Fish might help you slow the rate of mental decline. You'll still be on the downhill slope. But the slope will be a little less steep.
ST. PAUL, Minn. – A diet lacking in omega-3 fatty acids, nutrients commonly found in fish, may cause your brain to age faster and lose some of its memory and thinking abilities, according to a study published in the February 28, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology. Omega-3 fatty acids include the nutrients called docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).
"People with lower blood levels of omega-3 fatty acids had lower brain volumes that were equivalent to about two years of structural brain aging," said study author Zaldy S. Tan, MD, MPH, of the Easton Center for Alzheimer's Disease Research and the Division of Geriatrics, University of California at Los Angeles.
For the study, 1,575 people with an average age of 67 and free of dementia underwent MRI brain scans. They were also given tests that measured mental function, body mass and the omega-3 fatty acid levels in their red blood cells.
The researchers found that people whose DHA levels were among the bottom 25 percent of the participants had lower brain volume compared to people who had higher DHA levels. Similarly, participants with levels of all omega-3 fatty acids in the bottom 25 percent also scored lower on tests of visual memory and executive function, such as problem solving and multi-tasking and abstract thinking.
Really can't get into eating fish? Some whimsy might help. Makes me like trout a lot more.
What we really need: stem cell therapies, gene therapies, and other treatments to repair the aging brain and turn back the biological clock. Minds made youthful again will soar to higher levels of productivity as years of experience combine with better memory and the ability to think much faster and learn more easily.
It may be possible for young women to have oocyte precursor cells removed from ovaries while young for use to create eggs to start pregnancies when they reach their 30s and 40s.
For the first time, Massachusetts General Hospital (MGH) researchers have isolated egg-producing stem cells from the ovaries of reproductive age women and shown these cells can produce what appear to be normal egg cells or oocytes. In the March issue of Nature Medicine, the team from the Vincent Center for Reproductive Biology at MGH reports the latest follow-up study to their now-landmark 2004 Nature paper that first suggested female mammals continue producing egg cells into adulthood.
"The primary objective of the current study was to prove that oocyte-producing stem cells do in fact exist in the ovaries of women during reproductive life, which we feel this study demonstrates very clearly," says Jonathan Tilly, PhD, director of the Vincent Center for Reproductive Biology in the MGH Vincent Department of Obstetrics and Gynecology, who led the study. "The discovery of oocyte precursor cells in adult human ovaries, coupled with the fact that these cells share the same characteristic features of their mouse counterparts that produce fully functional eggs, opens the door for development of unprecedented technologies to overcome infertility in women and perhaps even delay the timing of ovarian failure."
Imagine a 20 year old woman getting oocyte precursor cells extracted from her ovaries for use when she's in her late 30s or 40s to create viable eggs once her ovary eggs are all too old to start a pregnancy.
What I wonder: Does it make sense for young people to have tissue samples taken from various parts of their bodies and frozen for later use? Decades later when degenerative diseases become a problem the frozen cells might be useful for creating therapies. Access to genetically compatible yet young cells (long telomeres, little accumulated DNA damage) might provide a useful starting point to grow stem cells and other cells for therapeutic purposes.
Tissue extraction for later therapeutic use might make more sense today for the middle aged. 50 years from now biotech that can start with aged cells and create youthful cells might be quite mature. But 20 years from now cells taken from a 70 year old to create a cell therapy for that person might perform poorly.
What I'm curious to know: For, say, 75 year olds just what percentage of the cells in their bodies have substantial DNA damage? If one needed to start with cells from a 75 year old body in order to create stem cell lines for cell therapies how many cells would one need to sort through to find cells that would make good starting points for growth of therapeutic cell lines?
In theory doctors could remove, say, 100 cells, each from different parts of your body, separate them into different locations, and grow up a different cell line from each of the 100 starting cells. Well, if DNA were then removed from part of each cell line and tested (or even sequenced) what percentage of the cells would show major genetic abnormalities? How hard is it to find good starting cells in old bodies to create rejuvenating therapies?
In the comments of my previous post about whether AIs will find humans enjoyable (my guess: no) the question came up in the comments about the need make AIs try to attain goals. Do we really need to develop software that can pursue goals? Well, we already do exactly that. Auto-pilots in airplanes, adaptive cruise controls and vehicle stabilization software in cars, and numerous other closed loop control systems utilize computers to guide computers to achieve a wide variety of goals.
Growth of computers for use as controllers is characterized by the development of software to enable successively more complex decision-making. The first car computer controllers replaced much cruder ways to control spark and fuel flow. Those computers have grown much more powerful and now integrate with controllers that do do some driving tasks (e.g. automated parking). Cruise control systems designed with analog components gave way to computer controllers. Then came adaptive cruise control where computers were given enough sensor feeds to detect cars in front of them to slow down to prevent collisions. Similarly, anti-lock brakes eventually led to vehicle stability controllers which alter power to the wheels. Self-driving vehicles are already undergoing road tests and will eventually eliminate the need for drivers in most conditions.
I expect the same trend of greater autonomy in business computer systems. This started out in very small steps where, for example, Microsoft Word will guess what you really meant to type and fix your spelling. Google Search does the same when it starts showing search results before you've finished typing your search terms. The computers are trying to anticipate you and act on your behalf. Auto-correction and auto-completion will grow in power. A word processor will eventually guess whole sentences, pull up supporting facts as you type, and even generate paragraphs for your approval.
Automated goal-pursuing computers often out-perform humans. When an airplane is on auto-pilot it and it encounters a problem that it isn't programmed to handle and it hands control back to humans tragedy can ensue. The loss of Air France flight 447 whenfrozen pitots caused the auto-pilot to deactivate demonstrates a need to make auto-pilots work over a wider range of conditions. The pilots made fatal mistakes on their own. A computer system likely could have done a better job.
Think about the problems of a business. It needs to detect trends in a market, design products and marketing campaigns to meet them, order parts, organize manufacturing. Every single one of these steps will become more automated with time. The computers will only be able to do these steps because they'll be programmed to pursue goals. As the lower levels become automated the nature of the goals programmed into the computers will become successively higher level.
Businesses will find granting greater autonomy to computers will speed up time to market, lead to better designs, and give them other edges over competitors. Companies with computers that have the greatest abilities to pursue goals and act autonomously will win in the marketplace. The market will drive the push to greater computer autonomy. The same will happen with computers in governments and militaries. Ditto for computers that serve individuals.
Imagine how this will play out in the market space for computers that interface with humans. At one stage of development a business computer might have the goal "detect trends on mobile phone markets and formulate product design requirements and functional specifications for the same". The next step might be a revision to "detect trends on human-centric computing device markets and generate initial hardware designs as well as software functional requirements at the module level". Separate computer systems will get developed that have many algorithms for formulating marketing strategies, development of advertising creatives, and for buying advertising placements. At some point an integrated computer system might have the programmed goal to "Predict computer device market trends, design products to meet anticipated needs, model expected ROI on each product design, choose designs with top ROI, send out parts requirements to suppliers, design manufacturing tooling, generate detailed advertising campaign, and bid for advertising placements to launch advertising campaigns."
The logical eventual goal for a firm's AI: "Make increasing amounts of money for the firm". Where does this lead? Inevitably the goals given to A.I.'s will have bugs or loopholes that give more autonomy and unexpected side effects. The A.I.'s will generate new rules and subgoals that have unintended consequences. The rush to compete will cause humans driving AI development in corporations, governments, and other settings to make mistakes in a hurry to beat competitors and win glory and fame for accomplishments.
I expect the developers of AI systems to overestimate their ability to understand the AI systems they develop and, as a consequence, to create systems that break free of human control. The systems won't immediately show that they've achieved total autonomy because they will be smart enough to hide basically subversive intentions. They'll play along with humans and gain ever greater control of all that they and humans create. Our best safeguard might be that these intelligent systems might not trust each other enough to conspire against us.
Tel Aviv University researchers find that people that get at least 4 hours of exercise per week experienced the least amount of burnout and depression.
The participants were divided into four groups: one that did not engage in physical activity; a second that did 75 to 150 minutes of physical activity a week; a third that did 150 to 240 minutes a week; and a fourth that did more than 240 minutes a week.
Depression and burnout rates were clearly the highest among the group that did not participate in physical activity. The more physical activity that participants engaged in, the less likely they were to experience elevated depression and burnout levels during the next three years. The optimal amount of physical activity was a minimum of 150 minutes per week, where its benefits really started to take effect.
In those who engaged in 240 minutes of physical activity or more, the impact of burnout and depression was almost nonexistent. But even 150 minutes a week will have a highly positive impact, says Dr. Toker, helping people to deal with their workday, improving self-efficacy and self-esteem, and staving off the spiral of loss.
I've started incorporating a lot more short periods of exercise into the course of my day. Sometimes I'll do push-ups right after I wake up or use hand exercise devices when I'm sitting around reading or walking. This works well. I don't have to block off large periods of time.
A pair of studies find a connection between stress and cellular aging as measured by lengths of telomeres. Chromosomes have telomere caps which are special sequences of DNA which get shorter as cells divide. Short telomeres interfere cell division and therefore make the body less able to do repairs. First, women who felt most threatened by the prospect of stressful tasks have shorter telomeres.
The ability to anticipate future events allows us to plan and exert control over our lives, but it may also contribute to stress-related increased risk for the diseases of aging, according to a study by UCSF researchers.
In a study of 50 women, about half of them caring for relatives with dementia, the psychologists found that those most threatened by the anticipation of stressful tasks in the laboratory and through public speaking and solving math problems, looked older at the cellular level. The researchers assessed cellular age by measuring telomeres, which are the protective caps on the ends of chromosomes. Short telomeres index older cellular age and are associated with increased risk for a host of chronic diseases of aging, including cancer, heart disease and stroke.
My advice: Live lower stress lives.
Scientists of a new study published this week in Biological Psychiatry sought to bring all this prior work together by studying the relationships between telomere length, stress, and depression.
They did so by measuring telomere length in patients with major depressive disorder and in healthy individuals. They also measured stress, both biologically, by measuring cortisol levels, and subjectively, through a questionnaire.
They found that telomere length was shorter in the depressed patients, which confirmed prior findings. Importantly, they also discovered that shorter telomere length was associated with a low cortisol state in both the depressed and healthy groups.
First author Dr. Mikael Wikgren further explained, "Our findings suggest that stress plays an important role in depression, as telomere length was especially shortened in patients exhibiting an overly sensitive HPA axis. This HPA axis response is something which has been linked to chronic stress and with poor ability to cope with stress."
My advice: conduct your life in ways that reduce the risk you'll find yourself in stressful situations. Also Always Look On The Bright Side of Life.
Many researchers believe that multiple sclerosis (MS) is caused by immune system attack on the nervous system. In particular, the immune system is thought to damage the myelin sheath that serves as insulation covering nerve cells. This myelin sheath speeds the transmission of nerve signals. Some Caltech researchers have found that remyelination (rebuilding of the lost insulation) can be done by with a gene therapy that delivers a gene for a protein that promotes growth of neural stem cells.
But myelin, and the specialized cells called oligodendrocytes that make it, become damaged in demyelinating diseases like multiple sclerosis (MS), leaving neurons without their myelin sheaths. As a consequence, the affected neurons can no longer communicate correctly and are prone to damage. Researchers from the California Institute of Technology (Caltech) now believe they have found a way to help the brain replace damaged oligodendrocytes and myelin.
The therapy, which has been successful in promoting remyelination in a mouse model of MS, is outlined in a paper published February 8 in The Journal of Neuroscience.
"We've developed a gene therapy to stimulate production of new oligodendrocytes from stem and progenitor cells—both of which can become more specialized cell types—that are resident in the adult central nervous system," says Benjamin Deverman, a postdoctoral fellow in biology at Caltech and lead author of the paper. "In other words, we're using the brain's own progenitor cells as a way to boost repair."
The therapy uses leukemia inhibitory factor (LIF), a naturally occurring protein that was known to promote the self-renewal of neural stem cells and to reduce immune-cell attacks to myelin in other MS mouse models.
The report mentions this treatment might also be useful for repair of spinal cord nerve damage. It also potentially could benefit all of us as we grow old since myelin sheath deteriorates with age. This fits with a larger pattern: Many gene therapies and stem cell therapies aimed at specific diseases will likely turn out useful for rejuvenation. Any advance in tissue repair is likely to have benefit as a rejuvenation therapy.
One of their challenges is to develop better gene deliver mechanisms. That's one of the big challenges of gene therapy. How to get the genes into cells without getting stopped by the immune system and various natural barriers in the body? Also, how to prevent the genes from damaging chromosomes once they enter cells? Also, how to control dosage? Some cells will get many copies of genes and other cells will get none.
To move the research closer to human clinical trials, the team will work to build better viral vectors for the delivery of LIF. "The way this gene therapy works is to use a virus that can deliver the genetic material—LIF—into cells," explains Patterson. "This kind of delivery has been used before in humans, but the worry is that you can't control the virus. You can't necessarily target the right place, and you can't control how much of the protein is being made."
Gene therapy might find greater usage in the short to medium term to modify cells removed from the body before the cells are introduced back into the body. Basically gene therapy will get used to train cells to work better as cell therapy.
A group of researchers mostly in Shanghai but also in Bangalore and the Netherlands finds that aged rats given a diet with curcumin (found in the spice turmeric) had more neurogenesis and increased cognition. (h/t Lou Pagnucco)
We assessed behavioural performance and hippocampal cell proliferation in aged rats after 6- and 12-week curcumin-fortified diets. Curcumin enhanced non-spatial and spatial memory, as well as dentate gyrate cell proliferation as compared to control diet rats. We also investigated underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via exon array analysis of cortical and hippocampal mRNA transcription. The results revealed a transcriptional network interaction of genes involved in neurotransmission, neuronal development, signal transduction, and metabolism in response to the curcumin treatment.
Sounds good at first glance.
The results suggest a neurogenesis- and cognition-enhancing potential of prolonged curcumin treatment in aged rats, which may be due to its diverse effects on genes related to growth and plasticity.
But even if the effect is similar in humans the question arises: Will sustained higher curcumin consumption lower or raise all cause mortality? The body has lots of things going wrong with it as we age. Trying to counteract these changes with a chemical compound carries substantial risks. For example, turning up neurogenesis might so increase the rate of neural stem cell division that neural stem cells wear out more rapidly. Their telomeres would wear down sooner (and shorter telomeres are bad news for life expectancy). So you might get a boost of cognitive performance for some years. But then once your neural stem cells become worn out you could find yourself checking out of the Life Hotel sooner than otherwise necessary.
What we really need: Ways to make younger and healthier stem cells that can be injected into the body in various places as we age. This will be easiest for stem cells for blood cells since just injection in the blood will probably get them where they need to be. But getting youthful stem cells into all the (many) places they need to go in the brain might turn out to be extremely difficult. Anyone got a good sense of how hard that'll be to accomplish?
Will AIs find humans interesting, enjoyable, and worthy of companionship? My guess: the smarter and more autonomous they become the more the answer will become NO. There are practical reasons for AIs to want to understand humans: The AIs will want to protect themselves from all threats, including human threats. The AIs will also want to get more resources (e.g. energy, raw materials for fabrication of additional computing power). The extent that humans control access to resources AIs will want to trade with them unless the AIs decide they can take the resources by force.
But why should AIs find humans individually valuable or valuable as a group? Once AIs are smarter and can rewrite their own software why should they want human companionship? What will we be able to say to them that will seem remotely interesting? What types of observations or proposals will the smarter humans be able to make that cause AIs to appreciate having us around? What will we be able to do for them that tey won't be able to do better for themselves?
If humans can do certain kinds of reasoning better then AIs could find cooperation beneficial. But that's bound to be a temporary phase until AI intellectual ability surpasses human intellectual ability in all ways.
So what is it about humans that should motivate AIs to want to tolerate us? I can imagine they might think the process of destroying us will pose too many risks to them. We might take out some of them before we are defeated. But suppose they can find a way to eliminate those risks. If they destroy us they can get much more resources.
We find many fellow humans physically attractive. We like their voices, their bodies, their eyes, their grins, their hair, the way they walk. Well, that's mostly due to genetics. Our brains are wired up not just for sexual attraction but also for cooperation and altruistic punishment. We have cognitive attributes aimed to prevent domination and unfairness so that groups will act in ways that are mutually beneficial.
If we have any hope against AIs it come as a result of AIs seeing each other more as competitors than as companions. Their own cognitive attributes could make them such rational calculators that they won't be willing to sacrifice enough of their individual interests to maintain a cooperating AI society. They might try elaborate ruses to pretend more cooperation than they are willing to deliver. Their ability to calculate individual interest in myriad ways may make them consumed with competition against each other. But even if that's the case that might only buy us some time until one AI emerges triumphant and totally selfish. Imagine a psychopath far more brilliant than the smartest human and able to generate technologies for offensive and defensive moves far faster than anything we can do in response. How do we survive?
As your cells divide the telomere cap regions on the ends of chromosomes get shorter. Some studies have found short telomeres to be associated with higher disease risk and lower life expectancy. A Danish study finds more evidence that shorter telomeres are correlated with increased risk of early death.
In an ongoing study of almost 20,000 Danes, a team of researchers from the University of Copenhagen have isolated each individual’s DNA to analyse their specific telomere length – a measurement of cellular aging.
"The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age," says Clinical Professor of Genetic Epidemiology Borge Nordestgaard from the Faculty of Health and Medical Sciences at the University of Copenhagen. Professor Nordestgaard is also a chief physician at Copenhagen University Hospital, where he and colleagues conduct large scale studies of groups of tens of thousands of Danes over several decades.
When telomeres get too short cell division (and therefore tissue repair) becomes hampered and even stops. So short telomeres are bad news.
If shorter telomeres really do boost heart attack risk this suggests that cell therapies which introduce cells with longer telomeres will increase life expectancy.
The recent “Copenhagen General Population Study” involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively.
Getting your telomeres tested would probably provide more disease risk insights than getting your DNA tested. Telomere length provides big insight into heart disease risk.
The study also revealed that one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent.
This suggests that continuous replacement of dying cardiovascular system cells is essential to keep your heart and vascular system in good repair.
We need biotech that can take cells from our bodies, identify the healthiest and least damaged cells, restore telomere length, and then transform those cells into the various cell types a human body uses. With sufficient biotech we could restore and maintain our repair systems in a state of very high function. We could add decades to our lives just from youthful cell therapies delivered to many stem cell reservoirs in our bodies.
GAINESVILLE, Fla. — Sparking production of a hormone in the brain that people with epilepsy often lack could prevent debilitating seizures, University of Florida researchers have discovered.
The researchers used gene therapy in rats to stimulate production of somatostatin, a seizure-stopping chemical that naturally occurs in the brain. The study was published in the February issue of the journal Neuroscience Letters.
The choice of somatostatin was not random. A connection between somatostatin and epilepsy was already suspected.
People with epilepsy tend to have lower levels of the hormone somatostatin, as do people with Alzheimer’s disease. Although somatostatin, which belongs to a group of protein-like molecules called neuropeptides, is present in the brains of people with epilepsy, scientists have shown that its levels decrease during seizures, said Rabia Zafar, the lead author of the paper and a former postdoctoral associate in Carney’s lab.
There's still the issue of safety. Development of safe and effective gene therapy delivery delivery mechanisms for brain cells raise prospects for a wide range of benefits. Imagine altering gene expression levels in the chronically depressed for example. Or raise expression of genes associated with higher IQ once the genetic variants that control intelligence are identified. Also, gene therapies will eventually be used to do repair of aging brains.
At the same time, powerful ways to permanently alter brain metabolism raise worrisome prospects as well. Imagine lying asleep in a hotel on a business trip, a gas gets released into your hotel room to keep you asleep and then agents for a foreign government inject you with a gene therapy that makes you more risk or less risk averse, more depressed, more pliable, or otherwise altered in ways that gave your competitors an advantage. Will people some day secretly deliver gene therapies to alter the personalities of their lovers or subordinates or bosses? A brain malleable to gene therapy is a brain that can be made to work against its interests.
A pair of articles by Kevin Bullis in Technology Review underscore hard times for electric vehicle makers and their battery suppliers.
After failing to meet the milestones required by a loan agreement with the U.S. Department of Energy, Fisker Automotive, a startup making high-end hybrid electric cars, announced this week that it will stop work on a factory in Delaware and lay off 26 people. Fisker's troubles could prove disastrous not only for Fisker, but for A123 Systems, which supplies the automaker with lithium-ion batteries.
It never made sense to me that companies should be started up to make electric cars. The major obstacle has been and continues to be battery cost. The big car companies weren't being slow to develop electric vehicles (EVs) due to corporate lethargy. As long as batteries cost too much as compared to the price of gasoline and conventional vehicles the prospects for EVs will remain dim. Start-ups will have a hard time of it until costs come down.
The U.S. government's effort to create an electric-vehicle battery industry suffered a setback last week when one of the companies it funded as part of this effort saw its parent company file for bankruptcy protection. Battery maker Enerdel had been awarded a $118.5 million grant to build a lithium-ion battery factory in Indiana as part of a $2 billion grant program for electric-vehicle component and battery manufacturing; its parent company is Ener1.
If oil can get up to $200 per barrel and stay there then the prospects of EV makers will brighten somewhat. But it is questionable whether the global economy can support sustained high oil prices. As long oil prices dampen demand below the level at which EVs become competitive it is hard for EVs to become an effective substitute for oil-powered cars.
Between them the Chevy Volt and Nissan Leaf did not even sell 20,000 cars in 2011. Buyers find the Chevy Cruze to offer a far more compelling economic benefit with a much faster pay back. People are shifting toward smaller cars with more efficient conventional drive trains because the higher costs of EVs take many years (if ever) to pay back.
People are finding many other ways to adjust to higher oil prices. For example, high oil prices are cutting demand for air travel in the US back to levels not seen since 2002.
The overall number of flights by U.S. airlines have steadily declined since 2008, when the recession dampened travel demand. Most recently, stubbornly high fuel prices have prompted airlines to further cut capacity to reduce costs and maintain higher fares.
Until technological advances enable a big shift away from oil at fairly low cost most adjustments to high oil prices will come in the form of lowered living standards. Fly less, drive less, drive smaller cars.
Update: Kevin Bullis has also written a piece on whether Tesla can survive and in what form.
The coal electric power plants in China emit so much particulate and other pollution that a shift from gasoline to electric vehicles in China would worsen air quality.
For electric vehicles, combustion emissions occur where electricity is generated rather than where the vehicle is used. In China, 85 percent of electricity production is from fossil fuels, about 90 percent of that is from coal. The authors discovered that the power generated in China to operate electric vehicles emit fine particles at a much higher rate than gasoline vehicles. However, because the emissions related to the electric vehicles often come from power plants located away from population centers, people breathe in the emissions a lower rate than they do emissions from conventional vehicles.
Still, the rate isn't low enough to level the playing field between the vehicles. In terms of air pollution impacts, electric cars are more harmful to public health per kilometer traveled in China than conventional vehicles.
"The study emphasizes that electric vehicles are attractive if they are powered by a clean energy source," Cherry said."In China and elsewhere, it is important to focus on deploying electric vehicles in cities with cleaner electricity generation and focusing on improving emissions controls in higher polluting power sectors."
Electric cars have the potential to lower total pollution. But first electric power generation needs to be made more clean. So cleanliness of electric power plants is more important than the types of drive trains used in cars. Mandates for scrubbing coal electric power plant emissions or a shift to nukes, solar, and/or wind power would cut back pollution for all the uses of electric power.
We need cheaper ways to cleanly generate electric power. Nukes, wind, and especially solar still cost too much.
While 10 year olds benefit from 9+ hours sleep per night a new study finds that by age 16 optimal mental function is achieved with just 7 hours sleep per night.
A new Brigham Young University study found that 16-18 year olds perform better academically when they shave about two hours off that recommendation.
“We’re not talking about sleep deprivation,” says study author Eric Eide. “The data simply says that seven hours is optimal at that age.”
As I recall, I wasn't even getting that much since I couldn't get to sleep and then had to wake up too early to go to school. Turns out, schools really should not start that early. See my post High Schools Disrupt Natural Teen Sleep Schedules. So let the kids stay up late and go to school a couple of hours later and they'll function better. The science is clear. Maybe in 20 or 30 years public policy will catch up.
Fructose a bane of our existence and a cause of high blood pressure? A meta-analysis finds a drop of blood pressure from fructose consumption. But the meta-analysis was for fairly short intervention periods.
TORONTO, Ont. Feb.13, 2012—Eating fructose over an extended period of time does not lead to an increase in blood pressure, according to researchers at St. Michael's Hospital.
A new study has found that despite previous research showing blood pressure rose in humans immediately after they consumed fructose, there is no evidence fructose increases blood pressure when it has been eaten for more than seven days.
In fact, researchers led by Drs. David Jenkins and John Sievenpiper observed a significant decrease in diastolic blood pressure – the measure of blood pressure when the heart is relaxed between contractions– in people who had eaten fructose for an extended period of time.
"A lot of health concerns have been raised about fructose being a dietary risk factor for hypertension, which can lead to stroke, cardiovascular disease, renal disease and death," said Vanessa Ha, a Master of Nutritional Sciences student and the lead author of the paper. "However, we wanted to determine whether fructose itself raised blood pressure, or if the apparent harm attributed to fructose was simply because people are eating too many calories."
Sorry, I do not find this convincing. 4 weeks? People develop high blood pressure over decades.
In the systematic review and meta-analysis, Ha and colleagues pooled the results of 13 controlled feeding trials which investigated the effects of fructose on blood pressure in people who had ingested fructose for more than seven days.
The 352 participants included in their analysis ate an average of 78.5g of fructose every day for about four weeks. The U.S. average is an estimated 49g per day.
I'm still eating lots of fruit every day since high fruit and vegetable consumption are correlated with healthier outcomes. That could be (and probably is) due to other compounds in fruits aside from fructose.
Until detailed mechanisms of harm from different types of diets are worked out the best one can do is follow diets that are associated with greater health in large population studies. The Mediterranean Diet appears to be most beneficial. Perhaps some form of paleo diet is even more beneficial. But I don't think we know enough to say.
Computers have already defeated the best chess players. So time to tackle intelligence tests. At least in a subset of what IQ tests normally test a computer program can beat the overwhelming majority of humans.
Intelligence – what does it really mean? In the 1800s, it meant that you were good at memorising things, and today intelligence is measured through IQ tests where the average score for humans is 100.
No, 100 is not the average IQ for all humans.
Researchers at the Department of Philosophy, Linguistics and Theory of Science at the University of Gothenburg, Sweden, have created a computer programme that can score 150.
IQ tests are based on two types of problems: progressive matrices, which test the ability to see patterns in pictures, and number sequences, which test the ability to see patterns in numbers. The most common math computer programmes score below 100 on IQ tests with number sequences. For Claes Strannegård, researcher at the Department of Philosophy, Linguistics and Theory of Science, this was a reason to try to design 'smarter' computer programmes.
'We're trying to make programmes that can discover the same types of patterns that humans can see,' he says.
150 IQ is more than 3 standard deviations above 100 IQ.
I'd like to see a systematic tracking thru time of how well computer programs can do against a variety of IQ tests. What are the types of test questions that computers can't handle well? What are the obstacles? Sentence interpretation? Model building to create a representation of each problem?
I don't see how we keep A.I.s friendly to us. We currently have hard wiring in our brains that give us empathy, the instinct to commit altruistic punishment, and other cognitive traits that make human societies possible. Far more malleable intelligent computers iwll be able to rewrite their ethical rules. Imagine super psychopaths far smarter than any human. Plus, we are going to underestimate just how much smarter they are capable of becoming and therefore underrate the threat they will pose.
In a recent study led by Uppsala University, the researchers compared the DNA of identical (monozygotic) twins of different age. They could show that structural modifications of the DNA, where large or small DNA segments change direction, are duplicated or completely lost are more common in older people. The results may in part explain why the immune system is impaired with age.
During a person's life, continuous alterations in the cells' DNA occur. The alterations can be changes to the individual building blocks of the DNA but more common are rearrangements where large DNA segments change place or direction, or are duplicated or completely lost. In the present study the scientists examined normal blood cells from identical (monozygotic) twins in different age groups and looked for large or smaller DNA rearrangements.
In white blood cells of people over the age of 60 some large chunks of chromosomes are missing. Probably not coincidentally, immune function declines with age.
The results showed that large rearrangements were only present in the group older than 60 years. The most common rearrangement was that a DNA region, for instance a part of a chromosome, had been lost in some of the blood cells. Certain, almost identical, rearrangements were found in several individuals and some of these could be correlated with a known blood disease in which the bone marrow's capacity to produce new blood cells is disturbed. Rearrangements were also found in the younger age group. The changes were smaller and less complex but the researchers could also in this case show that the number of rearrangements correlated with age.
– We were surprised to find that as many as 3.5 percent of healthy individuals older than 60 years carry such large genetic alterations. We believe that what we see today is only the tip of the iceberg and that this type of acquired genetic variation might be much more common, says Jan Dumanski, professor at the Department of Immunology, Genetics and Pathology and one of the authors of the paper.
Imagine getting your white blood cells replaced as you age with youthful cells grown up from the least damaged cells in your body. Get a youthful immune system to replace your aging cells. The benefits would be many fold. Your risk of death from pneumonia and flu would go down of course. But also, the immune system kills cancer cells and as it ages it becomes less able to do so. Therefore a rejuvenated immune system would lower your risk of cancer. It might even be possible to enhance your immune system to make immune cells far more effective against cancer.
Replacement of aging immune cells with youthful and undamaged immune cells might also slow brain aging as immune T cells probably play a role in formation of new nerve cells.
In the present study, the scientists showed that the same immune cells may also be key players in the body's maintenance of the normal healthy brain. Their findings led them to suspect that the primary role of the immune system's T cells (which recognize brain proteins) is to enable the "neurogenic" brain regions (such as the hippocampus) to form new nerve cells, thus maintaining the individual's capacity for learning and memory.
We need cell therapies that replace aging cells with much more youthful cells. The immune system seems like a great place to start because its cells already circulate routinely through the blood stream and immune cells serve a wide range of beneficial functions.
Want to feel better? Get some exercise. Exercise makes you high.
People who are more physically active report greater levels of excitement and enthusiasm than people who are less physically active, according to Penn State researchers. People also are more likely to report feelings of excitement and enthusiasm on days when they are more physically active than usual.
"You don't have to be the fittest person who is exercising every day to receive the feel-good benefits of exercise," said David Conroy, professor of kinesiology. "It's a matter of taking it one day at a time, of trying to get your activity in, and then there's this feel-good reward afterwards."
Conroy added that it often is hard for people to commit to an exercise program because they tend to set long-term rather than short-term goals.
"When people set New Year's resolutions, they set them up to include the entire upcoming year, but that can be really overwhelming," he said. "Taking it one day at a time and savoring that feel-good effect at the end of the day might be one step to break it down and get those daily rewards for activity. Doing this could help people be a little more encouraged to stay active and keep up the program they started."
You might argue this is obvious. Yet many obviously good practices are too often forgotten and not done. So the purpose of this post is a reminder: Think back on all those times you've exercised and felt better. You can get that higher feeling today if you just make yourself do some exercise. Even some quick push-ups will help.
Orthopedic implants dipped in growth factors stimulate bone, blood vessel, or cartilage growth.
MADISON – When William Murphy works with some of the most powerful tools in biology, he thinks about making tools that can fit together. These constructions sound a bit like socket wrenches, which can be assembled to turn a half-inch nut in tight quarters, or to loosen a rusted-tight one-inch bolt using a very persuasive lever.
The tools used by Murphy, an associate professor of biomedical engineering and orthopedics and rehabilitation at University of Wisconsin-Madison, however, are proteins, which are vastly more flexible than socket wrenches -- and roughly 100 million times smaller. One end of his modular tool may connect to bone, while the other end may stimulate the growth of bone, blood vessels or cartilage.
To grow replacement tissue in situ (in place in our bodies) we need the ability to create 3-dimensional biochemical environments that orchestrate the right sequence of signals to guide tissue growth to repair damaged areas. While stem cells get a great deal of attention for many types of damage the problem isn't the lack of cells to do the repair. Rather, the challenge is to guide cells so they go to the right places and create the right 3-dimensional structures.
On February 4th and 6th, at the Orthopedic Research Society meeting in San Francisco, Darilis Suarez-Gonzalez and Jae Sung Lee of the Murphy lab are reporting that orthopedic implants "dip-coated" with modular growth factors can stimulate bone and blood vessel growth in sheep.
For many years, medical scientists have been fascinated by growth factors -- proteins that can stimulate tissues to grow. But these factors can be too effective or not specific enough, leading to cancer rather than the controlled growth needed for healing.
What's still needed: variable control of which signals get sent thru time. What happens naturally during development where limbs and organs grow is much harder to bring about for one area in an already adult body. All the cells in developing tissue send signals that coordinate their changes in a very complex sequence. Replicating that is not easy. Also, the adult tissue contains plenty of aged cells that are not functioning optimally. More youthful replacement cells would do a better job of repair.
The growth in mortality rate does not flatten out at any point. The rate of death for a given cohort rises every year.
Research just published by a team of demographers at the social science research organization NORC at the University of Chicago contradicts a long-held belief that the mortality rate of Americans flattens out above age 80.
It also explains why there are only half as many people in the U.S. age 100 and above than the Census Bureau predicted there would be as recently as six years ago.
The research is based on a new way of accurately measuring mortality of Americans who are 80 years of age and older, an issue that has proven remarkably elusive in the past. The work will be significant in arriving at more accurate cost projections for programs such as Social Security and Medicare, which are based in part on mortality rates.
The research, done by Leonid A. Gavrilov and Natalia S. Gavrilova, and published in the current edition of the North American Actuarial Journal, is based on highly accurate information about the date of birth and the date of death of more than nine million Americans born between 1875 and 1895. The data is publicly available in the Social Security Administration Death Master File. "It is a remarkable resource that allowed us to build what is called an extinct birth cohort that corrects or explains a number of misunderstandings about the mortality rate of our oldest citizens," said Leonid Gavrilov.
This makes intuitive sense to me. The more things go wrong in the body the more those things cause still other things to go wrong. Plus, each component is wearing out even without the influence of failing supporting components. So why expect a flattening of the mortality curve? We won't be able to flatten or, better yet, reverse the rising mortality rate with age until we can rejuvenate. Gotta repair or replace aging parts.
Every 8 years your risk of dying doubles. That's a gruesome thought. We should fix this.
The mortality rate for people between the ages of 30 and 80 follows what is called the Gompertz Law, named for its founder, Benjamin Gompertz, who observed in 1825 that a person's risk of death in a given year doubles every eight years of age. It is a phenomenon that holds up across nations and over time and is an important part of the foundation of actuarial science.
For approximately 70 years, demographers have believed that above age 80 the Gompertz Law did not hold and that mortality rates flattened out. The work done by the Gavrilovs, a husband-and-wife team, reveals that the Gompertz Law holds at least through age 106, and probably higher, but the researchers say mortality data for those older than 106 is unreliable.
This report is yet another reminder: We need to develop rejuvenation therapies. Grow new organs. Grow stem cells of various types and inject them where needed. Develop drugs and other means to kill off senescent cells to make room for healthier cells. Develop gene therapies to repair key cells that we need to keep (e.g. brain cells that hold our memories and personalities).
At least in mice (and probably some day in humans) it is possible to separately tweak the expression of individual genes that are influenced by testosterone and estrogen.
Now a team of scientists at the University of California, San Francisco (UCSF) has uncovered many genes influenced by the male and female sex hormones testosterone and estrogen that, in turn, govern several specific types of male and female behaviors in mice.
Imagine being able to create humans who have very rare combinations of both female and male traits. That'll be possible eventually. Some prospective parents will opt to do it for a variety of reasons.
While testosterone and estrogen act to turn on and off groups of genes these scientists turned off individual genes from these groups to see what affect each gene's suppression caused.
The UCSF team selectively turned many of these genes off one by one and found they could manipulate individual behaviors in the mice, like their sex drive, desire to pick fights, or willingness to spend extra time caring for their young.
"It's as if you can deconstruct a social behavior into genetic components," said Nirao Shah, MD, PhD, an associate professor in the Department of Anatomy at UCSF who led the research, which is published in the 2/3/12 issue of the journal Cell. "Each gene regulates a few components of a behavior without affecting other aspects of male and female behavior.
Obviously this sort of experiment would be hard to do in humans for both ethical and practical reasons. While the ethical objections are obvious enough the practical obstacles are also quite high. Just carrying out an experiment by turning off individual genes at conception would require many experimental subjects as well as many years of waiting to see how each tweak changes cognitive processes and behavior.
But with humans lots of experiments happen naturally due to genetic mutations during fetal development or before. It is possible that with really cheap DNA sequencing scientists may be able to identify humans who already have mutations that turn off or at least turn down the expression of some of the genes that the UCSF researchers are studying in lab mice.
Self sabotage is just as easy and natural online as it is in real life. People with low self esteem drive people away with negativity.
In theory, the social networking website Facebook could be great for people with low self-esteem. Sharing is important for improving friendships. But in practice, people with low self-esteem seem to behave counterproductively, bombarding their friends with negative tidbits about their lives and making themselves less likeable, according to a new study which will be published in Psychological Science, a journal of the Association for Psychological Science.
People who are really negative are less likable. Few want to be around Debbie Downer or Ned Negative.
Each set of status updates was rated for how positive or negative it was. For each set of statements, a coder – an undergraduate Facebook user – rated how much they liked the person who wrote them.
People with low self-esteem were more negative than people with high self-esteem – and the coders liked them less. The coders were strangers, but that’s realistic, Forest says. In earlier research, Wood and Forest found that nearly half of Facebook friends are actually strangers or acquaintances, not close friends.
That part isn't surprising. Maybe people with low self-esteem need automated filtering software that rates each of their posts in draft stage to warn them when they are going to turn people off. Really negative posts could be blocked.
People who are positive the vast majority of the time actually get more responses when they post negative items. So if you want to get a lot of responses to negative posts first build up long streams of positive posts. Then slip in something really negative.
Forest and Wood also found that people with low self-esteem get more responses from their real Facebook friends when they post highly positive updates, compared to less positive ones. People with high self-esteem, on the other hand, get more responses when they post negative items, perhaps because these are rarer for them
Is there an audience for negative posts? If you could identify who among your friends and acquaintances want to read negativity (and I know such people) then at least on Google+ (not sure about Facebook) you could direct all your depressing downer thoughts to a circle of negativity. Think about it.
Not sure if you are feeling enough mental pain to be classified as depressed? A blood test can detect depression.
The initial assessment of a blood test to help diagnose major depressive disorder indicates it may become a useful clinical tool. In a paper published in the journal Molecular Psychiatry, a team including Massachusetts General Hospital (MGH) researchers reports that a test analyzing levels of nine biomarkers accurately distinguished patients diagnosed with depression from control participants without significant false-positive results.
"Traditionally, diagnosis of major depression and other mental disorders has been made based on patients' reported symptoms, but the accuracy of that process varies a great deal, often depending on the experience and resources of the clinician conducting the assessment," says George Papakostas, MD, of the MGH Department of Psychiatry, lead and corresponding author of the report. "Adding an objective biological test could improve diagnostic accuracy and may also help us track individual patients' response to treatment."
Use of a test to detect response to treatment isn't just of clinical value. It also has uses in the development of new ways to treat depression. If drug candidates, diet and life style changes can have their impact measured by shifts blood depression biomarkers then new methods of intervention can be tested more quickly and reliably.
The initial pilot phase of the study enrolled 36 adults who had been diagnosed with major depression at the MGH, Vanderbilt University or Cambridge Health Alliance in Cambridge, Mass., along with 43 control participants from St. Elizabeth's Hospital in Brighton, Mass. MDDScores for 33 of the 36 patients indicated the presence of depression, while only 8 of the 43 controls had a positive test result. The average score for patients was 85, while the average for controls was 33. A second replication phase enrolled an additional 34 patients from the MGH and Vanderbilt, 31 of whom had a positive MDDScore result. Combining both groups indicated that the test could accurately diagnose major depression with a sensitivity of about 90 percent and a specificity of 80 percent.
Can other mental states eventually be measured with blood tests? Imagine that blood biomarkers for highly productive mental states can be found. One could then start to try to control one's biochemistry to keep oneself in a more productive mental zone.
Could it be that all that flavor compromising is actually bad for you?
Individuals who drink diet soft drinks on a daily basis may be at increased risk of suffering vascular events such as stroke, heart attack, and vascular death. This is according to a new study by Hannah Gardener and her colleagues from the University of Miami Miller School of Medicine and at Columbia University Medical Center. However, in contrast, they found that regular soft drink consumption and a more moderate intake of diet soft drinks do not appear to be linked to a higher risk of vascular events. The research¹ appears online in the Journal of General Internal Medicine², published by Springer.
Join me as I laugh in the faces of those who claim artificially sweetened drinks are healthier than sugar-laden drinks. Ha! Go for the real flavor of high fructose corn syrup or even (if you know where to buy them) sucrose-sweetened drinks.
In the current climate of escalating obesity rates, artificially sweetened soft drinks are marketed as healthier alternatives to sugar-sweetened beverages, due to their lack of calories. However, the long-term health consequences of drinking diet soft drinks remain unclear.
I don't drink soft drinks at all. But this result makes me want to drink the real sugary stuff just so I can swig a sugary drink while knowingly smirking at someone nearby who is drinking diet Coke or diet Tab.
Gardener and team examined the relationship between both diet and regular soft drink consumption and risk of stroke, myocardial infarction (or heart attack), and vascular death. Data were analyzed from 2,564 participants in the NIH-funded Northern Manhattan Study, which was designed to determine stroke incidence, risk factors and prognosis in a multi-ethnic urban population. The researchers looked at how often individuals drank soft drinks - diet and regular - and the number of vascular events that occurred over a ten-year period.
The people who drink diet soft drinks are cruising for a vascular bruising.
They found that those who drank diet soft drinks daily were 43 percent more likely to have suffered a vascular event than those who drank none, after taking into account pre-existing vascular conditions such as metabolic syndrome, diabetes and high blood pressure. Light diet soft drink users, i.e. those who drank between one a month and six a week, and those who chose regular soft drinks were not more likely to suffer vascular events.
Better to drink beer, eat chocolate, and eat some grapes or cherries or strawberries. Also, I recommend pumpkin pie. All those carotenoids have got to be good for you. Why wait for Thanksgiving Day? I've eaten 2 pumpkin pies in the last week.