There's been controversy on whether those who take selective serotonin reuptake inhibitor (SSRI) antidepressants are at greater risk of thinking suicidal thoughts. It is a difficult effect to tease out since people depressed enough to take SSRIs are already at greater risk of depression and some of them probably become less at risk of suicide because SSRIs brighten their mood. But maybe others react to SSRIs by becoming more suicidal. Well, genetic testing might have allowed some scientists to discover who will be at greater risk of suicidal thoughts as a result of taking an SSRI. People taking the SSRI drug citalopram who have certain variants of glutamate receptor genes are at much higher risk of suicide thoughts.
Specific variations in two genes are linked to suicidal thinking that sometimes occurs in people taking the most commonly prescribed class of antidepressants, according to a large study led by scientists at the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH). Depending on the particular mix inherited, these versions increased the likelihood of such thoughts from 2- to15-fold, the study found. About 1 percent of adult patients were deemed to be at high genetic risk, 41 percent at elevated risk and 58 percent at lower risk.
If confirmed, the findings may hold promise for genetic testing, as more such markers are identified.
The "If confirmed" is important. They looked at many genes and so a false positive just by chance is possible.
Risk increased proportionately if a participant had two, as opposed to just one of the suspect versions. Both genes code for components of the brain’s glutamate chemical messenger system, which recent studies suggest is involved in the antidepressant response.
Overall, about 6 percent of 1,915 patients with depression reported that they started to have suicidal thoughts while taking an antidepressant. This rate soared to 36 percent among the few patients with both of the suspect gene versions; 59 percent of the patients who had suicidal thoughts had at least one of the versions.
Francis J. McMahon, M.D., Gonzalo Laje, M.D., NIMH Mood and Anxiety Disorders Program, and colleagues at the National Human Genome Research Institute (NHGRI), Mount Sinai School of Medicine, and the University of Texas Southwestern Medical Center, report on their findings in the October, 2007 issue of The American Journal of Psychiatry.
We are well within 10 years of widespread use of genetic testing when choosing between drugs and making other treatment decisions. Clinical practice will take a big turn when genetic tests can predict which drugs will cause which side effects in each patient.
The researchers found that certain versions of two genes that code for glutamate receptors – the receiving stations for the neurotransmitter’s chemical messages – were more prevalent in patients with suicidal thinking. How the newly identified versions affect the workings of glutamate receptors to confer increased risk remains to be discovered. It’s also not yet known whether the findings generalize to other antidepressants.
One percent of the study participants had a version of the kainate receptor gene, GRIK2, that increased the odds for suicidal thinking more than 8-fold. Forty-one percent of participants had a version of the AMPA receptor gene, GRIA3, that raised the odds nearly 2-fold. About one-half of 1 percent of participants had both high risk gene versions, boosting the odds 15 fold – but this was the case for only 11 participants, of whom four developed suicidal thinking.
The size of the observed effects makes it likely that their finding is real. It is the sort of result that could be confirmed pretty quickly with sufficient funding.
A discovery like this one is not just useful for making drug choices. It also provides clues about what causes people to become suicidal. A better understanding of the mechanisms which cause suicidal thoughts will lead to ways to stop suicidal thoughts.
People with Alzheimer's Disease who ate a Mediterranean diet (more monounsaturated fats, more fruits and vegetables, beans, whole grains, less meat and dairy) lived 4 years long than those not on a the Mediterranean diet.
Scarmeas' group found that patients whose consumption habits most closely tracked that of the Mediterranean diet were 76 percent less likely to die in the study period than those whose food intake least mimicked the diet.
Compared with those whose diets most closely resembled a Western diet, Alzheimer's patients who most closely followed the Mediterranean diet lived an average of four years longer.
A more moderate degree of adherence to the Mediterranean diet still translated into extra 1.3 years of survival, the researchers said. That's equal to a 29 percent to 35 percent reduced risk for dying during the study period.
The same Columbia University Medical Center team led by Nikolaos Scarmeas previously reported that the Mediterranean diet appears to lower the risk of getting Alzheimer's in the first place.
Compared to the third of people who scored worst on the Mediterranean diet scores, those in the mid-ranking group had a 15% to 21% lower risk of developing Alzheimer's disease, and those with the highest score had a 39% to 40% lower risk.
Also see this abstract of some of their previous work on this topic.
The Mediterranean diet is a more doable kind of diet than a lot of others. It doesn't eliminate fats. It just shifts which ones you eat. Ditto for carbs. A lot of people can eat a Mediterranean diet without feeling heavily deprived. But you have to commit to doing it. Cook the beans, buy the nuts and seeds. Switch from polyunsaturated oils to monounsaturates like olive oil and canola. Also, cut back on meat and dairy and eat more fish.
Periodically I try to find ways to improve my diet. It is already pretty good. But I just ordered a flax seed grinder. I'll let you all know how flax seed grinding works out.
Update: Reminder: Not excited about the notion of eating a better diet in order to slow the inevitable decay of old age? Feel like, hey, what's the point? The point is to live long enough to still have a functioning mind when rejuvenation therapies become available. Yes, the rejuvenation therapies are coming. They aren't distant science fiction prospects. We'll have at least some useful stem cell therapies in 10 years and many more in 20 years. We will have gene therapies and methods for growing replacement organs too. Hang in there and slow the decay. Eventually it'll be possible to reverse the decay.
More nuclear power plants are on the way.
With this week's application to build a new nuclear plant – the first such filing in nearly 30 years – the industry says the US is on the verge of a nuclear power renaissance.
With virtually no greenhouse-gas emissions, reactors are touted as part of the solution to global warming. Over the next 15 months, the Nuclear Regulatory Commission expects a tidal wave of similar permit applications for up to 28 new reactors, costing up to $90 billion to build.
These reactors are going to be larger than the existing 104 reactors. They'll also be safer and require less maintenance.
The nuclear power industry is being helped by federal loan guarantees.
Now, the Senate version of a new energy bill includes a provision that could provide tens of billions of dollars more in federal-loan guarantees. On Tuesday, the Energy Department announced it would provide up to $2 billion in federal risk insurance for the first six new nuclear-plant projects, protecting them against losses from regulatory or legal delays.
Those loan guarantees do not cost the federal government billions of dollars. Their main effect is to lower the interest rates on bonds sold by nuclear reactor builders. Since capital costs are such a huge part of total nuclear power costs the reduction of loan interest rates via loan guarantees cuts new nuclear power plant electric costs from 6.33 cents per kilowatt-hour (kwh) to 4.78 per kwh. That cut in capital costs makes nuclear power cheaper that coal. By contrast, electric power from a new pulverized coal plant would be 5.36 cents per kwh. Without loan guarantees nuclear power costs more than coal electric.
The biggest argument for the loan guarantees is that new coal plants are both dirtier with conventional pollutants (e.g. particulates) and also emit large amounts of carbon dioxide which many want to cut back due to its global warming effects. Now, we could instead just require new coal plants to not pollute at all (or just plain ban new coal electric plants). But the political will does not exist to block new polluting coal electric plants (and if I was king that political will would exist to stop coal electric pollution - but the peoples of the world haven't yet realized that they should make me king for their own good). Given current circumstances I see the nuclear loan guarantees as the most politically feasible way to cut back on the construction of new coal plants.
A House-passed farm bill would give corn growers $10.5 billion over the next five years, even if prices stay high. These "direct payments," a kind of annual allowance, are set by formula and go out automatically, regardless of prices, profits, yields or weather.
...
The rural prosperity is due in large measure to billions of dollars in federal subsidies and incentives for corn-based energy. These include a 51-cent tax credit that gasoline manufacturers get on every gallon of ethanol they mix with their blends, and more than $500 million in federal cash to ethanol refiners between 2001 and 2006.
In 2005, Congress required the use of at least 7.5 billion gallons of ethanol a year by 2012. Then in 2006 came new demand for ethanol as a pollution-curbing additive, along with a jump in gasoline prices that made the corn-based fuel competitive.
Corn ethanol is a bad idea. Biomass energy boosts nitrous oxide emissions and by causing the cutting down of lots of forests a big shift to biomass will even boost carbon dioxide emissions. But the tax dollars flowing into it make nuclear subsidies small potatoes in comparison.
Will construction of the next round of nuclear power plants lead the nuclear industry down a learning curve to where it can construct reactors eventually build them for lower costs and compete with dirtier coal electric even without loan guarantees? Or will people become sufficiently opposed to air pollution that resulting tougher emissions cutting regulations will drive coal electric costs above nuclear electric?
David Pogue of the New York Times interviews Martin Eberhard, a top executive at Tesla Motors about their pure electric sports car.
David Pogue: So give me the gist of the Tesla Roadster. Zero to 60 in...?
Martin Eberhard: This is zero to 60 in under four seconds.
DP: And the range of the battery is?
ME: It's over 200 miles. [DP note: This week, the Environmental Protection Agency concluded its testing of the Tesla. Its official measurement: 245 miles per charge.]
That range is telling. They've got a car they've designed with very light and expensive materials. They probably have little or no luggage space. I bet it doesn't do well in crash tests either. They are using the best batteries they can find. Yet it is good for only 245 miles. Plus, once you've driven three and a half to four hours with it you've got to stop and wait just as long for it to recharge. This is a local car, not suitable for cross-country travel. In order for batteries to totally replace liquid fuels future batteries have got to store more electric power per unit weight and be capable of recharge in 1% of the time of current best-of-breed batteries. Is this physically possible?
DP: And time to recharge the battery?
ME: From empty to full, about three and a half hours.
DP: O.K. And price of the car?
ME: This is a $98,000 base model.
Tesla claims to have over 500 orders and that they will start shipping first quarter of 2008.
Tesla can afford to charge a hundred grand for a high end sports car. But obviously this sports car isn't going to revolutionize transportation at that high end price. The Roadster has a carbon fiber body that contributes to its high cost along with the pricey lithium ion batteries. The key question here: How fast will lithium battery prices fall? That's the multi-billion dollar question.
Given cheap high density batteries we would not have to worry about Peak Oil. Why? We do not face a general energy shortage. But we seem to be facing a growing liquid fuel energy shortage. Great batteries would make that shortage irrelevant. With the ability to move around using electricity our energy cost per mile will actually drop. A full sized SUV might use only 460 watt-hours/mile (0.46 kwh/mile) (warning: PDF file). Well, assume 11 cents per kwh for the electric cost (I'm rounding up a bit since I'm expecting higher electric prices). So then 0.46 wh/mile times 11 cents/kwh gives us a cost of about 5 cents a mile. Even if we add another penny in for recharge heat losses we are still at 6 cents per mile. Though in a higher electric cost state like New York we'll be at .46*17 + 1 = 9 cents per mile to push a big SUV around. How does that work out? If you drive 12,000 miles per year and live in New York you will spend $1080 per year to move your SUV around and you'll lose more money to depreciation. In a cheap electric state like Washington you'll pay less than half that amount. If you live in Washington state and drive a compact electric car it'll probably cost you less than $300 per year to keep it charged up. Your car insurance will cost more.
Since electricity is so cheap for transportation the biggest issue with electric cars is battery cost. Other notable issues include battery weight, safety, and longevity. Lithium batteries are much lighter than lead acid batteries and probably light enough at least for medium range cars. EnerDel claims to have solved the heat safety problem. Other battery makers such as A123Systems might have solved the heat safety problem too. EnerDel also claims to have solved the longevity problem. But cost continues to be a problem. Will A123Systems, EnerDel, and other competitors solve the cost problem?
Update: If you are wondering how urgently we need electric cars to replace gasoline-powered and diesel-powered vehicles read here and here for some recent analyses of oil production trends. Scary stuff if you ask me.
Looking out 30 or 40 years I do not see the human race limited by energy availability. Nuclear and solar power will become much cheaper and we'll find ways to convert those sources of power into forms usable for transportation. But I'm less sure about the next 5 to 10 years. We could be headed for a wrenching readjustment replete with severe recessions and declining living standards. Also, biomass ethanol is not the answer and hydrogen looks like a longer term prospect at best. So do we get great batteries in a timely manner or do our economies go through much more severe restructurings?
Brain scans of pedophiles shown adult porno demonstrate less reaction to the pictures.
Philadelphia, PA, September 20, 2007 – Pedophilia, the sexual attraction of adults to children, is a significant public health concern and it does not respond well to treatment. Additionally, the brain mechanisms underlying pedophilia are not well understood. A new study being published in the September 15th issue of Biological Psychiatry is the first of its kind to use functional brain imaging to describe neural circuits contributing to pedophilia.
I've long expected scientists will find that peds are wired up differently than the rest of us. Since I suspect the cause of their behavior comes from how their brains are wired I do not see that it makes sense to let them back out into society once they've been identified and served jail sentences. Okay, so what I do propose to do with them instead? Put them in isolated communities where they can't possibly get near children but where they are otherwise able to move about and live freely. Set aside a pedophile island where they would get relocated. Put buildings, infrastructure, other elements need to create a functional economy on that island.
I think the "isle of the damned" approach makes a lot of sense for certain types of crimes where people have unacceptable and unrepairable obsessions and criminal tendencies. If they are threats to only a portion of humanity (e.g. children, women) then put them somewhere that has none of their preferred targets.
Will we some day use brain scans to identify who should get sent to the "isle of the damned"?
Using functional magnetic resonance imaging, or fMRI, Walter and colleagues report that pedophilic patients showed reduced activation of the hypothalamus, a brain region involved in regulating physiologic arousal and hormone release, as compared to healthy individuals when they were viewing sexually arousing pictures of adults. Deficits of activation in the frontal cortex were associated with the extent of pedophilic behavior. In other words, when shown erotic pictures of adults, the brains of the pedophilic patients had reduced reactions in the pleasure center of the brain, indicating an altered sexual interest.
Is it possible to develop a brain scanning technology that will identify pedophiles without any false positives?
The scientists obviously want “the ability to intervene rationally in this disorder".
John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments that, “the ability to intervene rationally in this disorder is limited by shortcomings in our understanding of its neurobiology. The findings provide clues to the complexity of this disorder, [and] this deficit may predispose individuals who are vulnerable to pedophilia to seek other forms of stimulation.” It is important to acknowledge and consider however, that it is currently unknown “whether this pattern of brain activation is a risk factor for the development of pedophilia or a consequence of their pedophilic sexual experiences,” according to Dr. Krystal, and future research will be needed.
Therapy in this case would result in reordering of neurons in the brain. These researchers sound like their ultimate goal is to reshape human desires that are considered morally unacceptable.
One of the study’s authors, Georg Northoff, M.D., Ph.D., adds, "[These findings] may open the door for better understanding the neurobiology of this disorder which is of forensic, criminal and public concern. Our results may thus be seen as the first step towards establishing a neurobiology of pedophilia which ultimately may contribute to the development of new and effective means of therapies for this debilitating disorder.”
Therapies for a brain disorder that causes undesired behavior? Any such therapy would involve reshaping the brain to change emotional reactions and desires. Is this acceptable to do to criminals without their consent?
Make sure you get enough vitamin D.
HONOLULU, Sept. 20 – Women with low levels of vitamin D have an increased risk of hip fracture, according to a study led by the University of Pittsburgh Graduate School of Public Health presented this week at the 29th annual meeting of the American Society for Bone and Mineral Research at the Hawaii Convention Center.
Jane A. Cauley, Dr.P.H., professor of epidemiology, and colleagues evaluated patient data on 400 women enrolled in the Women’s Health Initiative Observational Study Cohort who had experienced hip fracture, confirmed by their medical record, over a median of 7.1 years. Levels of 25 hydroxyvitamin D, an indicator of vitamin D status, in the bloodstream were measured for these patients and compared with those of a control group matched for age, race, ethnicity and the date of relevant blood work. As vitamin D concentrations decreased, the risk of hip fractures climbed.
“The risk of hip fractures was 77 percent higher among women whose 25 hydroxyvitamin D levels were at the lowest concentrations,” said Dr. Cauley, who has spent much of the past 15 years investigating the physical changes that take place in postmenopausal women. “This effect persisted even when we adjusted for other risk factors such as body mass index, family history of hip fracture, smoking, alcohol use and calcium and vitamin D intake.”
Vitamin D deficiency might well cause more damage than any other nutrient deficiency in industrialized countries.
Juvenile onset type 1 diabetes is an auto-immune disease where the body's immune cells attack pancreatic cells that make insulin. Omega-3 fatty acids, which are known to have anti-inflammatory properties, appear to substantially reduce risk of type 1 diabetes.
Preliminary research suggests that in children at increased risk for type 1 diabetes, dietary intake of omega-3 fatty acids was associated with a reduced risk of pancreatic islet autoimmunity, which is linked to the development of diabetes, according to an article in the Sept. 26 issue of JAMA.
“Type 1 diabetes mellitus is an autoimmune disease that is characterized by the destruction of insulin-producing beta cells in the pancreatic islets. Although it is not yet known what initiates the autoimmune process, it is likely that both genetic background and environmental factors contribute to the disease process,” the authors write. Certain dietary factors have been associated with the onset of type 1 diabetes as well as the autoimmune process that leads to the disease.
Jill M. Norris, M.P.H., Ph.D., of the University of Colorado at Denver and Health Sciences Center, Denver, and colleagues examined whether consumption of omega-3 and omega-6 fatty acids are associated with the development of pancreatic islet autoimmunity (IA; development of antibodies against the cells in pancreas that produce insulin) in children. The study, conducted between 1994 and 2006, included 1,770 children at increased risk for type 1 diabetes, defined as either possession of a high diabetes risk HLA (human leukocyte antigen) genotype or having a sibling or parent with type 1 diabetes. The average age at follow-up was 6.2 years. Islet autoimmunity was assessed in association with reported dietary intake of polyunsaturated fatty acids starting at age 1 year. Fish is the primary source of marine polyunsaturated fatty acids. Childhood diet was measured using a food frequency questionnaire (FFQ).
A case-cohort study (n = 244) was also conducted in which risk of IA by polyunsaturated fatty acid content of erythrocyte membranes (outer portion of the red blood cell) was examined.
Fifty-eight children became positive for IA during follow-up. Adjusting for HLA genotype, family history of type 1 diabetes, caloric intake, and total omega-6 fatty acid intake, total omega-3 fatty acid intake was inversely associated with IA risk (a 55 percent reduced risk). The association was strengthened when the definition of the outcome was limited to those positive for two or more autoantibodies. In the case-cohort study, omega-3 fatty acid content of erythrocyte membranes was associated with a 37 percent decreased risk of IA.
Children who eat fish are also getting more vitamin D and hence might have less auto-immune disease for that reason. It has long been noticed that in the United States the incidence of multiple sclerosis (such is very likely an auto-immune disorder) is higher at northern latitudes. Further north people spend more time in-doors and get less vitamin D made in their skin as a result of sunlight hitting their skin. So the effect here might not entirely come from the omega-3 fatty acids. Either way, this result is an argument for eating fish. The research on omega 3 fatty acids and chronic inflammatory diseases also supports the idea that fish oil delivers real benefit.
Both reported diets and blood tests correlated with measured autoimmune response.
Parents were surveyed annually about what their children ate and children were tested for specific antibodies in the blood that marked the destruction of the cells that make insulin (i.e. diabetes autoimmunity). In a subset of this population, the researchers also examined whether risk of diabetes autoimmunity was associated with omega-3 fatty acid content of red blood cell membranes, which is a marker of omega-3 fatty acid status.
Of the children followed, those who reported eating more omega-3 fatty acids were less likely to develop diabetes autoimmunity. The investigators also showed that omega-3 fatty acid content of red blood cell membranes was inversely associated with risk of diabetes autoimmunity.
I go out of my way to make sure I get enough omega 3 fatty acids and eat salmon several times a week. Suggest you do the same.
Rather than check out provided references after interviewing some employers are using social networking sites to find work acquaintances to ask about prospective employees even before calling them in for interviews.
Job interviewees, beware: Your prospective boss may have called your references before you walk through the door -- and they may not be the contacts you provided.
Professional networking sites such as LinkedIn Corp. and Jobster Inc. are making it easier for employers to get in touch with people who have worked with job candidates in the past or know them personally. Recruiters say they use such sites -- where people create online profiles and then link to professional colleagues who are also members -- to find mutual connections they can hit up for information. Many hiring managers say they even check to see if they have mutual connections with a candidate on Facebook and MySpace, the popular social-networking sites.
Companies are even trolling social networking webs to find job candidates. So you can get your references checked out before you even know about a job opening.
This is an automation of what has gone on informally and less efficiently for years. A person who has previously worked at companies Y and Z gets a job at company X and tells people in company X who the big talents are in former employers Y and Z. Then company X personnel call up these talents and try to recruit them. This is great fun when you are the person who gets asked to come in and interview for a position in a company you never heard of before. Well, the web is going to make this so9rt of thing happen more often. Want to find out who is good at company W? Find connections between current and former employees and then start trying to email and call them. In many cases just one or two names will be enough to start the process of finding lots of connections.
This ability to find out the appraisals of more former colleagues will increase the value of working hard wherever you are. Each job becomes more of an audition for other jobs.
This phenomenon is part of a larger trend: the death of privacy. Communications and computing advances mean that more about us gets recorded and knowable by electronic means.
CORK, IRELAND, Sept. 17 /CNW/ - CIBC (CM: TSX; NYSE) - Oil prices are likely to hit US$100 a barrel by the end of next year as soaring rates of domestic oil consumption in the world's leading oil producing nations cuts into their export capacity, forecasts the chief economist at CIBC World Markets.
Speaking at the 6th Annual Association for the Study of Peak Oil & Gas conference in Cork, Ireland, CIBC World Markets chief economist, Jeff Rubin told delegates that the export capacity of OPEC, Russia and Mexico will drop by 2.5 million barrels per day by the end of the decade.
"Domestic demand growth of as much as five per cent per year in key oil producing countries is already beginning to cannibalize exports and will increasingly do so in the future as production plateaus or declines in many of these countries," says Mr. Rubin. "OPEC members together with independent producers Russia and Mexico consume over 12 million barrels per day, surpassing Western Europe to become the second largest oil market in the world.
"At current rates of domestic consumption the future export capacity of OPEC, Russia and Mexico must be increasingly called into question. These trends are likely to result in a sharp escalation in world oil prices over the next few years."
He noted that while he expects today's US$80 barrel of oil will reach as high as US$100 a barrel by the end of 2008, consumers in many major oil producing countries pay nothing near the global price for crude. He finds that highly subsidized gasoline prices are often a significant factor in surging rates of domestic oil consumption. In many countries prices are as little as US$10 a barrel.
With exports from OPEC, Russia and Mexico expected to decline by seven per cent over the next three years, markets will seek greater reliance on higher cost unconventional deposits. He expects that Canadian oil sands will surpass deep water wells as the single largest source of new oil exports by decade end.
Governments of many big oil exporters sell petroleum products for a loss in domestic markets. They use lower prices to buy domestic support for their governments. So gasoline is cheaper in Venezuela, Iran, Saudi Arabia, and Russia than in the oil importing countries. As a result domestic demand for oil products is growing more rapidly in the oil exporting countries than in most of the rest of the world. This has hugely important implications. Oil exporters will reduce their oil exports years before their domestic production peaks. Also, once their domestic production peaks their oil exports will decline much more rapidly than their production.
Rubin sees Canada has holding over half the oil that private investors can bring into production.
NEW YORK, Sept. 27 /PRNewswire-FirstCall/ - CIBC - Six of the largest oil suppliers to the U.S. are poised to significantly cut exports by 2012, ramping up pressure on supply and price, and intensifying the focus on one of the last great deposits open to private investment: Canada's oil sands.
The forecasted cuts by Mexico, Saudi Arabia, Venezuela, Nigeria, Algeria and Russia are the subject of a keynote address that Jeff Rubin, chief market strategist and chief economist at CIBC World Markets will deliver at the firm's Industrial Conference Oct. 2 in New York City. In his remarks, Mr. Rubin will share his latest research on the global oil supply/demand balance, with specific focus on the size and scope of the oil supply crunch facing the U.S. over the next five years.
On the bright side, Americans can downshift to much smaller cars. Our profligacy makes it easier for us to adjust to oil shortages. We have that so much energy usage that is easy to curtail. If we were already all driving European sized small cars with diesels we wouldn't be able to downsize as easily as we can now.
This argument is similar to the argument made by The Oil Drum bloggers westexas (Jeffrey J. Brown) and khebab (Samuel Foucher). In a recent post they elaborate on their Export Land Model of how the big exporters will gradually stop exporting due to growing domestic demand coupled by stagnate or declining production.
The current top five net oil exporters--Saudi Arabia, Russia, Norway, Iran and the UAE--account for about half of world net oil exports. From 2000 to 2005, they showed a combined 3.7% per year increase in consumption.
From 2005 to 2006, their combined consumption showed an accelerating rate of increase, to +5.3% per year. From 2005 to 2006, the top five showed a net export decline rate of -3.3% per year. Based on year to date data, it is a near certainty that this net export decline rate will accelerate from 2006 to 2007.
Basically, khebab and westexas divide the world into Export Land (e.g. Saudi Arabia, Russia) and Import Land (e.g. the United States, European countries, Japan, China). They see the supply of oil for Import Land countries dwindling much more rapidly than the total world production of oil. While some dispute their time scales (e.g. when exactly will world oil production peak?) it is harder to dispute the logic for their argument. The exporters will cut their exports more rapidly than they cut domestic consumption and their domestic consumption will even continue to rise beyond the point in time when they start reducing exports. That's a big "ouch" for the rest of us.
As I see it the world is in a race between declines in oil exports on one hand and the development of non-oil methods do to things that we now do with oil. Most notably, we need non-oil ways to power transportation and cars in particular. When will workable batteries for cars become available? If the Export Land Model is correct then the answer to the battery question is enormously important.
Faster and cheaper continues to be the story for genetic sequencing technology.
BRANFORD, Conn., Sept. 27, 2007 – 454 Life Sciences, a Roche company, in collaboration with Yale University researchers today announced that they have developed a method, using the company’s Genome Sequencer system, to identify significant human genetic variability with an unprecedented level of detail. The new method enables researchers to analyze genome-wide structural variations (SV), the gross changes to the genetic code much faster and economically than existing techniques. The study, entitled "Paired-End Mapping Reveals Extensive Genomic Structural Variation in Humans," appears online (ahead of print) today in the journal Science.
Structural variations in chromosomes are things like variable number of repeats of whole genes. We do not all have equal numbers of copies of each gene. People who have more copies of a gene can get more proteins and other pieces made from their greater number of copies. The ability to detect more structural variations and to do so more cheaply and rapidly will speed up the identification and characterization of structural variations in the genome.
Previous studies of human genomic variation tended to look at changes called single nucleotide polymorphism, variations that involve just one nucleotide, commonly referred to as SNP. However, the study published today suggests that structural variation is responsible for a larger number of differences between the genomes of two individuals than SNPs. Furthermore, structural variation may have notable physical effects on an individual. The role that SV plays in human variability has not been well understood because of cost-prohibitive and imprecise technology used in previous research. The novel approach described today in Science, called Paired End Mapping (PEM), used 454 Sequencing to comprehensively study SV at an unmatched level of precision, detecting most of the structural variation in the human genome.
“454 Sequencing enabled us to efficiently identify over 1000 structural variations in two individuals. Our study demonstrates that a large number of SVs are present in the human population and that SV plays a greater role in genetic diversity than SNP,” explained Michael Snyder, PhD., senior author and Lewis B. Cullman Professor of Molecular, Cellular and Developmental Biology and Professor of Molecular Biophysics and Biochemistry; Director of the Yale Center for Genomics and Proteomics. “The widespread occurrence of structural variation and the observation that many genes are affected, suggests that SV is likely to be a major form of human variation. It will be essential to incorporate SV detection in human genome sequencing projects.”
Advances in technologies for genetic sequencing and genetic testing are more important than any of the discoveries that these advances enable. The discoveries become increasingly easier to make as the genetic sequencing equipment becomes increasingly powerful. As the sequencing devices become more powerful we are going to reach a point where the rate of discovery per day will exceed the rate of discovery of the previous decade.
The Cheap DNA sequencing technology we will have 10 to 20 years hence will enable us each to have detailed profiles of all of our individual genetic variations. The low cost and exhaustive identification of genetic differences between humans will allow scientists to do massive comparisons between millions of people of genetic differences, health histories, personalities, cognitive abilities, and other characteristics. Those comparisons will allow us to learn the significance of most genetic differences.
Knowledge about the meaning of genetic differences will lead to widespread use of sperm, egg, and embryo screening when starting pregnancies. People will want to choose which genes they pass on to their offspring. The ability to knowledgeably make such choices will accelerate the rate of human evolution by orders of magnitude. Humans born 50 years from now (assuming the Singularity does not put a stop to human reproduction) will differ greatly from humans today. Future humans (transhumans?) will be far smarter, mentally healthier, better looking, healthier, stronger, and less susceptible to death from accidents or suicide.
Here is more evidence htat Alzheimer's Diseases is a type of insulin resistant diabetes.
EVANSTON, Ill. --- Insulin, it turns out, may be as important for the mind as it is for the body. Research in the last few years has raised the possibility that Alzheimer’s memory loss could be due to a novel third form of diabetes.
Now scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer’s disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer’s removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)
With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer’s disease, the Northwestern study sheds light on the emerging idea of Alzheimer’s being a “type 3” diabetes.
Insulin serves multiple functions. The best known is that it binds on the surface of cells and causes the cells to pull sugar out of the bloodstream. But the lack of binding by insulin on neurons in Alzheimer's might wreak damage due to interference with other processes which insulin helps regulate.
Development of the ability to block the accumulation of these ADDL proteins might provide a way to stop Alzheimer's. But the research on insulin resistance in Alzheimer's suggests that treatments used for type 2 insulin resistant diabetes might help also. Or drugs could be developed to block ADDL binding to insulin receptors.
“We found the binding of ADDLs to synapses somehow prevents insulin receptors from accumulating at the synapses where they are needed,” said William L. Klein, professor of neurobiology and physiology in the Weinberg College of Arts and Sciences, who led the research team. “Instead, they are piling up where they are made, in the cell body, near the nucleus. Insulin cannot reach receptors there. This finding is the first molecular evidence as to why nerve cells should become insulin resistant in Alzheimer’s disease.”
ADDLs are small, soluble aggregated proteins. The clinical data strongly support a theory in which ADDLs accumulate at the beginning of Alzheimer’s disease and block memory function by a process predicted to be reversible.
Alzheimer's is a horrible disease. Your brain slowly dies while your body remains living. You know it is happening until you reach the point where you can't even remember that much.
Why do the ADDLs accumulate in the first place? We need treatments that will stop Alzheimer's by stopping the very earliest steps in the disease. Is toxic protein accumulation the earliest step? Or is the earliest step something that causes the toxic proteins to start accumulating?
Moderate exercise appears to reduce the risk of developing osteoarthritis.
For a clearer picture of the impact of physical activity on the knee joint, a team of researchers in Australia turned to magnetic resonance imaging (MRI). This highly accurate high-tech tool makes it possible to directly visualize joint structures, detect early and pre-disease states of OA, and assess the influence of potential risk factors. Taking advantage of this novel methodology, the researchers studied the effect of physical activity, in various degrees of intensity, frequency, and duration, on knee structures in a total of 257 healthy adults between the ages of 50 and 79, with no history of knee injury or OA. Their findings, presented in the October 2007 issue of Arthritis Care & Research, suggest that exercise that is good for the heart is also good for the knee.
Obviously the exercise an NFL quarterback gets while getting slammed into by an offensive lineman isn't covered by this study. Those guys do real damage to each other and live to suffer the results the rest of their lives.
Exercise that gets the heart pumping builds up cartilage volume in joints.
Among the notable findings, both baseline and current vigorous physical activity— exercise that gets the heart pumping and the body sweating—were associated with an increase in tibial cartilage volume, free from cartilage defects. What’s more, tibial cartilage volume increased with frequency and duration of vigorous activity. Recent weight-bearing exercise was also linked to increased tibial cartilage volume and reduced cartilage defects. Finally, moderate physical activity, including regular walking, was associated with a lower incidence of bone marrow lesions.
So exercise probably reduces the risk of bone fractures as well.
Sweat it up at least 20 minutes per week.
“Our data suggest that at least 20 minutes once per week of activity sufficient to result in sweating or some shortness of breath might be adequate. This is similar to, if not somewhat less than, the recommendations for cardiovascular health,” Dr. Cicuttini observes.
You already ought to be getting as much or more exercise for your heart anyway.
Philadelphia, PA, September 26, 2007 – Do gene variants that convey risk for schizophrenia affect apparently healthy individuals" Although these genes are present in every human, individuals may have different versions of these genes, called alleles. While many people who possess these “risk alleles” do not end up with schizophrenia, this does not mean they are unaffected by the presence of the risk allele. In the largest study of its kind to date, scheduled for publication in the October 1st issue of Biological Psychiatry, researchers sought to examine the impact of a few particular genes, known to be associated with a diagnosis of schizophrenia, on a healthy population.
Stefanis and colleagues recruited more than 2000 young men and measured dimensions of their cognitive abilities that tend to be impaired in individuals diagnosed with schizophrenia. The authors also measured schizotypal personality traits, which represent behaviors that are associated with schizophrenia, such as atypical behaviors and beliefs, suspiciousness or paranoia, and discomfort in social situations. They then genotyped these volunteers in relation to the four most prominent schizophrenia candidate genes: Neuregulin1 (NRG1), Dysbindin (DTNBP1), D-amino-acid oxidase activator (DAOA), and D-amino-acid oxidase (DAAO). According to Nicholas Stefanis, the lead author on the paper, their study showed “that apparently normal individuals who posses several risk alleles within these susceptibility schizophrenia genes, have indeed minute decrements in cognitive ability such as decreased attentional capacity and worse performance on memory tasks, and alterations in schizotypal beliefs and experiences.” In other words, they found that the healthy individuals who possessed the risk variants within the DNTBP1, NRG1, and DAAO genes exhibited small reductions in their cognitive performance and had atypical experiences that might be associated with schizophrenia.
How many people have atypical beliefs because they are smart enough to think their way outside the box of the conventional consensus? How many have atypical beliefs because they carry genetic variations that alter the way they view evidence?
Do we as a total society benefit from some people carrying alleles that make them think atypical thoughts? Are smart people with schizophrenia risk genes who do not get schizophrenia more creative, on average, than smart people without these schizophrenia risk genes? Is there some optimal small dose schizophrenia risk alleles that, when combined with high IQ, produces great scientists, inventors, and innovators? Whatever genes made the unusual mind of Vincent Van Gogh might get clipped out of future generations of humanity.
One of my concerns with mental illness risk genes going forward comes from the ability we are gaining to screen and choose amongst our genes to decide what to pass on to our offspring. Will prospective parents take such a risk minimizing approach to offspring genetic allele selection that future generations will have brains that make them more likely to accept the conventional wisdom and to go along with the consensus of elites and masses? Will future societies become more sheepish and less free as a result?
Lycopene was hyped as a potential risk reducer for prostate cancer. But then studies came out suggesting that maybe it doesn't help after all. The real answer has remained less than totally clear. The European Prospective Investigation into Cancer and Nutrition, being a pretty decent sounding prospective study, might provide the answer: lycopene and a bunch of anti-oxidant micronutrients don't appear to lower prostate cancer risks.
Objective: We aimed to examine the associations between plasma concentrations of 7 carotenoids, retinol, alpha-tocopherol, and gamma-tocopherol and prostate cancer risk.
Design: A total of 137 001 men in 8 European countries participated. After a mean of 6 y, 966 incident cases of prostate cancer with plasma were available. A total of 1064 control subjects were selected and were matched for study center, age, and date of recruitment. The relative risk of prostate cancer was estimated by conditional logistic regression, which was adjusted for smoking status, alcohol intake, body mass index, marital status, physical activity, and education level.
Results: Overall, none of the micronutrients examined were significantly associated with prostate cancer risk. For lycopene and the sum of carotenoids, there was evidence of heterogeneity between the associations with risks of localized and advanced disease. These carotenoids were not associated with the risk of localized disease but were inversely associated with the risk of advanced disease. The risk of advanced disease for men in the highest fifth of plasma concentrations compared with men in the lowest fifth was 0.40 (95% CI: 0.19, 0.88) for lycopene and 0.35 (95% CI: 0.17, 0.78) for the sum of carotenoids.
Conclusions: We observed no associations between plasma concentrations of carotenoids, retinol, or tocopherols and overall prostate cancer risk. The inverse associations of lycopene and the sum of carotenoids with the risk of advanced disease may involve a protective effect, an association of dietary choice with delayed detection of prostate cancer, reverse causality, or other factors.
I really wish they had looked at plasma vitamin D concentrations.
Taking most micronutrients in pills (vitamin D being a notable exception) doesn't serve as a substitute for eating foods that are health promoting or for avoiding foods that seem to harm health. You need to eat lots of fruits and vegetables and eat less highly fatty charbroiled beef. There's no pill substitute for avoiding saturated fats or for eating lower glycemic index foods. Macronutrients matter.
Widespread use of influenza vaccines haven't lowered death rates among old folks.
Researchers are questioning how much the flu vaccine prevents flu-related deaths among older people, saying it may provide less protection starting around age 70, as immune systems decline with age.
In a review article in the October issue of Lancet Infectious Diseases, researchers including Dr. Lisa Jackson, a senior investigator at the Group Health Center for Health Studies, say evidence that all older people should get flu vaccines is weak.
Read the full article for the details.
The problem is rickety old immune systems.
A further piece of research found that over-65s produced only half or a quarter of the antibodies to flu vaccines that younger people did. Vaccination coverage has risen steeply in the US, from 15% of the target population in 1980 to 65% today, they write. But there has been no matching drop in influenza deaths.
We need the ability to rejuvenate our immune systems. In particular we need a way to kill old immune cells that are too worn out so that healthier immune cells can take their place. Plus, we need the ability to grow replacement thymus glands. All of this will come with time. But we could get these advances sooner if we pushed harder for them.
For most of the remaining unconquered diseases we aren't going to cure them or prevent them without developing the ability to do rejuvenation on each portion of the body which malfunctions with each disease. Attempts to cure the many diseases and disorders of old age will inevitably lead to efforts to rejuvenate various malfunctioning parts of the body. Successful efforts to rejuvenate various parts of the body will lead us to the point where we can fix so many parts that full body rejuvenation becomes possible.
Skimping on the sleep might kill you.
Researchers from the University of Warwick, and University College London, have found that lack of sleep can more than double the risk of death from cardiovascular disease. However they have also found that point comes when too much sleep can also more than double the risk of death.
In research to be presented on Monday 24th September 2007, to the British Sleep Society, Professor Francesco Cappuccio from the University of Warwick’s Warwick Medical School will show the results of a study of how sleep patterns affected the mortality of 10,308 civil servants in the “Whitehall II study”. Amongst other things the data they used provided information on the mortality rates and sleep patterns on the same group of civil servants at two points in their life (1985-8 and those still alive in 1992-3).
The researchers took into account other possible factors such age, sex, marital status, employment grade, smoking status, physical activity, alcohol consumption, self-rated health, body mass index, blood pressure, cholesterol, other physical illness etc. Once they had adjusted for those factors they were able to isolate the effect that changes in sleep patterns over 5 years had on mortality rates 11-17 years later.
Taking those who had not made any change in their sleeping habits between 1985-8 and 1992-3 as their baseline (7 hours per night being the figure normally recommended as an appropriate period of sleep for an adult) they were able to see what difference having reduced the amount of sleep over time made to mortality rates by 2004.
Those who had cut their sleeping from 7h to 5 hours or less faced a 1.7 fold increased risk in mortality from all causes, and twice the increased risk of death from a cardiovascular problem in particular.
People who sleep less could conceivably have diseases that are disrupting their sleep and eventually killing them. But that seems an unlikely explanation given the stress effects of sleep deprivation. Get enough sleep. It ight save your life.
Hamilton, ON. Sept. 24, 2007 – Men who have lower-pitched voices have more children than do men with high-pitched voices, researchers have found. And their study suggests that for reproductive-minded women, mate selection favours men with low-pitched voices.
The study, published in Biology Letters, offers insight into the evolution of the human voice as well as how we choose our mates.
In previous studies, David Feinberg, assistant professor in the Department of Psychology, Neuroscience and Behaviour at McMaster University, and his colleagues have shown that women find deeper male voices to be more attractive, judging them to be more dominant, older, healthier and more masculine sounding. Men, on the other hand, find higher-pitch voices in women more attractive, subordinate, feminine, healthier and younger sounding.
“While we find in this new study that voice pitch is not related to offspring mortality rates,” says Feinberg,” we find that men with low voice pitch have higher reproductive success and more children born to them.”
What I really want to know: If deep voiced men and high pitched voiced women make babies then are the male babies not as deeped voiced as their dads and are the female babies not as high pitched voiced as their moms? To put it another way: Do more masculine mothers give birth to more masculine sons and do more feminine fathers sire more feminine daughters?
Some day prospective parents will genetically engineer their male offspring to have deeper voices and female offspring to have higher pitched voices. How many parents will give their daughters deeper voices to perhaps help them do better in work careers?
Also, once plastic surgery for voice tone modification becomes safe and effective how many people will change their voice pitch and in which direction?
Of course, if you want to increase your satisfaction with romantic relationships some day there'll be another option besides body alterations that enhance your appeal to others: modify your brain so that you find more kinds of human body shapes appealing. Then you could find easy pickings and satisfaction with those who are less attractive to the majority. Though that approach will become less valuable once most people get their appearances enhanced. You won't be able to find as many lonely people who others find unattractive. Jack Black's distorted view of a fat Gwyneth Paltrow will some day become achievable in real life. But before that happens obesity will become easily curable.
New York City hedge fund managers Robert Goldstein and Joel Greenblatt have created an annual $1 million prize for the best idea for cancer research of the ideas which researchers (and even the rest of us) post on their Gotham Prize web site.
A managing partner at the hedge fund Gotham Capital in New York, Mr. Goldstein recognized similarities with his own profession. Money managers also were reluctant to share investment ideas. A few years earlier, Mr. Goldstein's business partner and friend, Joel Greenblatt, the 49-year-old founder of Gotham Capital, had created an online, selective group called the Value Investors Club, to spur idea sharing. Members shared investing strategies and commented on each other's research. A cash prize was awarded for the best idea of the week.
The two men thought that perhaps a similar model would work in cancer research. So this year they agreed to put up $1 million of their own money every year to fund the Gotham Prize for Cancer Research. Modeled on the Value Investors Club, the annual prize will go to the person who posts the best new cancer-research idea, judged by a board of respected scientists, at the prize's Web site by the end of December.
The winner of the Gotham Prize doesn't have to present a shred of evidence that the premise will work. To attract ideas from people outside the field of cancer research, there is no requirement that the winner be capable of seeing the idea through. And the prize money is earmarked for personal use, to be spent on anything the winner wants, even a fancy car or a bigger house.
Got a good idea for cancer research that you think might be worth a cool million bucks? Now's your chance.
Some researchers quoted in the article are skeptical that prize money for ideas is the most efficacious way to fight cancer. But as the article also points out, lots of researchers keep their ideas secret because they want to be first to publish and get credit for a discovery that follows from a good idea. Getting more ideas out into the public domain might speed up the rate of researchers by allowing teams to incorporate more ideas from other teams into their experimental designs and strategies.
More generally, prizes for scientific discoveries are a great idea because humans respond to incentives and produce more when properly incentivized. The incentives facing academic researchers are not entirely directed toward increasing the motive to make useful discoveries. Also, academics have incentives to make their own labs look more productive even if they might have an idea that would be better tested in another lab. Academic politics and other influences create incentives that reduce the motive to discover. The need to get grants renewed can lead to conservative choices that are more likely to produce tangible results even if not immediately useful results. Tenure reduces the need to perform in research. With all these influences financial incentives can make a big difference.
Update: Modest proposal for the Gotham Prize folks: Most researchers aren't going to take the time to read all the submissions that are publically posted. You ought to provide a way for readers to assign scores to the quality of ideas so that others with limited time can come in and read, say, all the 5 star submissions. Then you run into the problem of the quality of the reviewers. Let people see who is scoring the submissions and if they recognize some name they respect let them view the list of submissions that a given reviewer scored and what score he or she assigned to each submission.
Few of the more than two dozen climate experts interviewed disagree with the one-meter projection. Some believe it could happen in 50 years, others say 100, and still others say 150.
Sea level rise is "the thing that I'm most concerned about as a scientist," says Benjamin Santer, a climate physicist at the Lawrence Livermore National Laboratory in California.
"We're going to get a meter and there's nothing we can do about it," said University of Victoria climatologist Andrew Weaver, a lead author of the February report from the Intergovernmental Panel on Climate Change in Paris. "It's going to happen no matter what - the question is when."
If you click through to the article you'll see what would get submerged along the US East and Gulf coasts by a 1 meter risk in the level of the ocean. But this claim by Andrew Weaver is a little annoying. We have the capability to put the entire planet into an Ice Age for cheap. There's nothing inevitable about global warming or the melting of glaciers on Greenland and the Antarctic continent.
Using either silicon dioxide or iron dumped in the ocean to produce dimethyl sulfide (DMS) we can make the Earth so cold that we bring on a new ice age. This can be done for a yearly cost of less than the United States wastes to subsidize corn ethanol production. For a few billion dollars per year we can turn much of the planet into an ice cube. For a smaller figure we could cancel out the amount of warming that might be caused by CO2 build-up.
One problem with this scheme: If we want to cancel out the effects of CO2 emissions then we have the problem of not really knowing how much an effect the CO2 is actually having. We do not know what the average global temperature would be in a given year minus the CO2 effect (or minus the effect of nitrous oxide or methane or other gases released by humans into the atmosphere). Still, presumably climate models will get better and in 20 or 30 years climate scientists create realistic simulations of Earth's climate with the ability to measure the effects of human intervention. Or we could just intervene by however much is necessary to ensure sea levels do not rise.
Suppose that the amount of CO2 already released into the air is already enough to raise temperatures at the poles enough to cause lots of water to flow into the oceans and raise water levels and flood low lying regions. Is that outcome so terrible that we should do climate engineering to prevent it from happening?
Should we do climate engineering to prevent the flooding Miami? Should we do climate engineering to prevent massive dislocations of humans in Bangladesh? Should we do climate engineering to prevent lots of high priced choice ocean front property from being destroyed by the waves and tides?
I'm thinking the world is going to run out of oil before some of the more pessimistic projections of carbon dioxide build-up can happen. So if we have a warming problem that'll cost us a lot of choice real estate (though while making colder places more livable and valuable to humans) then we could deal with that transitory trend toward warming by using climate engineering. On the other hand, we could instead opt to make the weather of Northern Europe, Siberia, Alaska, Canada, Minnesota and Maine more livable.
Biogerontologist Aubrey de Grey and assistant Michael Rae have a new book out on how aging can be stopped and reversed entitled Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging In Our Lifetime. I'm only on page 18 but it is pretty good so far. I'm going to write a series of posts about it as I read through the book.
In chapter 2 Aubrey discusses why people accept aging as inevitable and for the most part resist hearing arguments for why aging is defeatable.
There is a very simple reason why so many people defend aging so strongly - a reason that is now invalid, but until quite recently was entirely reasonable. Until recently, no one has had any coherent idea how to defeat aging, so it has been effectively inevitable. And when one is faced with a fate that is as ghastly as aging and about which one can do absolutely nothing, either for oneself or even for others, it makes perfect psychological sense to put it out of one's mind - to make one's peace with it, you might say - rather than to spend one's miserably short life preoccupied by it. The fact that, in order to sustain this state of mind, one has to abandon all semblance of rationality on the subject - and, inevitably, to engage in embarrassingly unreasonable conversational tactics to shore up that irrationality - is a small price to pay.
Most of us do need peace of mind. But watching people decay from aging does not give me peace of mind. Just how much aging causes pain and suffering is not something that most people appreciate. Do you know people who have daily pain from osteoarthritis? I do. Since friends know I follow things medical and biological I get requests from friends to look up on the internet info about side effects of pain killers and the like. Start taking note of people around you who use pain killers. You might be surprised at what you tally up.
Then there are the various infirmities and disablements. Know men who can't go far between toilet stops? Women who wake in the middle of the night from hot flashes that last for years? How about decaying eyes that need more kinds of corrective glasses for more reasons? The list goes on. Walk through a store and you'll see lots of people with lots of infirmities. The older they look the more problems you should suspect they have.
Some people say that aging is a graceful process that has dignity. Ever helped a person or a dog die from cancer? I've done both. Nothing graceful about it. Not dignified about it. I hate to recall the images of what I saw.
Aubrey calls on us to wake up out of our "aging is inevitable" trance. I'm hearing a variation on John Lennon in my mind: "Imagine there's no aging, It's easy if you try".
I've told you that we've recently reached the point where we can engage in the rational design of therapies to defeat aging: most of the rest of this book is an account of my favored approach to that design. But in order to ensure that you can read that account with an open mind, I need to dispose beforehand of a particularly insidious aspect of the pro-aging trance: the fact that most people already know, in their heart of hearts, that there is a possibility that aging will eventually be defeated.
Why is this a problem? Indeed, at first sight you might think that it would make my job easier, since surely it means that the pro-aging trance is not particularly deep. Unfortunately, however, self-sustained delusions don't work like that. Just as it's rational to be irrational about the desirability of aging in order to make your peace with it, it's also rational to be irrational about the feasibility of defeating aging while the chance of defeating it any time soon remains low. If you think there's even a 1 percent chance of defeating aging within your lifetime (or within the lifetime of someone you love), that sliver of hope will prey on your mind and keep your pro-aging trance uncomfortably fragile, however hard you've worked to convince yourself that aging is actually not such a bad thing after all. If you're completely convinced that aging is immutable, by contrast, you can sleep more soundly.
Aubrey argues that the chance of defeating aging within our lifetimes is a lot higher than 1% and on that I agree. Scientists are making advances in development of the tools we'll need to defeat aging. Impressive results are getting reported on stem cell therapies, growth of replacement organs in labs, and other pieces of the puzzle. We are looking at a scale of time that is on the order of decades, not centuries.
Anyway, the book is a good read so far. I recommend it.
Growing and burning many biofuels may actually raise rather than lower greenhouse gas emissions, a new study led by Nobel prize-winning chemist Paul Crutzen has shown.1 The findings come in the wake of a recent OECD report, which warned nations not to rush headlong into growing energy crops because they cause food shortages and damage biodiversity.
Crutzen and colleagues have calculated that growing some of the most commonly used biofuel crops releases around twice the amount of the potent greenhouse gas nitrous oxide (N2O) than previously thought - wiping out any benefits from not using fossil fuels and, worse, probably contributing to global warming. The work appears in Atmospheric Chemistry and Physics and is currently subject to open review.
'The significance of it is that the supposed benefits of biofuel are even more disputable than had been thought hitherto,' Keith Smith, a co-author on the paper from the University of Edinburgh, told Chemistry World. 'What we are saying is that [growing many biofuels] is probably of no benefit and in fact is actually making the climate issue worse.'
Biodiesel and corn ethanol both suffer from the same problem. Good, two stupid government programs to kill off.
Crutzen, famous for his work on nitrogen oxides and the ozone layer, declined to comment before the paper is officially published. But the paper suggests that microbes convert much more of the nitrogen in fertiliser to N2O than previously thought - 3 to 5 per cent or twice the widely accepted figure of 2 per cent used by the International Panel on Climate Change (IPCC).
For rapeseed biodiesel, which accounts for about 80 per cent of the biofuel production in Europe, the relative warming due to N2O emissions is estimated at 1 to 1.7 times larger than the quasi-cooling effect due to saved fossil CO2 emissions. For corn bioethanol, dominant in the US, the figure is 0.9 to 1.5. Only cane sugar bioethanol - with a relative warming of 0.5 to 0.9 - looks like a viable alternative to conventional fuels.
Some previous estimates had suggested that biofuels could cut greenhouse gas emissions by up to 40 per cent.2
So unfortunately bioethanol advocates in Europe can still rationalize incentives that encourage Brazilians to tear down rain forests to plant more sugar cane for ethanol.
When the extra N2O emission from biofuel production is calculated in "CO2-equivalent" global warming terms, and compared with the quasi-cooling effect of "saving" emissions of fossil fuel derived CO2, the outcome is that the production of commonly used biofuels, such as biodiesel from rapeseed and bioethanol from corn (maize), can contribute as much or more to global warming by N2O emissions than cooling by fossil fuel savings. Crops with less N demand, such as grasses and woody coppice species have more favourable climate impacts. This analysis only considers the conversion of biomass to biofuel. It does not take into account the use of fossil fuel on the farms and for fertilizer and pesticide production, but it also neglects the production of useful co-products. Both factors partially compensate each other. This needs to be analyzed in a full life cycle assessment.
Biomass energy is not the answer. Biomass energy is probably not even part of the answer. We need to move to a more electrified economy. The billions of dollars of US taxpayer subsidies for corn ethanol would be better spent on moving to nuclear, wind, and solar power.
The federal government heavily subsidizes corn growers and ethanol producers. Rolling Stone reporter Jeff Goodell observed in the July 24 issue that ethanol receives more than 200 tax breaks and at least $5.5 billion in subsidies per year.
According to Goodell, ethanol production represents only 3.5 percent of the nation's gasoline consumption, but it consumes 20 percent of the entire U.S. corn crop. The Energy Information Administration reported that "Ethanol relies heavily on Federal and State subsidies to remain economically viable as a gasoline blending component."
Congress is about to decide whether to give fast-growing biofuels a new supercharger by requiring that the nation use 36 billion gallons yearly by 2022 — 15 billion gallons from corn.
That is six times what is used today. Next in the schedule: The Senate and the House appoint members to decide whether the Senate-passed, 36 billion-gallon mandate survives.
Bio energy subsidies are huge and growing.
If extended through 2022, as the Senate bill provides, the ethanol subsidies will cost taxpayers an estimated $131 billion, according to the Tax Foundation. Subsidies under the Lugar-Harkin measure would cost as much as $205 billion over the next 15 years.
$205 billion is a lot of money to waste.
The madness for biomass energy is international and shows how foolish elite crowds can be together.
The European Union has announced that it wants to replace 10 percent of its transport fuel with biofuels by 2020. China is aiming for a 15 percent share. The United States is already on track to exceed Congress' 2005 goal of doubling the amount of ethanol used in motor fuels to 7.5 billion gallons by 2012. In his State of the Union speech in January, President George W. Bush set a new goal of 35 billion gallons of biofuels by 2017. In June, the Senate raised it to 36 billion gallons by 2022. Of that, Congress said that 15 billion gallons should come from corn and 21 billion from advanced biofuels that are nowhere near commercial production.
Just because lots of governments decide some path is a good idea doesn't mean they all aren't being stupid.
The first stage of the technique involves removing slivers of ovarian tissue through keyhole surgery.
Although these would be just millimetres wide, each sample would contain thousands of immature eggs.
The ovarian tissue is then frozen until the woman is ready to try for a baby. At that time, it will be stimulated with hormone chemicals to grow the immature eggs into mature ones ready for IVF treatment.
Mind you, the fertility researchers working on this problem think they are still 5 years away from offering this as a service. But I wonder: Are they trying to solve problems associated with initial extraction and freezing? Or are they working on how to solve the later stage of how to thaw out and grow eggs to maturity? If the latter then a woman who gets some ovarian tissue frozen today can probably count on the technology 5 to 10 years hence to thaw out and create eggs from that frozen tissue. If your biological clock is ticking then taking the first step might already make sense.
Dr Alan Thornhill, scientific director of the Bridge Fertility Centre, said: "It would mean we have got a pool of thousands of eggs at very little risk to the woman and relatively low cost because you avoid the huge drug costs. Instead of having up to 10 eggs to work with, with this you can have lots of eggs without the risk of over-stimulation.
Some day women in their 20s might routinely get their ovary tissue frozen in order to guarantee future availability of youthful eggs which have few genetic mutations. This will certainly enable many women to make babies in middle age. But it doesn't solve all the problems created by aging reproductive systems and aging bodies. The uterus ages as does the rest of the body and that aging reduces the ability of women to bring babies to term and increases the risk of defects.
The researchers working on this problem at the British clinics Bridge Fertility Centre and Care Fertility clinic are chasing a big market of affluent professional thirty something women who hear their clocks ticking. These women either haven't yet found Mr. Right (he's probably unlisted in the phone book or living under an assumed name) or the women first want to arrive at a place in their careers where they feel financially secure enough to make babies.
In the medium term biotechnologies will be developed that can turn normal cells from anywhere in the body into eggs. Also, as part of the general drive to grow replacement organs techniques will be developed to grow replacement ovaries and even replacements for other reproductive organs. Going out 30 to 40 years full body rejuvenation will totally eliminate age-related limits on reproduction. Then population growth will then become a huge problem. That will necessitate government-mandated limits on reproduction.
At the the third conference for Strategies for Engineered Negligible Senescence (SENS) Dr. Zheng Cui of Wake Forest University reported on impressive progress of his research team toward use of immune cells to defeat cancer.
Attendees at SENS3 heard first-hand about an extremely exciting approach to cancer treatment that has not yet hit the scientific literature or the press. In 2003, Dr. Zheng Cui and his colleagues at the Comprehensive Cancer Center of Wake Forest University reported the discovery of mice with immune cells that rendered them invulnerable to cancer: they had been intentionally giving mice cancer by injecting them with virulent cancer cells as part of a separate study, when they discovered a single mouse in the colony that was completely immune to the invasive cells.
His curiosity piqued, Dr. Cui went on to show that it could resist multiple rounds of such injections, and were so impressed that they used him to father a whole colony of mice, all of whom shared this remarkable invulnerability to cancer. Based on that ability, he calls them spontaneous regression/complete resistance (SR/CR) mice.
Last year, Dr. Cui electrified the world when he showed that the new strain's cancer-fighting abilities were caused by a particular subset of their immune cells -- members of a class of white blood cell known as neutrophil granulocytes.
You might be among the lucky few who have immune systems with especially high competence at defeating cancer.
At SENS3, Dr. Cui presented the next logical step in his research: work demonstrating the existence of, and characterizing, high-potency cancer-killing granulocytes in humans.
Dr. Cui's team first went looking for the existence of potent cancer-killing granulocytes in a group of healthy volunteers. This was done by testing the volunteers' granulocytes' ability to destroy cancer cells in a petrie dish. They found that, unlike in mice (who seem to have an all-or-nothing effect), there appears to be a classical bell-shaped distribution of cancer-killing ability in the granulocytes of people in the population: a few people have white blood cells extremely weak cancer-killing activity, the great majority have an 'average' competence, and a very small group of outliers have the kind of overwhelming search-and-destroy activity (at least in a test tube!) that is seen in the SR/CR mice.
Winter gives you cancer by weakening your immune system.
Surprisingly, they found that the ability of peoples' granulocytes to kill cancer is very sensitive to the season. Looking at the efficacy of granulocytes drawn at samples taken year round, he found that the activity is strong in the sunnier months (May to September) and falls off dramatically in the gloomier ones (November through April). The reason for this effect is unknown, but it could be connected to other things that vary with the number of hours of daylight and that are connected to cancer risk, such as the circadian-rhythm hormone melatonin or the "sunshine vitamin," vitamin D3.
He also found that the cancer-killing capacity could be "abolished" by stress: in one anecdote, a grad student from his lab at Wake Forest had been tested just after making his first presentation at a scientific conference, and the normally high level of cancer-fighting activity in his granulocytes was severely depressed. Re-testing him several days later, the activity of his granulocytes had bounced back to normal.
Stress is bad. Stress gives you cancer. But then that only makes sense. As Joe Jackson sang "Everything gives you cancer".
An immune method to defeat cancer would be great. Cui's about to start a clinical trial on 22 humans to try to see if immune system components from people with super immune systems can defeat cancer when separated out and injected into people with cancer.
The difference in potency of cancer killing cells between people is enormous.
Cui took blood samples from more than 100 people and mixed their granulocytes with cervical cancer cells. While granulocytes from one individual killed around 97 per cent of cancer cells within 24 hours, those from another healthy individual only killed around 2 per cent of cancer cells. Average cancer-killing ability appeared to be lower in adults over the age of 50 and even lower in people with cancer. It also fell when people were stressed, and at certain times of the year.
Maybe most of the increase of cancer with age is due to weakening immune systems. Immune system rejuvenation would probably reduce the incidence of cancer. Also, these people who have super anti-cancer immune systems have something that can be replicated in other people. Maybe gene therapy or vaccines could tune up our immune systems to make them more like the immune systems of the rare few whose immune systems are especially aggressive against cancer.
Cui's group is giving a "GIFT" (Granulocyte InFusion Therapy) to the rest of us.
Neutrophils and macrophages, as major components of infiltrating leukocytes, migrate to the site of cancer cells, capture the cancer cells by making tight physical contact with the cancer cell surface and destroy them via cytolysis. The leukocytes of these cancer-resistant mice can be used as therapeutic agents to cure several forms of highly aggressive cancers in wild type mice without any sign of adverse side effects. This leads to the apparent question of whether we can find cancer-resistant humans to test a similar cancer treatment via allogenic innate white cell transfer. Using a newly developed in vitro assay to measure the ability of white cells to kill various cancer cell line targets, we surveyed human volunteers and found that a significant number of healthy humans have cancer-killing activity (CKA) similar to that of cancer-resistant mice. There seems to be a bell-shaped distribution of CKA in the population of healthy humans. The CKA average appears to be lower in older human populations and to be even lower in human cancer patients. The CKA can also be abolished by stress and change of seasons. Based on these findings and the ability to screen for cancer-resistant humans as allogenic white cell donors, we proposed a new cancer treatment strategy, termed "GIFT" (Granulocyte InFusion Therapy), that will soon enter phase II clinical trials.
“About 1/3 of the CO2 from fossil-fuel burning is absorbed by the world’s oceans,” explained lead author Ken Caldeira from the Carnegie Institution Department of Global Ecology. “When CO2 gas dissolves in the ocean it makes carbonic acid which can damage coral reefs and also hurt other calcifying organisms, such as phytoplankton and zooplankton, some of the most critical players at the bottom of the world’s food chain. In sufficient concentration, the acidity can corrode shellfish shells, disrupt coral formation, and interfere with oxygen supply. ”
Most of the research today points to a future where, in the absence of a major effort to curtail carbon dioxide emissions, there will be double the atmospheric concentrations of CO2 (760 parts per million, or ppm) by century’s end. Atmospheric carbon dioxide concentrations could reach 500 ppm by mid-century. Pre-industrial concentrations, by comparison, were 280 ppm and today's concentration is about 380 ppm.
The acidity from CO2 dissolved in ocean water is measured by the pH scale (potential of Hydrogen). Declines in pH indicate that a solution is more acidic. The U.S. Environmental Protection Agency [1976] Quality Criteria for Water state: “For open ocean waters where the depth is substantially greater than the euphotic zone, the pH should not be changed more than 0.2 units outside the range of naturally occurring variation …” The euphotic zone goes to a depth of about 650 feet (200 meters), where light can still reach and photosynthesis can occur.
“Atmospheric CO2 concentrations need to remain at less than 500 ppm for the ocean pH decrease to stay within the 0.2 limit set forth by the U.S. Environmental Protection Agency [1976],” remarked Caldeira. “If atmospheric CO2 goes above 500 ppm, the surface of the entire ocean will be out of compliance with EPA pH guidelines for the open ocean. We need to start thinking about carbon dioxide as an ocean pollutant. That is, when we release carbon dioxide to the atmosphere, we are dumping industrial waste in the ocean.”
I have previously argued that since we can easily cool the Earth (even cause an Ice Age for less than $1 billion per year) using either silicon dioxide or dimethyl sulfide (DMS) that the main problem with atmospheric CO2 build-up the dissolving of atmospheric CO2 into the oceans making them too acidic. I've yet to come across any proposed methods for preventing ocean acidification. Also, it is not clear how much harm to marine life will come from a shift of pH down by 0.2.
Atmospheric CO2 might never reach 500 ppm. The rising cost of oil extraction will combine with future declines in the costs of nuclear and solar power to cause a shift away from fossil fuels and toward energy sources which are not net producers of carbon dioxide emissions.
Does the FDA really think that imported sperm create a risk of spreading Creutzfeldt-Jakob disease?
Cryos International, based in the Financial District, has gone to seed because the Food and Drug Administration banned sperm samples from 30 countries to prevent the spread of Creutzfeldt-Jakob disease, a rare, fatal disorder caused by eating beef contaminated with mad-cow disease.
Two years after the measure, Cryos has run out of offerings from such prized blond Norsemen as "Oluf," "Dagh," "Finn," "Ingi," "Jorn" and "Ante."
Speaking as someone who really appreciates blue and green eyed women I protest yet another example of overregulation by the US Food and Drug Administration. The Nordic blond hair and blue eyes are in short enough supply as it is. Why make the problem worse?
Sperm banks should consider opening up offices out in the upper plains states to recruit Nordic men. Some genetic testing could even provide genetic measures of just how Nordic is each donor.
Enough balls reach near the outer edge of the playing field that a few percent increase in ball speed coming off the bat is enough to increase home runs by 50% to 100%.
MEDFORD/SOMERVILLE, Mass. -- Steroid use by a Major League Baseball slugger may produce only modest increases in muscle mass and bat and ball speed but still boost home run production by 50 percent or more, according to a new study by Tufts University physicist Roger Tobin.
Tobin, a specialist in condensed matter physics with a long-time interest in the physics of baseball, will publish his paper "On the potential of a chemical Bonds: Possible effects of steroids on home run production in baseball" in an upcoming issue of the American Journal of Physics.
As Tobin's paper notes, Babe Ruth's record of 60 home runs in a single season stood for 34 years until Roger Maris hit 61 homers in 1961. For the next 35 years, no player hit more than 52 home runs in one season. But between 1998 and 2006, players hit more than 60 home runs in a season six times. Barry Bonds hit 73 home runs in 2001—topping Maris' mark by an astonishing 20 percent.
According to Tobin, the explosion in home runs coincides with the dawn of the "steroid era" in sports in the mid-1990s, and that surge quickly dropped to historic levels in 2003, when Major League Baseball instituted steroid testing.
What happens once parents start genetically engineering their kids at the stage of embryos to contain genes that make them super athletes? One solution: create baseball leagues where everyone genes genetically tested and people with closely equivalent genetic potentials play each other. But will the audience want to watch any league aside from the top league?
A 10% increase in muscle mass produces a 4% increase in ball speed as the ball leaves the bat.
Tobin reviewed previous studies of the effect of steroid use and concluded that muscle mass, the force exerted by those muscles and the kinetic energy of the bat could each be increased by about 10 percent through the use of steroids. According to his calculations, the speed of the bat as it strikes the pitched ball will be about 5 percent higher than without the use of steroids and the speed of the ball as it leaves the bat will be about 4 percent higher.
To determine the ultimate impact on home run production, Tobin then analyzed a variety of models for trajectory of the baseball, accounting for gravity, air resistance and lift force due to the ball's spin. While there was considerable variation among the models, "the salient point," he says, "is that a 4 percent increase in ball speed, which can reasonably be expected from steroid use, can increase home run production by anywhere from 50 percent to 100 percent."
The article also provides an estimate of speed increases of balls thrown by juiced up pitchers.
One way to cut down on home runs on juiced up or genetically enhanced teams is to just make the playing field bigger. But a higher rate of home runs might be a good idea for a sport that has a fairly slow speed of play as compared to many other sports. So the genetically engineered players of the future might increase audience satisfaction.
When people start genetically engineering highly athletic offspring this is going to create some pretty big disagreements between nations over international sports. Will the Olympics try to remain genetically natural? They'll have to get genetic samples from parents to prove whether an athletic as a particular combination of athletics enhancing genetic alleles naturally or not. But even such a test won't work entirely. Two prospective parents could choose the ideal combination of their chromosomes to have a child who has the most ideal combination of genes from the two parents.
Genetic testing of parents also won't be possible for offspring whose mothers used sperm donors. Johnny doesn't know who his Dad is. Should that fact rule him ineligible for going to the Winter Olympics as a skier? Of course some moms will choose sperm donors based on great genetic profiles for athletics. So the use of sperm donors will allow natural babies will be born with athletic abilities at a higher rate than is currently the case.
We are living in the end of the era of "wild type" humans. The people around you all carry genes that they got as a result of natural mutations. We are approaching the era where wild type gradually (or not so gradually) gets replaced with the engineered and chosen. This conversion will happen in a very uneven fashion across the world due to differing levels of affluence, regulations, and beliefs.
Not everyone will use offspring genetic engineering. Of those who use it not all will use it as extensively and different people will use it to achieve different goals. Even athletic goals will differ. People who want tall basketball players will chose different genetic alleles than those who want ballet dancers or tennis players or swimmers or golf players. Will more people choose the muscle type ideal for sprints or the muscle type ideal for long distance runners? Will more go for basketball height or defensive lineman solidness? What will be the most popular athletic forms for genetically engineering parents?
Using concentrating parabolic reflectors and a thermal storage system Palo Alto California company Ausra claims to have a workable way for solar power to supply electricity 24 hours per day.
Ausra claims to have solved the storage problem without using molten salts or other expensive means of conserving heat. In fact, the company estimates that the price of its electricity will drop to roughly 8¢ per kilowatt hour if it can store heat for 16 hours. "Thermal storage is generally considered to be quite a bit cheaper than electrical storage," says Nate Blair, a senior analyst at NREL. "There isn't a lot of power generation combined with storage systems that can take advantage of that. [Concentrated solar power] has a leg up on storage in the grid or flow batteries or even ultracapacitors."
The system will employ pressure and a steam accumulator to accomplish the trick. "You allow some of the steam to recondense," O'Donnell explains. "It flashes back to steam when you reduce the pressure just by opening the valve to the turbine."
Such long-term steam storage, however, is unproved. "Steam storage is currently feasible at small levels, for example, one hour or so," NREL's Mehos notes. "Due to large volumes and high pressures involved with steam storage, scaling up steam storage to baseload applications is very high risk."
Water boils at different temperatures at different atmospheric pressures. At high altitudes with thinner air and less atmospheric pressure water boils at lower temperatures. But put water under a sufficiently intense pressure and it will not boil into vapor. The idea is to store the water under high pressure so that it won't convert to steam and then release some of the water into a lower pressure area at night to allow the water to convert into high pressure steam and power turbines to generate electricity.
I don't know whether they can make it work. But this is an interesting approach. Store the energy as hot water rather than as hydrogen or electrochemically in a battery. Can they make this approach work? The storage container has to meet cost, pressure, and longevity goals. What sort of storage material could do this? Steel? Is insulation needed?
Once we can coax stem cells to go into places in the body and repair decayed tissue we are well on the way toward achieving the ability to do full body rejuvenation. Granted, we'll need other capabilities as well. But the ability to coax and direct stem cells is going to be one of the key pieces of the rejuvenation puzzle. With that in mind, this report about a special class of adult stem cells which can repair muscles is intriguing. Adult myoendothelial stem cells isolated from blood vessel walls can form muscle strands.
In a study using human muscle tissue, scientists in Children's Stem Cell Research Center - led by Johnny Huard, PhD, and Bruno Péault, PhD - isolated and characterized stem cells taken from blood vessels (known as myoendothelial cells) that are easily isolated using cell-sorting techniques, proliferate rapidly and can be differentiated in the laboratory into muscle, bone and cartilage cells.
These characteristics may make them ideally suited as a potential therapy for muscle injuries and diseases, according to Drs. Huard and Péault. Results of the study are published in the September issue of the journal Nature Biotechnology.
"Finding this population of stem cells in a human source represents a major breakthrough for us because it brings us much closer to a clinical application of this therapy," said Dr. Huard, the Henry J. Mankin Professor and vice chair for Research in the Department of Orthopaedic Surgery at the University of Pittsburgh School of Medicine. "To make this available as a therapy, we would take a muscle biopsy from a patient with a muscle injury or disease, remove the myoendothelial cells and treat the cells in the lab. The stem cells would then be re-injected into the patient to repair the muscle damage. Because this is an autologous transplant, meaning from the patient to himself, there is not the risk of rejection you would have if you took the stem cells from another source."
Muscles shrivel with age. Can myoendothelial stem cells restore muscles to something approaching their youthful glory? One problem is going to be that the myoendothelial stem cells will also age and myoendothelial stem cells isolated from a 70 or 80 year old might grow slowly and form tired muscle fibers.
But combine isolation of myoendothelial stem cells from an old body with some gene therapies to repair those stem cells and youthful stem cells for body repair could become available. How to develop those cellular rejuvenating gene therapies will probably turn out to be the hardest problem to solve to make adult stem cells fully useful in rolling back the ravages of aging.
Other types of adult stem cells can also form muscle. But the other types of adult stem cells form muscle much less efficiently.
Working in dystrophic mice while searching for a cure for Duchenne muscular dystrophy (DMD), Dr. Huard's laboratory team first identified a unique population of muscle-derived stem cells with the ability to repair muscle 8 years ago.
Dr. Péault, a professor in the Department of Pediatrics, Cell Biology and Physiology at the University of Pittsburgh School of Medicine, recognized the importance of determining the origin of these muscle-derived stem cells. His team applied, among others, techniques of confocal microscopy and cell sorting by flow cytometry which led to the discovery in human muscle biopsies that these myoendothelial cells are located adjacent to the walls of blood vessels.
According to their study, myoendothelial cells taken from the blood vessels are much more efficient at forming muscle than other sources of stem cells known as satellite and endothelial cells.
A thousand myoendothelial cells transplanted into the injured skeletal muscle of immunodeficient mice produced, on average, 89 muscle fibers, compared with 9 and 5 muscle fibers for endothelial and satellite cells, respectively. Myoendothelial cells also showed no propensity to form tumors, a concern with other stem cell therapies.
These researchers are chasing after better treatments for Duchenne muscular dystrophy (DMD). The development of stem cell treatments for DMD will inevitably lead to stem cell treatments to treat aged muscles. That is the way many rejuvenation therapies will come about. Efforts to repair damage caused by trauma, infection, and genetic defects will produce therapies that work to repair the damage caused by aging.
If you think someone smells sweet it might be down to genes.
To many, urine smells like urine and vanilla smells like vanilla. But androstenone, a derivative of testosterone that is a potent ingredient in male body odor, can smell like either - depending on your genes. While many people perceive a foul odor from androstenone, usually that of stale urine or strong sweat, others find the scent sweet and pleasant. Still others cannot smell it at all.
New research from Rockefeller University, performed in collaboration with scientists at Duke University in North Carolina, reveals for the first time that this extreme variability in people's perception of androstenone is due in large part to genetic variations in a single odorant receptor called OR7D4. The research is reported September 16 as an advance online publication of the journal Nature.
Combine bind genetic tests for OR7D4 with genetic tests for genes that regulate Androstenone secretion and you have the beginnings of a genetic compatibility test. Online match-making services will some day include genetic profile matching. Why go to the trouble of meeting someone you get matched with online if one of you is going to think the other one has a really disgusting smell?
So now we need scientists to discover genetic variations that regulate androstenone production and secretion.
Androstenone, found in higher concentrations in the urine and sweat of men than of women, is used by some mammals to convey social and sexual information, and the ability to perceive androstenone's scent may have far-reaching behavioral implications for humans.
In the largest study ever conducted of its kind, researchers at Rockefeller University presented nearly 400 participants with 66 odors at two different concentrations and asked them to rate the pleasantness and intensity of each odor. When scientists at Duke University identified OR7D4 as a receptor that androstenone selectively activates, Leslie Vosshall, Chemers Family Associate Professor and head of the Laboratory of Neurogenetics and Behavior at Rockefeller University and Andreas Keller, a postdoc in her lab, formed a collaboration with them, and began collecting blood samples from participants and isolated their DNA. The Duke team, led by Hiroaki Matsunami, used DNA from each participant to sequence the gene that encodes the OR7D4 receptor.
You can bet that many more genetic variations that influence physical attraction will be found.
More fun with human sexuality and attraction.
Whether we are seeking a mate or sizing up a potential rival, good-looking people capture our attention nearly instantaneously and render us temporarily helpless to turn our eyes away from them, according to a new Florida State University study.
“It’s like magnetism at the level of visual attention,” said Jon Maner, an assistant professor of psychology at FSU, who studied the role mating-related motives can play in a psychological phenomenon called attentional adhesion. His findings are published in the September issue of the Journal of Personality and Social Psychology.
The paper, “Can’t Take My Eyes Off You: Attentional Adhesion to Mates and Rivals,” is one of the first to show how strongly, quickly and automatically we are attuned to attractive people, he said. FSU graduate students Matthew Gailliot, D. Aaron Rouby and Saul Miller co-authored the study.
In a series of three experiments, Maner and his colleagues found that the study participants, all heterosexual men and women, fixated on highly attractive people within the first half of a second of seeing them. Single folks ogled the opposite sex, of course, but those in committed relationships also checked people out, with one major difference: They were more interested in beautiful people of the same sex.
Why the attention paid to same sex attractive people? Jealousy.
In the experiments, study participants -- 120 people in the first study and 160 and 162 in the second and third studies, respectively -- completed questionnaires to determine the extent to which they were motivated to seek out members of the opposite sex. They then took part in a series of “priming” activities before they were shown photos of highly attractive men, highly attractive women, average-looking men and average-looking women.
After a photo of one of the faces flashed in one quadrant of a computer screen, the participants were required to shift their attention away from that face to somewhere else on the screen. Using a precise measure of reaction time, Maner found that it took the participants longer to shift their attention away from the photos of the highly attractive people.
Maner said he was surprised that his studies showed little differences between the sexes when it came to fixating on eye-catching people.
“Women paid just as much attention to men as men did to women,” he said. “I was also surprised that jealous men paid so much attention to attractive men. Men tend to worry more about other men being more dominant, funny or charismatic than they are. But when it comes to concerns about infidelity, men are very attentive to highly attractive guys because presumably their wives or girlfriends may be too.”
So then can one measure loss of attraction to one's own mate by measuring how much people pay attention to same sex attractive people? Do people who are ready to file for divorce pay less attention to same sex attractive people?
Also, when people become involved in a relationship do they become more averse to spending time with their more attractive friends?
I'd also like to see this phenomenon measured as a function of blood sexual hormone levels. Do people with more testosterone pay more attention to same and opposite sex attractive pictures?
But since we just hit $80 per barrel $150 is less than a doubling. What, me worry?
Lord Oxburgh, the former chairman of Shell, has issued a stark warning that the price of oil could hit $150 per barrel, with oil production peaking within the next 20 years.
He accused the industry of having its head "in the sand" about the depletion of supplies, and warned: "We may be sleepwalking into a problem which is actually going to be very serious and it may be too late to do anything about it by the time we are fully aware."
Oxburgh argues that it isn't so much that we are running out of oil but that we are running out of oil that is cheap to extract. But we really are running out of oil too. Though new enhanced extraction methods such as toe to heel air injection (THAI) for heavy oil might delay the point of peak oil production.
As far as being too late to do anything about it: Well, the start-ups that are developing next generation batteries are doing the most to prepare us for declining oil production. Once we can shift most transportation energy usage to electric cars and electric trains declining oil production won't put an end to our mobile lifestyles.
The world will produce 118 million barrels of oil a day, up from its current 85 million barrels per day, just to satisfy projected demand by 2030, according to the Energy Information Agency.
"That's never going to happen," said Richard Heinberg, a research fellow at the Post Carbon Institute and author of three books on peak oil.
Heinberg says world production of regular crude oil actually peaked in May 2005. He also says production in 33 of the 48 largest oil producing countries is in decline, and that global oil discoveries peaked in 1964.
The people who see Peak Oil as happening in the next 10 years might be right. Suppose for the moment they are. Does that mean we will see $150 per barrel oil or even $200 or $300 per barrel? I have a hard time believing the higher price predictions because substitutes will become cost competitive below those higher prices and also because there are limits on how much people can afford to spend on oil.
The longer we go before world oil production peaks the easier the peak will be to handle. With time we'll get more technologies for producing and storing and using non-oil energy. We'll also gain technologies for using energy much more efficiently. So I'm not a doomster about Peak Oil even though I find the arguments for an earlier peak to be plausible.
If we hit an earlier peak (e.g. if it is happening right now) the economic cost will be substantial since we won't have as much technology to deal with it as we will if the peak comes 10 or 20 years from now. A peak in the next few years would cause a pretty sharp recession and require a lot of investment in more efficient vehicles and capital plant. But for the United States our profligate usage of gasoline actually makes adjustment easier. We could switch from bigger conventional cars to compact hybrid diesels and double or triple our miles per gallon. Countries whose populaces already drive compact diesels (e.g. about half of European car sales today are diesel) can't adjust as easily since they already are being relatively frugal in their oil usage.
Privacy protection advocates worry about intrusive governments and nosy corporations. But spouses looking at divorce have the keenest interest in electronic secrets.
“In just about every case now, to some extent, there is some electronic evidence,” said Gaetano Ferro, president of the American Academy of Matrimonial Lawyers, who also runs seminars on gathering electronic evidence. “It has completely changed our field.”
Privacy advocates have grown increasingly worried that digital tools are giving governments and powerful corporations the ability to peek into peoples’ lives as never before. But the real snoops are often much closer to home.
“Google and Yahoo may know everything, but they don’t really care about you,” said Jacalyn F. Barnett, a Manhattan-based divorce lawyer. “No one cares more about the things you do than the person that used to be married to you.”
Spying gets used in many ways. First off, spouses check up on each other to look for evidence of an affair in order to decide whether to divorce. But even if they decide to divorce before getting such evidence they still want evidence of affairs both to justify to themselves that they are the offended party and also to strengthen their position in bargaining for divorce settlement terms.
Another purpose for spying is purely financial. If the spouse has hidden assets then discovery of the assets creates the potential for a more advantageous settlement. One story mentioned in the Times article has a surgeon secretly buying a $3 million condo in order to continue an affair while denying that the affair is still happening. Cheeky devil.
The electronic trails left by emails, phone records, hidden recording devices, and the like create a fuller picture of just what humans have been doing on the sly.
Electronic means of surveillance are only going to grow more powerful, cheaper, and easier to use. Electronic devices mountable under vehicles provide a way for spouses to track each other's movements. But in the future smaller devices will be embeddable in clothing and other personal items to record sound and video of a person's day and form a much fuller image of what people do when their spouse is not around.
Surveillance technology will also transform the handling of paroled criminals. Already some criminals have to wear a ring around their leg or mounted in some other way on them to track their movements. But imagine when a ring worn around an extremity will be able to record all video and audio for a person for days and weeks. Recidivists who commit crimes while on parole will almost always get caught. You might think that crimes could still be concealed by briefly covering up a ring. But how about miniature video recorders mounted behind eyeballs? A person couldn't conceal where they are without closing their own eyes.
Epidemiologist John Ioannidis says most claimed research findings are wrong due to mistakes made by researchers in design and in analysis of results.
Dr. Ioannidis is an epidemiologist who studies research methods at the University of Ioannina School of Medicine in Greece and Tufts University in Medford, Mass. In a series of influential analytical reports, he has documented how, in thousands of peer-reviewed research papers published every year, there may be so much less than meets the eye.
These flawed findings, for the most part, stem not from fraud or formal misconduct, but from more mundane misbehavior: miscalculation, poor study design or self-serving data analysis. "There is an increasing concern that in modern research, false findings may be the majority or even the vast majority of published research claims," Dr. Ioannidis said. "A new claim about a research finding is more likely to be false than true."
The hotter the field of research the more likely its published findings should be viewed skeptically, he determined.
Should government agencies that hand out research grants hand out parallel grants to independent groups to do parallel analyzes of data produced by funded researchers to find errors?
I suspect peer reviewers lack the time, data, and incentives needed to catch errors in research papers. Given the relative cheapness of data storage and data transmission technologies at least for some types of research independent parties should be given a crack at analyzing the same data to see if the results drawn by original researchers are warranted.
Another thought: Could some types of studies have agreed standard data formats with standard analyzes written ahead of time so that different studies could be compared automatically and so that bias would not enter as much into the analysis phase?
Ioannidis published a paper in Plos Medicine in August 2005 entitled Why Most Published Research Findings Are False.
There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.
Step up a level and use the kind of thinking a business executive steeped in the wisdom of W. Edwards Deming would bring to a manufacturing quality problem: Huge amounts of labor goes into conducting scientific studies and therefore a high error rate represents a huge amount of waste of labor and supplies. Science needs more automation and other process improvements to raise quality control and reduce waste.
Writing in The Scientist Frederick Sachs argues that the large increase in funding for the US National Institutes of Health did not produce a commensurate increase in scientific productivity as measured by papers published.
Since the NIH budget doubled from $15 billion to $26.4 billion from 1999 to 2003 (Figure 1), I reasoned that there should have been a corresponding jump in productivity. The test was the simplest measure of productivity: the number of publications.
Here's what I found: The number of biomedical publications from US labs did in fact increase from 1999-2004. However, so did the number of publications from labs outside the US where the research budget did not double. Figure 2 shows a parametric plot of the number of scientific papers indexed in the ISI Web of Science database by the keyword "biology" that were published each year from US labs and non-US labs. There is no upward jump that you would expect to see with a sudden increase in productivity.
So are the brains in science tapped out already? Why didn't the rate of papers published increase?
I would have expected an increase in the rate of research papers getting published as a result of more powerful scientific instrumentation. But maybe the brains that used to try to figure out how to tease out smaller answers from lousier tools now publish the same number of papers but with bigger findings per paper on average? Certainly that happens with a lot of genetics papers which describe findings about hundreds and thousands of genes at a time. 10 or 20 years ago a single research paper couldn't report about many genes at once because the tools for sequencing and measuring genes were too primitive.
Any speculations on what is going on with the result Sachs reports?
An article in the Wall Street Journal relays the claim that changes to recordings to make them sound better when played from MP3 format causes the pre-MP3 original releases to sound worse.
"Right now, when you are done recording a track, the first thing the band does is to load it onto an iPod and give it a listen," said Alan Douches, who has worked with Fleetwood Mac and others. "Years ago, we might have checked the sound of a track on a Walkman, but no one believed that was the best it could sound. Today, young artists think MP3s are a high-quality medium and the iPod is state-of-the-art sound."
It isn't. Producers and engineers say there are many ways they might change a track to accommodate an iPod MP3. Sometimes, the changes are for the worse.
Is this claim true?
Eventually storage will become so cheap that compression of recordings will become less desirable. Also, newer formats will support more bits of resolution than CD offers and so especially at the lower frequencies sound quality should improve.
Nearly 40 years after the USA beat the Soviets to the moon Internet giant Google said Thursday it will give $20 million to the first private group to land a roving robot on the lunar surface — a prize likely to start a 21st-century space race.
...
For a team to win the $20 million grand prize, its vehicle must ramble at least a quarter-mile over the lunar surface and send video back to Earth. A $10 million second prize is reserved for the first spacecraft that can't rove but still transmits data from moon to Earth.
Another $10 million will go to super-rovers able to perform tasks such as roaming long distances or snapping pictures of equipment discarded by astronauts.
A prize goal should be achievable and preferably by a fairly small team. Prizes aimed at motivating large teams run up against limits to how many volunteers can work together and how they can agree on just distributions of prize money among other limits. Or the prizes just end up motivating a small number of large corporations. But a $20 million prize for the size of the task isn't profitable for a large corp even if they can be assured of success (which they can't for something this difficult).
David Noland of Popular Mechanics presents 5 reasons why no team will win this prize. Among the reasons? You have to succeed by 2012. Plus, the very obvious: $20 million is peanuts compared to the cost of designing all the hardware to get to the Moon and land and cruise around. The launch cost into orbit alone is going to be a lot more than $20 million.
Google is supposed to have a very smart staff. If those smarts really were applied to designing this X Prize and they really though this through then I'm left suspecting their motive. The prize is unworkable. It is a dumb way to try to achieve the stated goal. So are they just conning us? $20 million strikes me as a small amount of money for a large quantity of otherwise free publicity.
Prizes are better designed for more achievable smaller steps that take less time and resources so that individuals and small teams with the needed set of skills can get together and work toward some goal.
FORT COLLINS - Today, Colorado State University is taking another big step toward making Colorado a leader in sustainable energy production. Already internationally known for research in the development of clean energy solutions including alternative fuels, clean engines and intelligent power grids, Colorado State announced its innovative method for manufacturing low-cost, high-efficiency solar panels is nearing mass production - bringing hundreds of jobs to the region and potentially providing light and power for billions in the underdeveloped world.
In a new 200-megawatt factory, expected to employ up to 500 people, AVA Solar Inc. will start production by the end of next year on the pioneering, patented technology developed by mechanical engineering Professor W.S. Sampath at Colorado State. Based on the average household usage, 200 megawatts will power 40,000 U.S. homes.
Produced at less than $1 per watt, the panels will dramatically reduce the cost of generating solar electricity and could power homes and businesses around the globe with clean energy for roughly the same cost as traditionally generated electricity.
Cheap!
With installation the $2 per watt expected cost is still much lower than current photovoltaics.
The cost to the consumer could be as low as $2 per watt, about half the current cost of solar panels, and competitive with cost of power from the electrical grid in many parts of the world. In addition, this solar technology need not be tied to a grid, so it can be affordably installed and operated in nearly any location.
They say their manufacturing process will be highly efficient.
-Simple manufacturing process - fully automated and continuous production with no batch processing yielding high throughputs or production rates;
They also claim their process uses far less semiconductor material than crystalline silicon panels.
-Inexpensive, efficient raw materials - because they convert solar energy into electricity more efficiently, cadmium telluride solar panels require 100 times less semiconductor material than high-cost crystalline silicon panels.
The era of cheap solar photovoltaics is no longer a distant prospect.
Being lonely probably changes the level of expression of over 200 of your genes.
Cole and colleagues at UCLA and the University of Chicago used DNA microarrays to survey the activity of all known human genes in white blood cells from 14 individuals in the Chicago Health, Aging, and Social Relations Study. Six participants scored in the top 15 percent of the UCLA Loneliness Scale, a widely used measure of loneliness that was developed in the 1970s; the others scored in the bottom 15 percent. The researchers found 209 gene transcripts (the first step in the making of a protein) were differentially expressed between the two groups, with 78 being overexpressed and 131 underexpressed. “Leukocyte (white blood cell) gene expression appears to be remodelled in chronically lonely individuals,” said. Cole.
Genes overexpressed in lonely individuals included many involved in immune system activation and inflammation. But interestingly, several other key gene sets were underexpressed, including those involved in antiviral responses and antibody production. “These findings provide molecular targets for our efforts to block the adverse health effects of social isolation,” said Cole.
“We found that what counts at the level of gene expression is not how many people you know, it’s how many you feel really close to over time.” In the future, he said, the transcriptional fingerprint they’ve identified might become useful as a ‘biomarker’ to monitor interventions designed to reduce the impact of loneliness on health.
An obvious follow-up would be to find a way to make a group of lonely people a lot less lonely and then see if their gene expression levels change.
Being lonely is bad for your health and shortens your life expectancy.
It is already known that a person's social environment can affect their health, with those who are socially isolated suffering from higher all-cause mortality, and higher rates of cancer, infection and heart disease. Researchers are trying to determine whether these adverse health consequences result from of reduced social resources (e.g., physical or economic assistance) or from the biological impact of social isolation on the function of the human body. "What this study shows us," said lead author Dr. Steven Cole, of the University of California Los Angeles (UCLA) School of Medicine, "is that the biological impact of social isolation reaches down into some of our most basic internal processes - the activity of our genes."
Does some subgroup of isolated people have an immunity toward the effects of isolation? Do their genes express at levels similar to those of non-lonely people?
Also, why less immune activity in lonely people? Maybe that's an adaptation. If you aren't exposed to other people you are at lower risk of getting a disease from them. So maybe less immune response was needed in the past among lonely people. Though today with more urban environments even lonely people can frequently come into contact with others and therefore be at risk of getting infections.
Powered by $77 million in new investment, startup Heliovolt, based in Austin, TX, will build a factory next year for mass-producing a new type of solar cell that could, in much of the United States, make solar electricity as cheap as electricity from the grid. The company will be scaling up a new manufacturing technique that could produce high-performance thin-film solar cells more reliably than other methods.
Heliovolt is one of several startups developing a type of thin-film solar cell that converts light into electricity with a micrometers-thick layer of a copper-indium-gallium selenide (CIGS) semiconductor. Thin-film solar cells are attractive because they could produce electricity cheaper than conventional silicon solar cells.
Read the details in the linked MIT Technology Review article.
We have a problem with a looming fossil fuels shortage, especially for liquid fuel. But we do not face a general energy shortage or peak energy production problem. If necessary (or if we just get disgusted enough by conventional pollution) nuclear power could displace coal for electric power generation. Wind electric costs are going to go down and wind's role will grow. Also, one or more of an assortment of venture capital photovoltaics start-ups will bring low cost solar to the masses. With all the fine minds chasing this challenge I'll be surprised if photovoltaics aren't cost competitive for the American southwest within 5 to 7 years and for more temperate climates within 10 to 15 years.
Time for yet another FuturePundit post on why vitamin D is probably the best nutrient to take as a supplement. A meta-analysis of 18 randomized controlled trials using vitamin D supplements found a 7% lower risk of death among vitamin D supplement users.
Individuals who take vitamin D supplements appear to have a lower risk of death from any cause over an average follow-up time of six-years, according to a meta-analysis of 18 previously published studies in the September 10 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Past studies have suggested that deficiencies in vitamin D might be associated with a higher risk of death from cancer, heart disease and diabetes—illnesses that account for 60 percent to 70 percent of deaths in high-income nations, according to background information in the article. “If the associations made between vitamin D and these conditions were consistent, then interventions effectively strengthening vitamin D status should result in reduced total mortality,” the authors write.
Philippe Autier, M.D., of the International Agency for Research on Cancer, Lyon, France, and Sara Gandini, Ph.D., of the European Institute of Oncology, Milano, Italy, searched for randomized controlled trials of vitamin D supplements published before November 2006. They analyzed 18 separate trials that included 57,311 participants and evaluated doses of vitamin D ranging from 300 to 2,000 international units, with an average dose of 528 international units. Most commercially available supplements contain between 400 and 600 international units.
Over an average follow-up period of 5.7 years, 4,777 of the participants died. Individuals who took vitamin D had a 7 percent lower risk of death than those who did not. In the nine trials that collected blood samples, those who took supplements had an average 1.4- to 5.2-fold higher blood level of vitamin D than those who did not.
The reduction in all cause mortality suggests that vitamin D doesn't just reduce one risk while boosting another. Too many things that might help in some ways end up hurting in other ways. Vitamin D looks like a big net benefit.
Aside from vitamin D I'm hard pressed to think of a single vitamin that holds the promise of such a large benefit if taken as a supplement by most people in developed countries. Most likely you could do much better for your health by eating more vegetables and fruits than by taking any other vitamin.
Update: Vitamin D probably reduces the risk of preeclampsia too.
Vitamin D deficiency early in pregnancy is associated with a five-fold increased risk of preeclampsia, according to a study from the University of Pittsburgh Schools of the Health Sciences reported this week in the Journal of Clinical Endocrinology and Metabolism.
A Texas company might have an ultracapacitor design that will make electric cars a reality.
An Austin-based startup called EEStor promised ''technologies for replacement of electrochemical batteries,'' meaning a motorist could plug in a car for five minutes and drive 500 miles roundtrip between Dallas and Houston without gasoline.
Observers hesitate to dismiss this secretive company because they've managed to attract big name venture capital investors.
The deal with ZENN Motor and a $3 million investment by the venture capital group Kleiner Perkins Caufield & Byers, which made big-payoff early bets on companies like Google Inc. and Amazon.com Inc., hint that EEStor may be on the edge of a breakthrough technology, a ''game changer'' as Clifford put it.
A game changer advance in batteries would revolutionize transportation and make the coming of "Peak Oil" a small problem. The cost of electric power for electrically powered travel is cheap. A low cost technology that makes electric cars feasible will enable nuclear, solar, and wind power to push our vehicles down the road for two or three pennies per mile.
Over the last six years, hundreds of teenage boys have been expelled or felt compelled to leave the polygamous settlement that straddles Colorado City, Ariz., and Hildale, Utah.
Disobedience is usually the reason given for expulsion, but former sect members and state legal officials say the exodus of males — the expulsion of girls is rarer — also remedies a huge imbalance in the marriage market. Members of the sect believe that to reach eternal salvation, men are supposed to have at least three wives.
Does God stand in the way of efforts to stop death from disease or from problems during birth? Of course not. God doesn't stand in the way of progress. Surely God would approve of efforts to enlist technology to surpass the Beach Boys "Two Girls For Every Boy" (and yes it was Jan and Dean but Brian Wilson co-wrote it). This would work especially well if the boys were genetically engineered to think in six part harmony.
Nowadays if men want three girls for every boy they need to find out how to get rid of two boys out of three.
Mr. Gilbert estimates that 100 boys from his school class, or 70 percent of them, have been expelled or left on their own accord; there is no way to verify the numbers.
Sex selection would avoid the need to expel boys and therefore eliminate one cause of hostility toward the polygamists. They could create communities that have less internal strife as well. Parents who expel their sons can't be happy about it. Some of them must feel terrible about it.
I predict some polygamists will eventually embrace sex selection reproductive technologies. Also, once the neurological mechanisms behind jealousy are elucidated expect polygamists to genetically engineer girl offspring to not feel jealousy in polygamist marriages.
The question we need to ask: Will polygamy still pose a problem for the larger society if a society contains three times as many women as men and if women don't feel jealous in polygamous marriages? For example, will polygamous marriages make married people more inward oriented toward family and will this reduce the social capital of societies by reducing volunteerism and civic spirit?
Update: Some people are under the misimpression that the only way to do sex selection is either to selectively abort or to use in vitro fertilization and embryo selection before implantation. Not so. Microsort can partially separate X and Y carrying sperm and shift the odds of births heavily toward boys (73% accuracy) or girls (88% accuracy). Therefore only artificial insemination is needed for sex selection. Over 8 girls for every boy if only the X selected sperm are used.
Ghrelin, which appears to stimulate appetite, also prevents or slows shrinkage of the thymus (a key organ for regulating the immune system) which occurs with increasing age.
The deterioration in immune function that occurs as an individual ages is thought to occur because the thymus involutes with age, causing a dramatic decrease in T cell output. New data generated by Dennis Taub and colleagues from the National Institutes of Health, Baltimore, suggest that in mice, thymic involution is caused by a decrease upon aging in thymic expression of both a hormone that is better known as a stimulator of food intake (ghrelin) and its receptor. These results led them to caution that care should be taken when considering blocking ghrelin as a potential approach for treating individuals who are obese and to suggest that harnessing this pathway might provide a new approach to boost immune function in individuals who are elderly or immunocompromised.
The physiological relevance of the decrease, with age, in expression in the mouse thymus of both ghrelin and its receptor was highlighted by the observation that infusion of ghrelin into old, but not young, mice markedly increased thymic mass, improved thymic architecture, and increased thymocyte and thymic epithelial cell numbers. These changes were associated with increased T cell output and increased diversity of the TCR repertoire of the peripheral T cell population. Consistent with these observations, age-associated thymic involution was accelerated in mice lacking either ghrelin or its receptor.
This poses a quandary: Use ghrelin which will likely increase the fat and boost the immune system? Or cut the fat and reduce the immune system? The story is actually more complex than that. See this review of how ghrelin and leptin influence appetite for the details.
This reminds me of the potential risks of older people taking growth hormone and androgens. We have a hard time trying to use hormones to boost various metabolic processes without incurring some costs of bigger problems in other areas. We need orders of magnitude more information about how human metabolism really works so that we can know how and where to intervene to achieve desired changes in metabolism without producing dangerous and unpleasant side effects.
The abstract of the paper provides a helpful clue to the ghrelin quandary. Ghrelin promotes thymopoiesis (poiesis means creation or production) during aging - but leptin (an appetite suppressor) does too.
We have previously demonstrated that the orexigenic hormone ghrelin is expressed by immune cells and regulates T cell activation and inflammation. Here we report that ghrelin and ghrelin receptor expression within the thymus diminished with progressive aging. Infusion of ghrelin into 14-month-old mice significantly improved the age-associated changes in thymic architecture and thymocyte numbers, increasing recent thymic emigrants and improving TCR diversity of peripheral T cell subsets. Ghrelin-induced thymopoiesis during aging was associated with enhanced early thymocyte progenitors and bone marrow–derived Lin–Sca1+cKit+ cells, while ghrelin- and growth hormone secretagogue receptor–deficient (GHS-R–deficient) mice displayed enhanced age-associated thymic involution. Leptin also enhanced thymopoiesis in aged but not young mice.
So maybe we could use leptin to boost thymus size without boosting appetite. Then again, maybe boosting leptin would cause problems we don't even know about yet.
Women especially should try to get enough sleep.
The University of Warwick led research team looked at data from "The Whitehall II Cohort" which studied volunteers from 20 London-based civil service departments. There were a total of 6,592 participants (4,199 men and 1,567 women). The Warwick team defined hypertension as blood pressure equal to or higher than 140/90 mm Hg or if the subject made regular use of antihypertensive medications.
The researchers found that the those women in the study group who slept less than or equal to 5 hours a night were twice as likely to suffer from hypertension than women who slept for the more recommended seven hours or more a night. The researchers found no difference between men sleeping less than 5 hours and those sleeping 7 hours or more.
I wonder if the difference is due a difference in how male and female bodies react to sleep deficits. Or maybe the conditions that cause women to sleep less are different than the conditions that make men sleep less. Maybe stressful environments cause women to miss sleep but for men maybe the sleep is missed due to the desire to do more activities that are less stressful. Mind you, that's pure speculation. More likely female bodies react to lack of sleep in ways that do more damage to blood vessels.
Whether you are a man or women there are plenty of scientific reasons why you should get enough sleep. See my previous posts Less Sleep Increases Obesity, Sleep A Lot To Avoid Burn-Out From Stress And To Stay Skinny, and Lack Of Sleep Suppresses Neurogenesis And Memory Formation. Sleep is good.
After decades of experimentation scientists still do not have good ways to deliver gene therapy into cells in humans or other animals. Gene therapy is a crucial piece of the puzzle needed to cure many diseases (notably cancer) and to rejuvenate old bodies. Gene therapy is especially needed for brain rejuvenation. For the rest of the body cell therapies and replacement organs will provide easier ways to make worn out parts young again. But most neurons need to be repaired rather than replaced. So we need brain gene therapy to prevent our minds from growing old. With this thought in mind, recent MIT research looks promising for a better way to deliver gene therapy.
The new MIT work, published this week in Advanced Materials, focuses on creating gene carriers from synthetic, non-viral materials. The team is led by Daniel Anderson, research associate in MIT's Center for Cancer Research.
"What we wanted to do is start with something that's very safe--a biocompatible, degradable polymer--and try to make it more effective, instead of starting with a virus and trying to make it safer," said Jordan Green, a graduate student in biological engineering and co-first author of the paper.
The polymers self-assemble with DNA and package the DNA inside them.
Over 1,000 gene therapy clinical trials have failed so far.
Gene therapy has been a field of intense research for nearly 20 years. More than 1,000 gene-therapy clinical trials have been conducted, but to date there are no FDA-approved gene therapies.
A string of successful gene therapy clinical trials will some day mark a really big turn in the road toward the development of much more powerful medical treatments.
Key to this advance was the development of techniques to rapidly create and test large numbers of variations in polymers.
The researchers developed methods to rapidly optimize and test new polymers for their ability to form DNA nanoparticles and deliver DNA. They then chemically modified the very ends of the degradable polymer chains, using a library of different small molecules.
"Just by changing a couple of atoms at the end of a long polymer, one can dramatically change its performance," said Anderson. "These minor alterations in polymer composition significantly increase the polymers' ability to deliver DNA, and these new materials are now the best non-viral DNA delivery systems we've tested."
The polymers have already been shown to be safe in mice, and the researchers hope to ultimately run clinical trials with their modified polymers, said Anderson.
Even if this delivery vehicle turns out to work well to get DNA into cells that does not mean that a gene therapy which uses this delivery vehicle will be safe. Once the DNA gets into a cell it can integrate into a chromosome at a location that causes eventual cancer. So there's a second problem of how to get the newly introduced DNA to play nice with the cell it gets inserted into. Gene therapy is hard.
Viruses as gene therapy carriers are problematic because they usually cause an immune response. Plus, the amount of DNA which these polymers can carry looks to be larger than the amount that virus coatings can carry into cells.
Non-viral vectors could prove not only safer than viruses but also more effective in some cases. The polymers can carry a larger DNA payload than viruses, and they may avoid the immune system, which could allow multiple therapeutic applications if needed, said Green.
The researchers report success in getting their polymers to carry DNA into ovarian tumors. Gene therapy for cancer cells holds the promise of either reprogramming the cells to stop dividing or to even tell the cells to commit suicide.
2.5 year old children are better at following adult examples than are orangutans and chimpanzees.
Apes bite and try to break a tube to retrieve the food inside while children follow the experimenter's example to get inside the tube to retrieve the prize, showing that even before preschool, toddlers are more sophisticated in their social learning skills than their closest primate relatives, according to a report published in the 7 September issue of the journal Science, published by AAAS, the nonprofit science society.
This innate proficiency allows them to excel in both physical and social skills as they begin school and progress through life.
"We compared three species to determine which abilities and skills are distinctly human," explained Esther Herrmann of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany and lead author of the research paper. Humans differ from their great ape relatives because human brains are about three times the size of the closest primate relatives and humans have language, symbolic math and scientific reasoning.
That extra gray matter makes its presence felt at a very young age.
The human kids were equally in ability to the primates in many areas but showed a clear advantage in understanding and communicating.
About 230 subjects – chimps, orangutans and 2.5 year-old children – were compared using a battery of tests and found all to be about equal in the physical cognitive skills of space, quantities and causality. In the social skills of communication, social learning and theory-of-mind skills, the children were correct in about 74 percent of the trials, while the two ape species were correct only about 33 percent of the time.
The researchers chose to study children at an age when they have about the same physical skill level of chimpanzees. Children at 2.5 years are old enough to handle these tasks and people have not taught them too much so they provide a good comparison, Herrmann said. The apes ranged in age from 3 to 21.
Some day (maybe 50 to 75 years from now) some evolutionary anthropologists will perform a similar set of experiments comparing genetically natural 2 and 3 year old humans to genetically engineered 2 and 3 year old transhumans. I predict the gap in intellectual abilities between the humans and transhumans will be larger than the gap measured here between humans and other primates.
Do not overdrill on the same material over a short period of time.
Consider “overlearning.” That’s the term learning specialists use for studying material immediately after you’ve mastered it. Say you’re studying new vocabulary words, flash-card style, and you finally run through the whole list error-free; any study beyond that point is overlearning. Is this just a waste of valuable time, or does this extra effort embed the new memory for the long haul"
University of South Florida psychologist Doug Rohrer decided to explore this question scientifically. Working with Hal Pashler of the University of California, San Diego, he had two groups of students study new vocabulary in different ways. One group ran through the list five times; these students got a perfect score no more than once. The others kept drilling, for a total of ten trials; with this extra effort, the students had at least three perfect run-throughs. Then the psychologists tested all the students, some one week later and others four weeks later.
The results were interesting. For students who took the test a week later, those who had done the extra drilling performed better. But this benefit of overlearning completely disappeared by four weeks. In other words, if students are interested in learning that lasts, that extra effort is really a waste. They should instead spend this time looking at material from last week or last month or even last year.
In other words, as reported in the August issue of Current Directions in Psychological Science, “massing” all the study on a single topic into a single session reduces long-term retention. It’s better to leave it alone for a while and then return to it. Rohrer and Pashler also wanted to see if the duration of study breaks might make a difference in learning. It did. When two study sessions were separated by breaks ranging from five minutes to six months, with a final test given six months later, students did much better if their break lasted at least a month. So, rather than distribute their study of some material across just a few days, as millions of school children do when given a different list of vocabulary or spelling words each week, students would be better off seeing the same words throughout the school year.
All these experiments involved rote learning, but Rohrer and Pashler have also found similar effects with more abstract learning, like math. This is particularly troubling, the psychologists say, because most mathematics textbooks today are organized to encourage both overlearning and massing. So students end up working 20 problems on the same concept (which they learned earlier that day) when they should be working 20 problems drawn from different lessons learned since the beginning of the school year. In brief, students are wasting a lot of precious learning time.
Try to learn something a few times and then set it down and come back and try it again a few weeks later and do that again and again.
I see this as yet another reason why college lectures should all be recorded. You could watch all the material for semester in a single marathon session of a few days. Then watch all the material for another semester the next week and so on. Then eventually cycle back through and watch it all over again a month later.
The Hannaford Brothers Company grocery store chain in Maine tried putting stars on foods (the more stars the better the food) to steer customers toward healthier food choices. Given better information about the health benefits of foods while in grocery stores customers will select healthier meats but won't buy more vegetables.
After analyzing a year’s worth of sales data, Hannaford found that customers tended to buy leaner cuts of meat. Sales of ground beef with stars on their labels increased 7 percent, and sales of chicken that had a star rating rose 5 percent. Sales of ground beef labeled with no stars dropped by 5 percent, while sales of chicken that had a zero-star rating declined 3 percent. Similarly, sales of whole milk, which received no stars, declined by 4 percent, while sales of fat-free milk (three stars) increased 1 percent. Sales of fruits and vegetables, however, remained about the same as they did before the ratings were introduced. All fresh produce received stars.
People ask me to write a post describing the ideal diet. Well, the best thing you can do to improve your health is to eat lots more vegetables and fruits and less of just about everything else. But people want fats and red meat and starchy foods. They don't want vegetables. This latest result demonstrates this basic problem with the human diet. We have food instincts that are aimed at ensuring survival in environments where food is in short supply. So our instincts lead us to eat foods which are far from optimal for us today.
There'll be no need to force people to undergo Borg assimilation. The hive mind can take over by getting people addicted to computer games with brain-computer interfaces (BCIs).
Several makers of brain-computer interfaces, or BCIs -- devices that facilitate operating a computer by thought alone -- claim the technology is poised to jump from the medical sector into the consumer gaming world in 2008.
Companies including Emotiv Systems and NeuroSky say they've released BCI-based software-development kits. Gaming companies may release BCI games next year, but many scientists worry that users brains' might be subject to negative effects.
For example, the devices sometimes force users to slow down their brain waves. Afterward, users have reported trouble focusing their attention.
Trouble focusing their attention afterward? Maybe the games are so mentally demanding that playing them is akin to doing a physical work-out on one's muscles. The game work-out leaves the mind fatigued just like gym work-outs leave muscles fatigued.
Biofeedback was developed for medical purposes. Such serious technology shouldn't get treated like just another toy! Toys are undignified and medical technology should only be doled out by licensed doctors. Okay, I admit I'm exaggerating - there's a role for nurse practitioners in deciding how many hours a day Johnny can be jacked into the world wide head.
"Most biofeedback is used for clearly defined clinical purposes, specifically to try and eliminate or ameliorate a problem," says Alan Garos, president of the Association for Applied Psychophysiology and Biofeedback. "Using feedback of brain activity for non-therapeutic purposes is something that we have to look at carefully."
When LSD hit the streets of San Francisco that's kind of like what computers did when they became available for home use. The difference is that parents applauded the computer addiction craze. Therefore we can not expect a cautious approach toward BCI by electronic game playing addicts. BCI game playing will be seen as training for upscale jobs done through BCI devices.
Yet BCI poses problems We didn't evolve to handle computers. Therefore we aren't well adapted to their presence in our environments. We can either use genetic engineering to adapt ourselves to computers or let natural selection run its course. Eventually those who can't resist their addiction to brain-computer interfaces will die out due to failure to reproduce. Natural selection will spread genetic alleles that make people less susceptible to malfunction when connected to brain-computer interfaces.
Genetic engineering as the solution to weight control problems?
“From worms to mammals, this gene controls fat formation,” said Dr. Jonathan Graff, associate professor of developmental biology and internal medicine at UT Southwestern and senior author of a study appearing in the Sept. 5 issue of Cell Metabolism. “It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.
...
In the current study, the UT Southwestern researchers examined how adipose works by analyzing fruit flies, tiny worms called C. elegans, cultured cells, and genetically engineered mice, as well as by exploiting sophisticated molecular techniques. Using several methods, they manipulated adipose in the various animals, turning the gene on and off at different stages in the animals’ lives and in various parts of their bodies.
It was discovered that the gene, which is also present in humans, is likely to be a high-level master switch that tells the body whether to accumulate or burn fat.
In the mice, the researchers found that increasing adipose activity improved the animals’ health in many ways. Mice with experimentally increased adipose activity ate as much or more than normal mice; however, they were leaner, had diabetes-resistant fat cells, and were better able to control insulin and blood-sugar metabolism.
In contrast, animals with reduced adipose activity were fatter, less healthy and had diabetes.
Scientists might be able to find a drug that turns up the expression of adipose. Such a drug might cause weight loss.
Flies and mice react the same ways to higher and lower levels of adipose gene expression.
To explore Adp’s function even further, Graff and his colleagues produced a strain of mutant flies like those that Doane had found years earlier. They found that the mutant flies were indeed fat and also had trouble getting around. Flies with only one copy of the Adp mutation fell somewhere in between the fat and normal flies, evidence that the gene’s effects are “dose dependent,” they reported.
Treatments that increased Adp in the insects’ fat tissue led them to lose weight, evidence that the gene operates within fat cells themselves. In mice that expressed the gene in fat-storing tissues, the same patterns emerged.
“We made mice that expressed Adp in fat-storing tissues, and lo and behold, what happened"” Graff said. “They were skinny—weighed less with markedly less fat—and their fat cells were smaller.” Smaller fat cells usually translate into better metabolic function, he said, including better blood sugar control.
Imagine the selective use of gene therapy to turn up the adipose gene in some tissue and turn down adipose in other parts of the body. It could be used to sculpt desired body shapes.
While the days of high market growth, driven by the human genome project, are behind us, the era of personal genomics is yet to begin. Next generation genomics technologies are breathing new life into the market, and are expected to contribute to the robust growth of the U.S. genomics market between 2005 and 2012. Top industry participants are successfully developing specific applications for each evolutionary stage of the genomics research process, and are likely to maintain revenue streams, while strategically positioning themselves to penetrate the future markets for clinical applications of genomic technologies.
New analysis from Frost & Sullivan (drugdiscovery.frost.com), Strategic Analysis of U.S. Genomics Markets, reveals that revenues in this market totaled $1.85 billion in 2006, and is likely to reach $3.69 billion in 2012.
That doubling in revenue will occur along with a huge increase in the amount of DNA sequence produced per dollar spent. Leading industry figures expect a 3 order of magnitude drop in sequencing costs perhaps as soon as 5 years from now.
Scientists are doing most of the DNA sequencing for their own research purposes today. But at some point in the next 5 to 10 years the desire to learn one's own personal genome sequences will become the biggest source of demand for DNA sequencing services. Also demand will grow for surreptitious DNA sequencing services so that people can learn the DNA sequences of love interests, prospective employees, celebrities, and business competitors. Science will turn up all sorts of practical uses of DNA sequence information and your genetic privacy will become very hard to protect.
DALLAS — Sept. 4, 2007 — A simple imaging technique developed by UT Southwestern Medical Center researchers has revealed fat buildup in the hearts of pre-diabetic people long before symptoms of heart disease or diabetes appear.
This discovery fits a larger trend: in the future you'll be told sooner when parts of your body start breaking down. In fact, sensors will become so powerful that you'll be able to get daily measures (if you can stand to watch) of the many many small steps of your gradual decay into old age. This sort of advance will shift public perceptions about aging and cause younger people to see their bodies as gradually accumulating lots of small bits of old age. This will make people a lot more conscious of the aging process and reduce the feeling of invulnerability that younger people feel when looking at older people. I'm expecting this development and others like it to build support among younger people for a faster rate of research into techniques to slow, stop, and reverse the aging process.
Yet another impressive advance in scanning technology.
The technique detects fat accumulation in cells of the beating heart in a way no other clinical method can, the researchers said, and may provide a way to screen patients for early signs of heart disease in diabetes.
“Hearts beat; people breathe; and magnetic resonance imaging is very sensitive to motion, so we had to find a way to electronically ‘freeze’ the image of the heart,” said Dr. Lidia Szczepaniak, assistant professor of internal medicine at UT Southwestern and senior author of a study appearing in the Sept. 4 issue of Circulation.
“We wanted a noninvasive method to study the beating human heart,” Dr. Szczepaniak said.
Dr. Szczepaniak and her colleagues developed a technique that captures the signal from a beating heart as a person lies in an ordinary magnet used for MRI scanning.
The ability to detect the early stage development of insulin resistant (type 2) diabetes will serve the useful purpose of telling people to change their diets and lose weight. This capability should be more powerful than telling people they have high cholesterol and lipids in their blood since the report of fat build-up in heart muscle cells seems scarier. This MRI scan technique measures the early stage malfunction of a heart. Will you want to know about that?
Whilst we all know that tall parents are more likely to have tall children, scientists have been unable to identify any common genes that make people taller than others. Now, however, scientists have identified the first gene, known as HMGA2, a common variant of which directly influences height.
The difference in height between a person carrying two copies of the variant and a person carrying no copies is just under 1cm in height, so does not on its own explain the range of heights across the population. However, the researchers believe the findings may prove important.
Previous studies have suggested that, unlike conditions such as obesity, which is caused by a mix of genetic and environmental factors – so called "nature and nurture" – 90% of normal variation in human height is due to genetic factors rather than, for example, diet. However, other than very rare gene variants that affect height in only a small number of people, no common gene variants have until now been identified.
The research was led by Dr Tim Frayling from the Peninsula Medical School, Exeter, Professor Mark McCarthy from the University of Oxford and Dr Joel Hirschhorn from the Broad Institute of Harvard and MIT in Cambridge, US. Dr Frayling and Professor McCarthy were also part of a Wellcome Trust-funded study team that discovered the first common gene linked to obesity in April this year.
We are just now starting to see the results of big drops in the cost of DNA testing. The rate of discovery of the meaning of genetic variations is about to turn into a torrent. The discoveries will come so fast that only the most interesting ones will garner any press attention.
The findings, published in the September 2 advance online edition of Nature Genetics, stem from a large-scale effort led by scientists at the Broad Institute of Harvard and MIT, Children’s Hospital Boston, the University of Oxford and Peninsula Medical School, Exeter. Using a new “genome-wide association” method, the research team searched the human genome for single letter differences in the genetic code that appear more often in tall individuals compared to shorter individuals. By analyzing DNA from nearly 35,000 people, the researchers zeroed in on a difference in the HMGA2 gene — a ‘C’ written in the DNA code instead of a ‘T’. Inheriting the ‘C’-containing copy of the gene often makes people taller: one copy can add about a half centimeter in height while two copies can add almost a full centimeter.
These scientists think this gene's variants account for just 0.3% of all variability in human height. So many more genes that contribute to height are waiting to be found.
The genomic find, though, is not the only indication that HMGA2 affects height. Previous studies in mice and humans revealed that a handful of rare stature disorders result from severe mutations in the gene. Taken together, the findings provide strong evidence for a role for HMGA2 in height. However, the identified SNP accounts for just 0.3% of the normal variability in human stature, which means there are probably many others yet to be found. To do this, researchers will need to study even larger groups of individuals.
Imagine what happens when we discover all the genetic variations that influence height. A couple gets their DNA sequenced. A genetic counselor tells them if they have a son he could be anywhere from 5' 6" to 5' 11". But if they produce a dozen in vitro fertilization (IVF) embryos they've got a very high chance of getting a couple of embryos on the tall end. Suddenly IVF becomes a lot more attractive.
How far are we away from the deluge of genetic sequencing discoveries and the beginning of the shift toward IVF as the preferred way to start pregnancies? Maybe 5 years.
Having brought the cost down by three orders of magnitude, the aim is to drop it by another three, to $1,000, and also to speed things up. To that end, the X Prize Foundation, an innovative American charity, is offering a $10m prize to the first team to decode the DNA of a hundred people within ten days. Dozens of groups from around the world have signed up, and the organisers expect a winner in less than five years. And it may not take that long. George Church of Harvard University recently started what he calls the Personal Genome Project. This aims to decode the genetic material of 100,000 people over the next year or so.
We haven't even seen the full discovery effects of the last few orders of magnitude in DNA sequencing costs. The costs have dropped too recently for researchers to have made much use of the new affordability of genetic sequencing. Once the costs drop a few more orders of magnitude full genome sequencing of millions of people will become affordable and then will come the deluge of discoveries of what all the genetic variations mean.
British scientist Simon Hoeurstrup and heart surgeon Magdi Yacoub claim that in 3 to 5 years they will be able to grow replacement heart valves from a patient's own bone marrow stem cells.
In the tissue engineering approach favored by Yacoub and Hoerstrup, the patient's own stem cells -- taken from bone marrow -- are isolated and expanded in the laboratory using standard cell culture techniques.
They are then "seeded" onto a special matrix in the shape of a heart valve that is positioned in a device called a "bioreactor" that tricks the cells into growing in the right shape.
They've already tested this technique with sheep cells.
One problem with extracting bone marrow stem cells comes with age. Potential leukemia replacement cell donors are screened for age. People in their 60s aren't considered good bone marrow cell donors. Well, stem cells extracted from older people to grow heart valves might grow poorly. But given that the extracted cells won't be reimplanted the development of techniques to stimulate those cells (e.g. lengthen their telomeres) more rapidly would pose few risks.
As biogerontologist Aubrey de Grey points out once we can grow replacement parts we can keep our bodies youthful for many centuries.
In Europe more people are killed by cold weather than by warm weather.
How will heat and cold deaths change over the coming century with global warming? Let us for the moment assume—very unrealistically—that we will not adapt at all to the future heat. Still, the biggest cross-European cold/heat study concludes that for an increase of 3.6 degrees Fahrenheit in the average European temperatures, “our data suggest that any increases in mortality due to increased temperatures would be outweighed by much larger short-term declines in cold-related mortalities.” For Britain, it is estimated a 3.6°F increase will mean 2,000 more heat deaths but 20,000 fewer cold deaths. Likewise, another paper incorporating all studies on this issue and applying them to a broad variety of settings in both developed and developing countries found that “global warming may cause a decrease in mortality rates, especially of cardiovascular diseases.”
Mind you, this benefit of warmer weather might not be found in Africa, the Middle East, the Indian subcontinent, or other already very warm places.
In industrialized countries air conditioning appears to have decreased deaths from heat.
Yet something great happened in the decades following. Death rates in Philadelphia and around the country dropped in general because of better health care. But crucially, temperatures of 100°F today cause almost no excess deaths. However, people still die more because of cold weather. One of the main reasons for the lower heat susceptibility is most likely increased access to air-conditioning. Studies seem to indicate that over time and with sufficient resources, we actually learn to adapt to higher temperatures. Consequently we will experience fewer heat deaths even when temperatures rise.
Indeed humans live longer in warmer weather and cold weather seems to wear us out more quickly if we believe a paper by Olivier Deschenes and Enrico Moretti and published by the National Bureau of Economic Research:, Extreme Weather Events, Mortality and Migration.
We estimate the effect of extreme weather on life expectancy in the US. Using high frequency mortality data, we find that both extreme heat and extreme cold result in immediate increases in mortality. However, the increase in mortality following extreme heat appears entirely driven by temporal displacement, while the increase in mortality following extreme cold is long lasting. The aggregate effect of cold on mortality is quantitatively large. We estimate that the number of annual deaths attributable to cold temperature is 27,940 or 1.3% of total deaths in the US. This effect is even larger in low income areas. Because the U.S. population has been moving from cold Northeastern states to the warmer Southwestern states, our findings have implications for understanding the causes of long-term increases in life expectancy. We calculate that every year, 5,400 deaths are delayed by changes in exposure to cold temperature induced by mobility. These longevity gains associated with long term trends in geographical mobility account for 8%-15% of the total gains in life expectancy experienced by the US population over the past 30 years. Thus mobility is an important but previously overlooked determinant of increased longevity in the United States. We also find that the probability of moving to a state that has fewer days of extreme cold is higher for the age groups that are predicted to benefit more in terms of lower mortality compared to the age groups that are predicted to benefit less.
Global warming, by decreasing exposure to cold weather, should therefore increase life expectancies of people who now live in colder climates.
I wonder whether the real benefit of a southward migration is reduced exposure to the cold or increased exposure to the rays of the sun. Greater sunlight exposure reduces depression and also increases vitamin D production and therefore reduces incidence of cancer and other diseases. But even if life expectancy benefit comes from more sunlight exposure a warming of northern climes will get people outside sooner in springtime and hence up their vitamin D production.
Cold weather also probably reduces levels of exercise. Plus, in warmer climes locally grown vegetables and fruits are available more of the year. So diets might be better in warmer areas of industrialized countries.
Leonard "Bones" McCoy's medical tricorder couldn't do everything. After all, it didn't detect any readings from Trelane. But the tricorder didn't just have the ability to scan. The tricorder could heas as well (e.g. the doctor in Voyager used his tricorder to heal a "hairline fracture of the pre-maxilla bone" after Seven clobbered an alien). Well, the US Department of Defense is funding development of a portable high intensity ultrasound sound wave device to stop internal bleeding.
Engineers at the University of Washington are working with Harborview doctors to create new emergency treatments right out of Star Trek: a tricorder type device using high-intensity focused ultrasound rays. This summer, researchers published the first experiment using ultrasound to seal punctured lungs.
"No one has ever looked at treating lungs with ultrasound," said Shahram Vaezy, a UW associate professor of bioengineering. Physicists were skeptical it would work because a lung is essentially a collection of air sacs, and air blocks transmission of ultrasound. But the new experiments show that punctures on the lung's surface, where injuries usually occur, heal with ultrasound therapy.
"The results are really impressive," Vaezy said. He cautions that this is still in the early stages and the technique is not yet being tested on humans.
A focused beam of ultrasound could kill tumor cells better than x-rays because the heat of the ultrasound beam would only occur at the focus point. The intermediate tissue the ultrasound beams would pass through wouldn't suffer damage the way tissue gets damaged by radiation beams.
High-intensity focused ultrasound is now being investigated for a number of different treatments. It promises "bloodless surgery" with no scalpels or sutures in sight. Doctors would pass a sensor over the patient and use invisible rays to heal the wound. Researchers are exploring the use of high-intensity focused ultrasound - with beams tens of thousands of times more powerful than used in imaging - for applications ranging from numbing pain to destroying cancerous tissue.
In this case, lenses focus the high-intensity ultrasound beams at a particular spot inside the body on the patient's lungs. Focusing the ultrasound beams, in a process similar to focusing sunlight with a magnifying glass, creates a tiny but extremely hot spot about the size and shape of a grain of rice. The rays heat the blood cells until they form a seal. Meanwhile the tissue between the device and the spot being treated does not get hot, as it would with a laser beam.
"You can penetrate deep into the body and deliver the energy to the bleeding very accurately," Vaezy said. Recent tests on pigs' lungs showed that high-intensity ultrasound sealed the leaks in one or two minutes. More than 95 percent of the 70 incisions were stable after two minutes of treatment, according to results published this summer in the Journal of Trauma.
The University of Washington press release makes no mention of industry partners. But it does mention Department of Defense funding for this work. Well, a Seattle area company AcousTx Corporation, is working on development of an ultrasound bleed-stopping device for the Defense Advanced Research Projects Agency (DARPA) for DARPA’s Deep Bleeder Acoustic Coagulation (DBAC) program. Well it turns out that the DOD is so keen to get this technology that DOD is funding two different Seattle area teams to compete to achieve this goal.
The researchers at AcousTx, a small ultrasound company in Seattle, are funded by a four-year contract, worth up to $30 million, from the U.S. Defense Advanced Research Projects Agency (DARPA).
To underscore the pressing need, the agency gave another $21 million to a competing group, a partnership of Philips Research and the University of Washington's Center for Industrial and Medical Ultrasound.
"If this were to work, just think — just think — about the value it would have as a lifesaving device," said Michael Sekins, AcousTx vice president of research and development.
But how do they know where to focus the beam? They can't heat the entire chest without basically cooking the bleeding person to death. So how to locate the locations with dangerous bleeds?
Resveratrol continues to be the supplement which I'm not taking that I most wonder whether I should be taking. Resveratrol appears to confer some protection against prostate cancer.
BIRMINGHAM, Ala. – Researchers at the University of Alabama at Birmingham (UAB) have found that nutrients in red wine may help reduce the risk of developing prostate cancer.
The study involved male mice that were fed a plant compound found in red wine called resveratrol, which has shown anti-oxidant and anti-cancer properties. Other sources of resveratrol in the diet include grapes, raspberries, peanuts and blueberries.
In the study resveratrol-fed mice showed an 87 percent reduction in their risk of developing prostate tumors that contained the worst kind of cancer-staging diagnosis. The mice that proved to have the highest cancer-protection effect earned it after seven months of consuming resveratrol in a powdered formula mixed with their food.
Other mice in the study, those fed resveratrol but still developed a less-serious form of prostate cancer, were 48 percent more likely to have their tumor growth halted or slowed when compared to mice who did not consume the compound, the UAB research team said.
A pair of recent articles from MIT's Technology Review provide a broader look at the science and commercial development efforts around resveratrol. At Harvard Medical School researcher David Sinclair believes resveratrol might extend our lives.
Sinclair's basic claim is simple, if seemingly improbable: he has found an elixir of youth. In his Australian drawl, the 38-year-old Harvard University professor of pathology explains how he discovered that resveratrol, a chemical found in red wine, extends life span in mice by up to 24 percent and in other animals, including flies and worms, by as much as 59 percent. Sinclair hopes that resveratrol will bump up the life span of people, too. "The system at work in the mice and other organisms is evolutionarily very old, so I suspect that what works in mice will work in humans," he says.
Sinclair has co-founded a biotech start-up, Sirtris Pharmaceuticals, to try to develop variations on resveratrol to develop them into drugs.
Sinclair and a few other researchers involved in biotech start-ups around Boston argue that drugs can turn on the same genes that calorie restriction activates and thereby extend life just like calorie restriction does.
Only 20 years ago, aging was considered too complex for pharmacological intervention, involving thousands of genes and pathways. However, geneticists studying model organisms such as yeast and worms discovered several genes that can dramatically extend healthy life span1. There are proaging genes such as IGF-1 and antiaging genes such as SIRT1.
While genes that control aging have only recently been discovered, scientists have known for many decades that a simple change in diet can dramatically slow the pace of aging. "Calorie restriction" (CR), the diet wherein calories are reduced 20 to 40 percent, is the most robust means of extending healthy life span in mammals, and several of the key longevity pathways seem to underlie the beneficial effects of this diet. CR also improves health parameters in higher organisms including humans3.
There is controversy over whether calorie restriction delivers its benefits via SIRT1 activation. Researchers are chasing other genes as activators of CR's life extending effects. But resveratrol might deliver benefits even if it does not do so by emulating CR.
Extreme outcomes from fossil fuels burning are probably easily avoidable at low cost.. Ocean iron fertilization would cool the Earth by increasing natural sulfur aerosal production which would increase cloud formation and planetary reflectivity.
July 24, 2007 -- Prof. Oliver Wingenter of New Mexico Tech and his colleagues propose a limited iron fertilization of the Southern Ocean as a means to stimulate the natural sulfur cycle associated with marine phytoplankton which could result in increased cloud reflectivity that would slow down global warming and possibly decrease sea level rise.
Wingenter and his research colleagues Dr. Scott M. Elliot at Los Alamos National Laboratory and Prof. Donald R. Blake at University of California, Irvine report their research findings in an article published online July 18 in the journal Atmospheric Environment, titled "New Directions: Enhancing the natural sulfur cycle to slow global warming,".
The scientists base their plan on their observations made during the Southern Ocean Iron Experiments (SOFeX) research expedition, the longest and most comprehensive ocean iron fertilization experiment to date, which was carried out in 2002 aboard three research ships in the Southern Ocean, between New Zealand and Antarctica.
The scientists who conducted the SOFeX experiment were looking for a cheap way to cool the planet by pulling carbon dioxide out of the atmosphere. Instead they found a cheap way to pump a planet-cooling sulfide into the atmosphere.
Wingenter thinks we could delay global warming by 10 to 20 years at very low cost with iron fertilization of only 2% of the Southern Ocean. With just 30 ships and at most $100 million per year we could delay warming by 10 to 20 years.
"However, marine microorganisms not only consume inorganic carbon, but also produce and consume many climate-relevant organic gases," Wingenter continues. "The greatest climate effect of iron fertilization may be in enhancing dimethyl sulfide (DMS) production, leading to changes in the optical properties of the atmosphere and cooling of the region." Samples taken by Wingenter during SOFeX showed that the concentration of DMS increased about five times in the iron fertilized patch versus outside. Emissions of DMS are the main source of sulfate particle formation to the region and "seed" much of the cloud formation.
Wingenter and his research colleagues propose a limited fertilization of only about 2 percent of Southern Ocean---which would result in an estimated two degrees (Celsius) cooling of the region. A program of limited-scale iron fertilization in the Southern Ocean and perhaps a portion of the equatorial Pacific may have the potential to set back the tipping point of global warming from about 10 years to about 20 or more years," Wingenter estimates.
An iron-fertilization program of the scale envisioned by Wingenter and his fellow researchers would require about 30 ships, fertilizing the Southern Ocean with about 22 kilotons of iron sulfate, at an annual cost of anywhere between $10 million and $100 million, according to the article in Atmospheric Environment.
A program like this one could get tested at smaller scales and then scaled up very quickly as necessary. UC Irvine physicist Gregory Benford has proposed another cheap way to cool the planet as well. Cooling the planet down seems relatively easy. But I've yet to come across proposed engineering solutions for another consequence of atmospheric CO2 build-up: acidification of the oceans as atmospheric carbon dioxide dissolves into the oceans. What to do about that other than reduce CO2 emissions or accelerate the extraction of carbon from the atmosphere?
Writing in the Spring 2007 edition of the Wilson Quarterly scholar James R. Fleming argues that would-be climate engineers lack the ability to model all the side effects of climate engineering.
Yet thanks to remarkable advances in science and technology, from satellite sensors to enormously sophisticated global climate models, the fantasies of the weather and climate engineers have only grown. Now it is possible to tinker with scenarios in computer climate models—manipulating the solar inputs, for example, to demonstrate that artificially increased solar reflectivity will generate a cooling trend in the model.
But this is a far cry from conducting a practical global field experiment or operational program with proper data collection and analysis; full accounting for possible liabilities, unintended consequences, and litigation; and the necessary international support and approval. Lowell Wood blithely declares that if his proposal to turn the polar icecap into a planetary air conditioner were implemented and didn’t work, the process could be halted after a few years. He doesn’t mention what harm such a failure could cause in the meantime.
There are signs among the geoengineers of an overconfidence in technology as a solution of first resort. Many appear to possess a too-literal belief in progress that produces an anything-is-possible mentality, abetted by a basic misunderstanding of the nature of today’s climate models. The global climate system is a “massive, staggering beast,” as oceanographer Wallace Broecker describes it, with no simple set of controlling parameters. We are more than a long way from understanding how it works, much less the precise prediction and practical “control” of global climate.
Fleming also wonders who should control a climate engineering effort. The effects of climate engineering would create large numbers of both winners and losers. Cooling via engineering efforts would improve farming in some regions and make it much harder in other regions. Cooling would change costs of heating and air conditioning and air conditioning and change which structure designs are ideal in many areas.
Assume, for just a moment, that climate control were technically possible. Who would be given the authority to manage it? Who would have the wisdom to dispense drought, severe winters, or the effects of storms to some so that the rest of the planet could prosper? At what cost, economically, aesthetically, and in our moral relationship to nature, would we manipulate the climate?
But these questions which Fleming raises can already be raised about existing human activity. We build cities and cities cause severe thunderstorms. We plow fields on a massive scale to grow crops and farms reduce cloud cover and rainfall. In fact, humans might already have engineered the planet's climate thousands of years ago via farming and forest destruction that might have prevented an ice age. The difference with the modern would-be climate engineers isn't necessarily the scale on which they want to act. Rather, they want to intervene on purpose in a system to partially cancel out the effects of interventions we've already done by accident.
Given that our current industries, technologies, and lifestyles already generate lots of side effects and external costs (and not just due to climate effects) I do not see why we should oppose climate engineering just because it will inflict costs on some. If we took that approach on all environmental questions we'd have to abandon modern technology and force a huge contraction in the size of the human population. In many cases those costs will effectively come from returning a local environment to a state more like it would be absent human intervention. Though that would not always be the case.
Update: Climate cooling measures such as Gregory Benford and Oliver Wingenter propose can be implemented so quickly that we can wait to see whether global warming becomes a big problem before trying these methods. But it would be helpful to do research on these proposals to measure their effects and get a better handle on what undesirable side effects would arise from their use.
The best response I can see to rising CO2 levels is to try harder to develop cheaper substitutes to fossil fuels. Research that produces energy that is both cheaper and cleaner would give us the best of both worlds.
Moo cow fun with cloning science.
Two British scientists seeking permission to create cloned human embryos using cow eggs have renewed an old debate about these “chimeras,” which may offer a new embryonic stem cell source for research but are also a source of controversy.
Stem cell researchers Stephen Minger, director of the Stem Cell Biology Lab at King’s College London, and Lyle Armstrong, a researcher at the North East England Stem Cell Institute applied to the Human Fertilisation and Embryology Authority, the agency overseeing all British reproductive and embryo research, to carry out cloning experiments using human genetic material and cow eggs. The controversy surrounding the experiments has exploded on both sides of the Atlantic.
Do you object? If so, why? Does this seem like sacrilege? Or are you afraid where it might lead?
These scientists aren't trying to create fully formed creatures. The cell lines they might be able to create could reveal useful lessons about genetic regulation and interactions between different genetic variations that normally do not interact in nature. But this research sort of research will lead to the identification of compatibilities and incompatibilities between genes across species. That knowledge could some day be used to figure out how to make human compatible versions of genes from big cats, dogs, cows, monkeys, and many other species.
But why would we want to transfer genes from other species into humans? Some would do it to fulfill aesthetic desires. Someone might want a coat of fur made from the same genes as that beautiful coat of fur that their cat Fluffy has. Or how about a tail? Exotic dancers and prostitutes might find that the ability to look like female characters from the X-Men movies would boost their incomes by sizable amounts.
But transplantation of genes from other species into humans holds out the potential for very practical medical benefits as well. The Methuselah Foundation LysoSENS research initiative has as its goal to find genes in bacterial, molds, and other very small organisms that can be transferred into human cells to better break down trash that accumulates in cells as we age. Our own lysosomes contain lysozyme enzymes that break down junk. But over decades they encounter pieces of junk they can't break down and that junk accumulates in our cells and contributes to our aging. By isolating and studying lysozyme enzymes in other species the LysoSENS researchers hope to find enzymes we can transfer to humans with gene therapy to let us clean out our cells.