The reason cars can keep running indefinitely is because their worn out parts can be replaced. By contrast, we have very limited abilities to replace worn out human parts. The development of tissue engineering techniques for growing an implanting replacement parts holds the promise of making humans as repairable as cars. Some University of Washington researchers have developed human heart muscle patches that include blood vessels that allow larger patches to be grown.
University of Washington (UW) researchers have succeeded in engineering human tissue patches free of some problems that have stymied stem-cell repair for damaged hearts.
The disk-shaped patches can be fabricated in sizes ranging from less than a millimeter to a half-inch in diameter. Until now, engineering tissue for heart repair has been hampered by cells dying at the transplant core, because nutrients and oxygen reached the edges of the patch but not the center. To make matters worse, the scaffolding materials to position the cells often proved to be harmful.
The researchers were able to grow blood vessels along with the muscle. Then when they transplanted the tissue patches into rats the blood vessels in the patches formed connections with the blood vessels in the rats.
Stevens and her fellow researchers added two other types of cells to the heart muscle cell mixture. These were cells similar to those that line the inside of blood vessels and cells that provide the vessel's muscular support. All of the heart muscle cells were derived from embryonic stem cells, while the vascular cells were derived from embryonic stem cells or a variety of more mature sources such as the umbilical cord. The resulting cell mixture began forming a tissue containing tiny blood vessels.
Better techniques for tissue engineering are key to the development of human replacement parts. Replacement parts are key to human rejuvenation and the reversal of the aging process. Tissue engineering is more than just stem cell research (as important as that is). Tissue engineering involves the development of the ability to grow organized complex 3 dimensional groupings of cells that form a part equivalent to some existing part in our bodies.
Okay, time for yet another post on the glories of vitamin D. If you are already taking vitamin D you can still use this post to feel good about your wisdom and sagacity. Maintain your strength and balance in your old age so you don't fall down and go boom.
A daily supplement of vitamin D at a dose of 700-1000 IU reduces the risk of falling among older people by 19% according to a study published on bmj.com today. But a dose of less than 700 IU per day has no effect.
Sounds like D3 works better than D2. I happen to take D3. So I got that going for me. Which is nice. (who am I quoting?)
Supplemental vitamin D2 and Vitamin D3 were investigated. 700-1000 IU supplemental vitamin D per day (vitamin D2 or vitamin D3) reduced falls by 19% and up to 26% with vitamin D3.
This effect was independent of age, type of dwelling or additional calcium supplementation. The effect was significant within two to five months of starting treatment and extended beyond 12 months.
Supplemental vitamin D did not reduce falls at a dose of less than 700 IU per day.
Now if you are 20 years old the odds are that by the time you turn 60 you'll be able to get stem cell treatments that'll restore your skin's youthful ability to synthesize vitamin D. Plus, stem cell therapies to restore muscle strength along with stem cell therapies to repair joints and connective tissue will have you out playing beach volleyball. So you'll synthesize lots of vitamin D in your skin in your old age.
Resveratrol reduces the severity of type II insulin-resistant diabetes. A new study finds that resveratrol works against diabetes by altering brain metabolism.
Chevy Chase, MD—Resveratrol, a molecule found in red grapes, has been shown to improve diabetes when delivered orally to rodents. Until now, however, little has been known about how these beneficial changes are mediated in the body. A new study accepted for publication in Endocrinology, a journal of The Endocrine Society, shows that the brain plays a key role in mediating resveratrol's anti-diabetic actions, potentially paving the way for future orally-delivered diabetes medications that target the brain.
Resveratrol activates sirtuins, a class of proteins that are thought to underlie many of the beneficial effects of calorie restriction. Previous studies in mice have provided compelling evidence that when sirtuins are activated by resveratrol, diabetes is improved. Sirtuin activators are now being tested in humans as anti-diabetic compounds.
I continue to wonder whether I should take resveratrol. Anyone have well-informed views on this question?
Serious hikers and backpackers tend to become supporters of environmental and conservation groups while casual woodland tourists do not, a new study says -- and a recent fall-off in strenuous outdoor endeavors portends a coming decline in the ranks of conservation backers.
Oliver Pergams, visiting research assistant professor of biological sciences at the University of Illinois at Chicago, and Patricia Zaradic, director of the Red Rock Institute in Pennsylvania, made headlines in early 2008 with a study showing that a steady decline in nature recreation since the late 1980s correlated strongly with a rise in playing video games, surfing the Internet and watching movies -- an unhealthy trend they called "videophilia."
Now Pergams and Zaradic, along with Peter Kareiva, chief scientist at the Nature Conservancy, have found that only people who engage in vigorous outdoor sports, like hiking and backpacking, tend later to become supporters of mainline conservation groups, while those who only go sightseeing or fishing do not. Their findings are reported Oct. 7 in PLoS ONE, an online publication of the Public Library of Science.
I notice with some commenters a greater love of the creations of humans than of the natural wonders. This probably partly explains the indifference some express to the plight of nature due to human population growth and industrialization.
Will humans in the long term become less and less interested in natural environments and more supportive of artificial managed ecologies?
Using thin film copper indium gallium diselenide (CIGS) coated onto roof tiles Dow is going into the business of selling solar photovoltaic tiles for roofs.
The Dow Chemical Company (NYSE: DOW) today unveiled its line of DOW™ POWERHOUSE™ Solar Shingle, revolutionary photovoltaic solar panels in the form of solar shingles that can be integrated into rooftops with standard asphalt shingle materials. The solar shingle systems are expected to be available in limited quantities by mid-2010 and projected to be more widely available in 2011, putting the power of solar electricity generation directly and conveniently in the hands of homeowners.
Groundbreaking technology from Dow Solar Solutions (DSS) integrates low-cost, thin-film CIGS photovoltaic cells into a proprietary roofing shingle design, which represents a multi-functional solar energy generating roofing product. The innovative product design reduces installation costs because the conventional roofing shingles and solar generating shingles are installed simultaneously by roofing contractors. DSS expects an enthusiastic response from roofing contractors since no specialized skills or knowledge of solar array installations are required.
PV tiles have some advantages over PV panels. The most obvious is that the panels are an additional step to install and with additional bracketing. When a house is first constructed or it needs a new roof laborers already install tiles. The incremental labor cost of installing PV tiles rather than conventional tiles is smaller than the cost of of installing PV panels.
Dow claims their shingles cut labor installation costs by more than half.
The Dow shingles can be installed in about 10 hours, compared with 22 to 30 hours for traditional solar panels, reducing the installation costs that make up more than 50 percent of total system prices.
When you'll know solar PV has hit the mainstream: prefabricated housing will come with optional PV roofs. Seriously, house factories have lower labor costs because they can use much more automation. PV installation on pre-fab housing as shingles or other roofing material could be done at very low labor cost in a housing factory.
Global Solar Energy, the company which makes the PV material that Dow is using, has recently achieved 15.45% efficiency with their CIGS PV material. That's a substantial step up from the efficiency of the PV they are currently selling and close to the efficiency of silicon-based PV.
Global Solar Energy, Inc., the premier manufacturer of Copper Indium Gallium diSelenide (CIGS) thin film solar products, today announced that the U.S. Department of Energy’s National Renewable Energy Laboratory (NREL), the nation’s primary laboratory for renewable energy and energy efficiency research and development, confirmed 15.45 percent total area efficiency for Global Solar’s production level CIGS material. Adding to this news, Global Solar announces a peak efficiency of 11.7 percent for production CIGS solar cell strings manufactured at its 35-megawatt German and 40-megawatt U.S. plants.
Global Solar Energy's 75 MW yearly production capacity is small potatoes. Nanosolar's new PV plant in Germany has a yearly production capacity of 640 MW. Solyndra just started construction on a new production facility with a planned yearly 500 MW production capacity. While Showa Shell Sekiyu K.K. has announced plans for a thin film PV plant with a 900 MW yearly production capacity. Yet Dow is forecasting billions of dollars per year in sales for their PV shingles. If the demand develops then either Global Solar will have to scale up in a hurry or Dow's going to need another partner.
A New York Times article reports on other PV roofing material makers. For the home market PV tile will probably become the preferred choice.
Results: MIT engineers have boosted stem cells' ability to regenerate vascular tissue (such as blood vessels) by equipping them with genes that produce extra growth factors (naturally occurring compounds that stimulate tissue growth). In a study in mice, the researchers found that the stem cells successfully generated blood vessels near the site of an injury, allowing damaged tissue to survive.
The researchers used nanoparticles to deliver genes for an angiogenesis (stimulates blood vessel growth) compound to grow blood vessels using stem cells.
Methods: After removing stem cells from mouse bone marrow, the researchers used specially developed nanoparticles to deliver the gene for the growth factor VEGF (vascular endothelial growth factor). The stem cells were then implanted into damaged tissue areas. These nanoparticles, which the MIT team has also tested to deliver cancer treatments, are believed to be safer than the viruses often used for gene delivery.
Note that angiogenesis genes are problematic for therapies because mutations in angiogenesis genes are necessary steps for the development of killer cancers. Ideally to carry out safe the added genes need to break down after the repairs are completed.
Mercury is bad. If we got more electricity from nuclear power rather than coal we'd put less mercury into the environment.
DALLAS, Oct. 5, 2009 — The negative impact of high amounts of methylmercury in seafood on blood pressure may outweigh the protective effects of fish nutrients, researchers report in Hypertension: Journal of the American Heart Association.
Researchers found that even when blood pressure was within the normal range and numerous other factors, including omega-3 fatty acids (essential fats that your body needs to function properly but does not make) and selenium (a dietary essential mineral) were carefully controlled for, the environmental mercury was associated with higher blood pressure and pulse pressure among Nunavik Inuit adults in a recent study.
Keep in mind that few eat as much fish as the Nunavik.
Researchers conducted a survey in the 14 Nunavik communities in northern Quebec, Canada, where the traditional diet is based mainly on fish and marine mammals, and thus, residents regularly ingest higher levels of environmental mercury. Individuals taking medication for high blood pressure during data collection were excluded. The survey featured two-stage stratified random sampling and data from 732 Inuit adults (319 men and 413 women), average age 34.
The average total mercury blood concentration in people in the United States is now 4 nanomoles per liter (nmol/L) (NHANES study) compared to 50 nmol/L in the Inuit population.
Higher blood mercury means higher blood pressure.
Researchers found a 10 percent increase in blood mercury was associated with an increase of 0.2 mm Hg in systolic blood pressure after controlling for other factors.
You can get lots of omega 3 fatty acids by eating fish that have almost undetectable amounts of mercury such as sardines and salmon. Check out this US Food and Drug Administration chart of mercury levels in fish. The big fish at the top of the food chain such as shark and swordfish have high mercury levels. Compare them to tilapia and oysters. Salmon are the best to eat to my thinking because they have very low mercury while having some of the highest levels of omega 3 fatty acids such as DHA.
BOSTON – Eating salmon or other fatty fish just once a week helped reduce men's risk of heart failure, adding to growing evidence that omega-3 fatty acids are of benefit to cardiac health. Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and reported in today's on-line issue of the European Heart Journal, the findings represent one of the largest studies to investigate the association.
"Previous research has demonstrated that fatty fish and omega-3 fatty acids help to combat risk factors for a range of heart-related conditions, such as lowering triglycerides [fats in the blood] reducing blood pressure, heart rate and heart rate variability," explains first author Emily Levitan, PhD, a research fellow in the Cardiovascular Epidemiology Research Center at BIDMC. "Collectively, this may explain the association with the reduced risk of heart failure found in our study."
Studies of fish consumption are problematic because they typically do not collect detailed information about the types of fish consumed. Well, omega 3 fatty acid levels vary considerably between types of fish.Omega 3 fatty acid levels in fish vary over a few orders of magnitude. Caviar is the best followed by salmon.
There might be an ideal daily dose of omega 3 fatty acids.
The findings were similar when the researchers looked at fish oil consumption: Among five groups based on fish oil consumption, the middle group, who consumed 0.36 grams per day of omega-3 fatty acids showed a 33 percent reduced risk of heart failure, while the men who consumer greater quantities (approximately 0.46 grams per day or 0.71 grams per day) had a risk of heart failure similar to the men who consumed little or no fish oils.
Though the researchers leave open the possibility that people suffering from heart disease up their omega 3 fatty acid intake to help treat their disease. So the lack of benefit from the larger dose might not be real.
Writing in Scientific American David Biello presents the case that Thomas Malthus might be right after all.
MALTHUSIAN DILEMMA: How to feed a human population expected to reach 9 billion by 2050 while also grappling with poverty as well as climate change, dead zones, biodiversity loss and other environmental ills?
These problems won't all be solved. Technological advances will feed more humans while more species go extinct. Humans are not going to stop making babies so that orangutans or bonobo chimps can survive in the wild.
By 2050, the world will host nine billion people—and that's if population growth slows in much of the developing world. Today, at least one billion people are chronically malnourished or starving. Simply to maintain that sad state of affairs would require the clearing (read: deforestation) of 900 million additional hectares of land, according to Pedro Sanchez, director of the Tropical Agriculture and Rural Environment Program at The Earth Institute at Columbia University.
We are shifting more land into agricultural production and out-competing more species in the process. Land that used to support them now supports us.
"Agriculture is the main driver of most ecological problems on the planet," said economist Jeffrey Sachs, Scientific American columnist and Earth Institute director. "We are literally eating away the other species on the planet."
I think 6.6 billion people are enough. I do not see any personal benefit to myself from adding billions more humans to the planet. Rather, I see net costs. Look at pollution. The more people pollution the less pollution each can generate. But industrialization of previously undeveloped countries is increasing the amount of pollution per person while the total number of people keeps going up.
In 1980, Luis Alvarez and his collaborators stunned the world with their discovery that an asteroid impact 65 million years ago probably killed off the dinosaurs and much of the the world's living organisms. But ever since, there has been an ongoing debate about how long it took for life to return to the devastated planet and for ecosystems to bounce back.
I haven't kept up with the Cretaceous-Tertiary (K-T) boundary extinction debate. But some scientists argue the Chicxulub asterioid impact predates the K-T boundary by a few hundred thousand years. Has that paper stood the test of time? Massive volcanic eruptions are cited as another potential cause of the extinctions. Anyone know what the state of play is in that debate?
Whether or not an asteroid impact caused the K-T extinctions an asteroid impact as big as the Chicxulub impact could wipe out humanity. It strikes me we should pay attention to the past and potential future causes of mass extinctions. I do not want the human race to go extinct. I think we've got to make a conscious effort to avoid extinction. We need to better understand extinction events (including the one we are causing right now in other species) and try to avoid that fate.
Microorganisms can bounce back pretty quickly.
Now, researchers from MIT and their collaborators have found that at least some forms of microscopic marine life — the so called "primary producers," or photosynthetic organisms such as algae and cyanobacteria in the ocean — recovered within about a century after the mass extinction. Previous research had indicated the process might have taken millions of years.
Well great for algae and cyanobacteria. They were only down for a century before recovering. But what does that tell you about the scope of a really big asteriod impact? Forget about species like us surviving - unless you've got 100 years worth of food stored underground enough for a small community. We need to detect and deflect the next killer asteroid.
Sounds pretty severe.
The analysis clarified the sequence of events after the big impact. Immediately after the impact, certain areas of the ocean were devoid of oxygen and hostile to most algae, but close to the continent, microbial life was inhibited for only a relatively short period: in probably less than 100 years, algal productivity showed the first signs of recovery. In the open ocean, however, this recovery took much longer: previous studies have estimated that the global ocean ecosystem did not return to its former state until 1 to 3 million years following the impact.
Rather than spend money on another trip to the Moon or Mars we ought to take the same money and put it toward defense against space threats. Ditto for other extinction threats. My motto: First, don't die.
Will a baby born today live to 2109 on average? (or will AI robot terminators hunt them down and kill them?)
More than half of babies now born in the UK and other wealthy nations will live to 100 years, researchers say.
If we leave aside threats like robots, nanobots, quasars, asteroids, and VEI 8 volcanoes then I think an estimate of 100 year life expectancy is much too conservative. We are headed gaining the biotechnologies needed needed to do rejuvenation of worn out body parts. Look at the post I just did on ways to stimulate muscle stem cells to repair muscles. I expect eventual cures for cancer to enable safe restoration of youthful levels of stem cell activity and therefore much better body repair.
The leader of this study is making this prediction based on a long term trend toward longer life expectancy.
Professor Kaare Christensen, of the Danish Ageing Research Centre at the University of Southern Denmark, who led the study, said life expectancy had been increasing since 1840 and there was no sign of this trend slowing down.
The problem with this trend is that the types of advances that extend life will change with time. So far the sorts of tools used to extend life (e.g. clean water, antibiotics, vaccines, more and better foods) do not directly repair the effects of aging. But that's going to change in the lifetimes of most of the people reading this. Cures for cancer, therapies for muscle repair, and growth of replacement organs are among the treatments that'll come a lot sooner than 100 years. These therapies will extend life well beyond 100 years.
Biogerontologist Aubrey D.N.J. de Grey says we will achieve actuarial escape velocity where the rate of advance of biotechnology for repairing the body will extend life at least as fast as our bodies age. Repair rates will exceed aging rates and we will therefore effectively become younger each year. If that happens in the next 100 years (and I expect it will barring disasters that wipe out humans or destroy industrial civilization) then babies being born now will live thousands of years.
As we age changes in factors excreted by muscle cells suppress stem cells to make them do less repair. So our muscles decay. A change in biochemical signaling can activate stem cells to do more muscle repair.
Berkeley -- A study led by researchers at the University of California, Berkeley, has identified critical biochemical pathways linked to the aging of human muscle. By manipulating these pathways, the researchers were able to turn back the clock on old human muscle, restoring its ability to repair and rebuild itself.
The findings will be reported in the Sept. 30 issue of the journal EMBO Molecular Medicine, a peer-reviewed, scientific publication of the European Molecular Biology Organization.
"Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigor given the right mix of biochemical signals," said Professor Irina Conboy, a faculty member in the graduate bioengineering program that is run jointly by UC Berkeley and UC San Francisco, and head of the research team conducting the study. "This provides promising new targets for forestalling the debilitating muscle atrophy that accompanies aging, and perhaps other tissue degenerative disorders as well."
This builds on work stretching back to when Irina Conboy was at Thomas Rando's lab at Stanford about 6 years ago. This report shows how she and her collaborators are really rolling along progressively putting together more pieces of the puzzle needed to rejuvenate aging muscle. Conboy says she wants to eventually get into human trials with techniques to turn up muscle repair. I fear that getting to human trials will not be easy because the pathways that suppress stem cells in aged bodies do that in order to reduce cancer risk or perhaps other disease risks.
The problem is that aged muscle cells send the wrong mix of signals to neighboring stem cells. This turns down stem cell activity and reduces the amount of repairs that get done.
Previous research in animal models led by Conboy, who is also an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), revealed that the ability of adult stem cells to do their job of repairing and replacing damaged tissue is governed by the molecular signals they get from surrounding muscle tissue, and that those signals change with age in ways that preclude productive tissue repair.
Those studies have also shown that the regenerative function in old stem cells can be revived given the appropriate biochemical signals. What was not clear until this new study was whether similar rules applied for humans. Unlike humans, laboratory animals are bred to have identical genes and are raised in similar environments, noted Conboy, who received a New Faculty Award from the California Institute of Regenerative Medicine (CIRM) that helped fund this research. Moreover, the typical human lifespan lasts seven to eight decades, while lab mice are reaching the end of their lives by age 2.
An enzyme called MAP kinase (and kinases generally hook phosphates onto other proteins - often to regulate them) declines with age and this decline in MAP kinase (MAPK) appears to be key in turning down stem cell activity. The lowered stem cell activity means that muscle damage doesn't get repaired and therefore we accumulate more damage and muscle shrinkage as we age.
The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell's ability to divide.
The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells' capacity to effectively rebuild the body.
This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. MAP kinase (MAPK) is familiar to developmental biologists since it is an important enzyme for organ formation in such diverse species as nematodes, fruit flies and mice.
For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly, the researchers said.
In February 2005 Thomas Rando's group at Stanford showed that blood from young mice helped stimulate regeneration in muscle of old mice. I found that report to be really bad news because it suggests that even if we develop ways to make youthful stem cells programmed to become assorted cell types that by itself won't increase repair by all that much. Our problem is that cells throughout an aging body are either excreting factors into the bloodstream that dampen repairs or the cells are failing to excrete factors that stimulate repairs.
In 2008 Conboy and collaborators found that they could turn up repair capability of mouse stem cells. Now in this latest report they are working with human stem cells.
If the body is turning down MAPK and suppressing stem cells as we age there's probably a constructive reason for this. The most obvious possibility: the repair stem cells are turned down because as they age they become higher risks for turning cancerous. If that is the case (and I think it likely) then efforts to turn up stem cells to do more repair will put us at greater risk of cancer. Therefore we really need effective ways to kill pre-cancerous and cancerous cells as essential capabilities in order to do rejuvenation therapies.
One way to reduce the risk of cancer that likely would come from upregulating aged stem cells would be to replace the aged stem cells with young stem cells. Youthful stem cell lines selected for few mutations would pose less of a cancer risk. But even if suitable stem cell lines could be created for all the types of stem cells in the body getting the replacement stem cells to all the places where they are found is a daunting task. Also, getting existing stem cells to basically all die off to make room for their youthful replacements is similarly daunting.
In spite of the cancer risk for some people the benefits of therapy will outweigh the risks. If, for example, you have a failing heart that is going to kill you in a couple of years then, hey, a stem cell therapy combined with a drug therapy that upregulates stem cells will offer a very favorable ratio of benefits to risks. Stem cell therapies and other therapies to stimulate repair will make the most sense for the most unhealthy first.
A prospective study does not find a heart benefit from fish.
With heart failure treatments often limited to palliative care, much rests on prevention; this latest report from the Rotterdam Study was to investigate whether intake of the long-chain n-3 polyunsaturated fatty acids (PUFAs) found in fish conferred protection against heart failure as they seem to do against coronary heart disease.(3)
The analysis comprised 5299 subjects (41% men, mean age 67.5 years) who were free from heart failure and for whom dietary data were available. During 11.4 years of follow-up, 669 subjects developed heart failure. Their habitual diet had been assessed at baseline (in a self-reported checklist and by expert interview), with subjects specifically asked to indicate the frequency, amount, and kind of fish they had eaten, either as a hot meal, on a sandwich, or between meals.
Results showed that the dietary intake of fish was not significantly related to heart failure incidence. This relative risk was measured according to five levels of fish consumption as reflected in intake of two long chain n-3 PUFAs (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), both of which have been shown to exert some cardiovascular benefit via anti-inflammatory mechanisms, anti-arrhythmic effects and/or a reduction in serum triglycerides, blood pressure, and heart rate.
I am pretty confident that we should eat lots of fruits and vegetables and when eating grains they should be whole grain and high in fiber. But just how much omega 3 fatty acids to consume?
One of the problems is that there's genetic variability in determining what's the ideal diet. We need a level of understanding of nutritional genomics that does not exist yet. Though with the big drops in DNA sequencing costs I'm hopeful genetic alleles for dietary guidance will become known in a few years.
Update: Note that the problem with the Dutch study might be a dosing problem. Not enough people in the sample might have eaten enough fish for enough time to deliver a benefit. This study does contradict a lot of other studies. You can't conclude from just this study that eating fish doesn't help.
Also, omega 3 fatty acid concentrations vary greatly between species of fish. For example, you are going to get a lot more DHA and EPA from salmon than from tuna. Take a lot at the table at the bottom of this page for omega 3 in various fish. Salmon, anchovy, and sardines have the most omega 3 fats.
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“Over the next few years it's likely that this observed decline in the proportion of people with low cardiovascular risks will translate into increased cardiovascular disease,” said Professor De Backer, a former chair of the European Society of Cardiology (ESC) Joint Prevention Committee. “This paper should act as a wake-up call in Europe as well as the US, since overall European risk factors are not so different. While obesity may be higher in the US, Europe has been less successful in reducing smoking and cutting blood pressure.”
Indeed, the EuroAspire survey(2), which reviewed risk factors in patients with established coronary heart disease from 22 European countries, found that only 6 % of men and 4 % women were achieving lifestyle, risk factor and therapeutic targets for prevention.
“Health surveillance is essential for the development of good health policy. We need to know exactly what are the problems we are facing to determine the best ways of counteracting them,” said Professor De Backer.
The people in some European countries have porked out beyond US levels of porkiness. A whole lot of porking going on. Oink, oink. Plus, Europe has a lot more nicotine fiends. Gotta say I like California's legal hostility to cigarette smokers in workplaces.
Of course, if you are skinny non-smoker who gets a lot of exercise and eats a lot of fruits and vegetables your odds look a whole lot better. Drugs might even boost your odds of longer life even higher.
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Live near a major fault? When you read about distant earthquakes brace for the possibility of big local one as a result.
HOUSTON -- (Sept. 30, 2009) -- U.S. seismologists have found evidence that the massive 2004 earthquake that triggered killer tsunamis throughout the Indian Ocean weakened at least a portion of California's famed San Andreas Fault. The results, which appear this week in the journal Nature, suggest that the Earth's largest earthquakes can weaken fault zones worldwide and may trigger periods of increased global seismic activity.
"An unusually high number of magnitude 8 earthquakes occurred worldwide in 2005 and 2006," said study co-author Fenglin Niu, associate professor of Earth science at Rice University. "There has been speculation that these were somehow triggered by the Sumatran-Andaman earthquake that occurred on Dec. 26, 2004, but this is the first direct evidence that the quake could change fault strength of a fault remotely."
Live in an earthquake zone? I do. Want to be prepared? Look at the building you live in and the building you work in and ask yourself whether you are likely to die in either structure in event of an earthquake. If so, change jobs or move as appropriate. A really big quake in SoCal will take out water supplies in some areas. Think about putting in some big water storage bottles (appropriately padded and braced to prevent breakage) so you can keep drinking water after the Big One.
Last night I was watching a History Channel show about the odds of a really big earthquake in Southern California. One of the people on the show said the scientific consensus is for a 99% probability in the next 30 years. If you live in SoCal you really ought to prepare for it.
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Oklahoma State University researchers Melissa Burkley and Jessica Parker demonstrate an aspect of female desire that I've certainly experienced: women prefer taken guys.
Unknown to the participants, everyone was offered a fictitious candidate partner who had been tailored to match their interests exactly. The photograph of "Mr Right" was the same for all women participants, as was that of the ideal women presented to the men. Half the participants were told their ideal mate was single, and the other half that he or she was already in a romantic relationship.
"Everything was the same across all participants, except whether their ideal mate was already attached or not," says Burkley.
The most striking result was in the responses of single women. Offered a single man, 59 per cent were interested in pursuing a relationship. But when he was attached, 90 per cent said they were up for the chase.
You might think these women are unethical.
Roissy would not find these results surprising. Lots of us have had the experience of getting hit on by more women after they've seen a really attractive women hanging on us. That's been my experience.
So what's going on here? Women go with the herd. If some woman likes a guy enough to want to be attached to him this becomes evidence for other women that he's worth going after. For a guy a beautiful woman can serve as a powerful demonstration of higher value. I think there's a potential business here for a specialized escort service where women sell time with them in public places to guys who want to advertise their desirability.
A protein implicated in as a cause of Alzheimer's Disease increases in mice while they are away and declines while they are asleep. The implication here is that people who do not get enough sleep may be at increased risk of Alzheimer's.
While the occasional all-nighter to cram for exams or finish a grant proposal may seem like no big deal, losing sleep night after night could take its toll on brain health in later life, two new studies suggest. Based on microdialysis experiments in live mice, Dave Holtzman, Washington University, St. Louis, Missouri, and colleagues report in the current issue of Science that extracellular amyloid-beta levels in the brain fall during slumber and rise with wakefulness. They discovered that these Abeta dynamics rely on the hormone orexin, and that forcing animals to sleep or stay awake decreases or increases Abeta plaque formation accordingly in a mouse model for Alzheimer disease.
Lack of sleep increases inflammation and inflammation is also implicated in Alzheimer's. Lack of sleep also puts on the weight and increases obesity. This accelerates aging. So get lots of sleep. It is good for your brain.
Good news for Peak Oil doomsters: The Great Depression was accompanied by a rapid rise in life expectancies. So when oil production starts declining every year and most of us lose our jobs we'll live longer?
ANN ARBOR, Mich.—The Great Depression had a silver lining: During that hard time, U.S. life expectancy actually increased by 6.2 years, according to a University of Michigan study published in the current issue of the Proceedings of the National Academy of Sciences.
Life expectancy rose from 57.1 in 1929 to 63.3 years in 1932, according to the analysis by U-M researchers José A. Tapia Granados and Ana Diez Roux. The increase occurred for both men and women, and for whites and non-whites.
"The finding is strong and counterintuitive," said Tapia Granados, the lead author of the study and a researcher at the U-M Institute for Social Research (ISR). "Most people assume that periods of high unemployment are harmful to health."
Whereas mortality declined during economic expansions.
For the study, researchers used historical life expectancy and mortality data to examine associations between economic growth and population health for 1920 to 1940. They found that while population health generally improved during the four years of the Great Depression and during recessions in 1921 and 1938, mortality increased and life expectancy declined during periods of strong economic expansion, such as 1923, 1926, 1929, and 1936-1937.
We are presented such images of poverty back in the Great Depression. From a distance one might expect unemployed people to have starved to death. But hard to square that with a rise in life expectancies. Okay, why this result?
"Working conditions are very different during expansions and recessions," Tapia Granados said. "During expansions, firms are very busy, and they typically demand a lot of effort from employees, who are required to work a lot of overtime, and to work at a fast pace. This can create stress, which is associated with more drinking and smoking.
"Also, new workers may be hired who are inexperienced, so injuries are likely to be more common. And people who are working a lot may also sleep less which is known to have implications for health. Other health-related behaviors such as diet may also change for the worse during expansions."
In recessions, Tapia Granados noted, there is less work to do, so employees can work at a slower pace. There is more time to sleep, and because people have less money, they are less likely to spend as much on alcohol and tobacco.
In addition, economic expansions are also associated with increases in atmospheric pollution which has well-documented short-term effects on cardiovascular and respiratory mortality. Other reasons that periods of economic expansion may be bad for health could include increases in social isolation and decreases in social support that typically occur when people are working more.
What I wonder: Has this pattern held up in recent years?
Workplaces have become a lot safer since the 1920s. Also, hours worked are shorter now than back then. So people working longer hours during an upturn now are probably still working less than, say, workers in the 1920s. Also, economic upturns are less associated with pollution (at least in the United States, though obviously not in China) than was the case in the 1920s and 1930s. So has economic growth become relatively safer today?
