Here's a tour through a large assortment of studies on dietary and lifestyle factors that influence prostate cancer risks. Men who are willing to implement most of the recommendations here would greatly decrease their odds of getting prostate cancer. Note that many of the changes (e.g. less omega 6 fatty acids, more omega 3 fatty acids, less meat, more vegetables, more fruit, more vitamin D) would reduce the risks of other forms of cancer as well. Daily ground flaxseed made diagnosed prostate cancer cells less vigorous.
The researchers will present their results on Saturday, June 2, during a news briefing at the annual meeting of the American Society of Clinical Oncology, in Chicago. The multisite study, which was funded by the National Institutes of Health, also involved researchers at the University of Michigan and the University of North Carolina at Chapel Hill.
In the study, the researchers examined the effects of flaxseed supplementation on men who were scheduled to undergo prostatectomy -- surgery for the treatment of prostate cancer. The men took 30 grams of flaxseed daily for an average of 30 days prior to surgery. Once the men's tumors were removed, the researchers looked at tumor cells under a microscope, and were able to determine how quickly the cancer cells had multiplied.
Men taking flaxseed, either alone or in conjunction with a low-fat diet, were compared to men assigned to just a low-fat diet, as well as to men in a control group, who did not alter or supplement their daily diet. Men in both of the flaxseed groups had the slowest rate of tumor growth, Demark-Wahnefried said. Each group was made up of about 40 participants.
Study participants took the flaxseed in a ground form because flaxseed in its whole form has an undigestible seed coat, she said. Participants elected to mix it in drinks or sprinkle it on food, such as yogurt.
You'd probably need to get a seed grinder to make the ground seed once or twice a week. Though maybe freezing would let you make it less often.
Nutritionists recommend that people consume equal proportions of omega-3 and omega-6 PUFA. However, in current western diets, the proportion of omega-6 to omega-3 is between 30 and 50 to one.
The mice were fed either a diet high in omega-3 (ratio of omega-6 to omega-3 was 1:1) a diet low in omega 3 (ratio omega-6 to omega-3 was 20:1), or a diet high in omega-6 (ratio of omega-6 to omega-3 was 40:1). The scientists compared survival rates and weighed the animals’ prostates to measure tumor progression.
Mice with the tumor suppressor gene remained free of tumors and had 100 percent survival, regardless of diet. In mice with the gene defect, survival was 60 percent in animals on the high omega-3 diet, 10 percent in those on the low omega-3 diet and 0 percent in those on the high omega-6 diet.
“This suggests that if you have good genes, it may not matter too much what you eat,” said Chen, a professor of cancer biology. “But if you have a gene that makes you susceptible to prostate cancer, your diet can tip the balance. Our data demonstrate the importance of gene-diet interactions, and that genetic cancer risk can be modified favorable by omega-3 PUFA.”
The research team then progressed to tests in mice that had been injected with prostate cancer cells from humans and developed malignancies. The 24 mice were randomly divided into three groups. The control group received normal drinking water, while the animals in the second and third groups had their drinking water supplemented with .1 percent and .2 percent pomegranate extract respectively. The doses for the mice were chosen to parallel how much pomegranate juice a typical healthy human might be willing to eat or drink daily.
The results were dramatic: the mice receiving the higher concentration of pomegranate extract showed significant slowing of their cancer progression and a decrease in the levels of prostate-specific antigen (PSA), a marker used to indicate the presence of prostate cancer in humans. The animals that received only water had tumors that grew much faster than those in the animals treated with pomegranate extract.
Drinking an eight ounce glass of pomegranate juice daily increased by nearly four times the period during which PSA levels in men treated for prostate cancer remained stable, a three-year UCLA study has found.
The study involved 50 men who had undergone surgery or radiation but quickly experienced increases in prostate-specific antigen or PSA, a biomarker that indicates the presence of cancer. UCLA researchers measured "doubling time," how long it takes for PSA levels to double, a signal that the cancer is progressing, said Dr. Allan Pantuck, an associate professor of urology, a Jonsson Cancer Center researcher and lead author of the study.
Compound found in high-fiber foods shows promise against prostate cancer — A dietary component found in most whole grain foods, beans, nuts and other high-fiber items shows promise in animal studies as a potent weapon for preventing prostate cancer. The compound, inositol hexaphosphate (IP6), was fed to animal models of prostate cancer and resulted in up to a 66 percent reduction in tumor size in comparison to control animals that were given water instead, the researchers say.
Rutgers researchers have found that the curry spice turmeric holds real potential for the treatment and prevention of prostate cancer, particularly when combined with certain vegetables.
The scientists tested turmeric, also known as curcumin, along with phenethyl isothiocyanate (PEITC), a naturally occurring substance particularly abundant in a group of vegetables that includes watercress, cabbage, winter cress, broccoli, Brussels sprouts, kale, cauliflower, kohlrabi and turnips. "The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," said Ah-Ng Tony Kong, a professor of pharmaceutics at Rutgers, The State University of New Jersey.
SEATTLE – Drinking a glass of red wine a day may cut a man's risk of prostate cancer in half, and the protective effect appears to be strongest against the most aggressive forms of the disease, according to a new study led by investigators at Fred Hutchinson Cancer Research Center.
The study was directed by Dean Ornish, MD, clinical professor, and Peter Carroll, MD, chair of the Department of Urology, both of the University of California, San Francisco, and the late William Fair, MD, chief of urologic surgery and chair of urologic oncology, Memorial Sloan-Kettering Cancer Center.
The research team studied 93 men with biopsy-proven prostate cancer who had elected not to undergo conventional treatment for reasons unrelated to this study. The participants were randomly divided into either a group who were asked to make comprehensive changes in diet and lifestyle or a comparison group who were not asked to do so.
After one year, the researchers found that PSA levels (a protein marker for prostate cancer) decreased in men in the group who made comprehensive lifestyle changes but increased in the comparison group. There was a direct correlation between the degree of lifestyle change and the changes in PSA. Also, they found that serum from the participants inhibited prostate tumor growth in vitro by 70 percent in the lifestyle-change group but only 9 percent in the comparison group. Again, there was a direct correlation between the degree of lifestyle change and the inhibition of prostate tumor growth.
Participants in the lifestyle-change group were placed on a vegan diet consisting primarily of fruits, vegetables, whole grains, and legumes supplemented with soy, vitamins and minerals. They participated in moderate aerobic exercise, yoga/meditation, and a weekly support group session. A registered dietitian was available for consultation, and a nurse case manager contacted the participants once a week for the first three months and weekly thereafter.
The study, published in the September issue of Integrative Cancer Therapies, focused on the change in the levels of prostate-specific antigen (PSA), an indicator of the cancer, in response to a plant-based diet and stress reduction. Patients were taught to increase consumption of plant-based foods such as whole grains, cruciferous and leafy green vegetables, beans and legumes, and fruit, and to decrease the intake of meat, dairy products, and refined carbohydrates. They were also provided with stress management training, which incorporated meditation, yoga and Tai Chi exercises. The plant-based diet and stress reduction were effective in significantly reducing the PSA rate, indicating a reduction in the rate of progression of the prostate cancer.
My guess is you'll be much better off if you avoid grains and just eat non-grain plants. I wonder if the stress management techniques contributed to the benefit.
The diet changes were made for men with early stage prostate cancer. But the smarter thing to do is to make the diet changes before you get prostate cancer.
Up to 73% of men with prostate cancer take nonprescription supplements, and smaller numbers use diet, exercise, or both in the hope of improving their outcome. Most of these men also receive conventional therapy, but a few depend on lifestyle alone. The appeal of lifestyle therapy is obvious—but does it work? Experts don’t know, though research raises hope that it may have a beneficial impact, reports the July 2007 issue of Harvard Men’s Health Watch.
All of the 93 men who signed up for the trial had newly diagnosed low- to moderate-grade cancers that were localized to the prostate gland. Half were randomly assigned to a lifestyle program, and half got no advice on lifestyle changes. The program that researchers created included four elements: An ultra-low-fat vegan diet; supplements, including soy, fish oil, vitamins E and C, and selenium; an exercise program of walking 30 minutes six days a week; and stress reduction that included yoga-based stretching, breathing, and meditation for an hour a day.
At the end of a year, a small but significant difference was evident. The average PSA in the intensive lifestyle group fell, whereas the average PSA in the untreated men rose. The participants in the lifestyle group also showed favorable cancer-fighting changes in their blood.
“I was very surprised by the findings,” said Kristal, member and associate head of the Cancer Prevention Program in the Hutchinson Center’s Public Health Sciences Division. “We found the prostate-cancer-specific mortality risk associated with obesity was similar regardless of treatment, disease grade or disease stage at the time of diagnosis,” he said. “If a man is obese at the time of diagnosis, he faces a 2.6-fold greater risk of dying as compared to a normal-weight man with the same diagnostic profile, regardless of whether he has a radical prostatectomy or radiation therapy, whether or not he gets androgen-deprivation therapy, whether he has low- or high-grade disease and whether he has localized, regional or distant disease,” Kristal said, referring to the degree of cancer spread.
The researchers also found that obese men diagnosed with local or regional disease – that is, disease that is confined to the prostate or has spread to into surrounding tissue – face a 3.6-fold increased risk of cancer spreading into distant organs, or metastasis, as compared to prostate-cancer patients of normal weight.
PHILADELPHIA – The largest study examining the relationship between the traditional soy-rich Japanese diet and development of prostate cancer in Japanese men has come to a seemingly contradictory conclusion: intake of isoflavone chemicals, derived largely from soy foods, decreased the risk of localized prostate cancer but increased the risk of advanced prostate cancer.
The prospective study of 43,509 men, published in the March issue of Cancer Epidemiology, Biomarkers & Prevention, suggests that the effects of isoflavones on prostate cancer development may differ according to disease stage, say researchers at the National Cancer Center in Japan.
One possible explanation is that isoflavones may delay the progression of latent prostate cancer only; once tumors lose estrogen-receptor beta expression and become aggressive, isoflavones may fail to protect against the development of advanced cancer, and might even increase the risk of progression, possibly by reducing serum testosterone, researchers say. It is also possible that advanced and localized prostate cancer may be different tumor subtypes, which may react differently to isoflavones.
PHILADELPHIA -- Tomatoes might be nutritious and tasty, but don’t count on them to prevent prostate cancer. In the May issue of Cancer Epidemiology, Biomarkers & Prevention, researchers based at the National Cancer Institute and Fred Hutchinson Cancer Research Center report that lycopene, an antioxidant predominately found in tomatoes, does not effectively prevent prostate cancer. In fact, the researchers noted an association between beta-carotene, an antioxidant related to lycopene, and an increased risk for aggressive prostate cancer.
According to the researchers, the study is one of the largest to evaluate the role of blood concentrations of lycopene and other carotenoid antioxidants in preventing prostate cancer. Study data were derived from over 28,000 men enrolled in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, an ongoing, randomized National Cancer Institute trial to evaluate cancer screening methods and to investigate early markers of cancer.
Karla Lawson, Ph.D., of the National Cancer Institute in Bethesda, Md., and colleagues followed 295,344 men enrolled in the National Institutes of Health-AARP Diet and Health Study to determine the association between multivitamin use and prostate cancer risk. After five years of follow-up, 10,241 men were diagnosed with prostate cancer, including 8,765 with localized cancers and 1,476 with advanced cancers.
The researchers found no association between multivitamin use and the risk of localized prostate cancer. But they did find an increased risk of advanced and fatal prostate cancer among men who used multivitamins more than seven times a week, compared with men who did not use multivitamins. The association was strongest in men with a family history of prostate cancer and men who also took selenium, beta-carotene, or zinc supplements.
As long term readers know by now, the cancer risk reduction benefit from vitamin D is much clearer than that from other vitamins. See the posts 60% Cancer Drop From Vitamin D Supplements and Vitamin D Could Decrease Overall Cancer Risk 30%.
The younger among you may be thinking that by the time you reach the high cancer risk years we'll have effective cures for cancer. A person in their 20s isn't going to die from cancer they get in the year 2047. But keep in mind that cancer is a consequence of accumulated cell damage. We'll have cures for cancer before we get full body rejuvenation therapies. A diet that reduces your risk of cancer will slow your body aging and therefore if you eat a cancer risk reduction diet you won't grow as old while waiting for the rejuvenation therapies.
The selective serotonin reuptake inhibitor (SSRI ) antidepressant drugs (e.g. Paxil, Zoloft, Prozac) are known to stimulate replication of brain stem cells to produce new neurons. The delay in the antidepressant action of SSRIs might be due to the delay before they start causing substantial neuron creation. Well, exercise has an antidepressant effect and perhaps not coincidentally exercise also causes new neuron generation in the brain.
Exercise has a similar effect to antidepressants on depression. This has been shown by previous research. Now Astrid Bjørnebekk at Karolinska Institutet has explained how this can happen: exercise stimulates the production of new brain cells.
In a series of scientific reports, she has searched for the underlying biological mechanisms that explain why exercise can be a form of therapy for depression and has also compared it with pharmacological treatment with an SSRI drug.
The experiment studies were conducted on rats. The results show that both exercise and antidepressants increase the formation of new cells in an area of the brain that is important to memory and learning. Astrid Bjørnebekk’s studies confirm previous research results, and she proposes a model to explain how exercise can have an antidepressant effect in mild to moderately severe depression. Her study also shows that exercise is a very good complement to medicines.
“What is interesting is that the effect of antidepressant therapy can be greatly strengthened by external environmental factors,” she says.
There's a practical question here for people suffering from depression: Do exercise and SSRI add up together to an antidepressant effect that is greater than either of them alone?
What I want to know: How does exercise stimulate brain cell growth? Blood pressure changes? Increased oxygen into the brain? Other?
Also, does exercise increase memory formation even in the non-depressed?
Our brains have an inertial reference unit (and FuturePundit reacts by thinking it would be great to have a far better one bioengineered into us).
Researchers have discovered a sophisticated neural computer, buried deep in the cerebellum, that performs inertial navigation calculations to figure out a person’s movement through space.
These calculations are no mean feat, emphasized the researchers. The vestibular system in the inner ear provides the primary source of input to the brain about the body’s movement and orientation in space. However, the vestibular sensors in the inner ear yield information about head position only. Also, the vestibular system’s detection of head acceleration cannot distinguish between the effect of movement and that of gravitational force.
Dora Angelaki and colleagues published their findings in the June 21, 2007 issue of the journal Neuron, published by Cell Press.
But if this inertial reference unit (IRU) place in the brain was really great then it could integrate a history of motion for a long time and tell you how far you've travelled on a trip just like aircraft IRUs can. So this discovery makes me think some scientists have found the location of a brain subsystem that is in need of a great deal of design improvement.
Can we come up with micro-miniature gyroscopes that can out-perform the semicircular canal of the inner ear in detecting motion and rotation?
Angelaki and colleagues based their brain studies on the predictions of a theoretical mathematical model postulating that the brain could compute inertial motion by combining rotational signals from the semicircular canal in the inner ear with gravity signals.
We need better gyros and better accelerometers. Plus, we need a better integrating biocomputer that constantly calculates one's location and velocity.
Watching an episode of that tired prequel Star Trek: Enterprise where genetically engineered Suliban fought Jonathan Archer in temporal war got me thinking about genetic engineering for decreased susceptibility to death from accident or murder. The Suliban had rather unusual skin that seemed like it might form a protective plating. I can imagine some humans deciding to sacrifice their looks for a reduced risk of death.
So here's what I want to know: 50 or 100 years from now (assuming the robots or nanobots do not take over and that we don't all just live in virtual reality) will people choose to genetically engineer themselves and their offspring to have biological protective plating and other enhancements to make them harder to kill? You might argue that most people won't do that. But won't some people do it?
Some forms of protection won't have any esthetic costs and so should be pretty popular. For example, blood-borne nanodevices that can store many hours of oxygen will make people much less at risk from drowning or smoke inhalation. Also, people will go for nanobots that can seal off arteries and veins severed in accidents or shootings. One can imagine nanobots that can serve as distributed blood pumps so that a shot to the heart couldn't kill you either. But after getting all the invisible protective enhancements some people will desire even more security and even greater defenses against sudden death.
So how about biologically constructed nanosheet body armor skin made by your own cells? Surely enzymes that can construct carbon nanotubes are a pretty small jump from enzymes that can create carbon polymer lipids for fat storage.
Body armor nanosheet skin coating will come with some downsides such as less attractive visual appearances and less soft touch. Unless other humans get their brains reengineered to get a sexual turn-on from such skin anyone who walks around with unnatural-looking skin will find their sexual options much more limited. But not everyone has a strong sex drive and some will choose to use a gene therapy to turn down their sex drive even lower so that their reduced physical attractiveness won't leave them feeling frustrated.
Silk worms can synthesis incredibly strong silk and other organisms make other powerful structural materials. The goal of creating skin cells that create armor seems quite attainable. Powerful computer simulations will help guide bioengineers in their search of the solution space to produce designs that can create incredibly strong materials. All the naturally occurring biological materials will serve as starting points. So the question comes down to esthetics. How much will people trade off looks in order to reduce their odds of sudden death?
Dastardly humans won't be able to fry the world with excessive amounts of fossil fuels burning because we do not have enough fossil fuels left to burn to cause a first class disaster? Mother Gaia wisely limited the amount of fossil fuels she created because she knew her human progeny would wreak disaster if tempted with too much oil and coal to burn? Writing at The Oil Drum CalTech professor Dave Rutledge argues that the mathematical method which petroleum engineer King Hubbard used to predict the date of US oil production peak can also be used to predict how much coal will get burned in the world. Rutledge, Cal Tech Chair for the Division of Engineering and Applied Science, says the UN Intergovernmental Panel on Climate Change (IPCC) models for future climate change assume fossil fuels supplies available to raise atmospheric CO2 which overstate future hydrocarbon burning by a factor of 3 or 4 or more.
Often we do not have enough data to fit for remaining production this way. In these situations, I will use a Hubbert linearization to estimate the remaining production, like we often do for oil. Hubbert introduced this approach for modeling oil production in "Techniques of Prediction as Applied to the Production of Oil and Gas," in Saul I. Gass, ed., Oil and Gas Supply Modeling, pp. 16-141. National Bureau of Standards special publication 631. Washington: National Bureau of Standards, 1982. This is a great paper. It is difficult to find, but you can download it here (15MB file). Figure 2 shows a Hubbert linearization for world hydrocarbon production. The trend line is for 3.2 trillion barrels of oil equivalent (Tboe) remaining. We will use this number for our simulation of future atmospheric CO2 concentrations and temperature rise. This is 20% larger than the reserves given by the German resources agency BGR, 2.7Tboe. The BGR includes 500Gboe for unconventional sources. In contrast, the IPCC assumes that 11-15Tboe is available for production for its climate-change scenarios.
This fits with my intuition: We face such a huge looming problem with fossil fuels exhaustion that we should be thinking about moving away from fossil fuels due to rising costs and lowered production rather than because we might melt the polar ice caps. We need to embrace solar, nuclear, and wind because we just do not have as much fossil fuels left as the climate doomsters think we do.
If the Peak Oil, Peak Natural Gas, and Peak Coal folks are correct then why do the IPCC types spend so much time talking about climate catastrophe? My guess: Human-caused climate disaster makes for a far more dramatic moral story of human sin. Talk of using up all the coal and oil doesn't satisfy the need to see human action in such sinful terms. If we run out of oil then we suffer from the exhaustion of the oil but nature doesn't suffer as much as we do. We sin, but against ourselves. By contrast, if we heat up the planet the argument can be made for humans as massive sinners against nature.
Rutledge doesn't see how the IPCC scenarios for future atmospheric CO2 levels can happen given the amount of unburned and usable fossil fuels that are left.
Now we are in a position to see what some consequences for climate are. We convert future hydrocarbon and coal production to atmospheric carbon emission using EIA coefficients and plot them as the Producer-Limited Profile in Figure 10, together with the carbon emissions from the 40 scenarios. The Producer-Limited Profile has lower emissions than any of the 40 scenarios. This would be true even if we calculated the emissions with the full coal reserves. Jean Laherrere was the first to call attention to this anomalous situation. He has made the point forcefully and repeatedly, to no apparent effect.
Rutledge argues for carbon sequestration in order to avoid the 1.8 C heating. That amount of heating doesn't really alarm me. The biggest advantage I can see from carbon sequestration is that it will serve as a tax on coal and oil that will increase the incentives to develop energy replacements. A more rapid development of replacement energy sources will reduce the disruptions that will come with the exhaustion of oil, coal, and natural gas fields.
These two reports suggest to me a big future role for preventative gene therapy. The first report provides preliminary evidence that gene therapy can lessen the symptoms of Parkinson's Disease.
MANHASSET, NY -- A novel gene therapy technique is safe and may be effective at staving off worsening symptoms of Parkinson's disease, according to the first scientific review of a dozen patients who have received the treatment over the last three years. The results were published in the latest issue of Lancet.
The patients, half of whom live on Long Island, are in advanced stages of the illness and were no longer responding to medicines when they signed on for the experimental therapy. The study was conducted by Andrew Feigin, MD, director of Neuroscience Experimental Therapeutics at The Feinstein Institute for Medical Research and his colleagues in collaboration with Parkinson’s scientists at New York Presbyterian Hospital-Weill Cornell Medical Center in Manhattan.
One woman and 11 men received a surgical infusion of fluid containing a viral vector and genes for a protein called GAD, glutamic acid decarboxylase. This enzyme is critical in controlling a neurotransmitter called GABA. In Parkinson’s, GABA is reduced in an area of the brain called the subthalamic nucleus. This region is working on overdrive in the disease process and GABA is an inhibitory transmitter and is important in trying to calm this hyper-reactive circuit.
This particular gene therapy does not fix the genes that are contributing to the development of Parkinson's Disease. But the good news is that the therapy appears to successfully deliver genes into brain cells.
The gene therapy would be used to reduce symptoms and not alter the underlying disease process. Finding novel therapies are key as many Parkinson’s patients stop develop complications after prolonged use of traditional medicines.The Feinstein’s David Eidelberg, MD, took brain scans before, during and after the treatment and the scans show that the brain is re-working these abnormal circuits. Dr. Feigin said that patients had about a 27 percent improvement in symptoms, although the study was an open label design. The scientists are now designing a double-blind placebo controlled trial that would enroll far more patients in an attempt to see whether the gene therapy is effective in reducing symptoms.
A far better gene therapy would target the genes that contribute to the development of Parkinson's in the first place. Well, a Mayo Clinic group used the rapidly falling costs of genetic testing to look at lots of genes in Parkinson's sufferers and they found combinations of genetic variations highly predictive for the development of Parkinson's Diseases.
“By examining a large cluster of related genes, we found patterns that make people up to 90 times more likely to develop Parkinson’s than the average person,” says study co-author Timothy Lesnick, a Mayo Clinic biostatistician. “The size of the effects that we observed for genes within a pathway and the statistical significance of the predictive models were unprecedented.”The models were highly effective in predicting age of onset of the disease: by age 60, 91 percent of patients in the highest-risk group already had Parkinson’s, while only 11 percent of patients in the lowest-risk group did. By age 70, every member of the highest-risk group had the disease, whereas two-thirds of patients in the lowest-risk group still were disease-free. Members of the highest-risk group typically developed Parkinson’s more than 20 years earlier than the lowest-risk group.
These two reports are a great example of why personal genome sequencing will become useful. Once brain gene therapy becomes a safe reliable technology anyone with a genetic profile which puts them at high risk of Parkinson's Disease (or Alzheimer's or assorted other brain disorders) will be able to get gene therapy decades before they develop clinical symptoms of a brain disorder.
Preventative gene therapy. That's what I want. Only, I want it for every cell in the brain and for every single thing that ages in the brain. Plus, I want it for the rest of the body. Then we can stop and turn back the clock of biological aging and become youthful again.
The development of gene therapy treatments for most of the maladies of old age (and probably all the neurological maladies) will eventually provide us with most of the tools we'll need for full body rejuvenation. Development of stem cell therapies and techniques for growing replacement organs will provide most of the other tools we need to turn back the aging clock.
The New Jersey legislature has passed legislation that will require the New Jersey economy to cut greenhouse gas emissions and Governor Jon Corzine says he will sign it into law.
Under the new law, greenhouse gas emissions generated by every aspect of the state’s economy, not just electricity-generating stations, will have to drop about 13 percent, to 1990 levels, by 2020. The bill further requires that emissions be capped at 80 percent of 2006’s levels by 2050.
Whether the federal government will allow state governments to regulate emissions of CO2 and other gases for the purpose of avoiding climate change remains to be seen. California and a few other states have also adopted laws for greenhouse gas emissions reduction but none go as far as New Jersey's.
The eventual cap at 80% of 2006's level by 2050 is probably easier to achieve than the 13% reduction by 2020. Technologies developed in the 2010s and 2020s will greatly lower the costs of a switch to nuclear, solar, biomass, geothermal, and wind power.
The longer range goal is also easier to achieve because it is easier for energy-intensive industries to migrate out-of-state in the longer run. Companies can make plans to stop enhancing capital plant and not to initiate new plant construction, for example. Notably, this new regulatry policy will probably gradually drive much of the chemical industry out of the state.
If the US federal government allows individual states to enforce their own greenhouse gas emissions regulations then expect business executives to invest more in states that are big coal producers. Why? Because the states that are big coal (and oil and natural gas) producers have governments that favor the continuation of fossil fuels resource extraction and use. We see this in national politics where Barack Obama of Illinois favors federal subsidies for coal-to-liquid plants for example. West Virginia, Kentucky, North Dakota, and Wyoming all make good bets for energy intensive industries that want to avoid state-level green house gas emissions regulations and taxes.
What I want to know: Even if states gain some legal standing to regulation greenhouse gas (GHG) emissions how will that play out with electric power purchased across state lines? If, say, New Jersey requires a big reduction in GHG emissions in electric power plants can the state regulate utilities to require even out-of-state electric power brought into the state be made from plants that emit fewer GHG? My guess is the US constitution's Interstate Commerce Clause will pose an obstacle for that sort of regulation and therefore coal states like West Virginia and Kentucky might become big electricity exports to New Jersey and other northeastern states that also regulate GHG.
I'm especially interested in how this gets applied to the electric power industry because at a national level electric power accounts for 39% of total energy-related carbon dioxide emissions.
The data in Table 11 represent estimates of carbon dioxide emissions for the electric power sector. These emissions when taken as a whole account for 39 percent of total U.S. energy-related carbon dioxide emissions; in calculating sector-specific emissions, electric power sector emissions are distributed to the end-use sectors.
What I also want to know: How much is this law going to cost? Already New Jersey's electricity costs 12.8 cents per kwh as compared to coal-burning West Virginia at 6.2 cents per kwh or less than half New Jersey's cost. The people of New Jersey could find themselves paying New York prices (16.19 cents/kwh) or even Connecticut prices (18.51 cents/kwh - ouch). Though perhaps nuclear and wind power will put a ceiling on medium term electricity price rises.
Also see my post California Bill To Cut Greenhouse Gases 25% By 2020.
Heard the oft repeated claim that America has enough coal to last 250 years? A new report from the US National Academy of Sciences (NAS) claims recoverable US reserves are not nearly as large as has been claimed. Though another claim about America as "the Saudi Arabia of coal" might still be accurate. Why? If Matthew Simmons and other "Peak Oil" advocates are right then Saudi Arabia's oil reserves are also greatly exaggerated. The NAS report authors say attempts to spot check old recoverable coal reserves estimates have found far less recoverable coal than expected (PDF from Report Brief).
Present estimates of coal reserves— which take into account location, quality, recoverability, and transportation issues—are based upon methods that have not been updated since their inception in 1974, and much of the input data were compiled in the early 1970s. Recent programs to assess coal recoverability in limited areas using updated methods indicate that only a small fraction of previously estimated reserves are actually recoverable. Such findings emphasize the need for a reinvigorated coal reserve assessment program using modern methods and technologies.
Is this good news or bad news? I see it as good news. Coal is dirty. We have alternatives. The incremental cost difference going from coal to nuclear is probably at most 2 cents per kilowatt-hour (kwh). At the same time, wind and solar photovoltaics are declining in cost and photovoltaics probably can decline in cost by an order of magnitude. So coal has substitutes, at least for electric generation.
Small coal reserves seem more problematic for the coming peak in oil production. Coal-to-liquid (CTL) could help reduce the economic disruption that peak oil will cause to our living standards and lifestyles. Smaller coal reserves mean less CTL gasoline or diesel fuel. However Chevron and Shell research into oil shale extraction could provide another way to supply liquid fuels for that portion of transportation that does not go electric. Though the Natural Resources Defense Council (NRDC) argues that oil shale extraction will use too much of a limited supply of water in the Rocky Mountain states. What I'd like to know: at what price of oil and natural gas would nuclear energy become cheaper as a way to heat up tar sands in Alberta and oil shale in Colorado, Utah, and Wyoming?
The NAS coal report authors have revised US reserves from 250 years to 100 years at current consumption rates and so have reduced reserve estimates to only 40% of previous estimates.
The 250-year estimate was made in the 1970s and was based on the assumption that 25 percent of the coal that had been located was recoverable with current technology and at current prices, said one member of the study group, Edward S. Rubin, a professor of environmental engineering and science at Carnegie Mellon University.
But he said that more recent studies by the United States Geological Survey showed that at least in some areas, only 5 percent of the coal was recoverable with today’s technology and at current prices.
Even the 100 years estimate looks unrealistic given the boom in coal electric power plant construction now going on. But consumption could rise even higher if an oil production peak causes a building boom in coal-to-liquid plants to keep all the cars and trucks moving down the road.
The NAS coal report brief expects extracting difficult seams to cause more environmental and water problems. (PDF).
As mining activities extract coal from deeper and operationally more difficult seams, a range of existing environmental issues and concerns will be exacerbated and new concerns are likely to arise, particularly related to greater disturbance of hydrologic systems, ground subsidence, and waste management at mines and processing plants. Research activities should focus on developing techniques to mitigate the alteration and collapse of rock layers overlying mined areas, to model the hydrological impacts of coal mining, to improve mine mapping and void detection, to increase stability of waste heaps on steep slopes, and to improve the construction and monitoring of coal waste impoundments.
The money available for energy investments is enormous. Take the money spent on oil as a starting point. The current price for London Brent crude is over $71 per barrel and US oil is around $69 per barrel. Well, the United States uses over 20 million barrels of oil per day or over $1.4 billion dollars on oil alone per day. Add in coal, natural gas, nuclear, hydroelectric, and other sources of energy and the US economy spends billions of dollars per day on energy. If coal oil or shale oil can get made for $50 or $60 per barrel (and this seems likely from various reports) then the money can be found to build the capital plant to do the extraction and make the oil.
You can buy access to the full NAS report.
Update: If the Peak Oil pessimists (see here and here for Stuart Staniford on Saudi oil production) are right about an earlier date for a world oil production peak then it is it not too early to start talking about Peak Coal. If an oil peak comes sooner then we will not yet have the technologies needed to switch most transportation away from liquid fuel to electricity. Therefore big money will flow into coal-to-liquid (CTL) to make transportation fuels. As a result, coal reserves will decline much more rapidly.
But I'm not worried about Peak Coal. Coal, tar sands, and oil shale should buy us 2 or 3 decades to migrate to a much more electric economy. I think an early Peak Oil will be very costly if it comes as a surprise to most of industry. But my chief concern about a shift to coal is environmental. Coal is much dirtier.
Even if Peak Oil is still 20 years away Asian economic growth is pushing up the demand for energy so much that a shift to coal for liquid fuels could happen even before Peak Oil. I would rather the non-fossil fuels energy sources drop further in price and start putting a ceiling on energy prices than that coal consumption accelerates even more rapidly.
BEIJING (AP) - China has overtaken the United States as the world's top producer of carbon dioxide emissions - the biggest man-made contributor to global warming - based on the latest widely accepted energy consumption data, a Dutch research group says.
According to a report released Tuesday by the Netherlands Environmental Assessment Agency, China overtook the U.S. in emissions of CO2 by about 7.5 percent in 2006. While China was 2 percent below the United States in 2005, voracious coal consumption and increased cement production caused the numbers to rise rapidly, the group said.
What I want to know: how long will it take before China's emissions are twice as much as America's? Might be time to make a long term investment in a tropical Aleutian island.
China's per capita income and population size could grow for many years to come. If rising affluence make Chinese people more opposed to the One Child policy then China's population growth could accelerate and Chinese energy consumption could become a few times higher than that of the United States.
Jos Olivier, a senior scientist with the Dutch environmental agency, said those statistics are the most accurate but that he and others wanted to find a way to get more immediate figures. He relied primarily on energy data collected by British Petroleum and added information about cement production, a major source of greenhouse emissions from chemical reactions.
Olivier said he believed his figures were fairly reliable. In a telephone interview from his office in the Netherlands, he said his calculations showed that carbon dioxide emissions by the United States declined 1.4% in 2006 — very close to the official figure of 1.3% released in May by the U.S. Department of Energy.
U.S. emissions declined partly because of mild weather in 2006, and partly because of increased use of natural gas instead of dirtier forms of fossil fuel, the Energy Department said.
My guess is that some of that carbon emissions decline in the US is due to rising energy prices. If we really are approaching "Peak Oil" (watch for news about production peaking of the Saudi Ghawar oil field) then we will shift toward coal in a big way. Total carbon dioxide emissions could rise during the early years after oil production peaks as more coal gets used.
To reiterate my basic argument on this topic: The best way to lower carbon emissions is to develop technologies that make other energy sources cheaper than fossil fuels. Photovoltaics and nuclear power combined with next generation batteries could enable us to shift away from fossil fuels for transportation.
June 19, 2007 -- A probe of the upper echelons of the human brain's chain-of-command has found strong evidence that there are not one but two complementary commanders in charge of the brain, according to neuroscientists at Washington University School of Medicine in St. Louis.
It's as if Captains James T. Kirk and Jean-Luc Picard were both on the bridge and in command of the same starship Enterprise.
In reality, these two captains are networks of brain regions that do not consult each other but still work toward a common purpose — control of voluntary, goal-oriented behavior. This includes a vast range of activities from reading a word to searching for a star to singing a song, but likely does not include involuntary behaviors such as control of the pulse rate or digestion.
Brain scans show two separate networks of nodes making decisions.
Using an analytic technique originally developed by Raichle's group, scientists employed resting state functional connectivity MRI to identify pairs of brain regions where blood oxygen levels rose and fell roughly in synch with each other, implying the regions likely work together. They graphed the results, representing each brain region with a shape. They drew a line between paired brain regions if their blood oxygenation patterns correlated tightly enough. "You might expect that everything is connected to everything, and you would get sort of a big mess and not much information," Dosenbach says. "But that's not at all what we found. Even at low levels of correlation, there were two sides to these graphs. Brain regions on either side had multiple connections to other regions on their side, but they never connected to regions on the opposite side."
The two networks seem to have different purposes. The frontoparietal network sounds like it is more reactive.
Having established that two control networks existed, researchers turned back to their functional brain scans for insight into the networks' roles. One network, dubbed the cinguloopercular network, was linked to a "sustain" signal.
"When you start doing a task, this signal turns on," Petersen explains. "It stays constant while you're doing the task, and then when you're done it turns off."
In contrast, the frontoparietal network was consistently active at the start of mental tasks and during the correction of errors.
The balance between the two networks could vary from individual to individual. For example, some people might be better at maintaining a constant activity and others might be better at reacting to events.
Why can't libertarians persuade the majority to support libertarian economic and social policies? Most human brains are wired to give themselves pleasure when they commit altruistic acts including the paying of taxes.
Want to light up the pleasure center in your brain? Just pay your taxes, and then give a little extra voluntarily to your local food bank. University of Oregon scientists have found that doing those deeds can give you the same sort of satisfaction you derive from feeding your own hunger pangs.
A three-member team – a cognitive psychologist and two economists – published its results in the June 15 issue of the journal Science. The scientists gave 19 women participants $100 and then scanned their brains with functional magnetic resonance imaging (fMRI) as they watched their money go to the food bank through mandatory taxation, and as they made choices about whether to give more money voluntarily or keep it for themselves.
The participants lay on their backs in the fMRI scanner for an hour-long session and viewed the financial transfers on a computer screen. The scanner used a super-cooled magnet, carefully tuned radio waves and powerful computers to calculate what parts of the brain were active as subjects saw their money go to the food bank and made yes or no decisions on additional giving.
What I want to know: Who is having more kids? Those who enjoy taxpaying the most or those who get no pleasure from taxpaying? Is taxpaying getting selected for or against?
Libertarians can take small solace that voluntary altruism is more enjoyable than mandatory altruism.
“The surprising element for us was that in a situation in which your money is simply given to others – where you do not have a free choice – you still get reward-center activity,” said Ulrich Mayr, a professor of psychology. “I don’t think that most economists would have suspected that. It reinforces the idea that there is true altruism – where it’s all about how well the common good is doing. I’ve heard people claim that they don’t mind paying taxes, if it’s for a good cause – and here we showed that you can actually see this going on inside the brain, and even measure it.
I do not find this surprising. Economists need to adopt a much more realistic view of human nature so that this sort of result ceases to surprise.
When offspring genetic engineering becomes commonplace will parents choose to make their kids more or less altruistic? Will some genetic variations make people hate involuntary altruism while still enjoying voluntary altruism? If so, a libertarian society could be genetically engineered.
Nice, France: Children born after embryo biopsy for preimplantation genetic diagnosis (PGD) do not show any more major malformations than those born after artificial reproduction technologies (ART) without PGD, a scientist will tell the annual conference of the European Society of Human Genetics today. Professor Ingeborg Liebaers, from the Research Centre for Reproductive Genetics, Free University of Brussels, Brussels, Belgium, will say that the results of her study of 583 children born after PGD was reassuring.
PGD is a new option for couples at risk of transmitting genetic diseases. Instead of carrying out a prenatal diagnosis followed by a termination of pregnancy, in vitro fertilisation (IVF) with intracytoplasmic sperm injection (where a sperm is injected directly into an egg) is performed, followed by genetic testing of the embryos. Only unaffected embryos are subsequently transferred to the womb.
“Because embryos are biopsied in PGD procedures, and this constitutes an additional manipulation of a delicate organism, we set out to study whether this had any effect on the health of children who were born as a result of this procedure”, says Professor Liebaers. The scientists first collected data on the pregnancies by giving questionnaires to patients on the day of the embryo transfer. Additional questionnaires were sent during pregnancy, at delivery, and later on to the patients, their gynaecologists, and paediatricians. Children were examined at 2 months and 2 years old.
A low risk from PGD will make IVF much more attractive once genetic testing becomes cheap. Genetic researchers will discover the effects of hundreds of thousands of mutations and they will make these discoveries at an increasingly rapid rate as a result of falling costs for genetic testing. Those discoveries will allow prospective parents to compare the genetic profiles of multiple IVF embryos to select the one that delivers the most preferred combination of genes.
If other studies verify the low risk of PGD found in this study then once genetic testing becomes cheap that low risk will help make embryo selection with PGD the preferred way to start pregnancies. That, in turn, will cause a huge speed-up in the rate of human evolution.
Cold Spring Harbor, N.Y. -- Cold Spring Harbor Laboratory (CSHL) researchers led by Daniel Nolan and Assistant Professor Vivek Mittal have found that bone marrow (BM) derived endothelial progenitor cells (EPCs) play a critical role in the early stages of tumor progression and that eliminating EPCs stops cancer growth. Using sophisticated high-resolution microscopy and flow cytometry, they zeroed in on the earliest stages of cancer progression and identified the role of EPCs in generating blood vessels that allow cancers to grow. “If we selectively blocked the EPCs, tumors were unable to make blood vessels and could not sustain their own growth,” said Vivek Mittal, CSHL Assistant Professor.
But how to use this knowledge therapeutically? Usually early stage cancers go undetected. So suppression of stem cells in early stage cancers isn't a practical way to stop cancers. Scientists already know (and Judah Folkman gets much of the credit) that cancer cells mutate to release angiogenesis compounds to stimulate blood vessel growth. Some anti-cancer drugs work as angiogenesis inhibitors. We need more such compounds.
What this result makes me wonder: Once we can get youthful stem cell therapies will the stem cells up our cancer risk even if the stem cells themselves do not become cancerous? Maybe aging stem cells reduce the ability of tumors to spur blood vessel generation that tumors need to grow. Maybe young stem cells will more vigorously respond to angiogenesis compounds that cancer cells secrete and will build blood vessels more rapidly.
Some of the slowing down in the body that happens with age is likely an adaptation designed to reduce the risk of cancer spread. We need highly effective cures for cancer that cause little collateral damage. Those cancer cures will lower the risks of future rejuvenation therapies.
A new research report in Plos One provides support for the theory that abused children who have low level expression of the gene for monoamine oxidase A (MAOA) are more at risk of becoming violent and anti-social.
Previous research has reported that a functional polymorphism in the monoamine oxidase A (MAOA) gene promoter can moderate the association between early life adversity and increased risk for violence and antisocial behavior. In this study of a combined population of psychiatric outpatients and healthy volunteers (N = 235), we tested the hypothesis that MAOA genotype moderates the association between early traumatic life events (ETLE) experienced during the first 15 years of life and the display of physical aggression during adulthood, as assessed by the Aggression Questionnaire. An ANOVA model including gender, exposure to early trauma, and MAOA genotype as between-subjects factors showed significant MAOA×ETLE (F1,227 = 8.20, P = 0.005) and gender×MAOA×ETLE (F1,227 = 7.04, P = 0.009) interaction effects. Physical aggression scores were higher in men who had experienced early traumatic life events and who carried the low MAOA activity allele (MAOA-L). We repeated the analysis in the subgroup of healthy volunteers (N = 145) to exclude that the observed G×E interactions were due to the inclusion of psychiatric patients in our sample and were not generalizable to the population at large. The results for the subgroup of healthy volunteers were identical to those for the entire sample. The cumulative variance in the physical aggression score explained by the ANOVA effects involving the MAOA polymorphism was 6.6% in the entire sample and 12.1% in the sub-sample of healthy volunteers. Our results support the hypothesis that, when combined with exposure to early traumatic life events, low MAOA activity is a significant risk factor for aggressive behavior during adulthood and suggest that the use of dimensional measures focusing on behavioral aspects of aggression may increase the likelihood of detecting significant gene-by-environment interactions in studies of MAOA-related aggression.
The first report I came across a few years ago on a relationship between low levels of monoamine oxidase A (MAOA), abused children, and violent behavior came from a Dunedin New Zealand twins study. See my post A violence promoting gene and the follow-up and additional related info in the post Serotonin Transporter Gene Linked To Depression, Binge Drinking. Plus, see the post Initial Bullying In Late In Adolescence Causes Most Harm.
What I find interesting about the MAOA variations: The variation that makes one more violent in response to abuse basically makes humans more sensitive to environmental influence. The higher MAOA activity variation makes humans less sensitive to the environment. So the ability of humans to be influenced by the environment is under genetic control.
The fact that genetic variations cause differences in environmental sensitivity has future implications. When offspring genetic engineering enters the realm of the safely doable prospective parents are going to choose against genetic variations that cause environmental sensitivity for behavioral attributes where the parents have strongly held preferences. For example, parents who want total "Goodie Two Shoes" kids are going to choose against genetic variations that create the risk that the kids might turn out violent.
My prediction: Parents will choose genetic variations that make their kids more genetically determined, not less. Parents will choose against genetic variations that put them at 10% risk of some undesired attribute if some other genetic variations would make them at only 1% or a tenth of a percent risk of that the undesirable attribute. Similarly, parents will choose genetic variations that greatly increase the odds of various desired attributes. Basically, genetic variations that leave offspring at moderate odds (say 30% to 70%) of some outcome will get rejected in favor of genetic variations that make attributes either highly likely or highly unlikely.
From the heartland's whippoorwills and meadowlarks to the Northern bobwhite and common terns of the nation's coasts, 20 common bird species tracked by the National Audubon Society have seen their numbers fall 54 percent overall since 1967, with some down about 80 percent, the group reported Thursday.
Most of the trouble lies with loss of bird habitat, and has for decades, due to expanding agriculture and suburban development. The Rufous hummingbird's population has fallen 58 percent due to logging and development in its Pacific Northwest breeding range – and in its winter range in Mexico. The same thing has happened to whipporwills, whose numbers are down 57 percent due to loss of their forest habitat. At the same time, scientists say changes in migration patterns due to global warming are emerging, too.
"Habitat loss is still the major concern," says Greg Butcher, Audubon's bird conservation director in an interview. "But we're also seeing increasing impact from large-scale problems like global warming."
Losses due to global warming are speculative at this point. But loss of land to human use is not speculative. Destruction of rain forests in the tropics will drive many species to extinction. Both industrialization and population growth are driving the loss of land.
This trend could get much worse. My fear with biotechnology for biomass energy is that biotechnology will make more land useful for human purposes. If genetic engineers create plants that make land more usable for energy production then use of land for energy production will cause orders of magnitude greater loss of habitats than is caused by drilling for oil and construction of oil pipelines. Shifting of land into production for biomass energy will get added to expansion of land use for food crops, logging, and human settlements.
The habitat loss problem is going to get much worse even without a massive shift to biomass energy. The population of the United States will hit about 400 million by 2050. Most of that population growth will come from immigrants and from children of immigrants.
That population growth rate is probably going to go up if the S.1348 immigration amnesty bill passes Congress. Why? Immigration amnesties cause fertility spikes.
According to a 2002 study by demographers Laura E. Hill and Hans P. Johnson of the Public Policy Institute of California, due to the 1986 amnesty (another "comprehensive" compromise, combining legalization with enforcement provisions that were never enforced), "Between 1987 and 1991, total fertility rates for foreign-born Hispanics [in California] increased from 3.2 to 4.4" expected babies per woman over her lifetime.
I believe we already have too many people on planet Earth and that we are going to lose a large number of species due to population growth and industrialization. Eventually we are going to develop rejuvenation therapies and current projections of future population growth will turn out to be very low. Seems to me we have about 4 choices with population growth:
My guess is that the fourth option is the most likely. The instinct to reproduce is incredibly strong (even as many intellectuals erroneously claim we've somehow escaped our instincts). Also, the development of rejuvenation therapies seems inevitable barring a catastrophe that wipes out the human race.How can the fourth option be prevented? Maybe people will migrate to online virtual reality living and raise AI children. I doubt it. Maybe a Borg consciousness AI will take over a world government and control human behavior. For example, a massive AI (or a secret cabal of scientists and industrialists) could design viruses that infect the entire human race and reprogram their brains to dampen down desires to reproduce.
MIT's Technology Review reports on progress in raising solar photovoltaic cell efficiency.
The cell, which employs new "metamorphic" materials, is designed for photovoltaic systems that use lenses and mirrors to concentrate the sun's rays onto small, high-efficiency solar cells, thereby requiring far less semiconductor material than conventional solar panels. Last month Spectrolab published in the journal Applied Physics Letters the first details on its record-setting cell, initially disclosed in December, which converts 40.7 percent of incoming light into electricity at 240-fold solar concentration--a healthy 1.4 percent increase over the company's previous world-record cell. Other groups are developing promising cells based on the new type of materials, including researchers at the Department of Energy's National Renewable Energy Laboratory (NREL), in Golden, CO. The NREL researchers will soon publish results in the same journal showing that their NREL's designs are tracking Spectrolab's, improving from 37.9 percent efficiency in early 2005 to 38.9 percent efficiency today.
The Boeing subsidiary Spectrolab is keeping ahead of NREL. Are private sector workers more motivated or better funded? How about a hefty X Prize for the first group to exceed 50%, 51%, and so on?
Combine higher efficiency with solar concentrators for lower cost. Cheap solar power anyone?
Such high output may be just the beginning. Raed Sherif, director of concentrator products at Spectrolab, says there is every reason to believe that these metamorphic solar cells will top 45 percent and perhaps even 50 percent efficiency. Sherif says those efficiencies, combined with the vast reduction in materials made possible by 1,000-fold concentrators, could rapidly reduce the cost of producing solar power. "Concentrated photovoltaics are a relatively late entry in the field, but it will catch up very quickly in terms of cost," he predicts. (See "Solar Power at Half the Cost.")
Cheap solar power would favor a shift to electric cars. Combine cheap solar power with cheap, high capacity, and safe car batteries and market forces alone would make our environment much cleaner. We'd get cleaner air. But we'd also get cleaner water as the use of oil (leaks of which run off in rain) gradually dropped.
Cheap solar power would also lower costs and therefore accelerate economic growth and raise living standards. Cheap solar power with high conversion efficiency would use probably two orders of magnitude less land to produce the same amount of energy as biomass produces. So cheap solar power would reduce the demand for land for biomass energy. That would reduce habitat loss, especially in tropical lands such as Brazil, Malaysia, and Indonesia.
The rising price of oil and the expectation that oil production won't rise as fast as demand has powerfully concentrated many minds to look for alternative cheaper sources of energy. Cheap solar power is an achievable goal and I expect we will see it achieved by the 2020s at the latest.
Few older people die with brains untouched by a pathological process, however, an individual’s likelihood of having clinical signs of dementia increases with the number of different disease processes present in the brain, according to a new study. The research was funded by the National Institute on Aging (NIA), part of the National Institutes of Health, and conducted at the Rush Alzheimer’s Disease Center at Rush University Medical Center in Chicago. Julie Schneider, M.D., and colleagues report the findings in the journal Neurology online today.
Among their findings is the observation that the combination of Alzheimer’s disease and cerebral infarcts (strokes) is the most common mix of pathologies in the brains of people with dementia.
A diet to improve your blood lipid profile will help delay the day when strokes and other aging processes start you down the road to serious brain damage.
The implication of these findings is that public health efforts to prevent and treat vascular disease could potentially reduce the occurrence of dementia, the researchers say in the paper.
What would reduce the incidence of dementia: All the dietary, lifestyle, and drug factors that reduce the risk of stroke and heart disease. In this context I hear Ray Davies singing "I'm an ape man" since the Ape Diet of U Toronto researcher David Jenkins looks like a good bet for how to reduce the incidence of cardiovascular diseases.
The bad news is that most people have multiple serious brain diseases by the time they die.
The current study compared clinical and autopsy data on the first 141 participants who have died.
Annual physical and psychological exams showed that, while they were alive, 50 of the 141 had dementia. Upon death, a neuropathologist, who was unaware of the results of the clinical evaluation, analyzed each person’s brain. The autopsies showed that about 85 percent of the individuals had evidence of at least one chronic disease process, such as Alzheimer’s disease, strokes, Parkinson’s disease, hemorrhages, tumors, traumatic brain injury or others.
Comparison of the clinical and autopsy results showed that only 30 percent of people with signs of dementia had Alzheimer’s disease alone. By contrast, 42 percent of the people with dementia had Alzheimer’s disease with infarcts and 16 percent had Alzheimer’s disease with Parkinson’s disease (including two people with all three conditions). Infarcts alone caused another 12 percent of the cases. Also, 80 of the 141 volunteers who died had sufficient Alzheimer’s disease pathology in their brains to fulfill accepted neuropathologic criteria for Alzheimer’s disease, although in life only 47 were clinically diagnosed with probable or possible Alzheimer’s disease.
Growing oldn't isn't just about getting gray and wrinkled skin. Growing old is not graceful or dignified. Your brain becomes progressively more damaged.
Stem cell therapies, gene therapies, and other future therapies will eventually slow brain aging and in the longer run rejuvenation therapies together will reverse brain aging. We should demand greater efforts to develop all those brain rejuvenation therapies because currently we are all mentally decaying. Every day that goes by our brains get older and more dysfunctional.
ST. PAUL, MN- People who are easily distressed and have more negative emotions are more likely to develop memory problems than more easygoing people, according to a study published in the June 12, 2007, issue of Neurology®, the scientific journal of the American Academy of Neurology.
In the study, those who most often experience negative emotions such as depression and anxiety were 40 percent more likely to develop mild cognitive impairment than those who were least prone to negative emotions. Mild cognitive impairment is a transitional stage between normal aging and dementia. People with mild cognitive impairment have mild memory or cognitive problems, but have no significant disability.
Researchers analyzed the results from two larger studies, the Religious Orders Study and the Memory and Aging Project, which involved 1,256 people with no cognitive impairment. During up to 12 years of follow-up, 482 people developed mild cognitive impairment. Participants were evaluated on their level of proneness to distress and negative emotions by rating their level of agreement with statements such as “I am not a worrier,” “I often feel tense and jittery,” and “I often get angry at the way people treat me.”
Some people are probably innate worriers. So maybe the insight that negative emotions age your brain is hard to act upon. Still, you can try to make life choices that are less likely to put you in positions where you have to worry. For example, avoid lots of debt. Also, don't get hooked up with a romantic attachment that will stress you out. Sometimes you know what is coming and you do it anyway (and I'm speaking from personal experience). Don't do that. Also, stressful job? Start looking for another one.
DETROIT, June 11, 2007 -- Adding to a growing body of evidence, new research shows that a daily dose of pistachios may offer protective benefits against cardiovascular disease, according to a study published in the Volume 26, Number 2 issue of the Journal of the American College of Nutrition.
The study, conducted by James N. Cooper M.D., of George Mason University and Michael J. Sheridan, Sc.D., of Inova Fairfax Hospital, found that in people with moderately high cholesterol levels, a daily diet consisting of 15% of calories from pistachios (about two to three ounces or one to two handfuls of kernels) over a four-week period favorably improved some blood lipid levels.
"These results are exciting because the research indicates that adding pistachios to the daily diet can help protect the heart without a dramatic dietary lifestyle change," said Dr. James Cooper. "This research challenges the previously-held belief that a low-fat diet is best for heart health. Studies now show that a diet with a moderate amount of healthful monounsaturated fat, like the kind found in pistachios, is a more effective way to prevent heart disease than reducing overall fat intake. What's more, we noted very good compliance and a positive response from participants during the four-week period."
Nuts are good.
A new report on a set of genes discovered which contribute to a form of heart disease is less interesting for the discovery than for the tools developed which made the discovery possible. Development of a much cheaper and very sensitive technique for measuring message RNA expression levels enabled the discovery.
The one-gene, one-disease concept is elegant, but incomplete. A single gene mutation can cause many other genes to start—or stop—working, and it may be these changes that ultimately cause clinical symptoms. Identifying the complete set of affected genes used to appear impossible. Not anymore.
Studying genetically modified mice, researchers led by Christine E. Seidman, a Howard Hughes Medical Institute investigator at Brigham and Women's Hospital, and her husband Jonathan G. Seidman, who is at Harvard Medical School, have identified hundreds of genes with altered expression in preclinical hypertrophic cardiomyopathy. The study, which is coauthored by colleagues at Harvard Medical School, is published in the June 9, 2007, issue of the journal Science. The discovery could help scientists define the pathways that lead to the disease and lead to the discovery of targets for early detection, prevention, and treatment.
A new technique provides a highly sensitive way of measuring gene expression levels.
To obtain a complete picture of the genetic changes associated with the disease, the researchers developed a new gene sequencing technique called polony multiplex analysis of gene expression, or PMAGE. The technique can find messenger RNA transcripts—the directions for making a protein, spun out from the DNA of an active gene—that occur as rarely as one copy for every three cells.
PMAGE drops costs by an order of magnitude.
The industry standard for gene sequencing is serial active gene expression, or SAGE. "There are a couple of labs that have been dedicated to developing this technology," Seidman said, including HHMI investigator Bert Vogelstein at Johns Hopkins and George Church at Harvard. But PMAGE analysis costs between 1/20 and 1/9 of a comparable SAGE analysis, making it more appropriate for the kind of large-scale expression profiling undertaken in this study, she explained. "With SAGE, you can't afford to sequence 4 million transcripts."
These order of magnitude cost drops in assorted techniques for measuring genetic sequences and gene expression levels just keep coming. As the costs of measurement and data collection keep falling the rate at which scientists figure out what genes do keeps accelerating.
Many more order of magnitude cost drops for genetics and molecular biology lay in store in the future. A coming enormous flood of discoveries enabled by biotechnological advances will sweep through and revolutionize medicine.
Are you taking vitamin D yet? If not, here's yet another study finding a protective effect from vitamin D against cancer.
WASHINGTON, D.C. (June 8, 2007) – Key milk nutrients, calcium and vitamin D, may do more than just help keep your bones strong. Increasing intake of calcium and vitamin D could reduce the risk for cancer in women by at least 60 percent, according to a new study published in the American Journal of Clinical Nutrition. (1)
The four-year clinical trial included more than one thousand women over the age of 55 in one of three supplement groups: 1) calcium (1400-1500mg) plus vitamin D (1100 IU vitamin D) 2) calcium only (1400-1500 mg) or 3) a placebo. The researchers found that the risk of developing cancer was 60 percent lower for those who took calcium and vitamin D and 47 percent lower for those taking calcium alone, compared to the placebo.
Fifty women developed nonskin cancer through the course of the four-year study, including breast, colon, lung and other cancers. When researchers excluded the 13 cancers diagnosed during first year of the study, determining these cancers were likely present at the study onset, the protective effect of calcium and vitamin D was even greater, with a 77 percent lower risk for cancer for those taking calcium plus vitamin D compared to the placebo.
Taking the vitamin D and calcium long term might provide an even higher level of protection.
I found it interesting that calcium provides a protective effect and a substantial one. Almost all the studies I come across about the protective effect of vitamin D against cancer do not include a group that uses calcium. I wish this latest study had included a group that only took vitamin D. Then we'd know whether the calcium still provides a benefit on top of vitamin D.
Researchers at MIT have shown that it's possible to wirelessly power a 60-watt lightbulb sitting about two meters away from a power source. Using a remarkably simple setup--basically consisting of two metal coils--they have demonstrated, for the first time, that it is feasible to efficiently send that much power over such a distance. The experiment paves the way for wirelessly charging batteries in laptops, mobile phones, and music players, as well as cutting the electric cords on household appliances, says Marin Soljačić, professor of physics at MIT, who led the team with physics professor John Joannopoulos.
Notice at the bottom of this post that I filed it under "Energy Transportation". Why? They achieved 45% efficiency. But at a shorter distance they achieved 70% efficiency. Suppose they can get this up to 90+% efficiency. That would open up the possibility of recharging an electric car automatically when it parks in the right spot. That would solve a basic problem with shorter range electric cars that are used for daily short range commuting. Drive a 10 or 20 mile daily commute, park in the garage, and next morning the car will be fully recharged by an electric power transmission magnet in the garage. Ditto for, say, special parking spaces at workplaces.
Moffatt, an MIT undergraduate in physics, explains: "The crucial advantage of using the non-radiative field lies in the fact that most of the power not picked up by the receiving coil remains bound to the vicinity of the sending unit, instead of being radiated into the environment and lost." With such a design, power transfer has a limited range, and the range would be shorter for smaller-size receivers.
In contrast, WiTricity is based on using coupled resonant objects. Two resonant objects of the same resonant frequency tend to exchange energy efficiently, while interacting weakly with extraneous off-resonant objects. A child on a swing is a good example of this. A swing is a type of mechanical resonance, so only when the child pumps her legs at the natural frequency of the swing is she able to impart substantial energy. Another example involves acoustic resonances: Imagine a room with 100 identical wine glasses, each filled with wine up to a different level, so they all have different resonant frequencies. If an opera singer sings a sufficiently loud single note inside the room, a glass of the corresponding frequency might accumulate sufficient energy to even explode, while not influencing the other glasses. In any system of coupled resonators there often exists a so-called “strongly coupled” regime of operation. If one ensures to operate in that regime in a given system, the energy transfer can be very efficient.
While these considerations are universal, applying to all kinds of resonances (e.g., acoustic, mechanical, electromagnetic, etc.), the MIT team focused on one particular type: magnetically coupled resonators. The team explored a system of two electromagnetic resonators coupled mostly through their magnetic fields; they were able to identify the strongly coupled regime in this system, even when the distance between them was several times larger than the sizes of the resonant objects. This way, efficient power transfer was enabled. Magnetic coupling is particularly suitable for everyday applications because most common materials interact only very weakly with magnetic fields, so interactions with extraneous environmental objects are suppressed even further. “The fact that magnetic fields interact so weakly with biological organisms is also important for safety considerations,” Kurs, a graduate student in physics, points out.
I find the ability to use cordless appliances less interesting than charging cars because this approach sounds pretty directional.
The car charging problem has other potential solutions. For example, imagine a garage where a robotic apparatus automatically come down from the ceiling or up from the floor to plug into a receptacle.
What I wonder: Is there any health risk to an electromagnetic energy beam?
CHICAGO --- Northwestern University researchers have discovered a drug that slows – and may even halt – the progression of Parkinson’s disease. The drug rejuvenates aging dopamine cells, whose death in the brain causes the symptoms of this devastating and widespread disease.
D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University’s Feinberg School of Medicine, and his team of researchers have found that isradipine, a drug widely used for hypertension and stroke, restores stressed-out dopamine neurons to their vigorous younger selves. The study is described in a feature article in the international journal Nature, which will be published on-line June 10.
What would isradipine do for aging minds in general? We all have dopamine neurons. Those neurons age in all of us, albeit at a slower rate than they age in people who have Parkinson's.
Decades of research have not produced a single drug that slows the rate of neuronal cell death in Parkinson's.
“There has not been a major advance in the pharmacological management of Parkinson’s disease for 30 years,” Surmeier said.
Thousands of drugs exist in pharmacies. Why did it take decades before someone tried isradipine? Surmeier made a basic discovery about the behavior of adult dopaminergic neurons: unlike most neurons they use calcium for signaling rather than sodium.
First, Surmeier observed that dopamine neurons are non-stop workers called pacemakers. They generate regular electrical signals seven days a week, 24 hours a day, just like pacemaker cells in the heart. This was already known. But then he probed more deeply and discovered something very strange about these dopamine neurons.
Most pacemaking neurons use sodium ions (like those found in table salt) to produce electrical signals. But Surmeier found that adult dopamine neurons use calcium instead.
Actually, other types of neurons use calcium as well though in a more limited manner. My knowledge on this is rather dated at this point but calcium fluxes across membranes help initiate waves of depolarization at the dendrite end of neurons when neurotransmitters bind to a dendrite's receptors. But apparently dopamine neurons use calcium more extensively and instead of sodium.
Aged dopamine neurons switch to using calcium instead of sodium (why?) and this calcium has toxic effects on dopamine neurons that probably makes them wear out more rapidly.
When the neurons are young, Surmeier found they actually use sodium ions to do their work. But as the neurons age, they become more and more dependent on the troublesome calcium and stop using sodium. This calcium dependence – and the stress it causes the neurons --is what makes them more vulnerable to death.
So then would long term use of isradipine slow general brain aging?
Surmeier decided to block off calcium channels in dopamine cells by use of isradipine. The result: the dopamine cells switched over to use of less toxic sodium instead.
What would happen, Surmeier wondered, if he simply blocked the calcium’s route into the adult neuron cells" Would the neurons revert to their youthful behavior and start using sodium again"
“The cells had put away their old childhood tools in the closet. The question was if we stopped them from behaving like adults would they go into the closet and get them out again"” Surmeier asked. “Sure enough, they did.”
When he gave the mice isradipine, it blocked the calcium from entering the dopamine neuron. At first, the dopamine neurons became silent. But within a few hours, they had reverted to their childhood ways, once again using sodium to get their work done.
“This lowers the cells’ stress level and makes them much more resistant to any other insult that’s going to come along down the road. They start acting like they’re youngsters again,” Surmeier said.
Hat's off to this scientist and his team. Good job.
This week, General Motors (GM) announced its selection of battery makers to develop and test battery packs for use in its proposed electric vehicles. The selected battery makers, Compact Power, based in Troy, MI, and Continental Automotive Systems, based in Germany, say that they've overcome the performance and cost limitations that have been an obstacle to electric vehicles in the past.
A123 Systems will be supplying the battery cells which Continental will use to make full batteries for GM.
Pluggable hybrid electric vehicles (PHEVs) will allow people to recharge from a wall socket and run only on electricity on shorter trips. Though some PHEVs will require running their conventional engines at higher speeds . Then on longer trips the cars will run gasoline engines to recharge their batteries. GM will release 2 different kinds of PHEVs in 2010.
Factory-built, dealer-sold PHEVs are another story. General Motors says both an E-Flex car and a Saturn-branded plug-in, called the Vue Green Line, will be ready by 2010. The Vue, like models on the roads now, will follow a "parallel" design, in which both an electric motor and a gasoline engine drive the wheels, often working in concert. In contrast, the E-Flex cars will be "series" hybrids. Only the electric motor will turn the wheels. Then, once the battery runs low, a small engine — could be gas or diesel, or it could someday be replaced by a hydrogen fuel cell — fires to turn a generator that produces more electricity.
The auto industry expects battery costs for PHEVs and pure electric cars to drop to less than a third of current prices.
According to an industry rule of thumb, every kilowatt-hour of capacity adds about $1000 to the price of a battery. An E-Flex car, for instance, could cost $9000 to $10,000 more than a conventional gasoline-powered version of the vehicle. At least at first.
"If we're talking about 100,000 units or more, cost becomes less of an issue," says Altair head Alan Gotcher. The rough consensus among battery makers is that prices could drop to $5000 within a few years, and eventually dip below $3000.
Some "Peak Oil" doomsters see civilizational collapse in store when world oil production peaks and declines. But the advances in battery car technology makes that scenario unlikely. In 5 years time we will have millions of PHEV and pure electric vehicles. If we hit peak oil 5 years from now then we could shift to making only PHEV and pure electric vehicles. To generate the electricty we can use nuclear, wind, and (unfortunately) coal.
The global warming debate has focused on carbon dioxide emissions, but scientists at UC Irvine have determined that a lesser-known mechanism – dirty snow – can explain one-third or more of the Arctic warming primarily attributed to greenhouse gases.
If this is true it suggests we can greatly reduce ice melting by cutting back on particulates pollution from burning coal and other fossil fuels. Cutting back on the particulates would also reduce health harm from particulates. One of my recurring arguments on energy and environmental policy is that we should cut back on conventional air pollutants as a higher priority than reduction of carbon dioxide emissions. Here's evidence that cleaner burning of fossil fuels will reduce temperatures in the Arctic.
Snow becomes dirty when soot from tailpipes, smoke stacks and forest fires enters the atmosphere and falls to the ground. Soot-infused snow is darker than natural snow. Dark surfaces absorb sunlight and cause warming, while bright surfaces reflect heat back into space and cause cooling.
“When we inject dirty particles into the atmosphere and they fall onto snow, the net effect is we warm the polar latitudes,” said Charlie Zender, associate professor of Earth system science at UCI and co-author of the study. “Dark soot can heat up quickly. It’s like placing tiny toaster ovens into the snow pack.”
The study appears this week in the Journal of Geophysical Research.
The rapid rate at which China is building coal-fired electric power plants (1-2 per week) suggests the snow is going to get even more soot-infused in coming years.
Our snow is too dirty.
In the past two centuries, the Arctic has warmed about 1.6 degrees. Dirty snow caused .5 to 1.5 degrees of warming, or up to 94 percent of the observed change, the scientists determined.
Forest fires also generate soot that lowers albedo and heats up snow in the Arctic.
The Chinese aren't going to shift away from coal toward cleaner energy sources until the alternatives drop in price. However, as their living standards increase we can expect they will try harder to reduce emissions from their coal burning industries as their higher affluence causes them to see cleaner air as a higher priority. But their living standards have a long way to rise before they'll want to treat emissions controls as a high priority.
(PHILADELPHIA) – Researchers at the Abramson Family Cancer Research Institute of the University of Pennsylvania have found that deleting a gene important in embryo development leads to premature aging and loss of stem cell reservoirs in adult mice. This gene, ATR, is essential for the body’s response to damaged DNA, and mutations in proteins in the DNA damage response underlie certain types of cancer and other disorders in humans. This work appears in the inaugural issue of Cell Stem Cell.
Signs of aging come fast if an organism can't do tissue repair.
“The reason these mice age prematurely is that we’re exhausting their ability to renew tissues,” says Eric J. Brown, PhD, Assistant Professor of Cancer Biology. “These findings may be helpful to the aging and oncology fields since premature aging syndromes and many cancers involve the loss of DNA repair genes.”
When the researchers deleted ATR in the tissues of adult mice, they noticed that the mice showed signs of premature aging, such as hair graying, hair loss, and osteoporosis, within three to four months.
To be able to renew itself, most tissues have a reservoir of specific adult stem cells. These stem cells don’t divide as frequently as other cell types since they need to maintain the integrity of their DNA, and multiple divisions lead to natural breaks in DNA. But when these stem cells are needed, their progeny can rapidly divide and are able to replenish the tissue with new cells.
As we age our stem cells age right along with the rest of us. Aged stem cells gradually slow down and lose their ability to create replacement cells to repair damage caused by aging. As the repair systems slow down more damage accumulates and we get older.
This study supports the notion that replacement of aged stem cells with youthful stem cells will help slow and even reverse the process of aging. The development of the ability to create the various adult stem cell types is a crucial step in the development of full body rejuvenation therapies. Once we can create such cells on demand then their injection into our blood streams and into specific stem cell reservoirs will give our bodies the resources needed to repair worn out and failing body parts.
Time for another chapter in the on-going saga on which diet - if any - works to lose and keep off weight. Foods that provide lots of weight but few calories probably make weight loss easier.
Eating smart, not eating less, may be the key to losing weight. A year-long clinical trial by Penn State researchers shows that diets focusing on foods that are low in calorie density can promote healthy weight loss while helping people to control hunger.
Foods that are high in water and low in fat – such as fruits, vegetables, soup, lean meat, and low-fat dairy products – are low in calorie density and provide few calories per bite.
“Eating a diet that is low in calorie density allows people to eat satisfying portions of food, and this may decrease feelings of hunger and deprivation while reducing calories” said Dr. Julia A. Ello-Martin, who conducted the study as part of her doctoral dissertation in the College of Health and Human Development at Penn State. Previously, little was known about the influence of diets low in calorie density on body weight.
Whole grains lower calorie density because they have more fiber. Ditto lots of vegetables. These foods which are already considered better for other reasons are also better for weight loss.
The researchers compared the effects of two diets – one reduced in fat, the other high in water-rich foods as well as reduced in fat – in 71 obese women aged 22 to 60. The participants were taught by dietitians to make appropriate food choices for a diet low in calorie density, but unlike most diets, they were not assigned daily limits for calories.
At the end of one year, women in both groups showed significant weight loss as well as a decrease in the calorie density of their diets. However, women who added water-rich foods to their diets lost more weight during the first six months of the study than those who only reduced fat in their diets – 19.6 pounds compared to 14.7 pounds. Weight loss was well maintained by subjects in both groups during the second six months of the study.
I am guessing fiber will work as well or better than water as a substance to increase the weight of what you eat. The water-rich food eaters ate 25% more food by weight.
Records kept by the women showed that those who included more water-rich foods ate 25 percent more food by weight and felt less hungry than those who followed the reduced-fat diet. “By eating more fruits and vegetables they were able to eat more food, and this probably helped them to stick to their diet and lose more weight,” said Ello-Martin.
Yet another reason to eat more fruits and vegetables in place of other foods.
For several years here I've argued the ethical conflict over human embryonic stem cell research would get resolved by discovery of techniques to dedifferentiate adult cells (make cells less specialized and more flexible). Well, at least with mice a method has been discovered to do exactly that. The use of gene therapy to turn on 4 genes in adult mouse cells transforms those cells to make them as flexible as embryonic stem cells.
Now, in three papers published simultaneously this week, Yamanaka and two other groups report that by turning on expression of the same four chemicals in adult mouse cells, the cells run their differentiation process backwards, reverting to an ESC-like state (Nature, DOI:10.1038/nature05934 and DOI:10.1038/nature05944; Cell Stem Cell, DOI:10.1016/j.stem.2007.05.014). "We have shown that cells can be generated by these four factors, that are indistinguishable from embryonic stem cells," says Konrad Hochedlinger of the Harvard Stem Cell Institute, who wrote one of the papers (watch a video of Marius Wernig - first author on the same paper - describing the cells - 3.8 MB, .wmv).
These cells are pluripotent which means they are capable of turning into all the cell types in a body. Need new parts to replace old worn out organs, blood vessels, muscles, tendons, and joint tissue? Pluripotent cells will some day serve as starter cells for the growth of replacement parts. Replacement cells and organs will usher in the age of regenerative medicide and eventually full body rejuvenation.
What was the enabler that made these experiments possible? The discovery by Yamanaka's team that 4 genes could cause a cell to become pluripotent. As scientists discover more about which genes control cellular differentiation (how cells change to take on specialized jobs) more ways to manipulate cell type will come from use of this knowledge.
Using artificial viruses called vectors, the team activated the same four genes in a batch of mouse skin cells. These genes, Oct4, Sox2, c-Myc and Klf4, are called transcription factors, meaning that they regulate large networks of other genes. While Oct4 and Sox2 are normally active in the early stages of embryogenesis, they typically shut down once an embryo has developed beyond the blastocyst stage.
It says something about the immaturity of gene therapy techniques in the year 2007 that only 1 in 1000 cells exposed to viruses with the 4 genes got reprogrammed by the attempt to add genes to the cells.
“We were working with tens of thousands of cells, and we needed to devise a precise method for picking out those rare cells in which the reprogramming actually worked,” says Wernig. “On average, it only works in about one out of 1,000 cells.”
To test for reprogramming, the team decided to zero in on Oct4 and another transcription factor called Nanog. These two hallmarks for embryonic stem cell identity are only active in fully pluripotent cells. The trick would be to figure out a way to harvest Oct4- and Nanog-active cells from the rest of the population.
Nicholas Wade of the New York Times claims the technique, once replicated with human cells, will clost less and take less effort than cloning to create embryonic stem cells.
The technique, if adaptable to human cells, is much easier to apply than nuclear transfer, would not involve the expensive and controversial use of human eggs, and should avoid all or almost all of the ethical criticism directed at the use of embryonic stem cells.
“From the point of view of moving biomedicine and regenerative medicine faster, this is about as big a deal as you could imagine,” said Irving Weissman, a leading stem cell biologist at Stanford University, who was not involved in the new research.
Replicating this study with human cells poses some problems which scientists must solve. But some of the scientists are optimistic about solutions:
A third issue is that two of the genes in the recipe can cause cancer. Indeed 20 percent of Dr. Yamanaka’s mice died of the disease. Nonetheless, several biologists expressed confidence that all these difficulties would be sidestepped somehow.
“The technical problems seem approachable — I don’t see anyone running into a brick wall,” said Owen Witte, a stem cell biologist at U.C.L.A. Dr. Jaenisch, in a Webcast about the research, predicted that the problems of adapting the technique to human cells would be solvable but he did not know when.
The threat of cancer is a big problem with stem cells. We need better methods of doing gene therapy so that stem cells can get genetically altered to repair all genes that prevent cells from growing uncontrollably.
Thanks to Brock Cusick for the tip.
Low levels of testosterone may increase the long-term risk of death in men over 50 years old, according to researchers with the Department of Family and Preventive Medicine at the University of California, San Diego School of Medicine.
“The new study is only the second report linking deficiency of this sex hormone with increased death from all causes, over time, and the first to do so in relatively healthy men who are living in the community,” said Gail Laughlin, Ph.D., assistant professor and study author.
This result surprises me. I would have expected the testosterone to reduce life expectancies by upping the incidence of prostate cancer and by basically turning up the body's metabolism to a level that would cause the body to wear out more rapidly.
The men in this study have been tracked for the last 18 years.
“We have followed these men for an average of 18 years and our study strongly suggests that the association between testosterone levels and death is not simply due to some acute illness,” said Laughlin.
In the study, Laughlin and co-workers looked at death, no matter the cause, in nearly 800 men, ages 50 to 91 years, who were living in Rancho Bernardo, California. The participants have been members of the Rancho Bernardo Heart and Chronic Disease Study since the 1970s. At the beginning of the 1980s, almost one-third of these men had suboptimal blood testosterone levels for men their age.
The group with low testosterone levels had a 33 percent greater risk of death during the next 18 years than the men with higher testosterone. This difference was not explained by smoking, drinking, physical activity level or pre-existing diseases (such as diabetes or heart disease).
In this study, "low testosterone" levels were set at the lower limit of the normal range for young adult men. Testosterone declines slowly with aging in men and levels vary widely, with many older men still having testosterone levels in the range of young men. Twenty-nine percent of Rancho Bernardo men had low testosterone.
So them maybe testosterone patches would increase life expectancy in men who have lower levels of testosterone?
The men with lower testosterone had more fat on their wastes and more inflammation in their bodies.
Men with low testosterone were more likely to have elevated markers of inflammation, called inflammatory cytokines, which contribute to many diseases. Another characteristic that distinguished the men with low testosterone was a larger waist girth along with a cluster of cardiovascular and diabetes risk factors related to this type of fat accumulation.
This begs the question: If these low testosterone men took testosterone would their inflammation markers go down and their fat decrease? If so, would they then live longer? I would at least expect the reduction in body fat.
Folic acid supplementation can reduce the risk of stroke by 18% or more, conclude authors of an Article published in this week's edition of The Lancet.
But the authors and an accompanying comment caution that there remains controversy as to whether folic acid supplementation can lead to improved outcomes for other cardiovascular conditions.
Professor Xiaobin Wang, Children's Memorial Hospital and Children's Memorial Research Center, Northwestern University Feinberg School of Medicine, Chicago, USA, and colleagues did a meta-analysis (a study combining previous trials) of eight trials of folic acid that had stroke reported as one of the endpoints.
Folic acid supplementation lowers the concentrations homocysteine in the blood. High amounts of homocysteine in the blood are thought to increase the risk of stroke, as well as that of cardiovascular disease and deep vein thrombosis.
They found folic acid supplementation reduced the relative risk of stroke by an average of 18 per cent. In subgroup analyses, an even greater reduction of risk was seen when the treatment lasted over 36 months (29% less risk); if it reduced the concentration of homocysteine in the blood by more than 20% (23% less risk); or if the patient had no previous history of stroke (25% less risk).
The study also found that in areas that did not already have supplementation through fortified or partly fortified grain, folic acid supplementation decreased the risk of stroke by 25%.
Should blood tests for homocysteine levels become as commonplace as blood tests for cholesterol and lipids? Also, while I'm at it, should vitamin D blood tests also become commonplace?
Look ahead 20 years and I expect many people will walk around with implanted nanodevices that do in situ blood tests. People will get their blood tests and recommended dietary recommendations from their cell phones which will query their implanted nanodevices. Or maybe they'll have implanted headphones and the implants will tell us what we need? Or why not implant display devices on the optic nerves and just show the test results by stimulating a pattern on optic nerves to cause us to see test result data?
DNA double helix co-discoverer James D. Watson has had his DNA sequenced at a much lower cost than previous genome sequencing attempts.
On Thursday, James Watson was handed a DVD containing his entire genome, sequenced in the past few months by 454, a company based in Branford, CT, that's developing next-generation technologies for efficiently reading the genome. At a cost of $2 million, 454 sequenced Watson's genome for roughly an order of magnitude less than it would have cost using traditional machines.
The $2 million and two months that it took to sequence Watson's genome is a far cry from the more than ten years and $3 billion required for the Human Genome Project's reference genome, released in 2003.
454 Life Sciences Corporation, in collaboration with scientists at the Human Genome Sequencing Center, Baylor College of Medicine, announced today in Houston, Texas, the completion of a project to sequence the genome of James D. Watson, Ph.D., co-discoverer of the double-helix structure of DNA. The mapping of Dr. Watson's genome was completed using the Genome Sequencer FLX(TM) system and marks the first individual genome to be sequenced for less than $1 million.
And technology companies like Illumina, Applied Biosystems and 454 Life Sciences, which solicited Dr. Watson’s DNA to prove its abilities, say the price of a complete human genome has already dropped to $100,000. They are competing for a $10 million “X prize” to sequence 100 human genomes within 10 days. (Dr. Watson’s took about two months.)
The rapid advance of DNA testing technologies is possible because DNA is small and DNA testing relies on computer chip technologies. While I've made this claim for years this latest news provides a much dramatic demonstration that this trend is really happening. This rate of advance that bodes well for future advances across a wide range of biotechnologies.
What will come from very cheap DNA sequencing? Lots of things:
Most of us will live to see full genome testing become commonplace.
Will rise in atmospheric carbon dioxide (CO2) and consequent warming cause massive droughts and famine? Maybe not.
What goes up, must come down. This basic rule of gravity on Earth's surface also applies to water vapor in the atmosphere. And as the air, earth and sea warms with climate change the atmospheric water vapor load increases by as much as 6.5 percent per degree Celsius, according to satellite data from the past 20 years. As the water vapor increases, so, too, will rainfall, argues physicist Frank Wentz, director of Remote Sensing Systems (RSS) in Santa Rosa, Calif., a provider of climate data records contracted by NASA.
While global climate models predict less wind due to global warming Wentz and colleagues found that surface winds increased with recent warming. Winds will blow evaporated water from the oceans over land and hence winds create the potential for increased precipitation if the planet warms further.
But climate models project that global warming will also bring weaker winds, leading to less water evaporating from the ocean and counteracting the effect of warming. Models predict that worldwide precipitation — which must match the amount of evaporation — will increase by only 1-3% for each degree of future global warming.
They report in Science that the amount of water in the atmosphere, evaporation and precipitation all increased at the same rate, by about 1.3% per decade1 — or about 6.5% for every degree of warming. Surface winds increased, not decreased, with warming.
Why is this important: The "Apocalypse Soon" global warming doomsters predict global warming will lead to reduced precipitation and therefore crop failures and massive hunger. The official view of all Correct Thinking people is that global warming means massive droughts.
In February, the Intergovernmental Panel on Climate Change (IPCC) cited studies showing "extreme drought increasing from 1% of present-day land area to 30% by the end of the century."
The new study suggests models are flawed, underestimating how increased humidity in a warmer climate produces more rain clouds, Wentz said by e-mail.
Gavin Schmidt, a climatologist at the NASA Goddard Institute points out that the 20 years studied were dominated by a couple of El Niño events, which increased precipitation during that time. "The trends are not really significant," he says. "I think some more work would be necessary to really pin their argument down."
But if the warming brings more rain then more land might become usable for crops - especially lands closer to the north and south poles. Areas closer to the poles will gain longer growing seasons as nights get warmer in fall and spring and frost stops sooner and starts later. Massive farms in Siberia, Alaska, and northern Canada anyone?
Of course, that doesn't mean that a large increase in world temperatures will deliver net benefits. If Antarctica mostly melts then land areas will shrink due to rising ocean levels. Though we could build dikes to hold back the water ala Holland. Not sure that is feasible for Florida though. A cheaper solution for that problem: cool the poles with climate engineering to keep all the snow and ice frozen.
What worries me most about rising atmospheric CO2: Acidification of the ocean. That seems like a much tougher problem to prevent. Any ideas on that?
CHAMPAIGN, Ill. — All anxiety is not created equal, and a research team at the University of Illinois now has the data to prove it. The team has found the most compelling evidence yet of differing patterns of brain activity associated with each of two types of anxiety: anxious apprehension (verbal rumination, worry) and anxious arousal (intense fear, panic, or both).
Worriers have more activity in their left inferior frontal lobe. Whereas people feeling panic or fear are feeling the effects of activity in the right inferior temporal lobe.
The researchers used functional Magnetic Resonance Imaging (fMRI) to map the brain areas with heightened neural activity during a variety of psychological probes.
As the researchers had predicted, the anxious apprehension group exhibited enhanced left-brain activity and the anxious arousal group had heightened activity in the right brain. The anxious apprehension group showed increased activity in a region of the left inferior frontal lobe that is associated with speech production. The anxious arousal group had more activity in a region of the right-hemisphere inferior temporal lobe that is believed to be involved in tracking and responding to information signaling danger.
Better understanding eventually brings with it better ability to manipulate and control. Picture a future where nanotubes can get extended up arteries into the brain. The nanotubes could be used to locally deliver drugs or electrical pulses to excite or suppress activity in particular parts of the brain.
Of course the ability to stimulate particular kinds of emotions and mental states would enable some pretty severe abuse and manipulation of human behavior. But individuals could use such technology to control crippling emotional conditions. Plus, imagine turning up the motivation to work hard when you want to get more done.
ANAHEIM, Calif., May 21 -- Women with stress urinary incontinence (SUI) treated using muscle-derived stem cell injections to strengthen their sphincter muscles experience long-term improvements in their condition, according to a study led by researchers at the University of Pittsburgh School of Medicine and Sunnybrook Health Sciences Centre in Toronto. The study, which followed patients for more than one year, suggests that the approach is safe, improves patients’ quality of life and may be an effective treatment for SUI. The findings will be presented at the Tissue Engineering and Regenerative Medicine in Urology press briefing at the annual meeting of the American Urological Association (AUA) in San Diego, and will be published in Abstract 1331 in the AUA proceedings.
The results of this study illustrate a pattern: Stem cell therapies for maladies of aging bodies look like rejuvenation therapies. The development of stem cell therapies to treat various problems will produce treatments that do rejuvenation. As long as civilization isn't destroyed by a natural disaster such as an asteroid or massive volcanic eruption the development of rejuvenation therapies is inevitable.
Someone might object and argue that this treatment has a very narrow effect on one location in the body. But these researchers are developing a rather general capability where they can supply replacement muscle cells where lack of muscle cells is the problem. Well, as we grow old our muscle cells become hobbled by damage and die. This happens in all our muscles. The ability to grow stem cells and turn them into muscle cells is a key capability needed to rejuvenate our bodies.
In the study, Dr. Carr and colleagues took biopsies of skeletal muscle tissue from eight female patients and isolated and expanded the stem cells from the tissue in culture. In an outpatient setting, the patients then received injections of the muscle-derived stem cells into the area surrounding the urethra. Each patient received an equal dose of stem cell injections using three different injection techniques – a transurethral injection with either an 8-mm or 10-mm needle or a periurethral injection.
Five of the eight women who participated in the study reported improvement in bladder control and quality of life with no serious short- or long-term adverse effects one year after the initial treatment.
A future enhancement of this treatment will be to take the muscle stem cells, treat them with gene therapies to correct accumulated DNA damage, and then grow them up for injection. Eventually scientists will even discover genetic variations that enhance muscle performance and the stem cells will get genetically engineered to form better muscle cells than we were born with.
Over an average of 10 years of follow-up, 276 premenopausal women and 743 postmenopausal women developed breast cancer. Calcium and vitamin D intake were moderately associated with a lower risk of breast cancer before but not after menopause. The inverse associated in premenopausal women appeared more pronounced for more aggressive breast tumors.
"A possible explanation for the evident difference by menopause status may be related to the joint relationship among calcium, vitamin D and insulinlike growth factors (IGFs)," they continue. "In vitro studies have suggested that calcium and vitamin D exert anticarcinogenic effects on breast cancer cells expressing high levels of IGF-1 and IGF binding protein 3. Calcium, vitamin D and IGF binding protein 3 have been shown in vitro to interact with each other in promoting growth inhibition in breast cancer cells." Since blood levels of these compounds decline with age, they would be more prevalent in younger, premenopausal women.
This result does not necessarily mean that vitamin D and calcium have no anti-cancer benefit as women get older. As we age we suffer decreased ability to absorb nutrients. Maybe older women do not absorb vitamin D well enough to benefit from concentrations found in food and maybe they need higher doses to achieve the same benefit as they get older.