of dates. This option cuts the emotional cost of dating. With an easier exit ramp you are more likely to get on the highway in the first place.
“If it’s some jerk I went out on a couple of dates with, I can do without that drama,” she said.
“Text messaging someone ‘I would prefer not to see you again’ is really not my style,” she added. “But at the same time, I wanted to avoid an awkward conversation.”
I think the bigger problem with phone conversations is that they can be hard to end even with people you know you will speak with again. You might feel assorted obligations to the other person and don't want to signal that you are uninterested in hearing yet more of what they have to say. I didn't get a cell phone until last year for just this reason.
BTW, the New York Times picture of Ms. Gorman doesn't look as good as this Facebook picture which seems like it is her.
I'm seeing mention on a few blog sites of a sudden incompatibility between Site Meter and IE 6 and IE 7. Also, I just received an email report of IE access problems to this site that just started. Are you using IE6 or IE7? If so, are you having any sudden new site access problems here or elsewhere?
Also, if you are having any other problems accessing this site either new or old please let me know in comments.