Ray Kurzweil will be presenting his argument on why we are approaching the poit where technological advance starts accelerating so fast that society will be radically transformed in a very short period of time. Ramez Naam (a FuturePundit reader he tells me) will be presenting a talk called The Digital Biome about how sequencing all of the species of life will provide us with information that'll help us genetically reengineer the biosphere. A rather audacious line of argument.
Exponential technologies offer the promise not only of changing the human condition, but of radically altering the face of the planet on which we dwell. Within the next 20 years we will have sequenced the genome of every known species on the earth and tremendously advanced our understanding of how to utilize those genes and reprogram those organisms to alter the biosphere. Biosphere engineering will play a major role in overcoming current environmental and resource challenges, including finite reserves of fossil fuels and looming changes to the earth’s climate. That is just the beginning. An understanding of the complete biome genome will bring tremendous agility in combating future infectious disease outbreaks, in creating new sensors and manufacturing capabilities, and in revolutionizing food. Biosphere engineering and its underlying technologies will allow us to dramatically raise the population carrying capacity of the planet to tens of billions of individuals at least. With effective technology to sculpt the planetary biome, the limits of the number of humans that can live on the planet, and the quality of life of each, at tremendously higher than they appear to be today. This talk will explore some of the lower bounds of what's possible with control of the biome.
My own reaction: You know all those computer viruses? That's nothing compared to what will happen once really cheap microfluidic devices combined with really easy-to-use software enables teenagers to create new lifeforms. Throw in countries (and business interests) competing with each other by releasing highly well crafted organisms that reengineer the climate and ecosphere in ways that conflict with the national interests of other governments. In other words: The result is probably not going to be utopian.
As for raising the carrying capacity of the planet to tens of billions of people: If we raise our carrying capacity that high and then the number of humans on the planet increases into the tens of billions then we will end up returning to a Malthusian Trap. See Gregory Clark's A Farewell to Alms: A Brief Economic History of the World for an overview of why humanity spent most of its existence in Malthus' trap and how most of us have escaped it - at least for now. If we end up needing to support tens of billions of people then I think a return to that Malthusian Trap is inevitable. Either humanity eventually controls its growth or we run out of supplies once we've harnessed most of the solar system (and it takes too much mass and energy to leave to get more resources elsewhere).
If we are lucky or smart then in the future we will:
I think the odds are against us being that lucky and smart. I hope I'm wrong.
Clive Thompson argues voice phone calls are dying and deserve to die.
According to Nielsen, the average number of mobile phone calls we make is dropping every year, after hitting a peak in 2007. And our calls are getting shorter: In 2005 they averaged three minutes in length; now they’re almost half that.
This jibes with my experience. I rarely use the phone for voice calls and then mostly for people who for some bizarre reason have phones that can't handle SMS or email messages.
One obvious problem with voice phone calls is the need for both sides to be available at the same time. As Thompson points out, voice calls are more emotionally demanding. They pull us away from what we have in front of us (whether physically or more abstractly in front of us) to focus on trying to emotionally read what someone else is saying, when to interrupt with our one responses (harder when you can't see the other person's face), and whether we are being understood.
I find that when someone reaches me on the phone and I answer in case it is important then the result is often awkward. Sometimes I find out the purpose of the call is not important, that the person calling is just trying to kill time, and the call is not worth interrupting a conversation I'm having with someone I'm with. The caller then feels slighted when I beg off and ask them to call later.
Then there is the inefficient caller. They talk slowly, pause, provide too much set-up for their key message. The same person could provide the same information much more compactly in an email or SMS message. Same happens with voice mails. I want a way to tell the voice mail program to speed up playback and cut out pauses.
Parenthetically, I'd like the same capability to speed up Google Tech Talks and other lectures on YouTube (e.g. the rate of delivery in this video lecture is too slow. I've come across occasional political video sites that let you speed up playback. So this is technically possible.
Will video phone calls with phones like the HTC Evo 4G reverse the trend away from phone calls? You going to be more inclined to call people once you can watch their faces during the phone call? Or will Android's messaging features such as GMail integration make you even less inclined to do voice calling?
The number of Amish in North America has doubled since 1991 and their distinctive communities can now be found in Canada as well as 28 U.S. states, including unlikely ones like Texas and Maine.
That was a 19 year doubling. But their growth rate has increased and the next doubling will only take 14 years. If they keep that up they'll hit 1 million in 2038 and 2 million in 2052. By 2064 they could hit 4 million but still likely less than 1% of the US population at that time. It'll take them till 2078 before they are solidly over 1% of the American population at current rates.
My prediction: Groups that have high fertility will be selected for until the world human fertility decline reverses. Only a world dictatorship might prevent runaway population growth.
Naturally I flash on Weird Al Yankovic singing Amish Paradise. He's partying like its 1699.
The quickest, best way to slow the rapid melting of Arctic sea ice is to reduce soot emissions from the burning of fossil fuel, wood and dung, according to a new study by Stanford researcher Mark Z. Jacobson.
Since soot is bad for human health soot emissions reduction ought to go the head of the line of methods for cutting global warming. Even people who question the anthropogenic global warming theory should be able to see soot reduction as good public policy.
Only carbon dioxide causes a bigger warming effect.
His analysis shows that soot is second only to carbon dioxide in contributing to global warming. But, he said, climate models to date have mischaracterized the effects of soot in the atmosphere.
Because of that, soot’s contribution to global warming has been ignored in national and international global warming policy legislation, he said.
"Controlling soot may be the only method of significantly slowing Arctic warming within the next two decades," said Jacobson, director of Stanford’s Atmosphere/Energy Program. "We have to start taking its effects into account in planning our mitigation efforts and the sooner we start making changes, the better."
One estimate puts the number who die in the US each year from diesel soot at 21,000 people. Soot boosts the risk of lung cancer, heart disease, and other diseases. Soot elevates blood pressure. So I'm very keen to cut soot emissions.
A reduction in soot emissions would cool the Arctic.
Jacobson found that eliminating soot produced by the burning of fossil fuel and solid biofuel could reduce warming above parts of the Arctic Circle in the next 15 years by up to 1.7 degrees Celsius. For perspective, net warming in the Arctic has been at least 2.5 degrees Celsius during the last century and is expected to warm significantly more in the future if nothing is done.
The most immediate, effective and low-cost way to reduce soot emissions is to put particle traps on vehicles, diesel trucks, buses, and construction equipment. Particle traps filter out soot particles from exhaust fumes.
Soot could be further reduced by converting vehicles to run on clean, renewable electric power.
Biofuels burned by poor people in villages of undeveloped countries kills many more people than fossil fuel soot.
Jacobson found that although fossil fuel soot contributed more to global warming, biofuel-derived soot caused about eight times the number of deaths as fossil fuel soot. Providing electricity to rural developing areas, thereby reducing usage of solid biofuels for home heating and cooking, would have major health benefits, he said.
Short of electrification distribution of inexpensive but highly efficient wood-burning stoves could make a big difference.
A new Brigham Young University study adds our social relationships to the “short list” of factors that predict a person’s odds of living or dying.
In the journal PLoS Medicine, BYU professors Julianne Holt-Lunstad and Timothy Smith report that social connections – friends, family, neighbors or colleagues – improve our odds of survival by 50 percent. Here is how low social interaction compares to more well-known risk factors:
- Equivalent to smoking 15 cigarettes a day
- Equivalent to being an alcoholic
- More harmful than not exercising
- Twice as harmful as obesity
“The idea that a lack of social relationships is a risk factor for death is still not widely recognized by health organizations and the public,” write the PLoS Medicine editors in a summary of the BYU study and why it was done.
You could join a sun bathing club to get enough vitamin D. Double bonus points. Though skin cancer could be a problem. Or join a hunter-gatherer tribe and eat a natural Paleo Diet. Again, two birds with one stone.
Stop smoking or get some friends. If you are a smoker who opts to get some friends choose fellow smokers so that non-smokers don't have to breath in the second hand smoke.
Individuals with adequate social relationships have a 50% greater likelihood of survival compared to those with poor or insufficient social relationships. The magnitude of this effect is comparable with stopping smoking and exceeds many well known risk factors for mortality such as obesity and physical inactivity. These are the main findings of a meta-analysis of social relationships and mortality risk conducted by Julianne Holt-Lunstad (Brigham Young University, Utah, USA) and colleagues and published in this week's PLoS Medicine.
Pick up a new lover at a bar and start an affair. Anything to avoid loneliness.
If friendships lengthen life expectancies how do they do this? Being alone is probably more stressful for most people. Also, friends can help get you to a doctor or hospital or take care of you when you are sick. Plus, if your girlfriend is a good cook you'll eat better. Certainly has worked for me.
Want to spend (before tax credit) about $16k more than a Toyota Prius to get a pluggable hybrid that can go about 40 miles on electric power? Early adopters with moderately deep pockets please get in line.
General Motors began taking orders for the long-awaited Chevrolet Volt on Tuesday, pricing the plug-in hybrid car at $41,000.
A US federal tax credit of $7500 lowers a buyer's cost to $33.5k. A Volt fits well with a future full of parking lots covered with photovoltaic solar canopies. My expectation is that such solar canopies will become commonplace in 20 years along with electric cars.
So why buy a Volt? If you normally spend $50k or more on SUVs but want unusual bragging rights it is a cheap way to get them. Unlike the Nissan Leaf EV you can take the Volt on long trips. But if you only drive locally you can avoid a trip to a gas station.
Another reason to buy a Volt: world oil production has yet to surpass 2005 levels on a yearly basis. Peak Oil might already be in the rear view mirror. You can see the Volt as an insurance policy against Peak Oil. If oil production goes into decline then what looks now like an excess of federally subsidized electric battery factories could turn into a shortage.
Jane Brody of the New York Times takes a look at the evidence for benefits from raising blood vitamin D levels.
“As a species, we do not get as much sun exposure as we used to, and dietary sources of vitamin D are minimal,” Dr. Edward Giovannucci, nutrition researcher at the Harvard School of Public Health, wrote in The Archives of Internal Medicine. Previtamin D forms in sun-exposed skin, and 10 to 15 percent of the previtamin is immediately converted to vitamin D, the form found in supplements. Vitamin D, in turn, is changed in the liver to 25-hydroxyvitamin D, the main circulating form. Finally, the kidneys convert 25-hydroxyvitamin D into the nutrient’s biologically active form, 1,25-dihydroxyvitamin D, also known as vitamin D hormone.
A person’s vitamin D level is measured in the blood as 25-hydroxyvitamin D, considered the best indicator of sufficiency. A recent study showed that maximum bone density is achieved when the blood serum level of 25-hydroxyvitamin D reaches 40 nanograms per milliliter or more.
“Throughout most of human evolution,” Dr. Giovannucci wrote, “when the vitamin D system was developing, the ‘natural’ level of 25-hydroxyvitamin D was probably around 50 nanograms per milliliter or higher. In modern societies, few people attain such high levels.”
Note Giovannucci's reference to human evolution as relevant to discussions about human dietary needs. The Paleo Diet approach to looking at human nutrition is becoming mainstream. You can find knowledgeable writers on nutrition such as Stephan Guyenet basically taking an anthropological approach to identifying appropriate foods including the use of isotope ratios in predecessors to modern humans to discover how much of different food types they ate.
Brody also quotes noted vitamin D researcher Michael Holick. Worth a read to hear what he has to say about disease risks that are boosted by not getting enough vitamin D.
Check out this clip from Discovery Networks. Apex predators serve useful functions in ecosystems and should not be overfished. Currently dozens of shark species are being killed at unsustainable rates. Countries should stop doing this.
We need to stop overfishing the oceans.
Troy, NY – In the spring, later sunset and extended daylight exposure delay bedtimes in teenagers, according to researchers at Rensselaer Polytechnic Institute's Lighting Research Center (LRC).
"Biologically, this increased exposure to early evening light in the spring delays the onset of nocturnal melatonin, a hormone that indicates to the body when it's nighttime," explains Mariana Figueiro, Ph.D., associate professor. "This extended exposure adds to the difficulties teens have falling asleep at a reasonable hour."
The sleep-deprived brats become moody. How about totally covering the windows in their bedrooms to block out all light in the evening?
Over time when coupled with having to rise early for school, this delay in sleep onset may lead to teen sleep deprivation and mood changes, and increase risk of obesity and perhaps under-performance in school, according to Figueiro.
Kids are made to go to school too early. This is dumb. Too early rising even boosts teen car accidents.
Getting up late means less morning sun which just makes the problem worse.
"This is a double-barreled problem for teenagers and their parents," says Figueiro. "In addition to the exposure to more evening daylight, many teens also contend with not getting enough morning light to stimulate the body's biological system, also delaying teens' bedtimes."
Blue light at the right time in the morning (while in school) could shift teen clocks so they'd go to sleep earlier. Blocking blue light exposure delays onset of sleep. Got problems falling asleep? Adjust your light exposure. Be aware that evening exposure to computer screens might cause delay in sleep too.
We do not live in our natural environment. We need to engineer the environments that we do live in to match the designs of our bodies. We should engineer the intensity and frequency distribution of light across our days to control our biological clocks so that we get enough sleep and get up when we need to.
A 42% higher rate of childhood cancers among children conceived using In Vitro Fertilization (IVF). But in absolute terms the number of cancers was still very low. 15 more cancers out of 26,000 is 1 in 1733.
Swedish researchers used records of more than 26,000 children born after IVF treatment and linked them to registers of cancer diagnosis.
They found 53 children developed cancer, ranging from a very young age, up to 19-years-old, against an expected number of 38.
The team said this meant there was a 42 per cent increased risk of childhood cancer in these children.
The researchers do not know whether the IVF boosts cancer risk, It could be that women who have fertility problems might have wombs that alter development in ways that boost cancer risk. Or their eggs could have more problems than eggs of women who do not have fertility problems. Women using IVF are also older on average than women who are getting pregnant without use of IVF. More here.
The more troubling question: Do children who have higher risk of childhood cancer also have a similar higher risk of cancer in late middle are and old age? If IVF turns out to produce even a 10% increase in likelihood of cancers is one's 60s, 70s, and 80s that would come on top of a much higher base cancer rate.
For someone pondering IVF now higher rates of birth defects when using IVF also need to be taken into consideration.
Improving technologies for embryo testing and selection should go at least part of the way toward closing the risk gap between naturally started pregnancies and IVF pregnancies. While existing embryo genetic testing technologies might pose a risk to embryos in the long run I expect IVF conception to become lower risk than natural conception as IVF combined with advances in embryo genetic testing (more here) will enable a lowering of birth defect rates below the rates of birth defects seen with naturally started pregnancies.
The rapidly declining cost of full genome genetic sequencing technology is about to produce a flood of genetic data that will lead to the identification of what a large number of genetic variants mean. These findings will increase the value of IVF embryo testing as prospective parents gain the ability to select physical and mental traits of their future offspring by choosing which among several embryos to implant.
Technology Review has an article about an approach that might substantially boost the density of lithium batteries while also lowering their cost.
Planar Energy has developed a roll-to-roll process for making larger solid lithium-ion batteries. The company, which received $4 million in funding from the Advanced Research Projects Agency Energy program this spring, says it can print solid batteries that offer three times more storage than liquid lithium-ion batteries of the same size. This boost in energy storage is possible primarily because the company's all-solid batteries don't require many of the support structures and materials that take up space in conventional batteries, making more space for energy storage.
In the comments section John Pitts of Planar says the prototype Planar cell offers "substantial improvements over current, high-end Li-ion cells." He expects this prototype to enter durability testing in less than a year.
The design point for the prototype Planar cell, fully packaged, with a capacity of 5 Ah, is a specific energy of a little over 400 Wh/kg. The energy density of this cell is a little over 1200 Wh/l.
Since 2005's yearly oil production peak probably won't be surpassed in 2010 we might already be past the final world peak in oil production. So a lot is riding on efforts to cut the cost and boost the energy density of batteries. Electrification of more parts of our economies would do the most to insulate us from the effects of Peak Oil.
To explore the association between sitting time and mortality, researchers led by Alpa Patel, Ph.D. analyzed survey responses from 123,216 individuals (53,440 men and 69,776 women) who had no history of cancer, heart attack, stroke, or emphysema/other lung disease enrolled in the American Cancer Society's Cancer Prevention II study in 1992. They examined the amount of time spent sitting and physical activity in relation to mortality between 1993 and 2006. They found that more leisure time spent sitting was associated with higher risk of mortality, particularly in women. Women who reported more than six hours per day of sitting were 37 percent more likely to die during the time period studied than those who sat fewer than 3 hours a day. Men who sat more than 6 hours a day were 18 percent more likely to die than those who sat fewer than 3 hours per day. The association remained virtually unchanged after adjusting for physical activity level. Associations were stronger for cardiovascular disease mortality than for cancer mortality.
Think you can safely sit for many hours if you just get yourself a Hermann Miller Aeron chair then you are all set to sit for long hours? Nope, not that easy. Sitting is the problem. Worse yet, the classic 90 degree sitting angle is bad. Yup, all that advice about sitting up straight and rectangular was wrong. Those ram-rod straight sitters were all damaging their metabolism. Anyone know, does the Herman Miller Embody chair allow you to tilt back to 120 or 135 degrees? It appears to support more tilting back than the Aeron. But I can't tell how much from pictures.
Sitting combined with not exercising is an even speedier way to meet the Grim Reaper.
When combined with a lack of physical activity, the association was even stronger. Women and men who both sat more and were less physically were 94% and 48% more likely, respectively, to die compared with those who reported sitting the least and being most active.
"Several factors could explain the positive association between time spent sitting and higher all-cause death rates," said Dr. Patel. "Prolonged time spent sitting, independent of physical activity, has been shown to have important metabolic consequences, and may influence things like triglycerides, high density lipoprotein, cholesterol, fasting plasma glucose, resting blood pressure, and leptin, which are biomarkers of obesity and cardiovascular and other chronic diseases."
Hamilton, like many sitting researchers, doesn't own an office chair. "If you're standing around and puttering, you recruit specialized muscles designed for postural support that never tire," he says. "They're unique in that the nervous system recruits them for low-intensity activity and they're very rich in enzymes." One enzyme, lipoprotein lipase, grabs fat and cholesterol from the blood, burning the fat into energy while shifting the cholesterol from LDL (the bad kind) to HDL (the healthy kind). When you sit, the muscles are relaxed, and enzyme activity drops by 90% to 95%, leaving fat to camp out in the bloodstream. Within a couple hours of sitting, healthy cholesterol plummets by 20%.
I've gotten in the habit of getting up and walking around at least once every 2 hours. I'd really like a more flexible work environment that would make it easier to shift between sitting and standing during the course of the day.
We need surgical robots to make it very fast, cheap, and highly reliable to replace aging organs with new organs grown in vats outside the body. Automation is key to higher quality and lower error rates. With that thought in mind, some Duke researchers are developing autonomous surgical robots.
DURHAM, N.C. -- As physician-guided robots routinely operate on patients at most major hospitals, the next generation robot could eliminate a surprising element from that scenario -- the doctor.
Feasibility studies conducted by Duke University bioengineers have demonstrated that a robot -- without any human assistance -- can locate a man-made, or phantom, lesion in simulated human organs, guide a device to the lesion and take multiple samples during a single session. The researchers believe that as the technology is further developed, autonomous robots could some day perform many more simple surgical tasks.
"Earlier this year we demonstrated that a robot directed by artificial intelligence can on its own locate simulated calcifications and cysts in simulated breast tissue with high repeatability and accuracy," said Kaicheng Liang, a former student in the laboratory of Stephen Smith, director of the Duke University Ultrasound Transducer Group at the Pratt School of Engineering and senior member of the research team. "Now we have shown that the robot can sample up to eight different spots in simulated human prostate tissue."
Automation is needed in order to achieve the highest quality. So robotic surgeons don't just hold out the hope of lower costs. They'll also make fewer errors. The best human hand skilled at guiding a blade will inevitably be surpassed by a computer-controlled high precision device.
PASADENA, Calif.—Biologists at the California Institute of Technology (Caltech) have demonstrated a connection between multiple sclerosis (MS)—an autoimmune disorder that affects the brain and spinal cord-and gut bacteria.
The work—led by Sarkis K. Mazmanian, an assistant professor of biology at Caltech, and postdoctoral scholar Yun Kyung Lee—appears online the week of July 19-23 in the Proceedings of the National Academy of Sciences.
Our modern sterile environments might have shifted the make-up of our intestinal flora in a direction that causes immune system changes that increase the odds of MS.
Segmented filamentous bacteria induce an inflammatory cascade that leads to MS in lab animals created to study MS.
To find out, Mazmanian and his colleagues tried to induce MS in animals that were completely devoid of the microbes that normally inhabit the digestive system. "Lo and behold, these sterile animals did not get sick," he says.
Then the researchers decided to see what would happen if bacteria were reintroduced to the germ-free mice. But not just any bacteria. They inoculated mice with one specific organism, an unculturable bug from a group known as segmented filamentous bacteria. In prior studies, these bacteria had been shown to lead to intestinal inflammation and, more intriguingly, to induce in the gut the appearance of a particular immune-system cell known as Th17. Th17 cells are a type of T helper cell—cells that help activate and direct other immune system cells. Furthermore, Th17 cells induce the inflammatory cascade that leads to multiple sclerosis in animals.
"The question was, if this organism is inducing Th17 cells in the gut, will it be able to do so in the brain and central nervous system?" Mazmanian says. "Furthermore, with that one organism, can we restore to sterile animals the entire inflammatory response normally seen in animals with hundreds of species of gut bacteria?"
The answer? Yes on all counts. Giving the formerly germ-free mice a dose of one species of segmented filamentous bacteria induced Th17 not only in the gut but in the central nervous system and brain—and caused the formerly healthy mice to become ill with MS-like symptoms.
So this brings up the obvious question: Which types of bacteria will reduce our risks of MS? Anyone know much about popular yogurt bacteria? Which ones would be better to get more of? Any ones to avoid?
Update: A research report about probiotic (live lactic acid bacteria) use in pregnancy to cut the incidence of eczema in babies highlights how intestinal bacteria can influence immune system function.
(20.07.2010) Mothers who drank milk with a probiotic supplement during and after pregnancy were able to cut the incidence of eczema in their children by almost half, a new study published in the British Journal of Dermatology has shown.
The randomized, double-blind study, conducted by researchers at the Norwegian University of Science and Technology (NTNU), compared mothers who drank one glass of probiotic milk a day to women who were given a placebo. Use of the probiotic milk – which the mothers drank beginning at week 36 in their pregnancy up through to three months after birth -- reduced the incidence of eczema by 40 percent in children up to age two, the researchers found. The study is a part of a larger research project at the university called the Prevention of Allergy Among Children in Trondheim, or PACT, an ongoing population-based intervention study in Norway focused on childhood allergy.
Raising the albedo (reflectivity) of roofs and pavement with lighter colored and more reflective material could delay the effects of higher atmospheric CO2 by about 2 years.
In the latest study, the Berkeley Lab researchers and their collaborators used a detailed global land surface model from NASA Goddard Space Flight Center, which contained regional information on surface variables, such as topography, evaporation, radiation and temperature, as well as on cloud cover. For the northern hemisphere summer, they found that increasing the reflectivity of roof and pavement materials in cities with a population greater than 1 million would achieve a one-time offset of 57 gigatons (1gigaton equals 1 billion metric tons) of CO2 emissions (31 Gt from roofs and 26 Gt from pavements). That’s double the worldwide CO2 emissions in 2006 of 28 gigatons. Their results were published online in the journal Environmental Research Letters.
“These offsets help delay warming that would otherwise take place if actual CO2 emissions are not reduced,” says Surabi Menon, staff scientist at Berkeley Lab and lead author of the paper.
The benefits of this idea go beyond global warming. Another advantage would be cooler cities in the summer. Don't you just hate hot black pavement in the summer? The dark color of the pavement does less to warm up cold winters because there's less sun in the winter. So dark colors in building materials and pavement tend to intensify the difference between summer and winter weather.
Illumina now will charge $19,500 for the service. Users must follow a physician-mediated process. That's down from the $48,000 the firm was charging when actress Glenn Close revealed in March that Illumina had sequenced her genome.
But Illumina's price falls to $14,500 per person for groups of at least five that are referred by the same physician. And it falls to just $9,500 when a referring physician certifies that the sequencing could lead to a treatment for a patient's disease or condition.
Note the bit about "a physician-mediated process". Regulators won't let you find out our own genetic sequence without a visit to a doctor to get permission. What's the point of that visit? Will the doctor say no? If so, then what, you just don't get to know your own DNA sequence? If the doctor says no you can pay again to visit another doctor to try to get a yes. You can ask friends (or perhaps a social networking site) which doctors always say yes. The gatekeepers want to control the flow of medical information. I am opposed. What about you?
The US Food and Drug Administration has sent a letter to Illumina and other genetic sequencing companies telling them that their sequencing services for individuals falls under FDA authority. That does not bode well as I've previously discussed. Think my fears are overblown? Nope. In 2008 both California and New York State tried to prevent individuals from getting tests done on their own DNA. See this article from Wired and click thru on the links if you have any doubt.
When some overprotective Luddites from the California Department of Health Services sent cease-and-desist letters to thirteen genetic testing companies, they proved that someone in their office must have single nucleotide polymorphism that causes poor judgment. Interfering with the nascent industry is not a good idea for a plethora of reasons.
The messages, which were sent on June 9th, warned that each test must be ordered by a doctor and carried out in a laboratory that meets a strict set of standards. If not, the direct-to-consumer shops will face up to $3,000 per day in fines.
Hence the "physician-mediated process".
How most medical testing should work: Any drug store with a pharmacy department would be able to withdraw blood to submit for testing. Any pharmacist or suitably trained pharmacist's assistant should be able to take a blood sample (or a urine sample if they want to branch out). Then you pay and have the option of getting your results via a email, web site, physical mail, or a return visit. You should have the option of specifying which doctor(s) should also get your test results. You should also be able to have your results sent to an medical expert system web server that tracks all the medical information about you. Your medical history should reside in a cloud server that is independent any individual doctor's office.
The 1000 Genomes Project, an international public-private consortium to build the most detailed map of human genetic variation to date, announces the completion of three pilot projects and the deposition of the final resulting data in freely available public databases for use by the research community. In addition, work has begun on the full-scale effort to build a public database containing information from the genomes of 2,500 people from 27 populations around the world.
This sounds like an impressive scientific effort, right? In a few short years 100 times that many genomes will be sequenced each year and then sequencing rates will go up by more orders of magnitude. Though if the FDA stands in the way Americans will have to go on vacation to other countries to get our genomes sequenced.
Update: To the extent that the US FDA and like-minded agencies reduce the availability of DNA sequencing services they slow the rate of technological advance. Fewer people paying to get their DNA sequenced means less revenue to use to generate future generation sequencing devices. This delays the day various benefits of sequencing will be realized. We will be less healthy than we otherwise would be absent regulatory meddling.
I am looking forward to the day when full genome sequencing becomes affordable. If millions of people can get their DNA sequenced then the meaning of genetic variants will become known much sooner. We will be able to alter our diets and lifestyles and choose drugs and other treatments suited to our personal genetic profiles sooner. We will avoid more diseases. We will live with fewer ailments and pains.
Cheap DNA sequencing available to the masses will enable voluntary sharing of health and DNA sequencing information in order to discover which genetic variants matter. Imagine web sites where you submit your DNA (with appropriately privacy safeguards) along with disease history and physical and cognitive characteristics. Such a large scale cooperative effort will enable much faster discovery of what each genetic variant does. This can make DNA sequencing results more useful to more people sooner.
The firm GenomeQuest has a blog, and on that blog they have a post, Implications of exponential growth of global whole genome sequencing capacity. In that post there are some bullet points with numbers. Here they are:
* 2001-2009: A Human Genome
* 2010: 1,000 Genomes – Learning the Ropes
* 2011: 50,000 Genomes – Clinical Flirtation
* 2012: 250,000 Genomes – Clinical Early Adoption
* 2013: 1 Million Genomes – Consumer Awareness
* 2014: 5 Million Genomes – Consumer Reality
* 2015-2020: 25 Million Genomes And Beyond – A Brave New World
In light of the many orders of magnitude drop in DNA sequencing costs we've already witnessed in the last 30 years I find these numbers plausible. The 2010s are going to be a period in which the functional significance of tens or hundreds of thousands of genetic variants become known and DNA sequencing becomes affordable for the middle class.
There many reasons to do genome sequencing. Not all these reasons involve clinical applications by health care providers, though most do.
I expect DNA sequencing of cancer cells will become routine. Knowledge about cancer genome mutations will be used to choose treatments. I would not be surprised if DNA sequencing data gets used to design antibodies to attack cancer cells without attacking normal cells.
Since a person can have cancer for months or years and since cancer cells constantly mutate I expect oncologists to track cancers by using repeated sequencing of many cancer cell samples from each patient. Once full genome DNA sequencing costs just a few hundred dollars the cost will become a small fraction of total cancer treatment costs. So I do not see money as an obstacle to this style of usage of sequencing machines.
In a prelude to overhauling its regulatory oversight of genetic diagnostic testing, the U.S. Food and Drug Administration will convene a public meeting next week to gather input from test makers and others.
I would prefer the FDA and like regulatory agencies stay out of genetic testing except perhaps to test for error rates and publish the results. The rate of innovation will be faster with less regulatory involvement.
Yes, genetic testing will serve as a cornerstone of personalized medicine - but only if it is allowed to grow rapidly without big costs involved in getting regulatory approvals.
The event reflects a turning point in genetic testing, a cornerstone of personalized medicine. Once mainly the domain of rare diseases, scientists have discovered a growing number of genetic variations linked to both the risk of more common disease and patients' response to drugs. The number of genetic diagnostic tests has expanded rapidly, and tests have become increasingly complex, making it more challenging to interpret and act on the results.
Genetic tests are data. The flow of genetic testing information is like the flow of so many other kinds of information: increasing rapidly, growing by leaps and bounds. All that data should flow unhindered by regulations.
The FDA does not see doctors capable of interpreting genetic test results. I'm thinking they'll use web sites that will pop up to do genetic sequence data interpretation.
"We don't think physicians are going to be able to interpret the results; they are relying on the labs that make them," says Alberto Gutierrez, director of the Office of In Vitro Diagnostic Device Evaluation and Safety at the FDA. "So we think a third party should assess these devices."
Individuals shouldn't even need to go to a doctor in order to get their genes tested or fully sequenced. Testing and sequencing services should be available to accept tissue samples via web sites where people pay and then send in tissue samples.
Access to testing services without need to see a doctor should be allowed for much more than just DNA testing. Services for testing blood and assorted excretions (urine, stool, hair, nails, etc) should be available to the general public. Also, as microfluidic devices make mini home medical testing equipment practical we should be able to get a blood panel or other tests done at home.
Why can cars be kept operational decades longer than they were originally designed to last? Because repair shops can replace worn out and broken parts. We humans can't replace our worn out parts because we have no way to make replacements for most of our parts. With that thought in mind check out how researchers at Massachusetts General Hospital have grown replacement livers by using the vasculature and other structure of a freshly dead liver to grow a new liver.
Scientists at Massachusetts General Hospital in Boston have taken the first steps toward building functional, transplantable livers. In a study in rats, published online today by Nature Medicine, the researchers took donor livers, gently stripped them of their cells while leaving other material intact, and then used the remaining structure as a scaffold on which to grow healthy liver cells. The result was a nearly complete organ that was transplanted into the rats and remained functional for up to eight hours.
The strip away the liver cells to retain the scaffolding, add new liver cells and, and then grow a new liver in a nutrient bath.
One obvious problem with this approach is that it requires an existing organ to use as a starting point. Given that someone with a failing organ still typically needs the remaining functionality of their organ they can't use their own organ's blood vessels as a scaffolding to grow a replacement organ in a culture. The development of better artificial organs could enable the removal of more types of diseased organs without immediate death. Then a patient could be kept alive (albeit connected to machines) while a new replacement part is grown.
Of course, lots of people die every day who leave behind livers. If their liver cells could be removed and a person with a sick liver could donate their own cells to grow a new liver then the immune rejection problem would be much smaller even though the scaffolding used to grow the liver would be from a different person than the one who gets the new liver.
Click thru and read all the details. This approach still has some unsolved problems. But the scientists working on it are optimistic they can solve all these problems within 10 years. Then humans will become more like cars: able to be kept on the road with replacement parts.
Researchers at UCLA’s Jonsson Comprehensive Cancer Center created a large, well armed battalion of tumor-seeking immune system cells and watched, in real time using Positron Emission Tomography (PET), as the special forces traveled throughout the body to locate and attack dangerous melanomas.
But for now this sort of thing only gets done for those tricky lab mice who have done such a great job of convincing researchers into developing medical treatments for them first.
If I had terminal cancer and a large sum of money I'd hire medical researchers to do this to my own immune system.
The gene therapy work, done with melanomas grown in mice, employed a crippled HIV-like virus to serve as a vehicle to arm the lymphocytes with T cell receptors, which caused the lymphocytes to become specific killers of cancerous cells. A reporter gene, which glows “hot” during PET scanning, also was inserted into the cells so researchers could track the genetically engineered lymphocytes after they were injected into the blood stream, made their way to the lungs and lymph nodes and then specifically homed in on the tumors wherever they were located within the body.
“We’re trying to genetically engineer the immune system to become a cancer killer and then image how the immune system operates at the same time,” said Dr. Antoni Ribas, an associate professor of hematology/oncology, a researcher at UCLA’s Jonsson Comprehensive Cancer Center and the senior author of the study. “We knew this approach of arming the lymphocytes with T cell receptors showed significant anti-tumor activity based on studies in humans. Now, by tracking the immune system’s reaction to cancer and imaging it in real time, we can project how the same process that succeeded in mice might behave in people.”
The study is published July 12, 2010 in the early online edition of the journal Proceedings of the National Academy of Sciences.
I like the part in bold. Sure beats dying in a shriveled painful state of a horrible disease.
“The novelty of our work is that we were able to pack together the cancer specific T cell receptor and the PET reporter genes in a single vector and use it in mice with an intact immune system that closely resembles what we would see in real patients,” said Dr. Richard Koya, an assistant professor of surgical oncology at UCLA’s David Geffen School of Medicine and first author of the study. “We were also gladly surprised to see the targeted tumors literally melt away and disappear, underscoring the power of the combined approach of immune and gene therapy to control cancer.”
Time to do this in humans who have a few months to live. Maybe Chinese researchers will do it without waiting a long time to do more animal tests.
More than one-third of U.S. physicians responding to a survey did not agree that physicians should always report colleagues who are incompetent or impaired by conditions such as substance abuse or mental health disorders. The report from the Mongan Institute for Health Policy at Massachusetts General Hospital (MGH), published in the July 14 Journal of the American Medical Association, also finds that substantial numbers of physicians feel unprepared to report or otherwise deal with impaired or incompetent colleagues.
"Our findings cast serious doubt on the ability of medicine to self-regulate with regard to impaired or incompetent physicians," says Catherine DesRoches, DrPh, of the Mongan Institute, who led the study. "Since physicians themselves are the primary mechanism for detecting such colleagues, understanding their beliefs and experiences surrounding this issue is essential. This is clearly an area where the profession of medicine needs to be concerned."
The medical profession would prefer less outside judgment (e.g. fewer malpractice suits, less second-guessing by insurance companies) on the basis that only professionals are competent to judge other professionals. That sounds great if the professionals really step up to the plate to do that judging and do so objectively.
Pediatricians are least up to their responsibility. Which leads me to wonder: what's the split on male versus female reporting of incompetence?
Almost 1,900 surveys were returned, and only 64 percent of the respondents agreed that physicians should always report impaired or incompetent colleagues. About 70 percent of respondents indicated feeling prepared to deal with an impaired colleague, and 64 percent felt prepared to deal with an incompetent colleague in their practice. Pediatricians were the least likely to report feeling prepared to deal with impaired or incompetent colleagues, while psychiatrists and anesthesiologists felt most prepared.
In a given year about 6% of American physicians fail to report an impaired or incompetent physician.
Direct, personal knowledge of an impaired or incompetent physician during the past three years was indicated by 17 percent of respondents, but only 67 percent of those with such knowledge actually had reported the colleague.
One wonders how many people suffer or die as a result. One also wonders how much money is wasted as a result.
People who favor immigration restriction and an end to racial preferences will find support for their positions in this report.
The most frequently cited reason for not reporting was the expectation that someone else would report, indicated by 19 percent, followed by the belief that nothing would happen because of the report, cited by 15 percent, and a fear of retribution, 12 percent. Among factors associated with not reporting were belonging to one- or two-person practices and being a member of an underrepresented minority or a graduate of a foreign medical school. Whether respondents came from a state with high, medium or low rate of malpractice claims was not associated with failure to report.
Leave it to someone else, nothing would happen because the rest of the medical profession will ignore the report, and, hey, don't want doctors ganging up on you. This reminds me of the police with their thin blue line. As a practical matter I think police have such dangerous jobs dealing with such dangerous people that they need a considerable amount of solidarity against the world. Doctors have much higher status and cushier working conditions. They should step it up on enforcing performance standards on each other.
New and updated guidelines on recommended vitamin D intake have been published this week in the online issue of the Canadian Medical Association Journal (CMAJ).
Dr. David Hanley, professor at the University of Calgary Faculty of Medicine, and member of Osteoporosis Canada's (OC) Scientific Advisory Council, is the lead author of the paper on behalf of Osteoporosis Canada.
To take above 2000 IU per day the paper recommends medical supervision.
The new guidelines recommend daily supplements of 400 to 1000 IU for adults under age 50 without osteoporosis or conditions affecting vitamin D absorption. For adults over 50, supplements of between 800 and 2000 IU are recommended.
"A daily supplement of 25 mcg (800 IU) should now be regarded as a minimum dose for adults with osteoporosis," writes Hanley with co-authors. "Canadians can safely take daily vitamin D supplements up to the current definition of tolerable upper intake level (50 mcg [2000 IU]), but doses above that require medical supervision."
Blood tests can help guide decisions on how much vitamin D is needed.
But if you want to use the full range of your electric car, it could take over a day to recharge using a standard 110-volt power outlet.
The point was driven home Monday in an article in The Wall Street Journal, which described Nissan's efforts to break through bureaucracy to make it easier for homeowners to get special electric vehicle charging stations installed. Nissan, which is coming out with an electric vehicle this year called the Leaf, is concerned that customers will be put off from buying the car by the 20 hours required to recharge it from a standard outlet to get its full 100-mile range. Currently, it can take weeks for cities to issue the necessary permits for a fast charger that can cut recharging time to eight hours, the article said, and the price for the special charger, including installation, will range from about $1,200 (with a tax credit) to several thousand dollars if a electric panel upgrade is needed.
I've also covered this previously in my post Home Electric Upgrades For Electric Cars.
Who is the ideal Nissan Leaf electric car driver? Imagine you have the lifestyle characteristics for maximum ROI from driving an electric car. What does that the commuting pattern of that lifestyle look like?
Then if you go to work 250 days a year (quite the work-aholic) you travel about 45000 miles per year purely on electric power.
Okay, what's your best pure gasoline alternative? The Toyota Prius at about 50 mpg. Choosing a Leaf over a Prius would mean 900 gallons of gasoline avoided per year. Let us imagine that gasoline prices go back up and you pay an average of $4 per gallon for 5 years driving either the pure electric Nissan Leaf or hybrid Toyota Prius car. The Leaf lets you avoid 3600 gallons of gasoline for $14400 saved. But you have to subtract off maybe 250 watt-hours of cost per mile for the Leaf recharging. Say 2.6 cents per mile (it'll vary depending on where you live) or a total of $4680 for 5 years or 225000 miles of electric power. That yields a total savings of $9720. Given that the electric car's added cost is higher than that (I'm ignoring the cost reduction due to tax credits since somebody pays for the higher cost) you can see that electric cars take 5+ years to pay off for the really rare very high mileage drivers.
Of course I chose the ideal electric car driver to sketch out an ideal amount of money saved. In reality the average commuter is traveling less than half that distance per day and takes off more than 2 weeks for vacations, holidays, and sick time. So payback time is much longer, easily over 10 years. Plus, more money paid up front for a car is an opportunity cost since the money shelled out can't be invested elsewhere for a healthy ROI.
Most people do not match the ideal electric car driver profile in other ways as well. Renters aren't going to upgrade their apartment's or house's electric power. Until electric cars become extremely common not many landlords will invest in the upgrades either. People who see their house as a temporary abode for a few years until they move up or get transferred in their job similarly won't put in the 220V electric power. Ditto for people who are underwater in their mortgages (about a quarter of US mortgage holders last I checked). A suitable place to plug in at work with 220V and high amps is going to be even more rare than home 220V.
Another point: dynamic electric power pricing (which is going to become more widespread) will increase the cost of daytime recharging while lowering the price of night time recharging. So if your commute is so long that you need to recharge while at work your electric power cost per mile will be higher than if you only recharge while at home. So the ideal scenario of 2 recharges per day is really not as attractive as I sketched out above. The spread of wind power (which blows stronger at night) will widen the price gap between wholesale electric power prices from peak to bottom.
Also, if you will want to recharge your car when electric power is cheapest you'll need higher amp 220V power so that you can delay the start of recharging until after about 9 or 10 PM in order to get cheap late night electric power rates. But you'll have to weigh the difference in electric power costs versus the cost of electric wiring upgrades.
If you could jump into a time machine and come out 40 years from now you'd see a society where the shift to electric power for transportation has already happened and the cost problems outlined above are a faded memory. Battery cost drops, cheap solar photovoltaics, new houses built with 220V power, and other adjustments will enable much wider spread use of electric power for transportation. Peak Oil will help to accelerate the transition, meaning that many of the adjustments will happen under very trying circumstances.
One upbeat way to look at the costs of an electric car: Price insurance. If oil is going to back up near $150 per barrel and beyond (and I think it will) then an electric car would put a ceiling on your transportation costs that would let you adjust more easily to Peak Oil.
Update: Note that in my analysis above the high mileage driver can get a return on the EV investment. But the number of miles needed to get that return (ignoring tax credits) is so high I wonder whether the batteries will wear out before returning their costs. The Chevy Volt battery warranty will be 100,000 miles or 8 years.
But note that if you play the rational actor responding to the incentives created by tax policy then an EV pays back very quickly. Given the tax credit a Nissan Leaf will cost at most $1k more than a Prius (unless Toyota starts discounting). You get into the black pretty quickly on your investment. The Leaf and the Chevy Volt are both worth a serious look.
I expect the economics of PHEVs and EVs will become more favorable due to a combination of declining battery costs and rising oil costs. But electric cars have to fall by over $7k just to compensate for the eventual phase-out of EV and PHEV tax credits.
A new study on vitamin D levels and Parkinson's disease risk points to the need for further research on whether vitamin D supplements can protect against the movement disorder, according to an editorial in the July 2010 issue of Archives of Neurology.
The author of the editorial is Marian Evatt, MD, assistant professor of neurology at Emory University School of Medicine and director of the Atlanta Veterans Affairs Medical Center's Movement Disorders Clinic.
The study, also reported in Archives of Neurology, is the first to show that low vitamin D levels can help predict whether someone will later develop Parkinson's disease. Researchers at Finland's National Institute for Health and Welfare measured vitamin D levels from more than 3000 people, using blood samples taken between 1978 and 1980, and then followed those people to see whether they developed Parkinson's. People with the lowest levels of vitamin D were three times more likely to develop Parkinson's, compared to the group with the highest levels.
This report by itself does not prove a causal relationship where low vitamin D boosts Parkinson's risk. Other causal chains are possible. For example, it is possible some of the same genetic variants that cause differences in blood vitamin D level also separately cause changes in neuronal or immune system function and thereby change Parkinson's risk.
Vitamin D might provide protection by protecting dopaminergic neurons from toxins.
Research on animals suggests that vitamin D may protect neurons that produce dopamine from toxins. Besides vitamin D levels, factors such as genetics and exposure to pesticides also are associated with the risk for developing Parkinson's disease.
This report brings to mind a long studied link between multiple sclerosis and vitamin D. For example, a Canadian study found low vitamin D is linked to higher MS risk, MS is thought to be an auto-immune disorder, and vitamin D is thought to play a role modulating immune function. Curiously, a report in March 2010 found ultraviolet light might reduce the damage from MS independent of UV's stimulation of skin vitamin D synthesis. However, at least one study has found that vitamin D supplements appear to cut risk of MS relapse.
Ready for some scientific guidance to your golf game?Avoid repeatedly practicing just one shot. Sounds like good advice for life.
Struggling with your chip shot? Constant drills with your wedge may not help much, but mixing in longer drives will, and a new study shows why.
Previous studies have shown that variable practice improves the brain’s memory of most skills better than practice focused on a single task. Cognitive neuroscientists at USC and UCLA describe the neural basis for this paradox in a new study in Nature Neuroscience.
The researchers split 59 volunteers into six groups: three groups were asked to practice a challenging arm movement, while the other three groups practiced the movement and related tasks in a variable practice structure.
Volunteers in the variable practice group showed better retention of the skill. The process of consolidating memory of the skill engaged a part of the brain - the prefrontal cortex - associated with higher level planning.
Might this result also apply to purely intellectual learning where no physical skill is involved? Seems plausible.
You have to process what you are doing more deeply if you keep switching around between different physical activities.
The group assigned to constant practice of the arm movement retained the skill to a lesser degree through consolidation that engaged a part of the brain - the primary motor cortex - associated with simple motor learning.
“In the variable practice structure condition, you’re basically solving the motor problem anew each time. If I’m just repeating the same thing over and over again as in the constant practice condition, I don’t have to process it very deeply,” said study senior author Carolee Winstein, professor of biokinesiology and physical therapy at USC College.
“We gravitate toward a simple, rote practice structure because we’re basically lazy, and we don’t want to work hard. But it turns out that memory is enhanced when we engage in practice that is more challenging and requires us to reconstruct the activity,” Winstein said.
Don't let yourself get lazy. Mix it up.
With the exception of X and Y chromosome genes in men, we have copies of each gene from both parents. Researchers find that in mice (and likely in humans as well) specific genes from one or the other parent are silenced so that only one parent contributes to resulting phenotype (visible appearances and functionality).
The new findings, reported in two papers that appear in the early online edition of the journal Science on July 8, 2010, suggest that imprinting has a significant influence on brain development and behavior. It also likely contributes to diseases of the brain, since imprinting occasionally shuts down the only good gene in a pair.
Howard Hughes Medical Institute investigator Catherine Dulac led the team of scientists who conducted the ambitious analysis. Christopher Gregg, a postdoctoral fellow in her Harvard University lab, is the lead author on both of the publications.
“Essentially what we found with these two studies is that imprinting is not only very extensive but also seems to be subject to a lot of regulation, throughout the life of an individual and even according to brain region and gender,” says Dulac. “And that makes the phenomenon absolutely fascinating.”
This result helps explain why genetic causes of disease, IQ, physical appearances, and other qualities are so hard to track down. The simple Mendelian model of inheritance works in some cases. But for the genes identified in this study the Mendelian model doesn't predict what happens.
Whether the gene from mother or father gets expressed depends on the specific gene, whether the offspring is female or male, and even on stage of development.
Another striking finding was that paternal and maternal imprinting isn’t evenly mixed: About 60 percent of the imprinted genes in the mouse embryonic brain turned out to be maternal, while about 70 percent of the imprinted genes in the adult brain are paternal. Thus, in early life, it appears that imprinting mostly reflects the mother’s influence, and later gives way to the father’s. “But the majority of the genes that we found are imprinted during development, which is when mothers have the greatest influence,” says Dulac.
In their second paper, Dulac and her team reported that the gene imprinting in an animal can vary depending on whether the animal is male or female. Throughout the genome, they found 347 genes that appeared to be imprinted in adult female mice but not males, or vice versa. This sex-specific imprinting was particularly evident in females in the hypothalamic region of the brain, which mediates maternal and mating behaviors. One example of the complexity they encountered is the gene Mrpl48, which they found has a paternal expression bias in the hypothalamus of females, but not males.
Geneticists need to identify for about 20,000 human genes whether their maternal or paternal version is always active or suppressed in each tissue type at each stage of development and do this for men and women and across races.
Zaldy Tan, MD, MPH, of Brigham and Women's Hospital, GRECC, VA Boston, and Harvard Medical School, and colleagues estimated the levels of 24-hour physical activity of more than 1,200 elderly participants from the Framingham Study (742 female; age 76 +\-5) during the study's 20th examination cycle (1986-87) and followed them for the development of dementia. They divided the participants into five groups based on level of physical activity, from lowest (Q1) to highest (Q5).
Over two decades of follow-up (mean 9.9 +/-5 years), 242 participants developed dementia (of which 193 were Alzheimer's). The researchers found that participants who performed moderate to heavy levels of physical activity had about a 40 percent lower risk of developing any type of dementia. Further, people who reported the lowest levels of physical activity were 45 percent more likely to develop any type of dementia compared to those who reported higher levels of activity. Similar results were seen when analyses were limited to Alzheimer's alone. Analyses showed that the observed associations were largely evident in men in the study.
Hiking, biking, running, swimming, weight lifting, tennis, take your pick. Do it regularly.
Tea is associated with a reduction in cognitive decline. Note, though, that the biggest decline came from drinking only 1-4 times per week. That seems odd. Also, just drinking 1-3 times per month yielded almost as much benefit.
Lenore Arab, PhD, of UCLA, and colleagues used data on more than 4,800 men and women aged 65 and older from the Cardiovascular Health Study to examine the relationship between consumption of tea, coffee, and change in cognitive function over time. Study participants were followed up for up to 14 years for naturally-occurring cognitive decline using the Mini-Mental State Examination (3MSE) administered at baseline and annually up to 8 times. People scored on the average 1.17 points less per year. Tea and coffee drinking were assessed using a food frequency questionnaire.
The researchers found that people who consumed tea at a variety of levels had significantly less cognitive decline (17-37 percent) than non-tea drinkers. More specifically, study participants who drank tea 5-10 times/year, 1-3 times/month, 1-4 times/week, and 5+ times/week had average annual rates of decline 17 percent, 32 percent, 37 percent, and 26 percent lower, respectively, than non-tea drinkers.
Again, I find that an unusual result. Does daily tea have some sort of toxic effect?
My guess is you'd be better off eating blueberries and other potent berry sources of flavonoids. But fruits and vegetables in general are associated with very large decreases in dementia risks. More here.
Only the highest level of coffee consumption appears to cut dementia risk. But how are those people managing to sleep with all that caffeine in their bodies?
According to the scientists, coffee consumption did not show any effect except at the very highest level of consumption – where it was associated with significantly decreased decline of 20 percent.
Vitamin D deficiency is strongly associated with cognitive impairment.
David Llewellyn, PhD, of the University of Exeter Peninsula Medical School (UK), and colleagues examined information from 3,325 adults aged 65 years and older from the Third National Health and Nutrition Examination Survey (NHANES III), a study that was carefully designed to accurately represent the U.S. non-institutionalized population. Vitamin D levels were measured from blood samples and compared with performance on a measure of general cognitive function that incorporated tests of memory, orientation in time and space, and ability to maintain attention.
The researchers classified participants as being cognitively impaired if they scored in the worst 10 percent of older adults in the study. They found that the odds of cognitive impairment were about 42 percent higher in those people who were deficient in vitamin D, and 394 percent higher in people who were severely deficient.
If you do outdoor exercise in warm weather you can get more vitamin D and exercise at the same time.
Scientists have discovered a compound that restores the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain's memory hub. The research, funded in part by the National Institutes of Health, has turned up clues to a neuroprotective mechanism that could lead to a treatment for Alzheimer's disease.
"This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties," explained Steven McKnight, Ph.D., who co-led the research with Andrew Pieper, M.D., Ph.D., both of University of Texas Southwestern Medical Center, Dallas. "It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development."
a drug like this carries some risks. Most notably, by preventing cell death the drug increases the risk that mutated pre-cancerous cells will manage to survive and even start replicating. Brain cancer might be a real risk. This is the problem with any drug that improves cell replication and growth in old organisms. The most likely reason the stem cells become less able to replicate is a mechanism selected for by evolution to lower cancer risk.
Neurogenesis in the dentate gyrus is key to new memory formation.
Physical activity, social, or other enriching experiences promote neurogenesis – the birth and maturation of new neurons. This growth takes place in the dentate gyrus, a key area of the brain's memory hub, the hippocampus. But even in the normal adult brain, most of these newborn neurons die during the month it takes to develop and get wired into brain circuitry. To survive, the cells must run a gauntlet of challenges. Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer's, marked by runaway cell death.
Neuron formation was tripled in the dentate gyrus.
To find out if P7C3 could similarly stem aging-associated neuronal death and cognitive decline, the researchers gave the compound to aged rats. Rodents treated with P7C3 for two months significantly outperformed their placebo-treated peers on a water maze task, a standard assay of hippocampus-dependent learning. This was traced to a threefold higher-than-normal level of newborn neurons in the dentate gyrus of the treated animals. Rats were used instead of mice for this phase of the study because the genetically engineered mice could not swim.
Then the researchers developed a derivative drug that is even more potent. Imagine a black market in A20 for people in college.
The researchers pinpointed a derivative of P7C3, called A20, which is even more protective than the parent compound. They also produced evidence suggesting that two other neuroprotective compounds eyed as possible Alzheimer's cures may work through the same mechanism as P7C3. The A20 derivative proved 300 times more potent than one of these compounds currently in clinical trials for Alzheimer's disease. This suggested that even more potent neuroprotective agents could potentially be discovered using the same methods. Following up on these leads, the researchers are now searching for the molecular target of P7C3 – key to discovering the underlying neuroprotective mechanism.
Dr. McKnight was one of the first 12 recipients of the NIH Director's Pioneer Award, which is designed to allow researchers to pursue risky experiments that have the potential for producing highly innovative results.
"When I received the award, I thought 'I'm not going to waste it on something safe – I'm going to go for it. That's what the NIH expected of me and my team,' " Dr. McKnight said. "I'd like to give the NIH credit for betting on 'cowboy' science. If this pans out, it will be the most useful contribution of my career."
The discovery, made after researchers systematically and painstakingly infused each of 1,000 different chemicals into the brains of live mice, could point the way to a new type of neuroprotective drug for people with Alzheimer's or other neurodegenerative diseases, according to the report in the July 9th issue of the journal Cell, a Cell Press publication.
"We really didn't know if the screen would turn up a favorable compound or not," said Steven McKnight of the University of Texas Southwestern. "It was blind luck."
"Our chances were slim," added Andrew Pieper, also of UT Southwestern. "But we knew if we did find something, we would already have evidence that it worked in a living animal." Promising candidates landed in cell culture too often don't pan out.
We need the ability to rejuvenate the immune system in order to slash cancer risk. We can't turn up cell replication in aged stem cells without a way to prevent the rise in cancer risk that higher rate of cell division will otherwise bring.
Thanks to Lou Pagnucco for the heads up. Here's the open access research paper for this report: "Discovery of a Proneurogenic, Neuroprotective Chemical".
PHILADELPHIA — A recent report in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, adds to the growing evidence that fish oil supplements may play a role in preventing chronic disease.
Researchers at the Fred Hutchinson Cancer Research Center in Seattle, Wash., led by Emily White, Ph.D., a member of the public health sciences division, asked 35,016 postmenopausal women who did not have a history of breast cancer to complete a 24-page questionnaire about their use of non-vitamin, non-mineral "specialty" supplements in the Vitamins and Lifestyle (VITAL) cohort study.
After six years of follow-up, 880 cases of breast cancer were identified using the Surveillance, Epidemiology and End Results registry.
If this study's results turn out to be correct the risk reduction is substantial.
Regular use of fish oil supplements, which contain high levels of the omega-3 fatty acids, EPA and DHA, was linked with a 32 percent reduced risk of breast cancer. The reduction in risk appeared to be restricted to invasive ductal breast cancer, the most common type of the disease.
One study doesn't prove this result. But fish oil capsules are pretty cheap and probably won't hurt you. A randomized trial using vitamin D and omega 3 fatty acids that should answer this question more definitively is currently undergoing recruitment. But if you think your risk of breast cancer is substantial you might not want to wait years for the results from that study.
AUSTIN, Texas—As more women wait until their 30s and 40s to have children, they are more willing to engage in a variety of sexual activities to capitalize on their remaining childbearing years, according to new research by psychologists at The University of Texas at Austin.
Such "reproduction expediting" includes one-night stands and adventurous bedroom behavior, the research shows.
In a paper published in the July edition of Personality and Individual Differences, psychology graduate students Judith Easton, Jaime Confer and Cari Goetz, and David Buss, professor of psychology, found that women age 27-45 have a heightened sex drive in response to their dwindling fertility.
Is the heightened sex drive a consciously arrived at choice? I doubt it. Makes more sense for Mother Nature (a.k.a. Darwinian natural selection) to select for a strong desire to take one last shot at making babies before the reproductive machinery totally conks out.
What I'd like to know: Does the hormone that predicts earlier menopause also predict an earlier peaking of sexual desire in women who are going to have earlier menopause?
A specific and remarkably small fragment of RNA appears to protect rats against cocaine addiction - and may also protect humans, according to a recent study funded by the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health. The study was published today in the journal Nature.
RNA (ribonucleic acid) molecules are known to play critical roles in the translation of genetic information (DNA) into proteins, which are the building blocks of life. In the past decade, scientists have begun to notice, catalogue and characterize a population of small RNAs, called microRNAs, that represent a new class of regulatory molecules. In this study, researchers at The Scripps Research Institute in Jupiter, Florida found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, named microRNA-212. As its levels increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed. By contrast, as levels of microRNA-212 decreased, the rats consumed more cocaine and became the rat equivalent of compulsive users.
MicroRNA-212 is a type of small non-protein coding RNA that can regulate the expression levels of hundreds or even thousands of genes. As such, microRNA-212 and other types of microRNAs are considered "master regulators" of gene expression. Because of their ability to coordinate the expression of related genes responsible for brain structure and function, it is thought that microRNAs might play important roles in complex psychiatric disorders, but little has been known about their involvement in addiction—until now.
What the new findings suggest, Kenny said, is that individuals with serious addiction problems may have damaged supplies of this particular non-coding RNA, or the microRNA may not function properly.
"Looking into the future," he said, "It might be possible to develop a small molecule therapeutic that mimics or stimulates the production of this particular microRNA. Once we understand the precise mechanism, we might uncover novel targets that would have a similar effect to acting on the microRNA directly."
Addictions will become curable. Got an addiction you want to cure? If so, is it an interesting addiction?
Some Harvard and MIT researchers found that the type of object a person holds influences their judgment about resumes, stories, and other information they are asked to evaluate.
The researchers conducted a series of experiments probing how objects' weight, texture, and hardness can unconsciously influence judgments about unrelated events and situations:
- To test the effects of weight, metaphorically associated with seriousness and importance, subjects used either light or heavy clipboards while evaluating resumes. They judged candidates whose resumes were seen on a heavy clipboard as better qualified and more serious about the position, and rated their own accuracy at the task as more important.
- An experiment testing texture's effects had participants arrange rough or smooth puzzle pieces before hearing a story about a social interaction. Those who worked with the rough puzzle were likelier to describe the interaction in the story as uncoordinated and harsh.
- In a test of hardness, subjects handled either a soft blanket or a hard wooden block before being told an ambiguous story about a workplace interaction between a supervisor and an employee. Those who touched the block judged the employee as more rigid and strict.
- A second hardness experiment showed that even passive touch can shape interactions, as subjects seated in hard or soft chairs engaged in mock haggling over the price of a new car. Subjects in hard chairs were less flexible, showing less movement between successive offers. They also judged their adversary in the negotiations as more stable and less emotional.
Nocera and his colleagues say these experiments suggest that information acquired through touch exerts broad, if generally imperceptible, influence over cognition. They propose that encounters with objects can elicit a "haptic mindset," triggering application of associated concepts even to unrelated people and situations.
We believe we have more conscious control of our opinions and decisions than we really do. We are regularly doing things for reasons unknown to us. The human mind is a very flawed instrument for reasoning.
Update: If you get too worked up by tactile sensations you could always get botox treatment in order to dampen your emotions. If you can't smile or frown you can't feel all that happy or sad.
The telomere caps on chromosomes shorten as you age. A prospective study finds shorter telomeres are linked to a higher risk of cancer.
Peter Willeit, M.D., of Innsbruck Medical University, Innsbruck, Austria, and colleagues conducted a study to assess the association between leukocyte telomere length and risk of both new-onset cancer and cancer death. Leukocyte telomere length was measured by quantitative polymerase chain reaction (laboratory technique used to analyze DNA) in 787 participants, free of cancer in 1995, and part of the prospective, population-based Bruneck Study in Italy. The primary outcomes analyzed included the incidence of new cancer and cancer mortality over a follow-up period of 10 years (1995-2005).
During follow-up, a total of 92 of 787 participants (11.7 percent) developed cancer. Analysis indicated that short telomere length at the beginning of the study was associated with new cancer independently of standard cancer risk factors. Compared with participants in the longest telomere length group, participants in the middle length group had about twice the risk of cancer, and those in the shortest length group had approximately three times the risk. Cancer incidence rates were inversely related to telomere length, with participants in the group with the shortest telomere length having the highest rate of cancer.
The obvious question: what's the direction of causality? I am guessing that short telomeres are not causing cancer. One possibility: cells that have shorter telomeres have lived tougher lives (metaphorically speaking) and are more damaged than cells in same age people who have longer telomeres. While that's probably true of the cells of the body as a whole I suspect another mechanism is at work with leukocytes. More on this below
It would be interesting to know whether short telomeres in leukocytes is well correlated with short telomeres in other cell types, especially in the cell types listed here as having become cancerous.
Short telomere length was also associated with a higher rate of death from cancer. "Of note, telomere length was preferentially associated with individual cancers characterized by a high fatality rate such as gastric, lung, and ovarian cancer, but less so with tumors linked to better prognosis," the authors write. They add that telomere length had a similar predictive value for cancer in both men and women and in various age groups.
So what's the other mechanism of causation I suspect? Leukocytes are white blood cells. In other words, immune cells. White blood cells do not just kill invading cells. The immune system also (sometimes) goes after cancer. Leukocytes with short telomeres are less able to divide and therefore are less able to mount an attack against cancer cells. It could be that short telomeres matter because they indicate an aged immune system that won't fight cancer.
Dr. Zheng Cui of Wake Forest University has found that some special mice and rare people have extreme anti-cancer immune systems. He has also found that the anti-cancer capability of immune systems decline with age. That decline in anti-cancer capability is due in part to immune cells losing the ability to divide due to worn down telomeres.
What we need to slash our risks of cancer: Rejuvenated immune systems.
In 2009, and in absolute terms, about 19.9% (608 TWh) of Europe's total electricity consumption (3042 TWh) came from renewable energy sources. Hydro power contributed with the largest share (11.6%), followed by wind (4.2%), biomass (3.5%), and solar (0.4%).
With regards to the new capacity constructed that same year (27.5 GW), among the renewable sources, 37.1% was wind power, 21% photovoltaics (PV), 2.1% biomass, 1.4% hydro and 0.4% concentrated solar power, whereas the rest were gas fired power stations (24%), coal fired power stations (8.7%), oil (2.1%), waste incineration (1.6%) and nuclear (1.6%) (see figure1).
Sounds like big growth for renewables, right? But since the wind does not always blow and the sun does not always shine (especially so far north where Europe is located) new wind and new solar together will generate less electricity than new natural gas alone.
As not all installed technologies operate continuously 24 hours a day, figure 2 shows the expected yearly energy output (TWh) from the new capacity. The new gas-fired electricity plants will deliver yearly 28 TWh, followed by wind and PV with 20 TWh and 5.6 TWh, respectively.
New coal-fired plants (at a third of natural gas's capacity with similar or higher load factors) will probably generate more power than solar but less than wind.
In order for renewables to supply 35-40% of European power by 2020 current growth rates would need to be maintained. My guess is that'll be hard to do. Growth rates imply compound growth. So larger amounts get installed each year. Well, does Europe have enough wind sites to scale up that far?
If current growth rates are maintained, in 2020 up to 1400 TWh of electricity could be generated from renewable sources, the report concludes. This would account for approximately 35-40% of overall electricity consumption in the EU, depending on the success of community policies on electricity efficiency, and would contribute significantly to the fulfilment of the 20% target for energy generation from renewables.
Europe is not well situated for solar. Also, the place is very densely populated and does not feature an area equivalent to America's windy plains states with high quality wind. So wind power is more expensive in Europe. If the Europeans really want to displace fossil fuels they need to make a much harder look at nuclear. France leads the way on that score, already getting most of their electric power from nuclear power plants.
This post is written for chocolate lovers who need an excuse to eat dark chocolate. Research funded by Mars finds cocoa flavanols improved blood flow in heart disease patients at UC San Francisco.
A new study by UCSF cardiologists and researchers found that high concentrations of cocoa flavanols decrease blood pressure, improve the health of blood vessels and increase the number of circulating blood-vessel-forming cells in patients with heart disease. The findings indicate that foods rich in flavanols – such as cocoa products, tea, wine, and various fruits and vegetables – have a cardio-protective benefit for heart disease patients.
Findings will be published online July 5th and in the July 13, 2010 issue of the Journal of the American College of Cardiology (JACC).
One wonders whether most people who aren't currently suffering from known heart disease would benefit from the cardio-protective effects. My guess is that as you get older the odds rise that flavanols would benefit you. Anyone know how good the tests are at this point for measuring blood vessel health around the heart? Could test results point one in the direction of whether one should take steps to improve blood flow?
Cocoa is not the only source of flavanols.
Flavanols are phytonutrient compounds that are found naturally in apples, grapes, tea, cocoa and cherries, which account for the antioxidant effect provided by red wine and green tea. The study found a protective effect from a cocoa drink with 375 mg of flavanols, but according to researchers, a standard or recommended dosage has not yet been defined to achieve optimal health benefit.
For how to get the good stuff in food also see my previous post Flavonols In Cocoa Powder And Other Foods.
The flavanols appear to improve the process of angiogenesis (growth and repair of blood vessels by stem cells).
I worry a bit about the angiogenic effect of flavanols. Angiogenesis is essential for cancer growth. Tumor cells that haven't mutated to secrete angiogenesis compounds can't get the vascular growth they need to form bigger tissue masses. One can encourage too much vascular growth.
The UCSF team has shown for the first time that one of the possible mechanisms of flavanol's benefit is an increase in the circulation of so-called angiogenic cells in the blood. These cells, also known as early endothelial progenitor cells, are critical for the repair process after vascular injury, and perform function and maintenance roles in the endothelium. Endothelium is the thin layer of cells that line the interior wall of blood vessels.
A previous study in the Netherlands found a reduction in all cause mortality from cocoa consumption. It is not clear whether this finding would hold up in a larger scale trial.
While I write posts about the health benefits of individual foods I think one should try to improve one's diet in a general way rather than just focus on a few foods. Loren Cordain's Paleo Diet is worth considering if you want to eat a better diet. The general idea: eat foods that sustained pre-industrial cultures. Those are the foods we evolved to be adapted to. Also, read about which parts of the Mediterranean diet really matter. The devil's in the details. Even at the granularity of oil or olive oil the quality of the oil matters. See the discussion in the comments about phenolic compounds in types of olive oil and whole olives.
Try this as an exercise: put yourself in a situation where you feel anxious. Then introspect. When you feel anxious do you suddenly find yourself wanting to fly an airplane into a skyscraper?
TORONTO, July 6, 2010 – Anxiety and uncertainty can cause us to become more idealistic and more radical in our religious beliefs, according to new findings by York University researchers, published in this month's issue of the Journal of Personality and Social Psychology.
In a series of studies, more than 600 participants were placed in anxiety-provoking or neutral situations and then asked to describe their personal goals and rate their degree of conviction for their religious ideals. This included asking participants whether they would give their lives for their faith or support a war in its defence.
What do you think about when you struggle with difficult mathematical equations or proofs? Wiping out your enemies in an epic battle? Or the need for a couple of beers?
Across all studies, anxious conditions caused participants to become more eagerly engaged in their ideals and extreme in their religious convictions. In one study, mulling over a personal dilemma caused a general surge toward more idealistic personal goals. In another, struggling with a confusing mathematical passage caused a spike in radical religious extremes. In yet another, reflecting on relationship uncertainties caused the same religious zeal reaction.
I'm not remotely idealistic. So I'd go for the beer and think more about the potential for the beer silicon to make my bones stronger than the ability of a C4 vest to blow my bones and the bones of many others to bits. Some might fault me for my decadence.
Bottom line: Keep Muslims with bold personalities but low IQs out of Western math classes.
Researchers found that religious zeal reactions were most pronounced among participants with bold personalities (defined as having high self-esteem and being action-oriented, eager and tenacious), who were already vulnerable to anxiety, and felt most hopeless about their daily goals in life.
Bold guys need to be able to excel and dominate. It is an evolutionary imperative. Should they happen to believe a religion that leads them to see car bombs as the road to success then you've got a problem if they live near you. I would tend to want to keep them in smaller countries where they can achieve higher relative status. The desire for higher status causes all sorts of problems that capitalism does not solve.
Cocaine addiction and love are similar. So should love be banned along with cocaine? Or should the Betty Ford Center start treating jilted lovers?
July 6, 2010 – (BRONX, NY) – Researchers have linked rejection by a romantic partner to brain activity associated with motivation, reward and addiction cravings, according to a study published in the July issue of the Journal of Neurophysiology. Lucy Brown, Ph.D., clinical professor in the Saul R. Korey Department of Neurology and of neuroscience at Albert Einstein College of Medicine of Yeshiva University, is the corresponding author of the study. This is the third publication in which Dr. Brown and her research group demonstrated that primitive reward and survival systems are activated in people who look at their beloved.
Using functional magnetic resonance imaging (fMRI), researchers recorded the brain activity of 15 college-age adults who had recently been rejected by their partners but reported that they were still intensely "in love." Upon viewing photographs of their former partners, several key areas of participants' brains were activated, including the ventral tegmental area, which controls motivation and reward and is known to be involved in feelings of romantic love; the nucleus accumbens and orbitofrontal/prefrontal cortex, which are associated with craving and addiction, specifically the dopaminergic reward system evident in cocaine addiction; and the insular cortex and the anterior cingulate, which are associated with physical pain and distress.
It is only natural to stalk your dealer when you are being force to kick the addiction.
By tying these specific areas of the brain to romantic rejection, the research provides insight into the anguished feelings that can accompany a break-up, as well as the extreme behaviors that can occur as a result, such as stalking, homicide and suicide.
Hey, if love is a natural addiction and drugs are developed to cure drug addictions I bet these drugs will enable us to avoid falling in love and to fall out of love more quickly.
"Romantic love, under both happy and unhappy circumstances, may be a 'natural' addiction," said Dr. Brown. "Our findings suggest that the pain of romantic rejection may be a necessary part of life that nature built into our anatomy and physiology. A natural recovery, to pair up with someone else, is in our physiology, too."
Of course, a new hook-up can work. If you think you are going to get dumped then time to start cheating on the sly. Think of it as like methadone if you don't feel all that strongly for your new lay.
In the study, researchers used functional magnetic resonance imaging (fMRI) to record brain activity in 15 college-age, heterosexual men and women who had recently been rejected by their partners but reported that they were still intensely "in love." The average length of time since the initial rejection and the participants' enrollment in the study was 63 days, and all participants scored high on a psychological test called the Passionate Love Scale, which determines the intensity of romantic feelings. All participants said they spent more than 85% of their waking hours thinking of the person who rejected them, they yearned for the person to return and they wanted to get back together.
TORONTO, Ont., July 6, 2010 — Nearly 60 per cent of Ontarians with rheumatoid arthritis — an autoimmune disease that causes chronic inflammation of the joints — were not seen by a specialist within a one year period to treat the debilitating disease, according to a new study. Even more concerning is that women of child-bearing age are less likely to see a specialist than women 45 or older, say researchers from St. Michael's Hospital, the Institute for Clinical and Evaluative Sciences (ICES), and Women's College Hospital.
A Canadian friend (living in southern Ontario at the time) complained to me for years that he couldn't get a general practitioner. Without a general practitioner he couldn't get a referral to a specialist. He got his medical care by going to emergency wards. This all made me very unkeen on Canadian health care as a model for the US.
Of course US health care has big problems of its own. But if you've got the cash (and/or plush insurance policy) you're better off getting your care in the US. The value of cash will be even greater in the future as political systems ration care in order to cut costs. You can be for the miracle of more market forces or the miracle of government as single provider. But come what may you are better off if you have lots of cash to pay for care directly (possibly in other countries if you are like Canadians who have little access to pay-for-service health care).
My advice to Americans: accumulate cash in a Health Savings Account with a high deductible policy starting while you are young. Put in the max contribution every year. Save money in other ways too. The accumulated cash will help pay for your health care when you get older. If you are young then for sure that cash will help you pay for rejuvenation therapies. Someone in their 20s who doesn't die prematurely will live long enough to get excellent rejuvenation therapies.
If you save up big piles of money (and are willing to travel) you'll be able to get those rejuvenation therapies sooner. The time gap between narrow and wide availability might be wide enough to be a matter of life and death for you. In your 40s, 50s, 60s? It is especially true for you.
Blame your genes if you can't stop smoking cigarettes. Researchers at Duke University Medical Center and the National Institute on Drug Abuse (NIDA) find that the best dose nicotine patch for those quitting smoking depends on differences in genetic variants.
In the trial, 479 cigarette smokers who smoked at least 10 cigarettes per day and wanted to quit were categorized as either high- or low-dependence based on their level of nicotine dependence. The smokers in each group were then randomly assigned to wear two nicotine skin patches daily delivering a high dose ( (42mg) or a standard dose (21 mg). Patches were worn for two weeks prior to their quit date, and the nicotine doses were reduced gradually over the 10 weeks following their quit date. Participants were given denicotinized cigarettes during the two weeks before the quit date to minimize any potential adverse effects from the high dose nicotine patches. The treatment phase lasted for 12 weeks in all.
DNA was extracted from participants' blood and was used to assess a quit-smoking success genetic score.
At six months follow up, the researchers were able to confirm which smokers fared better or worse on the high-dose compared to the low-dose patch.
"The genotype score was part of what predicted successful abstinence. In the future such a score could help us make our initial treatment decisions," said Rose. "People who had both high nicotine dependence and a low or unfavorable quit success genetic score seemed to benefit markedly from the high-dose nicotine patch, while people who had less dependence on nicotine did better on the standard patch."
Genetic differences influence not only the difficulty in kicking an addiction but also the susceptibility to becoming addicted in the first place. For example, Mono Amine Oxidase (MAO) inhibition by tobacco compounds probably enhances addiction and genetic variants in MAO appear to influence risk of addiction.
Humans differ genetically in their capacity to be exposed to addictive drugs without becoming addicted. Keep this in mind the next time you see an addicted person acting destructive toward self and others. Some of those addicted people have genetic variants that make kicking their addiction especially difficult.
"You've got to ask yourself one question: Do I feel lucky? Well, do ya, punk?" Do you feel lucky enough to carry lots of long life genetic variants?
While environment and family history are factors in healthy aging, genetic variants play a critical and complex role in conferring exceptional longevity, according to a new study by a team of researchers from the Boston University Schools of Public Health and Medicine and the Boston Medical Center.
In a study released July 1 online by the journal Science, the research team identified a group of genetic variants that can predict exceptional longevity in humans with 77 percent accuracy – a breakthrough in understanding the role of genes in determining human lifespan.
Based upon the hypothesis that exceptionally old individuals are carriers of multiple genetic variants that influence their remarkable survival, the team conducted a genome-wide association study of centenarians. Centenarians are a model of healthy aging, as the onset of disability in these individuals is generally delayed until they are well into their mid-nineties.
Unfortunately we can't pick our own genetic variants (yet). To learn today whether you have shorter or longer life genetic is more akin to learning when your death sentence will be carried out.
At least 150 genetic variants matter for your odds of living a very long time. If you could know how many of these genetic variants you carry would you want to know?
Researchers led by Paola Sebastiani, PhD, a professor of biostatistics at the BU School of Public Health and Thomas Perls, MD, MPH, associate professor of medicine at the BU School of Medicine and a geriatrician at Boston Medical Center, built a unique genetic model that includes 150 genetic variants, known as single nucleotide polymorphisms (SNPs). They found that these 150 variants could be used to predict if a person survived to very old ages (late 90s and older) with a high rate of accuracy.
In addition, the team's analysis identified 19 genetic clusters or "genetic signatures" of exceptional longevity that characterized 90 percent of the centenarians studied. The different signatures correlated with differences in the prevalence and age-of-onset of diseases such as dementia and hypertension, and may help identify key subgroups of healthy aging, the authors said.
Notably, the team found that 45 percent of the oldest centenarians – those 110 years and older – had a genetic signature with the highest proportion of longevity-associated genetic variants.
The obvious question: What could we as individuals do with this information if we could know from our genetic profile how long we had to live? My first reaction: Not much. But wait. If you knew you had decent odds of living to 100 you'd know to save more for retirement and work more years before retiring. That's a good idea anyway (what with governments unable to afford to deliver all the promises they've made for old age benefits). But accumulation of big savings is an especially good idea if your genetic profile suggests you have higher odds of living into your 90s and possibly beyond. So genetic testing as retirement planning guide. That's the ticket.
Genetic profiles that predict longevity are initially more useful for researchers. That's part of a larger pattern where the tons of DNA sequencing information hasn't turned out to be immediately useful for treating diseases but is helping researchers learn which genetic variations cause which changes in gene expression and in differences in disease risks, special abilities (e.g. ability to live at high altitudes), personality traits, intelligence, and other ways in which humans differ.
How can researchers use genetic information linked to life expectancy to help those of us not born with genes that'll make us into centenarians? I see a few ways:
I am skeptical about the drug approach mostly because, if the study above is correct, the centenarians have many genetic differences which account for their longer lives. Many differences that matter mean many drug targets which means develop many drugs to make a big difference. Each drug would cost about $1 billion to develop and each would therefore be expensive to buy month after month, year after year. Even if a few drugs could target a few of those differences the drugs still wouldn't target all the differences. Plus, drugs frequently have side effects. Plus, the drugs would have to be taken for decades to make a difference which means the tedium of taking the drugs for decades as well as dealing with side effects for decades.
Similarly, I think there's a limit to what diet can accomplish. Those old Dannon yogurt commercials aside, it doesn't look like there's a diet that will enable most people to live to 90, let alone 100.
One might expect fewer of the already known disease-associated genetic variants to be found in centenarians. But the disease-associated genetic variants did not appear to make much of an impact.
Besides looking at which genetic variants were associated with longevity, the authors looked into whether the absence of disease-associated variants also played an important role. They did this by analyzing how many disease-associated variants each centenarian had, compared to each of the controls. Their analysis found little difference between the two groups, suggesting that the presence of genetic variants associated with longevity is of more importance than the absence of disease-associated variants.
Biogerontologist Aubrey de Grey argues that we should focus our efforts on developing treatments that repair the damage caused by aging. Even if we can eventually slow down the rate of aging using drugs we'll all be older by the time those drugs hit the market and those drugs won't reverse the damage already done. At best they'll make the downhill slope from that point on not as steep as it otherwise would be. We'll still grow old just like the centenarians.
Consider the idea of gene therapy and cell therapy to alter our metabolism to slow aging. Once researchers develop workable cell therapies it seems more sensible to first apply these cell therapies to repair of damage. If we can send in replacement cells that have also been altered to last longer (by, say, first altering the cells to contain the 150 genetic variants mentioned above) then all the better. But the capability to do repairs is more important than how long the repairs will last.
To examine whether increased fructose consumption has contributed to rising rates of hypertension, Diana Jalal, MD (University of Colorado Denver Health Sciences Center and her colleagues analyzed data from the National Health and Nutrition Examination Survey (2003-2006). The study involved 4,528 US adults 18 years of age or older with no prior history of hypertension. Study participants answered questions related to their consumption of foods and beverages such as fruit juices, soft drinks, bakery products, and candy. Dr. Jalal’s team found that people who consumed a diet of 74 grams or more per day of fructose (corresponding to 2.5 sugary soft drinks per day) had a 26%, 30%, and 77% higher risk for blood pressure levels of 135/85, 140/90, and 160/100 mmHg, respectively. (A normal blood pressure reading is below 120/80 mmHg.)
To put that 74 grams of fructose in context: You get about 11 grams of fructose in a medium sized apple. Will eating 7 apples a day harm you? Certainly it is better than eating 2.5 sugary soft drinks every day.
The health effects of fructose consumption have become a controversial topic. Robert Lustig most notably bashes fructose as a big cause of the obesity epidemic. But see Alan Aragon on fructose and be sure to read the exchange between him and Lustig in the comments.
Fruits have phenolics and other compounds in them that are probably good for your health. I'd really like to know how much fruits one should eat per day for optimal benefit. At what level of fruit consumption does fructose become a problem that outweighs the benefits of fruits?
A comparison of the genomes of 50 Tibetans and 40 Han Chinese shows that ethnic Tibetans split off from the Han less than 3,000 years ago and since then rapidly evolved a unique ability to thrive at high altitudes and low oxygen levels.
A common misperception is that evolutionary changes require tens or hundreds of thousands of years. Not so. Given strong enough selective pressures mutations can spread very rapidly. Humans have developed many adaptations to adjust them to local conditions. Altitude is just one of the environmental challenges which humans have evolved to handle in local regions. Among the many local adaptations: lactase enzyme upregulation among pastoral populations that derived a substantial fraction of their calories from animal milk. Differences in alcohol tolerance in northern and southern European peoples also probably comes as a result of selective pressures in areas where more alcohol was produced.
Many genes were involved in the evolution of Tibetan adaptation to high altitude living.
The genome-wide comparison, performed by evolutionary biologists at the University of California, Berkeley, uncovered more than 30 genes with DNA mutations that have become more prevalent in Tibetans than Han Chinese, nearly half of which are related to how the body uses oxygen. One mutation in particular spread from fewer than 10 percent of the Han Chinese to nearly 90 percent of all Tibetans.
Evolution happens due to different death rates between carriers of different genetic variations. Lots of people died early while others died later (after reproducing) to adapt Tibetans to their ecological niche.
"This is the fastest genetic change ever observed in humans," said Rasmus Nielsen, UC Berkeley professor of integrative biology, who led the statistical analysis. "For such a very strong change, a lot of people would have had to die simply due to the fact that they had the wrong version of a gene."
The fastest change observed in human evolution took place in 3000 miles? See this book for an example of a human evolutionary adaptation that took place in several hundred years.
The continued decline in DNA sequencing costs is set to unleash a huge flood of discoveries about human genetic adaptations which developed in ecological niches around the globe. I expect that every organ in the body has genetic variations that have adapted humans to different diets, weather, diseases, elevations, temperature ranges, local prey, and other local conditions.
Also see my previous post Tibetans Genetically Adapted To High Altitude.
OAK BROOK, Ill. – Arthroscopic surgical repair of torn anterior cruciate ligaments (ACL) or meniscal cartilage injuries in the knee does not decrease the chances of developing osteoarthritis, according to a new study published in the online edition and August print issue of the journal Radiology.
There's a lesson in this sort of report: Surgery falls way short of full repair of tissue damage. The long term effects of those injuries is to accelerate aging. Surgery is inadequate because surgeons can not instruct cells how to do repairs.
If you've had an ACL tear or cartilage damage then osteoarthritis lies in your future until cell therapies and gene therapies are developed that can do full repair.
A decade after the initial injuries were diagnosed using MRI, localized knee osteoarthritis was evident in patients, regardless of whether or not the injuries had been surgically repaired.
"This study proves that meniscal and cruciate ligament lesions increase the risk of developing specific types of knee osteoarthritis," said Kasper Huétink, M.D., the study's lead author and resident radiologist at Leiden University Medical Center in the Netherlands. "Surgical therapy does not decrease that risk."
Gotten yourself pretty banged up by sports, yard work, or an accidental fall? You need the development of gene therapies and cell therapies to render you fully repaired. Otherwise painful arthritis lies in your future.