2004 August 31 Tuesday
People More Unhappy From Wasted Money Than Wasted Time?

People do not know how to value their time and are less upset by wasted time than by wasted money.

"Our research shows that the concept of time is easier to write off than is money," said Erica Okada, a University of Washington assistant professor of marketing who co-authored the study with Stephen Hoch, professor of marketing at the University of Pennsylvania's Wharton School. "People are relatively certain about how much their money is worth, but when it comes to their time, people are less certain about its value."

Unlike previous research that focused almost exclusively on money-based transactions, this study used time as a form of currency. Researchers conducted five experiments to determine how the inherently ambiguous value of time influences consumer purchasing behavior.

Three hundred sixty undergraduate students completed a questionnaire that presented two scenarios in which they were told they had already consumed a product that they had acquired in exchange for either four hours of work or $50. In one scenario, the students were told their experience with the product was good, in the other negative.

Okada and Hoch noted a greater difference in reaction between a good experience and a bad experience among those who paid in money. The difference between the levels of satisfaction following a good experience and dissatisfaction following a bad experience was significantly less among those who paid in time.

As suspected, said Okada, the experiments revealed that consumers have an easier time rationalizing a bad outcome after paying with time than hard-earned cash. The ambiguity in the value of time allows people to do this, whereas it is more difficult to do so with money, she added.

I wonder whether older people and higher income people would react in the same way as these students. My guess is that students accustomed to treatment by educational institutions that place a low value on their time.

By Randall Parker 2004 August 31 01:55 AM  Brain Economics
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2004 August 30 Monday
Brain Rewards For Carrying Out Altruistic Punishment

Dominique de Quervain, Urs Fischbacher and Prof Ernst Fehr of the University of Zurich used Positron Emission Tomography (PET) brain scans to watch players carry out altruistic punishment against cheaters.

All 14 players chose revenge whenever the double-cross was deliberate and the retaliation free. Only three retaliated when the double-cross wasn't deliberate. Twelve of 14 players punished a deliberate double-cross even if it cost them more money.

The basic outline of the game which was played repeats the work of one these same researchers, Ernst Fehr, and Simon Gächter of the University of St. Gallen which I reported in my post Altruistic Punishment And Genetic Engineering Of The Mind. My guess is that there is genetic variation in the human population on the extent to which people will feel rewarded for meting out altruistic punishments. That opens up the possibility that once people can control which genetic variations their offspring get they may not opt to pass along all the genetic variations that cause altruistic punishment behavior. This could potentially destabilize society at some time in the future. Also see the related post Emotions Overrule Logic To Cause Us To Punish.

The added twist in the latest work is that the researchers were watching the brains of the players using PET scans while the players inflicted punishments at their own expense.

The researchers determined that deciding to impose this penalty, an altruistic punishment, activated a brain region, the dorsal striatum, involved in experiencing enjoyment or satisfaction.

The dorsal striatum and its most important part, the caudate nucleus, form part of a "reward circuit".

We are wired up to enjoy getting even. The term "sweet revenge" is entirely appropriate. I bet if the brain was scanned while someone ate sweets some of the same circuits would light up.

Altruistic punishment was selected for by evolution. (same article here)

"A lot of theoretical work in evolutionary biology and our previous experimental work suggest that altruistic punishment has been crucial for the evolution of cooperation in human societies," said Ernst Fehr, the senior author of the study who is director of the Institute for Empirical Research in Economics at the University of Zurich. "Our previous experiments show that if altruistic punishment is possible, cooperation flourishes. If we rule out altruistic punishment, cooperation breaks down."

Stanford University psychology professor Brian Knutson wrote an accompanying commentary noting that schadenfreude has now been captured in a brain scan.

The researchers also found that the fantasy of revenge is immensely satisfying: "The activation in the dorsal striatum reflects the anticipated satisfaction from punishing defectors" — or, it appears, from seeing them suffer.

As Knutson notes in his commentary, the Swiss researchers "appear to have captured this complex emotional dynamic of schadenfreude with a PET camera."

There are some interesting aspects of phenomenon. First of all, the brain does reward some types of altruism. But the altruistic act is not experienced subjectivly as a loss because the brain delivers an internal reward that compensates for the loss of resources caused by paying to punish others. Also, the actual act that the brain is rewarded for is essentially painful for the direct target of the act while being beneficial for others since it causes the targets of punishment to be less likely to cheat other people. Altruistic punishment then is quite a complex behavior in terms of its effects.

By Randall Parker 2004 August 30 03:37 PM  Brain Altruism
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Estrogen Benefits For Cognitive Performance Depend On Stress Level

In female rats running through water mazes higher estrogen estrogen levels helped boost performance only when the conditions were not stressful.

"Water temperature totally reversed who did better," said Janice M. Juraska, a professor of psychology and of neuroscience. "Proestrous rats, which have high hormone levels, did better when the water was warm, presumably because they were less stressed. Estrous rats did better when the water was cold, presumably because they are not as prone to get stressed during this time."

Proestrous rats are fertile and ready to mate, while estrous rats have low hormone levels and won't mate. For the study -- funded by a grant to Juraska from the National Science Foundation -- 44 female rats were divided into four groups. The two groups of rats in proestrus and the two groups in estrus had to learn the route and swim to a submerged platform in either warm (91 degrees Fahrenheit; 33 Celsius) or cold water (66.2 degrees Fahrenheit; 19 Celsius).

Many scientists have tried to answer the hormones-cognition question, but the various findings, measuring different tasks, have been inconsistent and often contradictory.

"These discrepancies of sometimes opposite results have been very difficult to resolve," Juraska said. "Even for simple tests of spatial behavior, high hormones can either help or hinder, and nobody has understood why."

What is the evolutionary adaptation that is causing this difference in performance under different conditions?

We already have fairly limited abilities to regulate the extent of our stress response. We can take drugs that make us more relaxed and also other drugs that suppress inflammation response. We will of course eventually achieve much more control over the body's stress response. One future use of the ability to regulate stress response will be to create levels of stress that have the effect of optimally tuning the mind to reach peak performance for specific types of cognitive tasks.

Of course hormones will be manipulated to produce differences in cognitive function as well. But what we really need with hormones is the ability to make different target tissue types see different hormone levels. Rather than the whole body seeing, for instance, pharmaceutically boosted levels of testosterone expect to see the development of means to target only muscles or only the brain to produce only a subset of all the effects that testosterone produces. Ditto for estrogen, progesterone, and other hormones. Lots of effects of these hormones go together in nature. But you can bet people will want to, say, enhance their physical appearance without changing their cognitive function and vice versa.

By Randall Parker 2004 August 30 03:00 AM  Brain Enhancement
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2004 August 27 Friday
Should Flying Cars Ever Be Allowed?

A story on flying cars includes a comment at the end pointing out that there are arguments to be made against flying cars.

Ken Goodrich, a senior research engineer at NASA, said one concept under discussion is technology that runs in "h" mode, which stands for "horse." The idea is that a horse, unlike a car, is more likely to try to avoid other objects and may even know how to find its way home.

But Goodrich said he's not sure that the fantasy of the flying car ever would or should become a reality. He questioned whether having flying/driving vehicles throughout the country might end up being too noisy, disruptive and impractical.

Noise is certainly an important issue. In the future we should have fewer and quieter disruptions from the noises generated by others. Certainly car locking horn blasts and car horn alarms should be banned as obnoxious public nuisances. But millions of flying vehicles taking off and landing daily next to every house in suburbs would make horn blasts seem like minor annoyances in comparison.

There is an even more important issue than noise: Safety of people on the ground. Right now a person can greatly reduce their risk of death or disablement from accidents by working at home or within walking distance of a job or in some rural environment where there are few cars. Whereas sky cars flying in and out of suburban housing tracts all day and night will bring a new risk to the lives of all the people who are now safe in their own homes from the risks of car accidents.

Flying cars might be safer for drunk drivers and their current day victims. But a better solution to that problem ought to be either to make smart cars down here on the ground that can take over for a drunk or make it impossible for a drunk to start a car in the first place (biosensors embedded in the steering wheel could detect the alcohol).

Failure modes such as engine failures which are almost always non-fatal in ground vehicles become potentially fatal not only to commuters but to anyone they are flying over in housing tracts. Plus, cars rarely hit houses and cause building structure damage today. But that would change if tens of millions of flying vehicles were passing over housing tracts every day.

Once we achieve perpetual youth with SENS (Strategies for Engineered Negligible Senescence) technologies a risk that is low in a single year will become orders of magnitude larger once human life spans are measurable in thousands or tens of thousands of years. People may become more risk averse when faced with longer lives (or maybe not). We ought to be looking ahead now and avoiding the spread of technologies that will make it hard to lower risks that would pose substantial cumulative risks to long lived humans. Count me in the ranks of opponents of sky cars.

Update: It is debatable whether people will become more risk averse when faced with longer lives. Some people, given younger bodies, will feel energetic and will have higher levels of hormones running through their bodies making their personalities younger again as well. So people may take more risks rather than less risks. However, there will be considerable variation between different people due to innate differences in what people find most rewarding.

Also, some people will seek out brain treatments that lower thrills they get from risky activity. Just as drug addicts will some day get gene therapies to change receptors to lower cravings for drugs so will thrill seekers. Expect to see gene therapies developed that lower the feeling of excitement that people get from dangerous activities.

Also, expect to see people migrate to jurisdictions that have safety regulation levels geared to their own levels of risk aversion. Highly dedicated long lifers will live in jurisdictions where sky cars are banned, cars have test devices to guarantee that drivers are cognitively competent to drive, speed limits are low, and commuter train systems are designed to be extremely safe. High safety jurisdictions will likely not allow violent criminals to ever be released onto the street without being subjected to gene therapies that reprogram their brains to make them non-violent.

By Randall Parker 2004 August 27 02:27 PM  Airplanes and Spacecraft
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2004 August 26 Thursday
Two New Hydrogen Generation Techniques

A pair of University of Wisconsin researcher claim they have developed a more efficient and less polluting way to convert hydrocarbons into hydrogen.

Carbon monoxide, or CO, has long been a major technical barrier to the efficient operation of fuel cells. But now, chemical and biological engineers at UW-Madison have not only cleared that barrier - they also have discovered a method to capture carbon monoxide's energy.

To be useful in a power-generating fuel cell, hydrocarbons such as gasoline, natural gas or ethanol must be reformed into a hydrogen-rich gas. A large, costly and critical step to this process requires generating steam and reacting it with carbon monoxide (CO). This process, called water-gas shift, produces hydrogen and carbon dioxide (CO2). Additional steps then are taken to reduce the CO levels further before the hydrogen enters a fuel cell.

James Dumesic, professor of chemical and biological engineering, postdoctoral researcher Won Bae Kim, and graduate students Tobias Voitl and Gabriel Rodriguez-Rivera eliminated the water-gas shift reaction from the process, removing the need to transport and vaporize liquid water in the production of energy for portable applications.

The team, as reported in the Aug. 27 issue of Science, uses an environmentally benign polyoxometalate (POM) compound to oxidize CO in liquid water at room temperature. The compound not only removes CO from gas streams for fuel cells, but also converts the energy content of CO into a liquid that subsequently can be used to power a fuel cell.

Note that their focus is on the development of supporting technologies aimed at making portable fuel cells more practical. Their approach does not generate any energy and they need hydrocarbon fuels to start with. Still, conversion of hydrocarbons to hydrogen to burn in fuel cells might some day make cars more efficient in their use of liquid hydrocarbons. At the very least their appoach might provide portable power sources for personal computers and other gadgets humans lug around.

WIth an aim of enabling solar power to be tapped as an economic source of energy a pair of Australian scientists claim they will be able to build solar power driven hydrogen generating titanium oxide ceramics.

Australian scientists predict that a revolutionary new way to harness the power of the sun to extract clean and almost unlimited energy supplies from water will be a reality within seven years.

Using special titanium oxide ceramics that harvest sunlight and split water to produce hydrogen fuel, the researchers say it will then be a simple engineering exercise to make an energy-harvesting device with no moving parts and emitting no greenhouse gases or pollutants.

It would be the cheapest, cleanest and most abundant energy source ever developed: the main by-products would be oxygen and water.

"This is potentially huge, with a market the size of all the existing markets for coal, oil and gas combined," says Professor Janusz Nowotny, who with Professor Chris Sorrell is leading a solar hydrogen research project at the University of New South Wales (UNSW) Centre for Materials and Energy Conversion. The team is thought to be the most advanced in developing the cheap, light-sensitive materials that will be the basis of the technology.

"Based on our research results, we know we are on the right track and with the right support we now estimate that we can deliver a new material within seven years," says Nowotny.

...

The UNSW team opted to use titania ceramic photoelectrodes because they have the right semiconducting properties and the highest resistance to water corrosion.

Solar hydrogen, Professor Sorrell argues, is not incompatible with coal. It can be used to produce solar methanol, which produces less carbon dioxide than conventional methods. "As a mid-term energy carrier it has a lot to say for it," he says.

Okay, seven years is some years out there with obviously a number of technical problems yet to be solved. They haven't proved they can really make their approach work or that their materials will really turn out to be cheap to manufacture. Still, they might succeed.

We need many more teams in research labs working on materials to use solar power to generate hydrogen, electricity, and hydrocarbons (artificial photosynthesis). We also need more teams working on fuel cell technologies and materials for newer lighter types of batteries. Many battery and fuel cell technologies would allow fossil fuels to be burned more efficiently while also acting as enabling technologies for solar power by allowing energy captured by solar technologies to be stored.

By Randall Parker 2004 August 26 03:49 PM  Energy Tech
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2004 August 24 Tuesday
Mouse Engineered For Marathon Running, Resistance To Obesity

Some researchers at the Salk Institute have developed a transgenic mouse with more slow twitching muscle fibers and a resistance to obesity when fed a high fat diet. (same article here)

LA JOLLA, CA — A molecular switch known to regulate fat metabolism appears to prevent obesity and turns laboratory mice into marathon runners, a Salk Institute study has found.

The discovery of the switch could lead to treatments for obesity and disorders associated with it, such as heart disease and type 2 diabetes. The study, led by professor Ronald Evans and his postdoctoral fellow Yong-Xu Wang, appears in the September issue of the Public Library of Science Biology journal (PLoS Biology). Evans is also an Investigator of the Howard Hughes Medical Institute.

Evans, Wang and team discovered that activation of the switch, a receptor called PPAR-delta, increases the rate at which the body burns fat. This makes PPAR-delta an exciting potential target for drugs that treat diabetes and lipid disorders. The team produced a genetically engineered mouse endowed with the activated form of PPAR-delta in its skeletal muscles. The result was a dramatic increase in "non-fatiguing" or "slow twitch" muscle cells and a mouse capable of running up to twice the distance of a normal littermate without training.

By expressing genes for an activated form of the receptor PPAR-delta, we created a mouse that could, compared to normal mice, run marathons, said Evans. The activated form of PPAR-delta produced muscle fibers that enhanced endurance exercise." By turning on PPAR-delta, the team had produced highly efficient muscle fibers that burned fat more rapidly. As a result, the mice were almost unable to gain weight even in the absence of exercise.

"These muscles also provided resistance to obesity, despite the level of exercise," said Evans. "By manipulating this receptor, it is possible to design treatments that change our muscle makeup and help resist obesity and associated metabolic disorders.

To test the concept, Evans and his team treated normal mice with an experimental drug called GW501516 that activates PPAR-delta. These mice also expressed genes for slow-twitch muscles and gained less weight when given a high-fat diet. This drug is now in the earliest stages of being tested on people for its effects on obesity and other disorders of fat metabolism such as high blood cholesterol.

This experiment underscores the importance of metabolism in fighting obesity and improving fitness, said Evans. Activating the PPAR switch may prevent physical fatigue and enhance the quality of exercise, which may lead to a new class of drugs to promote weight loss and treat diseases arising from an overweight population.

If GW501516 turns out to be safe to use then consider the benefits. The drug may increase your muscle mass, reduce your body fat, lower your cholsterol, and reduce your risk of insulin resistance all at the same time.

A substantial portion of the population of Western nations (and probably other nations as well) will embrace the use of drugs and gene therapy that alters muscle metabolism for health reasons alone. The prospect of competing in athletic competitions will not be the main allure of body engineering for most people. The ability to keep off excess fat, prevent the loss of muscle mass with age, lower cholesterol, and avoid type II insulin-resistant diabetes will together attract more people than the drive to perform better in competitive sports.

The research paper for this report was published in PLoS Biology which offers on-line access at no cost The full research paper drives home the point that upregulation of PPARδ (also spelled above as PPARdelta) made the transgenic mice resistant to obesity.

A number of previous studies have shown that obese individuals have fewer oxidative fibers, implying that the presence of oxidative fibers alone may play a part in obesity resistance. To test this possibility, we fed the transgenic mice and their wild-type littermates with a high-fat diet for 97 d. Although the initial body weights of the two groups were very similar, the transgenic mice had gained less than 50% at day 47, and only one-third at day 97, of the weight gained by the wild-type animals (Figure 4A). The transgenic mice displayed significantly higher oxygen consumption on the high-fat diet than the control littermates (unpublished data). By the end of this experiment, the control littermates became obese, whereas the transgenic mice still maintained a normal body weight and fat mass composition (Figure 4A). A histological analysis of inguinal fat pad revealed a much smaller cell size in the transgenic mice (Figure 4B), due to the increased muscle oxidative capacity. While there was no significant difference in intramuscular glycogen content, the triglyceride content was much less in the transgenic mice (Figure 4C and 4D), which may explain their improved glucose tolerance (Figure 4E). We also placed wild-type C57BJ6 mice on the high-fat diet and treated them with either vehicle or the PPARδ agonist GW501516 for 2 mo. GW501516 produced a sustained induction of genes for type I muscle fibers; this, at least in part, resulted in an only 30% gain in body weight, a dramatically reduced fat mass accumulation, and improved glucose tolerance, compared to the vehicle-treated group (Figure 5). Thus, muscle fiber conversion by stimulation with the PPARδ agonist or the activated transgene has a protective role against obesity.

A synopsis that accompanies the research paper makes the point that most people lack the ideal genetic coding to be a sprinter or to be a marathon runner or both.

Have you ever noticed that long-distance runners and sprinters seem specially engineered for their sports? One's built for distance, the other speed. The ability to generate quick bursts of power or sustain long periods of exertion depends primarily on your muscle fiber type ratio (muscle cells are called fibers), which depends on your genes. To this extent, elite athletes are born, not made. No matter how hard you train or how many performance-enhancing drugs you take, if you're not blessed with the muscle composition of a sprinter, you're not going to break the 100-meter world record in your lifetime. (In case you'd like to try, that's 9.78 seconds for a man and 10.49 seconds for a woman.)

Of course that doesn't prevent those at the highest levels from using the latest performance enhancer to get that extra 1% edge. But wait until trainers hear about the Marathon Mouse. A new study by Ronald Evans and colleagues provides evidence that endurance and running performance can be dramatically enhanced through genetic manipulation.

Skeletal muscles come in two basic types: type I, or slow twitch, and type II, or fast twitch. Slow-twitch fibers rely on oxidative (aerobic) metabolism and have abundant mitochondria that generate the stable, long-lasting supplies of adenosine triphosphate, or ATP, needed for long distance. (For more on muscle fiber metabolism, see synopsis titled “A Skeletal Muscle Protein That Regulates Endurance”) Fast-twitch fibers, which produce ATP through anaerobic glycolysis, generate rapid, powerful contractions but fatigue easily. Top-flight sprinters have up to 80% type II fibers while long-distance runners have up to 90% type I fibers. Coach potatoes have about the same percentage of both.

In the future we are going to be able to use drugs and gene therapy to tune our metabolisms to operate more like the metabolisms athletes who perform best in specific types of sports. But note that we will have to choose how we want to optimize our bodies. An ideal optimization for sprinting will reduce performance in distance running and vice versa.

The drug GW501516 which the Salk team used to upregulate PPARδ may not be causing its main anti-obesity effect by increasing the amount of slow twitch muscle. A different research team at the University of Queensland reports that GW501516 causes changes in lipid metabolism and in energy uncoupling.

Activation of PPARß/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, ß-oxidation, cholesterol efflux, and energy uncoupling. Furthermore, we show that treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARß/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPAR{gamma} induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage

The reference to energy uncoupling suggests that GW501516 and PPARδ might be causing more of the energy that is produced by breaking down sugars to be given off as heat.

By Randall Parker 2004 August 24 02:58 PM  Biotech Athletics
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2004 August 23 Monday
Genetically Enhanced Athletes In 2008 Olympics?

Some athletes may already be experimenting with gene therapy to enhance their performance.

"I wouldn't be surprised if somebody (in sports) is trying it as we speak," University of Western Ontario genetics expert Dr. Shiva Singh said. "If you can do it for a diseased muscle, why can't you do it for a normal muscle?"

Many of the therapies developed for muscular dystrophy, muscle injuries, aged muscles, and other muscle disorders will be easily adapted to enhance performance well beyond the natural level of performance. So banning the development of genetic enhancement therapies is not feasible.

Anne McIlroy of the Globe and Mail has an excellent overview of the developments that are leading toward the genetic enhancement of athletic performance. She reports that genetically enhanced athlets may show up at the 2008 Summer Olympics to compete.

Many experts believe that the first genetically modified athletes could be competing at next Summer Olympics.

"I would think the Beijing Olympics may be the time to pick it up on a widespread basis," says Geoffrey Goldspink, an expert in muscle regeneration at the University College Medical School in London. He is already working on a test to detect genetic cheaters for the U.S. anti-doping agency.

...

In 1964, Finnish cross-country skier Eero Mantyranta was suspected of blood doping after winning two gold medals because he had so many red blood cells in his system. Three decades later, he was cleared when researchers found that he and many of his family members have a genetic mutation that increases their red-blood-cell count by 20 per cent.

Eventually the World Anti-Doping Agency will have to face what to do about children genetically engineered to be faster, stronger, and more coordinated from birth. Take the mutation carried by someone like Eero Mantyranta (or the myostatin gene mutation that has produced a super-muscular baby in Germany) and imagine couples who decide to have children and choose to incorporate a mutation like Mantyranta's mutation in their offspring. The kids will never have been given the chance to turn down their performance enhancing genotypes. They may even have only naturally occurring enhancements - just not ones their own parents possess. Lots of performance-enhancing genetic variations are naturally occurring. We let people who by chance naturally get great genetic variations from their parents to compete at the Olympic level. Should people be banned from Olympic sports because their parents gave their kids the same exact variations using genetic manipulations of sperm or eggs or freshly fertilized embryos? If so, why?

Andy Miah argues that genetic enhancement ought to be allowed but genetically enhanced athletes ought to compete in separate categories.

Gene therapies hold so much promise for helping humanity, Dr. Miah says, that he has urged the WADA not to treat them simply as a new form of illegal doping. For example, gene therapy potentially could be used to repair the injured muscles of athletes. Would that use also be illegal? "It's that kind of boundary that's unclear from the present rulings," he says. By making genetic modification illegal, athletes may seek out "rogue scientists," he says. "If we do prohibit it, we push it underground, and we don't know what athletes are doing. They don't know what they're doing." If we regulate instead, "we can try to make sure they're doing it in a safe manner," he says.

Miah points to paralympics competitions where people with different kinds of disabilities compete in different classes. But there is an more striking way in which athletes have been put into different classes based on innate abilities: the division of athletes by sexes. Men have an innate advantage in musculature and even in the strength of some connective parts (e.g. the weaker Anterior Cruciate Ligament in women makes the frequency of ACL injuries much higher in women than in men). Most people (aside from some feminists) accept it as normal that men and women compete in separate groups in most sports. Why shouldn't we take the same approach with genetically modified athletes?

Shannon Klie has an excellent Better Humans article that reviews a number of the recent discoveries of genetic variations which enhance musculature and performance. Klie quotes the argument of USCD cancer research and WADA board member Theodore Friedmann, MD that sports is threatened by a loss in the belief of spectators that the contests are a measure of innate abilities and developed skills.

But while Friedmann thinks that it's inevitable that genetic therapies will be incorporated into international sports, he worries about their effect on the nature of sport. He says that instead of a feat of athleticism being the result of skill, training and dedication, in the future people will wonder if it's a simple product of bioengineering. "It's a threat to sport as we know it," he says.

But I think Friedmann is overlooking two obvious points:

  • As we learn more about existing genetic variations that show just how much individuals differ in their genetic potential the public will come to realize just how much of superior athleticism is due to factors that the athletes have no control over: their own genetic endowment. We will be seen as innately very unequal from each other in physical abilities for genetic reasons that do not reflect on our drive or personal conscious choices. Once DNA sequencing becomes cheap sports announcers will compare competitors in terms of their genetic advantages and disadvantages.
  • Tens or hundreds of millions of people already enjoy watching sports that have a very large element of engineering team competition as part of the total competition. The engineering competitions range across sports and encompass designs of shoes, bicycles, race cars, race boats, sail boats, and countless other items used in a variety of sports.

Once it becomes safe and easy to do genetic enhancement a large fraction of the population will choose to genetically engineer their bodies to improve their looks, strength, resistance to infections, and a great many other qualities. To keep genetic engineering out of professional sports will then require some small fraction of the human population to keep itself in "wild type" state so that "natural" sports can continue to be practiced. My guess is that most potential athletes will decide that is a sacrifice that is too large to be worth it. If existing sports organizations keep their bans on genetic enhancement in effect then new sporting organizations will be formed to hold competitions between the genetically enhanced and the crowds will shift their interests toward the competitions between genetically enhanced athlets. WADA is a reactionary organization in an ultimately futile fight for a type of sports that will eventually be seen as anachronistic.

What is the psychological basis of the opposition to genetic enhancement of athletic performance? Is genetic enhancement seen as a threat to athletics as a sort of folk religion aimed at the worship of what humans can accomplish if they will their selves to power with strong free wills? Or is genetic enhancement more threatening because it is perceived as reducing the role for chance in determining outcomes? Or is it born more from a desire to see human bodies and not machines as the height of human accomplishment? What do you see as threatened by genetic enhancement?

By Randall Parker 2004 August 23 12:00 AM  Biotech Athletics
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2004 August 20 Friday
People With Asymmetric Bodies More Aggressive?

Beware people with uneven body shapes.

Research showed that the farther certain paired body parts were from symmetry – if one ear, index finger or foot was bigger than another, for example – the more likely it is was that a person would show signs of aggression when provoked. The symmetry effects were different in men and women, however.

While the findings may seem strange, there is a plausible explanation, said Zeynep Benderlioglu, co-author of the study and a post-doctoral researcher at Ohio State University.

The physical attraction people have to highly symmetrical faces in the opposite sex is very likely the product of natural selection. The symmetry is a sign of health and reproductive fitness. This latest study shows that asymmetry is even a proxy for a tendency toward impulsiveness.

Body asymmetry is thought to be an indicator that the fetus was under stress (e.g. toxins, nutrient deficiencies or perhaps more stress hormones released by the mother) during development. The visible physical asymmetry is thought to be a proxy for malformations of other less visble parts of the body including the brain.

The study involved 100 college students (51 men and 49 women). Researchers measured differences in size of several paired body parts, including finger length, palm height, wrist diameter, elbow width, ear height and width, foot breadth and ankle circumference. The sum of all the differences in these pairs gave researchers a score of asymmetry for each participant.

The students, who were all volunteers, were told they were going to participate in a study of persuasive ability. They were given a list of phone numbers to call and attempt to raise funds for a fictitious charity organization. But they were actually calling two people involved in the study who were given instructions about how to respond to the study participants.

One of the people the participants called seemed friendly and amenable to giving, but said he didn’t have money to donate. But the second charity target was confrontational. He directly challenged the caller and the worthiness of the donation.

The researchers had rigged the phones so they could measure how hard the participants slammed the receiver down after the call – this was a measure of reactive aggression.

Results showed that, in general, the more asymmetry the participants showed in their body parts, the more force they used when hanging up the phone.

But there were also interesting gender differences.

In men, asymmetry was related to a more aggressive response when ending the phone call under the low-provocation condition – when the person simply didn’t have money to give. But there was no such association between asymmetry and aggression in the high-provocation condition -- when they talked with the rude charity target.

For women, it was just the opposite – there was no relation between asymmetry and aggression with the low-provocation caller, but women with higher asymmetry scores used more force when hanging up from the rude, high-provocation caller.

Benderlioglu said these results probably have to do with the different ways men and women respond to provocation in general.

“Research has shown that men are quicker to anger than are women,” she said. “But while unprovoked men are generally more aggressive than women, the gender differences either disappear under provocation, or women may actually become more aggressive than men.”

High testosterone made men more angry during low-provocation phone calls. But the opposite was the case with women.

Men with high levels of testosterone used more force when slamming down the phone only under the low-provocation condition. In women, higher levels of testosterone were associated with higher aggressiveness only under the high-provocation condition.

One of the most interesting twists is that confrontational behavior does not always elicit an aggressive response. But this makes sense intuitively. In many situations a person who shows fear is more likely to be attacked than a person who acts menacingly.

Update: Also see my related post Premature Birth Produces More Lasting Brain Effects In Boys. Factors that cause less than optimal conditions during pregnancies have the potential of creating behavior problems that will endure for life. Drug abuse, malnutrition, physical abuse of pregnant women, and other stressors on developing fetuses exact a very long term cost to society as a whole.

By Randall Parker 2004 August 20 04:56 PM  Brain Violence
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Variations In Sun's Magnetic Field Influence Climate Trends?

Some climate scientists are arguing that the intensity of cosmic rays from distant exploding stars varies over time to cause long term changes in Earth's climate.

The idea will also be backed up by Nigel Marsh of the Danish Space Research Institute in Copenhagen.

Marsh and his colleagues looked at satellite images of low-altitude clouds from the past 20 years. They noticed that the pattern of global cloud cover varied over a time scale of roughly 10 years, and found a correlation with the 11-year sunspot cycle.

The more sunspot activity there is, the greater the strength of the sun's magnetic field. And cosmic rays are deflected by this field, so the stronger it is, the fewer rays reach the Earth, and the lower the cloud cover.

The Copenhagen team also found that clouds were scarce near the equator and thicker towards the tropics. According to Marsh, this is because cosmic rays have a hard time punching through Earth's magnetic field at the equator, but can leak in through the relatively weaker field nearer the poles.

The Sun is known to go through periods of much lower sunspot activity. One such period is known as the Maunder Minimum coincided with the "Little Ice Age" back in 1645-1715. During low sunspot periods it is thought that the Sun puts out less light energy and hence causes a cooling effect on Earth's climate. But this theory about cosmic rays basically provides another way that sunspot activity fluctuations can cause climate fluctuations: low sunspot activity reduces the magnetic field of the sun and therefore lets more cosmic rays through to the Earth to increase cloud cover and therefore to cause reflection of light before it reaches the surface.

One of the proponents of this theory, Nir Shaviv of the Hebrew University in Jerusalem, Israel has an interesting set of web pages arguing his view point. See his graph of Earth climate cycles and Milky Way galaxy spiral arm rotations.

There are indications that Cosmic Rays affect climate on Earth. If this is true, then one should expect climatic variations while we roam the galaxy. This is because the density of cosmic ray sources in the galaxy is not uniform. In fact, it is concentrated in the galactic spiral arms (it arises from supernovae, which in our galaxy arise predominantly from the death of massive stars, which in turn form and die predominantly in spiral arms). Thus, each time we cross a galactic arm, we should expect a colder climate. Current data for the spiral arm passages gives a crossing once every 135+/-25 Million years.

A record of the long term variations of the galactic cosmic ray flux can be extracted from Iron meteorites. It was found in this work that the cosmic ray flux varied periodically (with flux variations greater than a factor of 2.5) with an average period of 143 +/- 10 Million years. This is consistent with the expected spiral arm crossing period and with the picture that the cosmic ray flux should be variable. The agreement is also with the correct phase.

The main result of this research, is that the variations of the flux, as predicted from the galactic model and as observed from the Iron meteorites is in sync with the occurrence of ice-age epochs on Earth. The agreement is both in period and in phase: (1) The observed period of the occurrence of ice-age epochs on Earth is 145+/-10 Myr (compared with 143 +/- 10 Myrs for the Cosmic ray flux variations), (2) The mid point of the ice-age epochs is predicted to lag by 31 +/- 8 Myr and observed to lag by 33 +/- 20 Myr. This can be seen in the following graph:

I am in no way qualified to comment on the plausibility of this particular theory. But there have been a number of surprising discoveries in recent years of unexpected factors that influence climate (see my Trends Climate category archives for interesting examples). This leads me to suspect that current climate models are too simple to use with a high level of confidence when making public policy decisions. There is a large degree of uncertainty when we look ahead at the future of Earth's climate.

By Randall Parker 2004 August 20 03:42 PM  Climate Trends
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Study Finds Embryo Screening Does Not Boost Birth Defect Rate

The use of Preimplantation genetic diagnosis (abbreviated PGD or PIGD) does not increase risk of birth defects.

The Reproductive Institute of Chicago study looked at 754 babies born after IVF pregnancies where preimplantation genetic diagnosis was used.

It found they were no more likely to suffer birth defects than babies born after natural pregnancies.

It is not clear that the BBC reporter got this story exactly correct. First of all, the risk of in vitro fertilization (IVF) pregnancy is hard to compare to natural pregnancy because people using IVF already have a problem getting a pregnancy started. IVF users tend to be older on average and to have problems starting and bringing a pregnancy to completion. I suspect that the original finding of the paper might support the idea that IVF with PIGD is no riskier than IVF alone. But I kinda doubt that they could prove that IVF is no riskier than normal pregnancy started with sexual intercourse.

The abstract does not provide enough details. Also, the Reproductive Institute referred to above is really the Reproductive Genetics Institute. They do not appear to have a press release on this paper on their site. (Though their site's layout could really stand for some improvement to make it easier to find stuff on it)

Once DNA testing becomes much cheaper and the significance of many more genetic variations becomes known expect to see embryo screening to become much more widely used. The advantage is that it allows people to control which genetic variations they pass along to their offspring. A person apprised of what is on each of their chromosomes is likely to decide for each pair of chromosomes that a particular one of each pair would make a much better choice to pass on to offspring. The decisions will be made for reasons of hair color, eye color, intelligence, personality, risk of skin disease, risk of depression, facial shape, height, tendency toward obesity, or countless other qualities.

One interesting aspect of this latest report may not be immediately apparent: On day 3 an embryo has 8 cells and one is removed to use to do the PIGD testing for genetic defects. Well, the embryo can continue to grow without problems even though one cell has been removed from it. Think about that 1 cell that has been removed. It could be stored. It could be grown up to produce a large number of cells to use in stem cell therapies. Currently there is a lot of opposition to the use of embryonic stem cells in large part because the creation of embryonic stem cell lines is seen as a procedure that destroyed a potential life. But if that single removed cell could be cultured and grown up to produce lots more additional cells then no potential life would need to be extinguished. Any IVF pregnancy could also produce useful stem cells.

Also see my previous post Fetuses Give Pregnant Women Stem Cell Therapy for another possible way around problem of the ethical opposition to embryonic stem cell therapy.

By Randall Parker 2004 August 20 01:33 PM  Biotech Reproduction
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2004 August 18 Wednesday
Gene Knock-Outs Reduce Age-Related Bone Loss, Obesity In Mice

Weight gain and thinning of bones was partially prevented in mice by suppression of a gene.

ROCHESTER, Minn. -- Weight gain and bone thinning may seem to be natural complications of aging in humans and mice. Now, Mayo Clinic researchers have discovered a genetic basis for this physical decline -- and have suggested that “silencing,” or turning off a specific gene complex, may halt weight gain and control bone loss. The team found laboratory mice without this gene function have 70 percent less body fat and exhibit the dense bones and lean bodies of young mice.

The researchers dub the mice “Adonis,” after the youth in Greek mythology who had an ideal, youthful physique. Their report appears in the August issue of FASEB Journal published by The Federation of American Societies for Experimental Biology. The work connects the function of genes important in the immune response with processes of physical development and aging. This functional linkage between the immune system, and on body plan and aging, was first described in fruit flies through the study of a gene called Toll. The mouse and human version of Toll is TLR4, which stands for “Toll-like Receptor 4.”

Mutations in either of two genes prevented much of age-related bone loss and increase in fat.

The Experiment
The group of mice under investigation was genetically the same as the healthy control mice except that they had mutations in TLR4 or in a signaling gene it needs called CD14. Bone density, bone mineral content, bone area, total body mass, fat body mass and fat-free body mass were tested and analyzed by computer with specialized software. Bone growth in the legs was evaluated. Physical activity was tracked with a computerized observational system. Food and water were provided throughout the experiment. Muscle mass was determined, but muscle strength was not checked. Eighteen tests were given to all mice to periodically check for bacteria, viruses and toxins.

Researchers found that the mutant mice whose TLR4 was silenced had:

  • Greater bone mineral content at 20 weeks of age compared to normal mice -- and that this relationship increased as both groups aged.
  • Larger bones at 20-24 weeks of age.
  • 70 percent less body fat than the control group as they grew and aged.

It would be interesting to know whether these mice will live any longer or shorter than wild type mice.

It might then seem logical for life extension advocates to advocate the development of drugs to silence TLR4 (perhaps based on DNA anti-sense technology or RNA interference technology). But keep in mind that TLR4 plays an important role in spurring the immune response to dangerous blood infections.

Background
Immunologists think that stimulation of TLR4 is a crucial first step in mounting an immune response in mice and in humans. TLR4 usually responds to endotoxins, which are carried by the bacteria that cause sepsis, a dangerous blood infection. Sepsis occurs in 400,000 people in the United States annually; as many as half may die. Because of its seriousness, Mayo Clinic immunology researchers were interested in understanding the mechanism of sepsis.

Perhaps this can be finessed somehow. If compounds that could act in place of TLR4 could be found then those compounds could be delivered to patients whose own TLR4 genes have been suppressed by a DNA anti-sense drug. Alternatively, perhaps a drug can be developed that will suppress TLR4's effects on fat cells or bone cells (aside: does TLR4 down-regulate osteoblasts or up-regulate osteoclasts?) without interfering with immune response.

Another possibility is to suppress whatever factors might be up-regulating TLR4 in aging bodies. But my guess is that the most likely factor for the cause of TLR4 expression in old folks is an accumulation of damage that causes an inflammation response. Generally speaking, as people age more of their inflammation and repair genes are activated. Possibly we can selectively suppress subsets of those genes to achieve some slowing of aging. But what we really need to do most of all is to be able to repair all the things that are breaking. Regular readers know that this means we need to develop therapies based on SENS (Strategies for Engineered Negligible Senescence).

By Randall Parker 2004 August 18 02:00 PM  Aging Studies
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2004 August 17 Tuesday
Glass Coating Reflects More Heat At Higher Temperatures

A vanadium dioxide derivative with a precise amount of added tungsten automatically lets in more infrared light when the temperature is cold than it does when the temperature is warmer.

Soaring air conditioning bills or suffering in the sweltering heat could soon be a thing of the past, thanks to University College London chemists.

Reporting in the Journal of Materials Chemistry, researchers reveal they have developed an intelligent window coating that, when applied to the glass of buildings or cars, reflects the sun’s heat so you don’t get too hot under the collar.

While conventional tints block both heat and light the coating, which is made from a derivative of vanadium dioxide, allows visible wavelengths of light through at all times but reflects infrared light when temperature rise over 29 degrees Celsius. Wavelengths of light in this region of the spectrum cause heating so blocking infrared reduces unwanted rays from the sun.

The coating’s ability to switch between absorbing and reflecting light means occupants benefit from the sun’s heat in cooler conditions but when temperatures soar room heating is reduced by up to 50 per cent.

Professor Ivan Parkin, of UCL’s Department of Chemistry and senior author of the paper, says:

“Technological innovations such as intelligent window coating really open the door to more creative design. The current trend towards using glass extensively in building poses a dilemma for architects. Do they tint the glass, which reduces the benefit of natural light or face hefty air conditioning bills?

Professor Parkin says the next item on their research agenda is to investigate the durability of the coating and also to change its color.

Better materials for windows, walls, ceilings, and doors could greatly reduce the amount of energy used for heating and cooling.

By Randall Parker 2004 August 17 06:35 PM  Energy Tech
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2004 August 16 Monday
Thin Film Fuel Cells May Obsolesce Large Electric Plants

Small thin film fuel cells may obsolesce large electric power generating plants based on fossil fuels.

"By using materials science concepts developed in our superconductivity research and materials processing concepts in our semiconductor research, we are able to reduce operating temperatures, eliminate steps and use less expensive materials that will potentially revolutionize from where we derive electrical energy," said Alex Ignatiev, director of TcSAM and distinguished university professor of physics, chemistry and electrical and computer engineering at UH. "While there are a number of fuel cell research programs at the university, ours focuses on the application of thin film science and technology to gain the benefits of efficiency and low cost."

Compared to the macroscopic size of traditional fuel cells that can take up an entire room, thin film SOFCs are one micron thick – the equivalent of about one-hundredth of a human hair. Putting this into perspective, the size equivalent of four sugar cubes would produce 80 watts – more than enough to operate a laptop computer, eliminating clunky batteries and giving you hours more juice in your laptop. By the same token, approximately two cans' worth of soda would produce more than five kilowatts, enough to power a typical household.

Keeping in mind that one thin film SOFC is just a fraction of the size of a human hair with an output of 0.8 to 0.9 Volts, a stack of 100 to 120 of these fuel cells would generate about 100 volts. When connected to a homeowner's natural gas line, the stack would provide the needed electrical energy to run the household at an efficiency of approximately 65 percent. This would be a twofold increase over power plants today, as they operate at 30 to 35 percent efficiency. Stand-alone household fuel cell units could form the basis for a new 'distributed power' system. In this concept, energy not used by the household would be fed back into a main grid, resulting in a credit to the user's account, while overages would similarly receive extra energy from that grid and be charged accordingly.

"The initial applications of our thin film fuel cell would probably be for governmental entities," Ignatiev said. "For instance, once the preliminary data satisfies the Department of Defense, we could see our fuel cell research in action in the backpacks of soldiers, replacing heavy batteries to power their computers and night vision goggles and such.

"NASA also is very interested in this research mainly because of the weight and size factors," he said. "Thin film SOFCs offer light, compact, low mass properties of significant interest to them. Right now, the shuttle routinely uses fuel cells that require ultrapure oxygen and hydrogen, use exotic materials and are massive and large. But the thin film SOFCs we are developing at UH are not as sensitive to contaminants and are highly efficient in their design and lightweight size, which is ideal for space applications."

Inherent to the more efficient design of these "cool" fuel cells is quite literally the fact that they operate at a much lower temperature than other solid oxide fuel cells, yet do not need a catalyst. Despite their 60 to 70 percent efficiency, SOFCs, in general, operate at 900 to 1,000 degrees Celsius, a very high temperature that requires exotic structural materials and significant thermal insulation. However, the thin film solid oxide fuel cell has an operating temperature of 450 to 500 degrees Celsius, one half that of current SOFCs. This lower temperature is largely a result of the drastically decreased thickness of the electrolyte-working region of these thin film SOFCs and negates the need for exotic structural materials and extensive insulation. The lower temperature also eliminates the need for catalysts (known as reformers) for the fuel cell. All of these features indicate a reduced cost for the thin film SOFC and positive future impact on the fuel cell market.

Note that SOFCs would not obosolesce nuclear power plants. If nuclear power could be made cheaper than coal or natural gas electric power plants then nuclear plants might still have a future. But as a means to generate electricity from fossil fuels large centralized plants are probably going to be obsolesced by smaller cheap and highly efficient fuel cells that can be located quite close to the devices that run off of electricity.

I think a really nice energy future would be based on the use of sunlight to run artificial photosynthesis systems to generate synthetic hydrocarbons. Such systems could be either biologically based with genetically engineered plants or the systems could be based on non-living catalyst materials that are like photovoltaic cells but which drive the fixing of hydrogen with carbon. Another approach would be to run nuclear power plants to generate power to supply the power to run artificial photosynthesis systems. All these approaches could produce gaseous and liquid hydrocarbons for burning in fuel cells and in existing engines while we transition to fuel cells.

Update: See Tim Worstall's post Solid Oxide Fuel Cells where after analysing the work of Professor Ignatiev he opines:

Insolation is at roughly one horsepower per hour per square yard for seven equator equivalent hours per day just about anywhere with extensive human habitation. That's 5 or so KWatts per sq yard per day. What's the size of the average American houses' roof? 1,000 sq foot? 100 or so sq yards? 500 Kwatts a day? Solar cells with 30% efficiencies are out there (Berkeley, GaAs/GaN/InN). 150 KWatts. As I don't know the efficiency of a process to separate the hydrogen from the water, I'll assume 50%. OK, we've got 75 KWatts of usable power now. Our SOFC produces electricity at 60% efficiency: 45 KWatts per day of storable power. From land that's already in use for something else. Average US household daily electricity usage? 30 KWatts.

OK, OK, there's a number of leaps in those numbers but we are getting there, we really just on the cusp of being able to power a household from the ground it already occupies.

By Randall Parker 2004 August 16 02:47 AM  Energy Electric Generators
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Gene Variants Influence Schizophrenia, Cognitive Abilities

A variant in the GRM3 glutamate receptor gene may increase the risk for schizophrenia while simultaneously lowering cognitive ability.

Glutamate is a key neurotransmitter long thought to play a role in schizophrenia. The gene identified in this study makes the glutamate receptor (GRM3) which is responsible for regulating glutamate in synapses — spaces in between brain cells — where chemicals like glutamate transfer information from cell to cell. The amount of glutamate remaining in the synapse may have a downstream impact on cognition.

...

GRM3 alters glutamate transmission, brain physiology and cognition, increasing the risk for schizophrenia. To pinpoint the section of the gene responsible for these changes, scientists are exploring a region where the gene may differ by one letter at a location called SNP4. The normal variation is spelled with either an 'A' — the more common of the two — or a 'G'. Patients with schizophrenia are more likely to inherit an 'A' from either parent, indicating the 'A' variant slightly increases risk. The 'A' variant is also associated with the pattern of traits linked with the disorder. This was true in patients, their healthy siblings, and normal volunteers.

In the study, people with an 'A' variant have differences in measures of brain glutamate. In a postmortem study of brain tissue, the 'A' variant was associated with lower levels of the chemical that promotes gene expression for the protein responsible for regulating the level of glutamate in the cell. N-acetylaspartate, a measure of cell health evaluated through the use of MRI spectroscopy, was lower in 'A' participants. 'A' carriers had poorer performance on several cognitive tests of prefrontal and hippocampal function than people with the 'G' variant. The 'G' marker was associated with relatively more 'efficient' processing in the prefrontal cortex. Those who inherit the 'G' variant scored higher on verbal and cognitive tests than those who have two of the 'A' variant. Scientists think the less common 'G' variant may exert a protective effect against the disease.

People with schizophrenia and their healthy siblings share the inefficient brain physiology, and cognition patterns, which suggests a link to genetic risk, though the disease itself is most likely caused by a combination of genetic and environmental factors. The gene seems to affect the mechanism of memory encoding only as there was no genotype effect seen during retrieval in the memory tests.

What I find more interesting than the link to schizophrenia risk is that these two genetic variants differ in their impact on normal cognitive function. GRM3 SNP4 looks like it will turn out to be one of the locations in the human genome which have variations that produce different levels of intelligence. In the next 10 years expect to see the identification of dozens and perhaps even hundreds more of additional locations of genetic variants that influence intellectual abilities and personality. Declining costs of DNA testing will drive the rate of such discoveries up by orders of magnitude.

By Randall Parker 2004 August 16 02:21 AM  Brain Genetics
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2004 August 13 Friday
Genetic Screen Identifies Compounds That Might Slow Aging

Calorie Restriction (CR) diets that reduce calories about 35% below normal have been shown to increase average life expectancy across a large assortment of animal species (though the longevity enhancing effect of CR has not yet been confirmed in humans). The life extending effect of CR has been the subject of a great deal of research attention as researchers have sought to find compounds that will throw the body into a metabolic state that is like the CR state. The hope is that a drug could provide the same life extending effects but without the need to feel perpetually hungry and to look gaunt.

Some researchers have been comparing the pattern of gene expression found in mice on CR diets with the patterns of gene expression found in mice given a variety of drugs. Some already used drugs may induce a metabolic state that will extend life expectancy by the same mechanism that CR diets extend life expectancy.

Investigators from an international consortium of research institutes, including the Johns Hopkins Bloomberg School of Public Health, have identified compounds that mimic the effects of a low-calorie diet without changing the amount of essential nutrients.

The lack of PPARalpha prevented some of the changes in metabolism normally seen on a CR diet.

Lead author, J. Christopher Corton, PhD, with ToxicoGenomics in Chapel Hill, NC, examined the genetic changes that occur during calorie restriction in mice that were fed a diet for one month containing about 35 percent fewer calories than a normal diet. He explained that these genetic changes, which are referred to as a transcript profile, can be used like a bar-code to distinguish a unique profile from other genetic changes that occur in the body. The researchers compared the profile of calorie restriction with the profiles produced by compounds known to have some properties similar to calorie restriction, including the ability to suppress factors that lead to a number of diseases.

The compounds that shared the greatest similarities in the bar codes included those that have activity toward receptors of interest to the pharmaceutical industry. The receptors include those that are targeted by drugs used to treat high cholesterol and triglyceride levels. One of the receptors, called PPARalpha, is a target for drugs that are currently used to treat high cholesterol and triglyceride levels in people at risk for heart disease.

The investigators also compared responses in normal mice to mice that lack a functional PPARalpha to determine if PPARalpha was directly involved in any of the responses that are induced by calorie restriction. They found that the PPARalpha-mutant mice lack many of the characteristics of calorie restriction, including changes in genes that may play important roles in heart disease and cancer. Calorie restriction is also known to protect animals from chemical exposure, and the investigators found that the protection afforded by calorie

It may turn out to be the case that some existing drugs that target PPARalpha are already benefitting their users by inducing a metabolic state that is similar to the state induced by calorie restriction.

The press release above does not indicate which cholesterol lowering drugs the researchers were using. However, my suspicion is that they were using statin drugs since statin drugs are known to activate PPARalpha. Well, Lipitor and Crestor users might be benefitting from CR-like effects on their bodies.

By Randall Parker 2004 August 13 04:14 AM  Aging Studies
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Quick Testosterone Muscle Boosting Makes Use Hard To Detect

The New Scientist reports on a surprising result where it was found that testosterone works so rapidl to boost muscle mass that athletes may be able to escape detection from blood tests by using testosterone for short periods.

The received wisdom is that testosterone must be injected weekly for at least 10 weeks. Yet sports scientist Robert Weatherby of Southern Cross University in Lismore, New South Wales, Australia, who conducted the study, found the biggest increase in performance came after just three weeks.

Taking testosterone for short periods only, taking smaller doses, or doing both, would reduce the chances of athletes getting caught by drugs testers. "Athletes have probably already figured this out, and we are just confirming that scientifically,"

More methods that increase athletic performance while leaving smaller chemical footprints will be found. It will becoe steadily more difficult to detect illegal drug use.

One factor that may shift the advantage back toward the anti-doping agencies is the identification of all the DNA sequence variations that have some effect on athletic performance. Once DNA sequences can be tested for each athlete it will become possible to state that for some athlete his performance exceeds his genetic potential and that therefore he must be cheating. But such DNA testing is still several years away and in the meantime banned performance boosting techniques will become harder to detect. So expect more successful cheating.

By Randall Parker 2004 August 13 03:27 AM  Biotech Athletics
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2004 August 11 Wednesday
Monkeys Turned Into Workaholics With Brain Gene Suppression

The future is going to be a very different place. We live on the verge of an age of genetically engineered emotion and motivation alteration.

Using a new molecular genetic technique, scientists have turned procrastinating primates into workaholics by temporarily suppressing a gene in a brain circuit involved in reward learning. Without the gene, the monkeys lost their sense of balance between reward and the work required to get it, say researchers at the NIH's National Institute of Mental Health (NIMH).

"The gene makes a receptor for a key brain messenger chemical, dopamine," explained Barry Richmond, M.D., NIMH Laboratory of Neuropsychology. "The gene knockdown triggered a remarkable transformation in the simian work ethic. Like many of us, monkeys normally slack off initially in working toward a distant goal. They work more efficiently – make fewer errors – as they get closer to being rewarded. But without the dopamine receptor, they consistently stayed on-task and made few errors, because they could no longer learn to use visual cues to predict how their work was going to get them a reward."

Richmond, Zheng Liu, Ph.D., Edward Ginns, M.D., and colleagues, report on their findings in the August 17, 2004 Proceedings of the National Academy of Sciences, published online the week of August 9th.

Richmond's team trained monkeys to release a lever when a spot on a computer screen turned from red to green. The animals knew they had performed the task correctly when the spot turned blue. A visual cue--a gray bar on the screen--got brighter as they progressed through a succession of trials required to get a juice treat. Though never punished, the monkeys couldn't graduate to the next level until they had successfully completed the current trial.

As in a previous study using the same task, the monkeys made progressively fewer errors with each trial as the reward approached, with the fewest occurring during the rewarded trial. Previous studies had also traced the monkeys' ability to associate the visual cues with the reward to the rhinal cortex, which is rich in dopamine. There was also reason to suspect that the dopamine D2 receptor in this area might be critical for reward learning. To find out, the researchers needed a way to temporarily knock it out of action.

They used DNA antisense oligonucleotides which are short stretches of DNA sequence which match with a target gene to bind to it to prevent ts expression.

Molecular geneticist Ginns, who recently moved from NIMH to the University of Massachusetts, adapted an approach originally used in mice. He fashioned an agent (DNA antisense expression construct) that, when injected directly into the rhinal cortex of four trained monkeys, spawned a kind of decoy molecule which tricked cells there into turning-off D2 expression for several weeks. This depleted the area of D2 receptors, impairing the monkeys' reward learning. For a few months, the monkeys were unable to associate the visual cues with the workload – to learn how many trials needed to be completed to get the reward.

Monkeys are usually procrastinators. But the lack of D2 receptors turned them into workaholics.

"The monkeys became extreme workaholics, as evidenced by a sustained low rate of errors in performing the experimental task, irrespective of how distant the reward might be," said Richmond. "This was conspicuously out-of-character for these animals. Like people, they tend to procrastinate when they know they will have to do more work before getting a reward."

Using the same technique to turn off NMDA receptors did to increase motive to work for a reward.

To make sure that it was, indeed, the lack of D2 receptors that was causing the observed effect, the researchers played a similar recombinant decoy trick targeted at the gene that codes for receptors for another neurotransmitter abundant in the rhinal cortex: NMDA (N-methlD-aspartate). Three monkeys lacking the NMDA receptor in the rhinal cortex showed no impairment in reward learning, confirming that the D2 receptor is critical for learning that cues are related to reward prediction. The researchers also confirmed that the DNA treatments actually affected the targeted receptors by measuring receptor binding following the intervention in two other monkeys' brains.

And you can bet these researchers are thinking about how to use this technique on people.

"This new technique permits researchers to, in effect, measure the effects of a long-term, yet reversible, lesion of a single molecular mechanism," said Richmond. "This could lead to important discoveries that impact public health. In this case, it's worth noting that the ability to associate work with reward is disturbed in mental disorders, including schizophrenia, mood disorders and obsessive-compulsive disorder, so our finding of the pivotal role played by this gene and circuit may be of clinical interest," suggested Richmond.

"For example, people who are depressed often feel nothing is worth the work. People with OCD work incessantly; even when they get rewarded they feel they must repeat the task. In mania, people will work feverishly for rewards that aren't worth the trouble to most of us."

Of course there is the classical science fiction threat of companies or governments taking over the minds of people to train them to work hard for the organization. The classical abuses will probably happen eventually and may lead to some pretty horrible outcomes. But I can easily imagine why lots of people (FuturePundit included) will choose to use drugs to motivate themselves. Looking at a big long work task? Know that you are hurting yourself by not working harder during the earlier stages? Well, take some DNA antisense drug and as your D2 receptor concentration drops you may find yourself working harder for distant rewards.

The problems with delivering DNA antisense oligonucleotides into cells will be solved in time as part of the larger push to develop techniques to deliver gene therapy into cells. Once the delivery vehicles are available the use of gene therapy will allowing temporary and permanent modification of personality, emotional state, and behavior on a scale that will make Prozac and Zoloft seem like primitive tools in comparison.

Update: And what about the economic impact of motivation enhancing gene therapy? While I'm bearish about the next 20 or 30 years due to aging populations and other demographic problems once we can raise IQ, increase motivation, and do other cognitive tweaking it is hard to see how economic output will not be greatly increased. Raising IQ is going to be harder to do than motivation alteration. But just reducing the amount of procrastination would be a big boost to productivity. Add in rejuvenation therapies, IQ enhancement of progeny (which will be easier to do than IQ enhancement of adutls), and even cognitive enhancement of adults and in a longer time frame the human part of the economic productivity equation looks much rosier. What is harder to predict is just when these various capabilities will be available.

Update II: Note that the level of motivation varies greatly from one person to the next. Also, some people are better set up to pursue longer term goals and others need more immediate rewards to get off their duffs and do anything. This latest result suggests a possible reason: differing levels of expression of genes that control dopamine D2 receptor concentrations. Once offspring genetic engineering becomes possible will people opt to have children who are more motivated than they are? Also, will employers surreptitiously take samples of DNA from job applicants to decide which applicants will be the hardest workers? Will some applicants even go so far as to state that while their natural DNA sequences tend to make them slackers and procrastinators they have permanently altered their personalities to turn themselves into workaholic maniacs? Will applicants even supply suitably certified medical records as evidence of their altered state? It all seems very plausible to me...

By Randall Parker 2004 August 11 11:57 AM  Brain Emotion Alteration
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2004 August 10 Tuesday
Premature Birth Produces More Lasting Brain Effects In Boys

Permanently smaller brain sizes in premature babies are an especially serious problem with premature boys.

STANFORD, Calif. – Kids on a playground can be hard to tell apart. But those who were born significantly preterm may be struggling with a hidden handicap that sets them apart from their peers: specific areas of the brain that are smaller than normal, even years later.

A collaborative study between the Stanford, Yale and Brown medical schools compared the brain volumes of two types of 8 year olds: those born prematurely and those born full-term. The researchers found significant, lingering reductions in the areas of the cerebral cortex responsible for reading, language, emotion and behavior. Even more surprising, the researchers discovered that the brains of preterm boys were more severely affected than were girls.

Boys born preterm do more poorly in school, have a harder time speaking, and are socially less able.

Doctors have known that preterm newborn boys fare more poorly than girls, but it’s not been clear why. The differences persist even after the early medical hurdles have been cleared: preterm boys struggle more than preterm girls with speech and language and have a harder time in academic and social situations as they grow older. Although it stands to reason that newborns making an unreasonably early appearance have smaller brain volumes than full-term babies, it wasn’t known that boys’ brains are more severely affected or that the disparity persists for so long.

By the description here among those born premature both males and females suffer from lower brain grey matter area. But only premature boys suffer from reduced white matter.

Reiss and Stanford co-investigator Shelli Kesler, PhD, collaborated with Laura Ment, MD, Betty Vohr, MD, and colleagues at Yale and Brown to compare brain-imaging data of 65 preterm children to 31 healthy, full-term children. Preterm babies were born at around 28 weeks of gestation and weighed about 2 pounds at birth. The study is published in the August issue of the Journal of Pediatrics.

“In the preterm group as a whole, we found the volumes of both grey matter and white matter were reduced,” said Reiss. “When we divided the preterm group by gender we found, bingo, the females had normal or preserved white matter volume, but the males’ volumes were reduced compared to their full-term peers.”

White matter is primarily made up of the axon connections and cells that facilitate communication between parts of the brain over distances, whereas grey matter consists of the cell bodies of the brain’s nerve cells, where signal processing and thinking happen. White matter lesions are responsible for the symptoms of multiple sclerosis, which compromise both mobility and cognitive functions.

“The adverse effects of preterm birth, such as hypoxia, expose the premature brain to an environment it’s not yet supposed to be in,” said Reiss. “Researchers have hypothesized that white matter might be preferentially affected, but sex-based differences have never been clearly shown until now.” Reiss speculates that girls may gain a measure of protection either through genetics or hormones.

The reduction in brain gray matter size that results from premature birth is also quite important because of the role that gray matter plays in determining intelligence. See my previous post Brain Gray Matter Size Correlated To Intelligence. Since intelligence is inversely correlated with criminality the increase in the number and survival rate of premature births may be boosting the crime rate.

The ability to save babies in troubled pregnancies using sophisticated medical technology is coming at a cost that includes not just the large sums of money spent on initial medical care but also the survival of babies that will grow up to be less intelligent, less socially adept, and economically less successful. At least some of the taxpayers money spent on funding the medical care that saves premature babies seems misplaced. The same number of dollars spent on isolating pregnant women who are cigarette smokers abusing drugs, and consuming alcohol would reduce the number of premature births and reduce the number of babies who will grow up with permanent mental and physical disabilities.

Premature births are now 12 percent of all births in the United States and cost $58,000 on average each as compared to $4,300 on average for normal births.

The five-year, $75 million awareness campaign was launched because premature births have risen 27 percent since 1981, resulting in tremendous cost to families, the medical system and society.

"Many of these babies come into the world with serious health problems. Those who survive may suffer lifelong consequences, from cerebral palsy and mental retardation to blindness," said Dr. Jennifer House, president of the March of Dimes.

Another factor contributing to the rising number of babies suffering from improperly developed brains is In Vitro Fertilization (IVF). Whether due to the age of the mother, other complications that prevented normal means of starting a pregnancy, or the IVF procedure itself, IVF pregnancies have at least double the rate of premature births.

There was limited evidence of a three times increased risk of having a very premature baby born prior to 32 weeks gestation.

In addition, there was just over a doubling of the risk of a "mildly" premature baby, born between 32 and 36 weeks.

What we need are technologies and practices that reduce the rate of premature births. So far most reproductive technologies appear to be making the problem worse. Technological advances are also making this problem worse by lowering the costs and increasing the availability of recreational drugs, alcohol, and cigarettes. My guess is that the reduction of exertion needed in daily life might also be contibuting to the problem. Technologies do not automatically make the human condition better. We need to develop technologies that adapt us better to those technologies that have caused many humans to behave in ways that are maladaptive and destructive.

By Randall Parker 2004 August 10 02:10 PM  Brain Development
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2004 August 09 Monday
Fluorescent Labelling Tracks Activity Of Multiple Genes In Single Cell

A team at UC San Diego has developed a technique in Drosophila fruit fly cells that can watch the level of gene expression for several genes at once in living cells.

“Multiplex labeling has allowed us to directly map the activation patterns of micro-RNA genes, which were hitherto undetectable,” says William McGinnis, a professor of biology at UCSD and co-principal investigator of the study. “Micro-RNAs were known to be important in development, but this is the first evidence indicating that these genes can control the embryonic body plan.”

Different colored fluorescent molecules can be used to identify transcripts from different genes in the same cell. It works even if one gene is much more active than another, because the amount of fluorescence of each color is quantified separately.

“When using the microscope to measure the fluorescence, the light is fanned out into a rainbow, and each color is read through a separate channel,” explains Bier. “That way if the light is 90 percent blue and ten percent yellow, it might look blue to the naked eye, but the microscope detects each color present.”

According to Bier, multiplex labeling fills a gap in developmental biologists’ toolkit between gene chips, which can identify several hundred gene transcripts at a time, but not their location, and methods that can reveal the identity and location of up to three gene transcripts simultaneously—though not if they are in the same cell. So far the researchers have used multiplex labeling to visualize the activity of up to seven genes at the same time, but they predict it will be possible to increase this to 50.

Newly developed, ultra-bright fluorescent molecules make the multiplex labeling technique possible. The fluorescent molecules were provided by Molecular Probes, Inc., and the company’s scientists also shared their expertise with the UCSD researchers. Developing an effective way to attach the fluorescent molecule to the RNAs complementary to the gene transcripts, and perfecting the overall labeling process were also pivotal in the development of the technique.

These researchers say additional work has to be done to adjust their technique to work in other species. They foresee its eventual use in the study of cancer tumor development and in other diseases and normal biological processes.

This research is yet example of how biologists are developing techniques that are speeding up the rate at which biological systems can be studied and understood.

By Randall Parker 2004 August 09 01:48 AM  Biotech Advance Rates
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2004 August 06 Friday
Key Reason Found For Paralysis After Spinal Cord Injury

Some types of spinal cord injury do not result in an immediate severing of the spinal cord and yet paralysis does eventually develop hours after the injury. A group of University of Rochester Medical Center researchers have pinpointed the reason for the neuronal cell death that produces paralysis: astrocyte support cells around a spinal injury respond to the injury by releasing ATP that signals to the neurons to kill themselves.

ATP, the vital energy source that keeps our body’s cells alive, runs amok at the site of a spinal cord injury, pouring into the area around the wound and killing the cells that normally allow us to move, scientists report in the cover story of the August issue of Nature Medicine.

The finding that ATP is a culprit in causing the devastating damage of spinal cord injury is unexpected. Doctors have known that initial trauma to the spinal cord is exacerbated by a cascade of molecular events over the first few hours that permanently worsen the paralysis for patients. But the finding that high levels of ATP kill healthy cells in nearby regions of the spinal cord that were otherwise uninjured is surprising and marks one of the first times that high levels of ATP have been identified as a cause of injury in the body.

The team found that excess ATP damages motor neurons, the cells that allow us to move and whose deaths in the spinal cord result in paralysis. Even more noteworthy was what happened when the research team from the University of Rochester Medical Center blocked ATP’s effects on neurons: Rats with damaged spinal cords recovered most of their function, walking and running and climbing nearly as well as healthy rats.

While the work opens up a promising new avenue of study, the work is years away from possible application in patients, cautions Maiken Nedergaard, M.D., Ph.D., the researcher who led the study. In addition, the research offers promise mainly to people who have just suffered a spinal cord injury, not for patients whose injury is more than a day old. Just as clot-busting agents can help patients who have had a stroke or heart attack who get to an emergency room within a few hours, so a compound that could stem the damage from ATP might help patients who have had a spinal cord injury and are treated immediately.

“There is no good acute treatment now for patients who have a spinal cord injury,” says Nedergaard. “We’re hoping that this work will lead to therapy that could decrease the extent of the secondary damage.

Anyone know how this team at Rochester blocked ATP's effects?

Neuronal support cells known as astrocytes release ATP that binds to the P2X7 receptor on neurons in such large concentraitions that the neurons interpret the binding as a signal to kill themselves in a cell suicide process known as apoptosis.

The findings come courtesy of the same technology that underlies the firefly’s mating habits. The firefly uses the enzyme luciferase to convert ATP to the glow it uses to light up and attract mates. Nedergaard’s team used the same enzyme to study the levels of ATP around the site of spinal cord injury, recording a very a bright signal for several hours around the site of injury.

While low levels of ATP normally provide a quick and primitive way for cells to communicate, Nedergaard says, levels found in the spinal cord were hundreds of times higher than normal. The glut of ATP over-stimulates neurons and causes them to die from metabolic stress.

Neurons in the spinal cord are so susceptible to ATP because of a molecule known as “the death receptor.” Scientists know that the receptor, also called P2X7, also plays a role in regulating the deaths of immune cells such as macrophages, but its appearance in the spinal cord was a surprise. ATP uses the receptor to latch onto neurons and send them the flood of signals that cause their deaths. Nedergaard’s team discovered that P2X7 is carried in abundance by neurons in the spinal cord.

The source of the ATP that kills the neurons provided another revelation for researchers. Star-shaped cells known as astrocytes, long considered simply as passive support cells for neurons in the nervous system, produce the high levels of ATP.

This discovery opens up several avenues of attack for the development of treatments. First of all, a method might be found to create a chemical environment around the astrocytes that looks like no injury has occurred. The astrocytes would not react to the injury because the chemical changes caused by the trauma effectively would be hidden from them. Another possibility would be a drug that would bind somewhere in astrocytes to suppress ATP release even though the astrocytes are getting external signals typical of trauma. At the intermediate point between ATP release and ATP binding methods of getting rid of the ATP might be employed. For instance, a drug that would catalyze the breakdown of ATP would eliminate the ATP after it was released by the astrocytes. Another possibility would be a drug that would compete with ATP to bind at the P2X7 site. Such a drug would need to be able to bind at the site while not triggering the receptor to change shape the way ATP does when ATP binds at the site. A fourth target area would be within the neurons. A cascade of events within neurons is set off by ATP binding to P2X7. It might be possible to find drugs that will interrupt that cascade at any number of stages to prevent cell death.

Discoveries that point in a clear direction for where to intervene in a disease process do not get as much attention as do actual treatments. Yet the identification of high quality targets for intervention greatly speed up the development of treatments. This discovery of the importance of ATP and the P2X7 receptor is probably going to lead to the development of a number of treatments that will prevent paralysis after many spinal cord injuries and other types of nerve injuries.

By Randall Parker 2004 August 06 02:13 PM  Biotech Therapies
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2004 August 05 Thursday
Earth-Like Planets May Be Rare Around Other Stars

So far most stars with planets oribiting around them have gas giants with highly elliptical orbits that prevent Earth-like planets from developing in less elliptical orbits.

Researchers from the UK believe that our Solar System could have formed differently from many other star systems, making places like our home much more rare in the Universe. After examining the 100 or so known extrasolar planetary systems, they found that they probably formed in a manner different from our own Solar System - in a way that's hostile to the formation of life. Planets could form in several different ways, and how the Earth formed is actually quite rare. It will still be 5 more years or so before astronomers have equipment with the resolution to confirm this.

Martin Beer thinks our solar system's planets may have formed in a way that is rare as compared to how planets form around most stars.

Martin Beer of the University of Leicester, UK, and co-workers argue that our Solar System may be highly unusual, compared with the planetary systems of other stars. In a preprint published on Arxiv1, they point out that the alien planets we have seen so far could have been formed by a completely different process from the one that formed ours. If that is so, says Beer, "there won't necessarily be lots of other Earths up there".

But current ways of detecting extrasolar (not from our solar system) planets are biased toward planets that are the sort being found so far.

It will take a few years to resolve this debate. The vast majority of extrasolar planets have been detected by measuring the way a star wobbles as a result of the gravity of an orbiting planet. This technique is inherently sensitive to heavy planets with short orbital periods, so those are the ones we are finding.

NASA's planned Kepler mission, to be launched tentatively in 2007, will be able to find more Earth-like planets.

Kepler also is being designed to detect planets in an orbit like the Earth at the same distance from their star as the Earth is from our Sun. With a measure of the orbit of the planet and with information about the planet's star, scientists can determine if the planet might have liquid water on its surface and, perhaps, sustain life.

This is a familiar story in one sense: More advanced scientific and technological capabilities are accelerating the rate at which scientific discoveries can be made. Any speculation about the odds on the existence of intelligent species around other planets is fairly uninformed at this point. We will have far more data about the frequency of extrasolar planets with promising conditions within several years and our ability to listen for signs of intelligent life will grow by leaps and bounds in the coming years as well.

Also see my recent post Will Intelligent Alien Life Be Discovered Within 20 Years?

By Randall Parker 2004 August 05 01:49 PM  Space Exploration
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2004 August 04 Wednesday
Long Droughts Were Common In American Great Plains Holocene Era

A team of Duke University researchers led by Jim Clark looking at core drillings found repeated dust bowl periods during "the mid-Holocene period of 5,000 to 8,000 years ago in parts of the Dakotas, Montana and western Minnesota".

PORTLAND, ORE. – Events like the great Dust Bowl of the 1930s, immortalized in "The Grapes of Wrath" and remembered as a transforming event for millions of Americans, were regular parts of much-earlier cycles of droughts followed by recoveries in the region, according to new studies by a multi-institutional research team led by Duke University.

Some of those prehistoric droughts in the northern Great Plains of what is now the United States also lasted longer than modern-day dry spells such as the 1930's Dust Bowl decade, according to sediment core studies by the team.

The group's evidence implies these ancient droughts persisted for up to several decades each. At their heights, prairie fires became uncommon because there was too little vegetation left to burn. The ages of charcoal deposits suggest instead that prairie fires occurred during intervening wet periods, with each wet-dry cycle lasting more than a century each.

Too many people believe that whatever weather one has seen in one's own lifetime is "normal". When weather suddenly veers from the pattern one has become accustomed to there is a human tendency to look for some exceptional cause such as human intervention. While human intervention may well be changing the climate the climate is not stable to begin with. We should expect large climate changes as natural.

Even the 1930s drought was not unique in modern times with the 1890s having gone through a drought period as well. But there was no John Steinbeck around to write a great novel about the 1890s drought let alone a silver screen adaptation of the story.

The regularity of these ancient droughts make much more recent Great Plains droughts in the 1890s and 1930s appear "unremarkable" by comparison, Clark said, even though the contemporary ones "walloped people."

The study did not speculate how the findings might relate to anticipated future climate change, when a surge of carbon dioxide from human activities is predicted to cause Earth's climate to warm appreciably.

"What we can say that is relevant is that these sort of drought cycles are common and most of the climate models predict increased aridity in continental interiors in the future," Clark said.

"One could speculate that the droughts could be all that much worse when you realize that it's not only climate change from changing CO2 content in the atmosphere, but also this natural variability out there that we don't fully understand."

Another drought on the Great Plains would wipe out agriculture over a large area and drive lots of people to migrate away from the region. It would also reduce river flow down the Missouri and Mississippi rivers and that would reduce the navigability of those rivers for shipping as well as reduce the amount of water that could be taken from the rivers for irrigation.

Whether or not humans reduce their emissions of green house gasses sooner or later the Earth is going to go through some large regional and eventually even global climate shifts. Those of us who live long enough to be around when rejuvenation therapies are developed will likely then live long enough to witness many large changes in Earth's climate.

However, not all the natural changes lying in our future will come to pass. At some point humans are going to start intervening to prevent some changes while perhaps in other cases humans will engineer other desired changes. Expect to see less desert in the future as some nations decide they would rather cause local climate changes to make their deserts more hospitable to human habitation. This will lead to international disagreements when other nations calculate how conversion of deserts to forests in some regions will cause changes they do not like in their own regions.

By Randall Parker 2004 August 04 12:31 PM  Climate Trends
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2004 August 02 Monday
Low Hormone Level Causes Mother Mice To Be Fearless

A reduction in corticotropin-releasing hormone (CRH) in mothers may explain the willingness of many mothers to fearlessly fight to protect their young.

MADISON - Everyone knows not to get between a mother and her offspring. What makes these females unafraid when it comes to protecting their young may be low levels of a peptide, or small piece of protein, released in the brain that normally activates fear and anxiety, according to new research published in the August issue of Behavioral Neuroscience.

"We see this fierce protection of offspring is so many animals," says Stephen Gammie, a University of Wisconsin-Madison assistant professor of zoology and lead author of the recent paper. "There are stories of cats rescuing their kittens from burning buildings and birds swooping down at people when their chicks are on the ground."

In terms of biology, it makes sense that mothers would lay down their own lives to protect their offspring, especially if it means the parents' genes will be passed down to the next generation, says Gammie. But he adds that despite all the observations and the theories explaining why mothers display this behavior - commonly known as maternal aggression - very little research has investigated the biological mechanisms that turn on this trait in new mothers.

"We've known for a long time that fear and anxiety decrease with lactation," explains Gammie. "Maybe it's this decrease that allows mothers to attack during a situation that normally would evoke a fear response."

Testing this hypothesis, the Wisconsin professor and his colleagues studied the link between maternal aggression in mice and levels of corticotropin-releasing hormone (CRH), a peptide that acts on the brain to control behavior.

About six days after a group of mice gave birth, the new mothers received injections containing either one of three doses of CRH or a saline solution with no amount of the peptide. Following each injection, which was given once a day for four consecutive days, the researchers returned the mother mice to their pups. Twenty-eight minutes later, the researchers removed the pups and introduced a male intruder.

Under normal conditions, female rodents will fiercely attack the males, says Gammie, noting that the males sometimes eat pups and that "the best defense for the mom is the offense."

For the study, only the mice that received either no dose or a low dose of the peptide displayed the expected behavior. As the levels of CRH increased, the number of attacks and the duration of them dramatically decreased.

The results show, for example, that while the mice with the lowest levels of CRH attacked more than 20 times for the duration of about 45 seconds, the mice with moderate levels of the peptide attacked about six times over about eight seconds. Mice with the highest levels of CRH didn't attack at all.

"When we put the male in the cage, some moms would just sit there. They weren't protective at all. If anything they were skittish. They showed a fear response," says Gammie.

The researchers note that altering the levels of the peptide appeared to affect only maternal aggression; normal maternal behaviors, such as nursing, were observed in all mothers both before and after the encounters with male mice.

Based on the results, Gammie says, "Low CRH levels appear to be a necessary part of maternal aggression. If you don't keep them low, you won't see this fiercely protective behavior."

Low CRH levels in some women suffering postpartum depression may explain child neglect and child abuse.

He adds that this finding - some of the first evidence suggesting a biological mechanism that enables parents, regardless of the potential danger, to defend their offspring - may also begin to explain why mothers occasionally neglect or harm their offspring.

"Postpartum depression in some individuals has been linked to higher levels of CRH release and an overly active stress response," explains Gammie. "If CRH needs to be low to see maternal protection of offspring, as our work suggests, then it explains why moms with high postpartum depression and high CRH not only may neglect, but also may abuse, their children."

At this point it doesn't sound like researchers have checked whether CRH production declines in nursing mothers.

Although the link between low levels of CRH and increased maternal aggression seems straightforward, Gammie admits that researchers do not know exactly how the process works. Perhaps lactation stimulates the brain to produce less CRH, he suggests. Or maybe the brain's cells simply become less responsive to the hormone.

It would be interesting to know whether nursing human mothers have lower CRH than mothers who use bottled formua and whether nursing mothers are less prone to postpartum depression, child neglect, and child abuse.

Perhaps at some point in the future women who neglect or abuse their kids will be given the option of either losing their children or taking drugs that make them feel more protective and caring toward their children.

A CRH blocker might make stressed out soldiers more aggressive.

“In war, soldiers are under high stress constantly,” says Tracy Bale, who works on CRH and depression at University of Pennsylvania. “In those cases, a CRH blocker might help.”

Given that the connection between soldiering and national security is more widely accepted than the connection between reproduction and national security it seems a safer bet to predict that while the use of drugs to reduce child neglect might be placed beyond the pale future soldiers will routinely be given drugs that control emotions and stress response on the battlefield. The benefits for soldiers will be more clearly understood and governments will be more motivated to tune the emotions of soldiers than of mothers. Drugs will be used to place upper limits on levels of stress response but when stress response is appropriate drugs may be used to heighten stress in order to increase alertness and motivation. Also, feelings of aggressiveness will be dialed up and down according to circumstances.

This reminds me: There is an on-going controversy about the use of drugs and other biotechnologies to enhance the performance of athletes. Well, the use of biotechnologies to enhance physical performance is yet another area where soldiers are going to have the edge on other potential users of human-altering tech. While sports organizations hold meetings and pursue increasingly more advanced methods to screen for the use of forbidden biotech military organizations will rush to embrace any tech that will improve the performance of soldiers.

By Randall Parker 2004 August 02 10:08 PM  Biological Mind
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2004 August 01 Sunday
What Will Be The Big Political Issues In Future Decades?

My readers, I have a speculative exercise for you: What will be the top 5 political issues 10, 20, 30, 40, and 50 years from now? Specify whether your list is for the United States, your own country, the world, or some other domain. For instance, if you think the United States won't exist as such 50 years from now you can state "North American Union" or Transatlantic Union". You can also specify more than one political unit for a list if you think the list will apply to more than one political unit. Post your own in the comments. I'll read what everyone posts and then come up with a new set of lists in a new post.

Here is my first set of guesses.

United States 2014:

  1. Rising costs of medical spending for old folks.
  2. Low salaries and low labor market participation rates for the bottom quarter of society.
  3. Islamic terrorism.
  4. United States debt to the rest of the world.
  5. Funding for rejuvenation research.

United States 2024:

  1. High costs of medical spending for old folks.
  2. Funding for rejuvenation research.
  3. The continuing decrease in the demand for the least skilled workers.
  4. Genetic engineering choices for offspring personalities, cognitive abilities, and physical attributes.
  5. Islamic terrorism.

United States, Europe, Australia, New Zealand, Canada 2034:

  1. Increased violence and other crime as all people become young, energetic, and motivated by youthful levels of desire once again. This will lead to a debate on whether governments should genetically reengineer the brains of criminals.
  2. Debate over reproductive rights as death due to aging becomes rare. Should people be allowed to have as many kids as they would like?
  3. Widening cognitive gap between the intellectually enhanced offspring and the older generations.
  4. Political rights of artificial intelligences and allowable programming for their motives and values.
  5. "Uplift" of other species with enhanced intelligence and allowable mental qualities of uplifted species. How smart are we going to allow our dogs to become? Even smarter than Border Collies?

World 2044:

  1. Migration of cognitive elites to other planets.
  2. Creation of new sovereign states by forced shifting of populations to separate cognitively incompatible groups. The sorting will be based not just on IQ (or even chiefly on IQ). Desires, values, religiosity, and other cognitive differences will become too great to allow harmonious existence of some groups with each other in the same society.
  3. Religious disagreements that escalate into armed conflicts will come about as a result of genetically engineered causes of differences in religious beliefs and values.
  4. Rivalry between large artificial intelligences.
  5. Debates about cognitive qualities allowable in new biological life forms.

World 2054:

  1. Humans controlled by artificial intelligences.
  2. Cyborgs that are smarter than any human.
  3. Wars between artificial intelligences.
  4. Possible devastation by nanotech goo.
  5. The high level of determinism achievable for the values and preferences of newly created intelligences both biological and artificial.

One theme running through these lists my view that cognition, whether human, animal, or artificial, will become the central issue of the future. What are allowable patterns of cognition? Once desires and values become programmable the Western rights-based view of the brain as a sovereign entity is going to run into the problem that technology will be able to be used to create intelligences that have little or no respect for the rights of others. Also, some intelligences will be engineered to have respect for the rights of only well-defined subsets of all sentient beings.

It is hard to guess the relative times at which various technologies will become available. For instance, as soon as personal DNA sequencing becomes cheap then each woman making a reproductive decision will be able to decide on a potential mate or sperm donor based on much more accurate projections of offspring intelligence and personality than is now the case. But when will DNA sequencing become cheap enough to provide a strong incentive for women to become aggressive practitioners of eugenics?

Also, when will rejuvenation therapies become available? That will determine how far the finances of Western nations deterioriate before rejuvenation therapies allow older folks to return to the labor force. When those rejuvenation therapies do become available how expensive will they be initially? How long will the expensive phase last and how much political conflict will it produce?

I have a harder time predicting when and if we will get wiped out by nanotech goo or taken over by artificial intelligences. The achievement of an artificial intelligence singularity where computers become smart enough to accelerate scientific and technological progress by orders of magnitude could make predictions about the 2040s and 2050s (or perhaps even the 2030s) impossible to make. Yet struggle between conflicting wills seems inherent to intelligences no matter how fast and powerful the intelligences become.

By Randall Parker 2004 August 01 02:20 PM  Trends Future Issues
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