Exercise Prevents Heart Disease as Effectively as Expensive Medications.


·         After reviewing 305 randomized controlled trials, researchers found no statistically detectable differences between physical activity and medications for prediabetes and heart disease, including statins and beta blockers

·         Exercise was also found to be more effective than drugs after you’ve had a stroke. The only time drugs beat exercise was for the recovery from heart failure, in which case diuretic medicines produced a better outcome

·         Exercise is in fact so potent, the researchers suggested that drug companies ought to be required to include it for comparison when conducting clinical trials for new drugs

·         High-intensity interval training, which requires but a fraction of the time compared to conventional cardio, has been shown to be FAR more effective. It’s also the only exercise that really gives you an efficient cardiovascular workout

Did you know that exercise is one of the safest, most effective ways to prevent and treat chronic diseases such as heart disease?

This common-sense advice was again confirmed in a meta-review conducted by researchers at Harvard University and Stanford University,1 which compared the effectiveness of exercise versus drug interventions on mortality outcomes for four common conditions:

·         Diabetes

·         Coronary heart disease

·         Heart failure

·         Stroke

After reviewing 305 randomized controlled trials, which included nearly 339,300 people, they found “no statistically detectable differences” between physical activity and medications for prediabetes and heart disease.

Exercise was also found to be more effective than drugs after you’ve had a stroke. The only time drugs beat exercise was for the recovery from heart failure, in which case diuretic medicines produced a better outcome.

The drugs assessed in the studies included:

·         Statins and beta blockers for coronary heart disease

·         Diuretics and beta blockers for heart failure

·         Anticoagulants and antiplatelets for stroke

Exercise Should Be Included as Comparison in Drug Development Studies

The featured review is a potent reminder of the power of simple lifestyle changes, as well as the shortcomings of the drug paradigm. If you’re interested in living a longer, healthier life, nothing will beat proper diet and exercise.

Exercise is in fact so potent, the researchers suggested that drug companies ought to be required to include it for comparison when conducting clinical trials for new drugs! As reported by Bloomberg:2

“The analysis adds to evidence showing the benefit of non-medical approaches to disease through behavior and lifestyle changes.

Given the cost of drug treatment, regulators should consider requiring pharmaceutical companies to include exercise as a comparator in clinical trials of new medicines, according to authors Huseyin Naci of Harvard and John Ioannidis of Stanford.

‘In cases where drug options provide only modest benefit, patients deserve to understand the relative impact that physical activity might have on their condition,’ Naci and Ioannidis said in the published paper. In the meantime, ‘exercise interventions should therefore be considered as a viable alternative to, or, alongside, drug therapy.’”

There are glimmers of hope that change is possible, slow and begrudging as it may be. Dean Ornish, founder of the Preventive Medicine Research Institute, spent 16 years proving that a vegetarian diet along with exercise and stress management is more effective than conventional care for the treatment of heart disease.

And, as of January 2011, Medicare actually began covering the Ornish Spectrum—Reversing Heart Disease program,3 under the benefit category of “intensive cardiac rehabilitation.”

How Exercise Benefits Your Heart and Health

Heart disease and cancer are two of the top killers of Americans, and exercise can effectively help prevent the onset of both, primarily by normalizing your insulin and leptin levels.

Other beneficial biochemical changes also occur during exercise, including alterations in more than 20 different metabolites. Some of these compounds help you burn calories and fat, while others help stabilize your blood sugar, among other things.

In a nutshell, being a healthy weight and exercising regularly creates a healthy feedback loop that optimizes and helps maintain healthy glucose, insulin and leptin levels through optimization of insulin and leptin receptor sensitivity.

And, as I’ve mentioned before, insulin and leptin resistance—primarily driven by excessive consumption of refined sugars and grains along with lack of exercise—are the underlying factors of nearly all chronic disease that can take years off your life.

Previous research has shown that exercise alone can reduce your risk of cardiovascular disease by a factor of three.4However, endurance-type exercise, such as marathon running, can actually damage your heart and increase your cardiovascular risk by a factor of seven…

Research5 by Dr. Arthur Siegel, director of Internal Medicine at Harvard’s McLean Hospital found that long-distance running leads to high levels of inflammation that can trigger cardiac events. Another 2006 study6 found that non-elite marathon runners experienced decreased right ventricular systolic function, again caused by an increase in inflammation and a decrease in blood flow.

All in all, such findings are a powerful lesson that excessive cardio may actually be counterproductive. In the featured review, the types of exercise, frequency, intensity and duration varied widely across the included studies, which made it impossible to ascertain the specifics of what was most or least effective for the prevention and treatment of disease.

However, it was clear that exercise in general is comparable to many of the drugs used for heart disease, heart failure, and stroke. That said, other research has clearly demonstrated that short bursts of intense activity is safer and more effective than conventional cardio—for your heart, general health, weight loss, and overall fitness.  One of the easiest ways to exercise is simply by performing body weight exercises.

Are You Exercising Effectively and Efficiently?

The answer is to exercise correctly and appropriately, and making certain you have adequate recovery, which can be as important as the exercise itself. There is in fact overwhelming evidence indicating that conventional cardio or long-distance running is one of the worst forms of exercise there is. Not only have other studies confirmed the disturbing findings above, but they’ve also concluded it’s one of the least efficient forms of exercise. Research emerging over the past several years has given us a deeper understanding of what your body requires in terms of exercise. 

High-intensity interval training, which requires but a fraction of the time compared to conventional cardio, has been shown to be FAR more efficient, and more effective. This type of physical activity mimics the movements of our hunter-gatherer ancestors, which included short bursts of high-intensity activities, but not long-distance running. This, researchers say, is what your body is hard-wired for. Basically, by exercising in short bursts, followed by periods of recovery, you recreate exactly what your body needs for optimum health. Twice-weekly sessions, which require no more than 20 minutes from start to finish, can help you:

·         Lower your body fat

·         Improve your muscle tone

·         Boost your energy and libido

·         Improve athletic speed and performance

This type of exercise will also naturally increase your body’s production of human growth hormone (HGH)—a synergistic, foundational biochemical underpinning that promotes muscle and effectively burns excessive fat. It also plays an important part in promoting overall health and longevity. Conventional cardio will NOT boost your HGH level.

Interval Training—A Much Better Cardio Workout

Most people still think that in order to improve your cardiovascular fitness, endurance training is a must. But this is actually not true. Quite the contrary. According to fitness expert Phil Campbell, getting cardiovascular benefits actually requires working ALL your muscle fibers and their associated energy systems. Interestingly enough, this cannot be achieved with traditional cardio, and here’s why: Your body has three types of muscle fibers: slow, fast, and super-fast twitch muscles, and your heart has two different metabolic processes:

·         The aerobic, which requires oxygen for fuel

·         The anaerobic, which does not require any oxygen

Slow twitch muscles are the red muscles, which are activated by traditional strength training and cardio exercises. The fast and super-fast twitch muscles are white muscle fibers, which are only activated during high intensity interval exercises or sprints. Activating the fast and super-fast muscles is also what causes the production of therapeutic levels of growth hormone, as mentioned earlier. Many athletes spend $1,000 a month on HGH injections, which carry certain health risks, but there’s really no need for that. With Peak Fitness exercises and the use of the Power Plate, you can increase your levels of HGH to healthy young normal’s.

Now, traditional cardio exercises work primarily the aerobic process, associated with your red, slow-twitch muscles. High-intensity interval training, on the other hand, work both your aerobic AND your anaerobic processes, which is what you need for optimal cardiovascular benefit. Quite simply, if you don’t actively engage and strengthen all three muscle fiber types and energy systems, then you’re not going to work both processes of your heart muscle. Many mistakenly believe that cardio works out your heart muscle, but what you’re really working is your slow twitch muscle fibers, associated with the aerobic process only. You’re not effectively engaging the anaerobic process of your heart…

Demonstration of an Effective High Intensity Interval Session

In the case of high intensity exercises, less is more, as you can get all the benefits you need in just a 20-minute session performed twice to three times a week. It’s inadvisable to do them more than three times a week. If you do, you may actually do more harm than good—similar to running marathons. Because while your body needs regular amounts of stress like exercise to stay healthy, it also needs ample recuperation, and if you give it more than you can handle your health will actually begin to deteriorate. As a general rule, as you dial up the intensity, you can dial back on the frequency. While the entire workout is only 20 minutes, 75 percent of that time is warming up, recovering or cooling down. You’re really only working out intensely for four minutes:

·         Warm up for three minutes

·         Exercise as hard and fast as you can for 30 seconds. You should feel like you couldn’t possibly go on another few seconds

·         Recover at a slow to moderate pace for 90 seconds

·         Repeat the high intensity exercise and recovery 7 more times

For Optimal Health, Add Variety to Your Fitness Routine

While high intensity interval exercises accomplish greater benefits in a fraction of the time compared to slow, endurance-type exercises like jogging, I don’t recommend limiting yourself to that alone. Of equal, if not greater importance, is to avoid being too sedentary in general. Compelling research now tells us that prolonged sitting can have a tremendously detrimental impact on your health even if you exercise regularly. The reason for this is because your body needs to interact with gravity in order to function optimally. Therefore, make sure to get out of your chair every 10 minutes or so, as suggested below.

Ideally, to truly optimize all aspects of your health, you’d be wise to design a well-rounded fitness program that incorporates a variety of different exercises. Without variety, your body will quickly adapt, so as a general rule, as soon as an exercise becomes easy to complete, you’ll want to increase the intensity and/or try another exercise to keep it challenging. I recommend incorporating the following types of exercise into your program:

1.    Interval (Anaerobic) Training: This is when you alternate short bursts of high-intensity exercise with gentle recovery periods.

2.    Strength Training: Rounding out your exercise program with a 1-set strength training routine will ensure that you’re really optimizing the possible health benefits of a regular exercise program. You can also “up” the intensity by slowing it down. For more information about using super slow weight training as a form of high intensity interval exercise, please see my interview with Dr. Doug McGuff.

3.    Avoid Sitting for More Than 10 Minutes. This is not intuitively obvious but emerging evidence clearly shows that even highly fit people who exceed the expert exercise recommendations are headed for premature death if they sit for long periods of time. My interview with NASA scientist Dr. Joan Vernikos goes into great detail why this is so, and what you can do about it. Personally, I usually set my timer for 10 minutes while sitting, and then stand up and do one legged squats, jump squats or lunges when the timer goes off. The key is that you need to be moving all day long, even in non-exercise activities.

4.    Core Exercises: Your body has 29 core muscles located mostly in your back, abdomen and pelvis. This group of muscles provides the foundation for movement throughout your entire body, and strengthening them can help protect and support your back, make your spine and body less prone to injury and help you gain greater balance and stability.

Foundation Training, created by Dr. Eric Goodman, is an integral first step of a larger program he calls “Modern Moveology,” which consists of a catalog of exercises. Postural exercises such as those taught in Foundation Training are critical not just for properly supporting your frame during daily activities, they also retrain your body so you can safely perform high-intensity exercises without risking injury. Exercise programs like Pilates and yoga are also great for strengthening your core muscles, as are specific exercises you can learn from a personal trainer.

5.    Stretching: My favorite type of stretching is active isolated stretches developed by Aaron Mattes. With Active Isolated Stretching, you hold each stretch for only two seconds, which works with your body’s natural physiological makeup to improve circulation and increase the elasticity of muscle joints. This technique also allows your body to repair itself and prepare for daily activity. You can also use devices like the Power Plate to help you stretch.

Exercise Tips for Those with Chronic Health Problems

Remember that even if you’re chronically ill, exercise can be a potent ally. That said, if you have a chronic disease, you will of course need to tailor your exercise routine to your individual scenario, taking into account your stamina and current health. For example, you may at times need to exercise at a lower intensity, or for shorter durations, but do make a concerted effort to keep yourself moving. Just listen to your body and if you feel you need a break, take time to rest. But even exercising for just a few minutes a day is better than not exercising at all.

In the event you are suffering from a severely compromised immune system, you may want to exercise in your home instead of visiting a public gym. But remember that exercise will ultimately help to boost your immune system, so it’s very important to continue with your program, even if you suffer from chronic illness.

Exercise Is More Effective Than Potent Medicines

The take-home message here is that one of the best forms of exercise to protect your heart is short bursts of exertion, followed by periods of rest. By exercising in this way, you recreate exactly what your body needs for optimum health. Heart attacks, for example, don’t happen because your heart lacks endurance. They happen during times of stress, when your heart needs more energy and pumping capacity, but doesn’t have it. So rather than stressing your heart with excessively long periods of cardio, give interval training a try.

During any type of exercise, as long as you listen to your body, you shouldn’t run into the problem of exerting yourself excessively. And, with interval training, even if you are out of shape you simply will be unable to train very hard, as lactic acid will quickly build up in your muscles and prevent you from stressing your heart too much.

Most importantly, the featured review is a powerful message to anyone considering taking a medication to address risk factors and lower your risk of heart disease. There’s simply no evidence suggesting that statins or beta blockers are any more effective than exercise, which means you can forgo all the side effects and exorbitant expense associated with such drugs.  

Remember what these Harvard and Stanford University researchers concluded after reviewing 305 studies comparing exercise versus drug treatment: “[E]xercise interventions should… be considered as a viable alternative to, or, alongside, drug therapy.” What could possibly be more empowering than that?!

Seeing light in a new light.


Scientists create never-before-seen form of matter

Harvard and MIT scientists are challenging the conventional wisdom about light, and they didn’t need to go to a galaxy far, far away to do it.

Working with colleagues at the Harvard-MIT Center for Ultracold Atoms, a group led by Harvard Professor of Physics Mikhail Lukin and MIT Professor of Physics Vladan Vuletic have managed to coax photons into binding together to form molecules – a state of matter that, until recently, had been purely theoretical. The work is described in a September 25 paper inNature.

The discovery, Lukin said, runs contrary to decades of accepted wisdom about the nature of light. Photons have long been described as massless particles which don’t interact with each other – shine two laser beams at each other, he said, and they simply pass through one another.

“Photonic molecules,” however, behave less like traditional lasers and more like something you might find in science fiction – the light saber.

“Most of the properties of light we know about originate from the fact that photons are massless, and that they do not interact with each other,” Lukin said. “What we have done is create a special type of medium in which photons interact with each other so strongly that they begin to act as though they have mass, and they bind together to form molecules. This type of photonic bound state has been discussed theoretically for quite a while, but until now it hadn’t been observed.

“It’s not an in-apt analogy to compare this to light sabers,” Lukin added. “When these photons interact with each other, they’re pushing against and deflect each other. The physics of what’s happening in these molecules is similar to what we see in the movies.”

To get the normally-massless photons to bind to each other, Lukin and colleagues, including Harvard post-doctoral fellow Ofer Fisterberg, former Harvard doctoral student Alexey Gorshkov and MIT graduate students Thibault Peyronel and Qiu Liang couldn’t rely on something like the Force – they instead turned to a set of more extreme conditions.

Researchers began by pumped rubidium atoms into a vacuum chamber, then used lasers to cool the cloud of atoms to just a few degrees above absolute zero. Using extremely weak laser pulses, they then fired single photons into the cloud of atoms.

As the photons enter the cloud of cold atoms, Lukin said, its energy excites atoms along its path, causing the photon to slow dramatically. As the photon moves through the cloud, that energy is handed off from atom to atom, and eventually exits the cloud with the photon.

“When the photon exits the medium, its identity is preserved,” Lukin said. “It’s the same effect we see with refraction of light in a water glass. The light enters the water, it hands off part of its energy to the medium, and inside it exists as light and matter coupled together, but when it exits, it’s still light. The process that takes place is the same it’s just a bit more extreme – the light is slowed considerably, and a lot more energy is given away than during refraction.”

When Lukin and colleagues fired two photons into the cloud, they were surprised to see them exit together, as a single molecule.

The reason they form the never-before-seen molecules?

An effect called a Rydberg blockade, Lukin said, which states that when an atom is excited, nearby atoms cannot be excited to the same degree. In practice, the effect means that as two photons enter the atomic cloud, the first excites an atom, but must move forward before the second photon can excite nearby atoms.

The result, he said, is that the two photons push and pull each other through the cloud as their energy is handed off from one atom to the next.

“It’s a photonic interaction that’s mediated by the atomic interaction,” Lukin said. “That makes these two photons behave like a molecule, and when they exit the medium they’re much more likely to do so together than as single photons.”

While the effect is unusual, it does have some practical applications as well.

“We do this for fun, and because we’re pushing the frontiers of science,” Lukin said. “But it feeds into the bigger picture of what we’re doing because photons remain the best possible means to carry quantum information. The handicap, though, has been that photons don’t interact with each other.”

To build a quantum computer, he explained, researchers need to build a system that can preserve quantum information, and process it using quantum logic operations. The challenge, however, is that quantum logic requires interactions between individual quanta so that quantum systems can be switched to perform information processing.

“What we demonstrate with this process allows us to do that,” Lukin said. “Before we make a useful, practical quantum switch or photonic logic gate we have to improve the performance, so it’s still at the proof-of-concept level, but this is an important step. The physical principles we’ve established here are important.”

The system could even be useful in classical computing, Lukin said, considering the power-dissipation challenges chip-makers now face. A number of companies – including IBM – have worked to develop systems that rely on optical routers that convert light signals into electrical signals, but those systems face their own hurdles.

Lukin also suggested that the system might one day even be used to create complex three-dimensional structures – such as crystals – wholly out of light.

“What it will be useful for we don’t know yet, but it’s a new state of matter, so we are hopeful that new applications may emerge as we continue to investigate these photonic molecules’ properties,” he said.

Marijuana Cuts Lung Cancer Tumor Growth In Half, Study Shows.


The active ingredient in marijuana cuts tumor growth in common lung cancer in half and significantly reduces the ability of the cancer to spread, say researchers at Harvard University who tested the chemical in both lab and mouse studies.

They say this is the first set of experiments to show that the compound, Delta-tetrahydrocannabinol (THC), inhibits EGF-induced growth and migration in epidermal growth factor receptor (EGFR) expressing non-small cell lung cancer cell lines. Lung cancers that over-express EGFR are usually highly aggressive and resistant to chemotherapy.

THC that targets cannabinoid receptors CB1 and CB2 is similar in function to endocannabinoids, which are cannabinoids that are naturally produced in the body and activate these receptors. The researchers suggest that THC or other designer agents that activate these receptors might be used in a targeted fashion to treat lung cancer.

“The beauty of this study is that we are showing that a substance of abuse, if used prudently, may offer a new road to therapy against lung cancer,” said Anju Preet, Ph.D., a researcher in the Division of Experimental Medicine.

Acting through cannabinoid receptors CB1 and CB2, endocannabinoids (as well as THC) are thought to play a role in variety of biological functions, including pain and anxiety control, and inflammation. Although a medical derivative of THC, known as Marinol, has been approved for use as an appetite stimulant for cancer patients, and a small number of U.S. states allow use of medical marijuana to treat the same side effect, few studies have shown that THC might have anti-tumor activity, Preet says. The only clinical trial testing THC as a treatment against cancer growth was a recently completed British pilot study in human glioblastoma.

In the present study, the researchers first demonstrated that two different lung cancer cell lines as well as patient lung tumor samples express CB1 and CB2, and that non-toxic doses of THC inhibited growth and spread in the cell lines. “When the cells are pretreated with THC, they have less EGFR stimulated invasion as measured by various in-vitro assays,” Preet said.

Then, for three weeks, researchers injected standard doses of THC into mice that had been implanted with human lung cancer cells, and found that tumors were reduced in size and weight by about 50 percent in treated animals compared to a control group. There was also about a 60 percent reduction in cancer lesions on the lungs in these mice as well as a significant reduction in protein markers associated with cancer progression, Preet says.

Although the researchers do not know why THC inhibits tumor growth, they say the substance could be activating molecules that arrest the cell cycle. They speculate that THC may also interfere with angiogenesis and vascularization, which promotes cancer growth.

Preet says much work is needed to clarify the pathway by which THC functions, and cautions that some animal studies have shown that THC can stimulate some cancers. “THC offers some promise, but we have a long way to go before we know what its potential is,” she said.

Source: http://www.sciencedaily.com

Harvard Study Shows “Marijuana Cuts Lung Cancer Tumor Growth In Half”.


The active ingredient in marijuana cuts tumor growth in common lung cancer in half and significantly reduces the ability of the cancer to spread, say researchers at Harvard University who tested the chemical in both lab and mouse studies.
They say this is the first set of experiments to show that the compound, Delta-tetrahydrocannabinol (THC), inhibits EGF-induced growth and migration in epidermal growth factor receptor (EGFR) expressing non-small cell lung cancer cell lines. Lung cancers that over-express EGFR are usually highly aggressive and resistant to chemotherapy.smoking_1117THC that targets cannabinoid receptors CB1 and CB2 is similar in function to endocannabinoids, which are cannabinoids that are naturally produced in the body and activate these receptors. The researchers suggest that THC or other designer agents that activate these receptors might be used in a targeted fashion to treat lung cancer.

“The beauty of this study is that we are showing that a substance of abuse, if used prudently, may offer a new road to therapy against lung cancer,” said Anju Preet, Ph.D., a researcher in the Division of Experimental Medicine.

Acting through cannabinoid receptors CB1 and CB2, endocannabinoids (as well as THC) are thought to play a role in variety of biological functions, including pain and anxiety control, and inflammation. Although a medical derivative of THC, known as Marinol, has been approved for use as an appetite stimulant for cancer patients, and a small number of U.S. states allow use of medical marijuana to treat the same side effect, few studies have shown that THC might have anti-tumor activity, Preet says. The only clinical trial testing THC as a treatment against cancer growth was a recently completed British pilot study in human glioblastoma.

In the present study, the researchers first demonstrated that two different lung cancer cell lines as well as patient lung tumor samples express CB1 and CB2, and that non-toxic doses of THC inhibited growth and spread in the cell lines. “When the cells are pretreated with THC, they have less EGFR stimulated invasion as measured by various in-vitro assays,” Preet said.

Then, for three weeks, researchers injected standard doses of THC into mice that had been implanted with human lung cancer cells, and found that tumors were reduced in size and weight by about 50 percent in treated animals compared to a control group. There was also about a 60 percent reduction in cancer lesions on the lungs in these mice as well as a significant reduction in protein markers associated with cancer progression, Preet says.

Source: realfarmacy.com

Nanodiamond thermometer can find the temperature inside a single living cell.


The mercury-in-glass thermometer has served us well for the past 270 years, but sometimes you need something smaller — say to find the temperature inside a single living cell. Researchers at Harvard have discovered a new technique using lasers and diamond nanocrystals to measure temperatures of microscopic structures, recording temperature fluctuations as small as 0.05 Kelvin (0.09ºF) in size.

The technique relies on the quantum properties of the diamonds’ tasty centers. In a diamond crystals with a nitrogen vacancy in its center — a kind of defect — the center’s electronic spin comes to depend on its temperature. Laser light bouncing out of one of these nanodiamonds shows up as a different color depending on the center’s temperature. And using diamonds also adds some other benefits. Because they’re highly chemically inert, changes in the surrounding chemistry don’t affect the outcome, and the method can be used over a broad range of temperatures, for the same reason. In one series of experiments (pictured above), the team implanted a human cell with a gold nanoparticle, used a laser to heat it up (thereby heating up the surrounding cell), and bounced a laser off a diamond implanted in the same cell to record the temperature difference. The results will be published in the August issue of Nature.

So why would you want to know the temperature inside a living cell? The team believes that the gold heating trick, precisely monitored with its diamond-and-laser nanothermometer, could make it possible to “engineer biological processes at the subcellular level,” possibly helping to screen for cancer, or cooking the perfect steak, one cell at a time.

Source: http://www.theverge.com

New theory uncovers cancer’s deep evolutionary roots.


A new way to look at cancer – by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago – has been proposed by Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science in collaboration with Charles Lineweaver of the Australian National University. If their theory is correct, it promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos.

Paul Davies

Davies and Lineweaver are both theoretical physicists and cosmologists with experience in the field of astrobiology – the search for life beyond Earth. They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology. The center is one of twelve established by the National Cancer Institute to encourage physical scientists to lend their insights into tackling cancer.

The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge. It might be triggered by a random accident, they say, but thereafter it more or less predictably unfolds.

Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies. It appears in a special July issue of Physics World devoted to the physics of cancer.

“We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells,” says Davies, an Arizona State University Regents’ Professor in ASU’s College of Liberal Arts and Sciences. “It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort.” As such, he describes cancer as a throwback to an ancestral phenotype.

The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years, with the help of Luis Cisneros, a postdoctoral researcher with ASU’s Beyond Center.

But if this is the case, then why hasn’t evolution eliminated the ancient cancer subroutine?

“Because it fulfills absolutely crucial functions during the early stages of embryo development,” Davies explains. “Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.”

The link with embryo development has been known to cancer biologists for a long time, says Davies, but the significance of this fact is rarely appreciated. If the new theory is correct, researchers should find that the more malignant stages of cancer will re-express genes from the earliest stages of embryogenesis. Davies adds that there is already some evidence for this in several experimental studies, including recent research at Harvard University and the Albert Einstein College of Medicine in New York.

“As cancer progresses through its various stages within a single organism, it should be like running the evolutionary and developmental arrows of time backward at high speed,” says Davies.

This could provide clues to future treatments. For example, when life took the momentous step from single cells to multicellular assemblages, Earth had low levels of oxygen. Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar.

Davies and Lineweaver predict that if cancer cells are saturated with oxygen but deprived of sugar, they will become more stressed than healthy cells, slowing them down or even killing them. ASU’s Center for the Convergence of Physical Science and Cancer Biology, of which Davies is principal investigator, is planning a workshop in November to examine the clinical evidence for this.

“It is clear that some radically new thinking is needed,” Davies states. “Like aging, cancer seems to be a deeply embedded part of the life process. Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”

Source: asunews.asu.edu

The Neuroscience of Everybody’s Favourite Topic.


Why do people spend so much time talking about themselves?

Human beings are social animals. We spendlarge portions of our waking hours communicating with others, and the possibilities for conversation are seemingly endless—we can make plans and crack jokes; reminisce about the past and dream about the future; share ideas and spread information. This ability to communicate—with almost anyone, about almost anything—has played a central role in our species’ ability to not just survive, but flourish.

the-neuroscience-of-everybody-favorite-topic-themselves_1

How do you choose to use this immensely powerful tool—communication? Do your conversations serve as doorways to new ideas and experiences? Do they serve as tools for solving the problems of disease and famine?

Or do you mostly just like to talk about yourself?

If you’re like most people, your own thoughts and experiences may be your favorite topic of conversation.  On average, people spend 60 percent of conversationstalking about themselves—and this figure jumps to 80 percent when communicating via social media platforms such as Twitter or Facebook.

Why, in a world full of ideas to discover, develop, and discuss, do people spend the majority of their time talking about themselves? Recent research suggests a simple explanation: because it feels good.

In order to investigate the possibility that self-disclosure is intrinsically rewarding, researchers from the Harvard University Social Cognitive and Affective Neuroscience Lab utilized functional magnetic resonance imaging (fMRI). This research tool highlights relative levels of activity in various neural regions by tracking changes in blood flow; by pairing fMRI output with behavioral data, researchers can gain insight into the relationships between behavior and neural activity. In this case, they were interested in whether talking about the self would correspond with increased neural activity in areas of the brain associated with motivation and reward.

In an initial fMRI experiment, the researchers asked 195 participants to discuss both their own opinions and personality traits and the opinions and traits of others, then looked for differences in neural activation between self-focused and other-focused answers. Because the same participants discussed the same topics in relation to both themselves and others, researchers were able to use the resulting data to directly compare neural activation during self-disclosure to activation during other-focused communication.

Three neural regions stood out. Unsurprisingly, and in line with previous research, self-disclosure resulted in relatively higher levels of activation in areas of the medial prefrontal cortex (MPFC) generally associated with self-related thought. The two remaining regions identified by this experiment, however, had never before been associated with thinking about the self: the nucleus accumbens (NAcc) and the ventral tegmental area (VTA), both parts of the mesolimbic dopamine system.

These newly implicated areas of the brain are generally associated with reward, and have been linked to the pleasurable feelings and motivational states associated with stimuli such as sexcocaine, and good food. Activation of this system when discussing the self suggests that self-disclosure, like other more traditionally recognized stimuli, may be inherently pleasurable—and that people may be motivated to talk about themselves more than other topics (no matter how interesting or important these non-self topics may be).

This experiment left at least one question unanswered, however. Although participants were revealing information about themselves, it was unclear whether or not anyone was paying attention; they were essentially talking without knowing who (if anyone) was on the other end of the line. Thus, the reward- and motivation-related neural responses ostensibly produced by self-disclosure could be produced by the act of disclosure—of revealing information about the self to someone else—but they could also be a result of focusing on the self more generally—whether or not anyone was listening.

In order to distinguish between these two possibilities, the researchers conducted a follow-up experiment. In this experiment, participants were asked to bring a friend or relative of their choosing to the lab with them; these companions were asked to wait in an adjoining room while participants answered questions in a fMRI machine. As in the first study, participants responded to questions about either their own opinions and attitudes or the opinions and attitudes of someone else; unlike in the first study, these participants were explicitly told whether their responses would be “shared” or “private”; shared responses were relayed in real time to each participant’s companion and private responses were never seen by anyone, including the researchers.

In this study, answering questions about the self always resulted in greater activation of neural regions associated with motivation and reward (i.e., NAcc, VTA) than answering questions about others, and answering questions publicly always resulted in greater activation of these areas than answering questions privately.  Importantly, these effects were additive; both talking about the self and talking to someone else were associated with reward, and doing both produced greater activation in reward-related neural regions than doing either separately.

These results suggest that self-disclosure—revealing personal information to others—produces the highest level of activation in neural regions associated with motivation and reward, but that introspection—thinking or talking about the self, in the absence of an audience—also produces a noticeable surge of neural activity in these regions. Talking about the self is intrinsically rewarding, even if no one is listening.

Talking about the self is not at odds with the adaptive functions of communication. Disclosing private information to others can increase interpersonal liking and aid in the formation of new social bonds—outcomes that influence everything from physical survival to subjective happiness. Talking about one’s own thoughts and self-perceptions can lead to personal growth via external feedback. And sharing information gained through personal experiences can lead to performance advantages by enabling teamwork and shared responsibility for memory. Self-disclosure can have positive effects on everything from the most basic of needs—physical survival—to personal growth through enhanced self-knowledge; self-disclosure, like other forms of communication, seems to be adaptive.

You may like to talk about yourself simply because it feels good—because self-disclosure produces a burst of activity in neural regions associated with pleasure, motivation, and reward.  But, in this case, feeling good may be no more than a means to an end—it may be the immediate reward that jump-starts a cycle of self-sharing, ultimately leading to wide varieties of long-term benefits.

Source: Scientific American

 

New hormone stimulates pancreatic β-cell proliferation.


Diabetes affects more than 360 million people worldwide and its prevalence is increasing, with 552 million diabetics predicted worldwide by 2030. Scientists recently discovered a hormone that could improve future diabetes management by stimulating replenishment of insulin-producing β cells in the pancreas.

The hormone, which has been named betatrophin, was discovered in studies of a mouse model of severe insulin resistance in which chemical blockade of insulin receptors induced pancreatic β-cell proliferation. Betatrophin was identified in murine liver and fat, and its stimulatory effect on cellular replication was limited to β cells. Its expression was also reported in human liver tissue.

Betatrophin treatment of mice increased proliferation of pancreatic β-cells by an average of 17-fold within a few days, causing an expansion of β-cell mass and increased insulin concentrations in the pancreas.

Betatrophin’s discovery “is a very exciting new development, and is only the beginning of the story”, says C Ronald Kahn (Joslin Diabetes Center, Boston, MA, USA). He adds that unanswered questions include whether “action on islets is direct or indirect. We don’t know how betatrophin works; is it only one growth factor or one of many? There is a lot of future work to be done”.

Senior author Douglas Melton (Harvard University, Cambridge, MA, USA) said: “It’s not often that one finds a new hormone, so it opens up all kinds of possibilities for new treatments”.

The most immediate application for betatrophin is for the “millions of prediabetics who are on their way to getting type 2 diabetes. If these individuals still have β cells, this hormone could give them more β cells and alleviate the need for insulin injections”, Melton continued. Betatrophin may also prove beneficial in type 1 diabetes, which is initiated by an autoimmune process. “If the disease is just starting, one could give an immunosuppressant and this hormone to forestall the onset of type 1 diabetes.”

Melton cautions that results from human studies should not be expected quickly. “We are currently working with our collaborators Evotec and Janssen to make the human betatrophin protein. This will take more than a year.” Results from studies in humans might be available “2—3 years from now, if all goes well”.

Source: Lancet

How Your Smartphone Could Get You a Job.


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Keith Gormley wasn’t looking for a new job on a day last fall when he used his iPhone to pull up the Indeed.com job-search app during his morning commute.

“I was bored, and maybe Twitter wasn’t as active as usual. I was just flipping through to see what jobs were out there,” he said.

A social-media position at Prudential Financial Inc. PRU +4.61% caught Mr. Gormley’s eye. He clicked through to the financial-services firm’s career site, then did some research on Twitter and LinkedIn. A few days later, he applied for the job from his home computer. By December the 31-year-old had been hired.

Technology-research firm IDC has predicted that mobile devices will overtake desktop and laptop computers as Americans’ preferred method for accessing the Internet by 2015. And as Web traffic migrates to smartphones and tablets, employers are rushing to develop mobile versions of their career websites, apps with interactive career content such as games and workplace tours, and simplified versions of job applications that can more easily be completed on a hand-held device.

Companies and recruiting experts believe mobile recruiting will help them engage candidates who may otherwise fall through the cracks: lower-wage and younger workers who may not have computers at home but are glued to their smartphones, as well as the coveted passive candidates—people like Mr. Gormley who are already employed—who might casually explore their options while they are off the clock.

“People are getting used to going online while sitting on a bus or waiting for an airplane. And if you hate your job, it’s so easy to pull out your phone and see what else is out there,” said Cindy Cloud, senior manager of employment-branding and marketing at Informatica Corp.,INFA -0.44% a Silicon Valley data integration firm. “We think mobile is the next big area for recruiting.”

That is good news for employers: A 2011 paper from economists Peter Kuhn and Hani Mansour shows that online job-search is now starting to make the labor market more efficient as candidates are more quickly matched to jobs. The development has likely increased because of the popularity of social networking, the authors said.

“Any company that hasn’t started to address mobile recruiting is at least a year behind,” said Elaine Orler, an expert in recruiting technology and president of the Talent Function Group, a human resources consulting firm. “This is the connectivity that job seekers expect now.”

That may be, but it isn’t widespread just yet. In January, iMomentous, a developer of mobile career sites, found that 167, or 33%, of Fortune 500 companies had career portals that were optimized in even the most basic way—that is, sized to fit a smartphone screen. Still, it was an improvement over a year earlier, when 65 companies had mobile optimized career sites.

The biggest challenge is creating a streamlined user experience. After all, filling in dozens of fields and taking assessment tests is annoying enough with a traditional keyboard; it is even more cumbersome with a tiny screen and touch-based keyboard.

McDonald’s Corp. MCD -0.93% tried to simplify the application process for mobile job candidates. While the mobile application asks for the same information as the desktop one—both versions take 30 to 35 minutes to complete—more than 30 fields were altered to provide dropdown menus rather than free-text boxes, and calendars were added that automatically populate queries in the correct format.

“With the hiring volume we have, it’s much easier when someone comes into a restaurant and can apply right there on a phone instead of filling out a paper application,” said Nicholas Statler, director of employment strategy at McDonald’s. It also cuts down on the time managers spend on new applicants since the managers no longer need to input all the information into a computer.

When the restaurant chain launched its first mobile career site in 2008, three million people visited it and 24,000 people used it to submit applications, said Mr. Statler. By 2012, those figures had jumped to 30 million visits and two million applications. Now, it brings in a little over 10% of total applications.

This development isn’t just about technology. Friction in the labor market—the phrase economists use to describe inefficiencies in matching employers with people looking for jobs—might be eased if companies with low-skill, high-turnover jobs make it easier for job seekers to find and apply for openings, said Richard Freeman, a labor economist at Harvard University who has studied online job markets.

Firms are finding that, for higher-skilled positions too, candidates now expect the easy access of mobile job-searching and applications.

Macy’s Inc. M +10.63% developed its first mobile optimized career page in 2011 to target 700 hires like software developers and marketers it was making for its e-commerce group. Only after that experiment worked did it roll out a mobile page for hourly workers, in 2012, said Michelle Cantor, director of employment process and jobs.com. Today, 20% to 25% of all applicants to Macy’s apply on mobile devices.

This development goes hand in hand with two other transformative technology trends: social networking and cloud computing.

A February 2013 report from market-research firm Nielsen found that 63% of Americans access social-networking sites like LinkedIn or Facebook FB -1.56% on their mobile devices. With job opportunities shared widely across these sites—and recruiters relying on them to reach out to prospects—more candidates are hearing about openings on their phones and tablets.

“If our recruiters send a message via LinkedIn, we know it’s likely they’re going to get it on their phone,” said Brett Underhill, director of recruiting programs at Prudential.

Employers are also starting to experiment with the next frontiers of mobile recruiting: using QR codes and text-messaging, two capabilities that are specifically geared to smartphones.

McDonald’s and Macy’s are both integrating QR codes into their hiring ads, so that job seekers or customers can walk into a store, scan the code they see on a poster, and be sent directly to the openings available at that location. With text messaging, applicants can text a phone number listed, for example, on a bus advertisement and immediately receive a link to job openings.

“These are marketing techniques that are now being applied to jobs,” said Ms. Orler.

Source: WSJ

 

Tiny robot flies like a fly.


Engineers create first device able to mimic full range of insect flight.

A robot as small as a housefly has managed the delicate task of flying and hovering the way the actual insects do.

“This is a major engineering breakthrough, 15 years in the making,” says electrical engineer Ronald Fearing, who works on robotic flies at the University of California, Berkeley. The device uses layers of ultrathin materials that can make its wings flap 120 times a second, which is on a par with a housefly’s flapping rate. This “required tremendous innovation in design and fabrication techniques”, he adds.

The robot’s wings are composed of thin polyester films reinforced with carbon fibre ribs and its ‘muscles’ are made from piezoelectric crystals, which shrink or stretch depending on the voltage applied to them.

Kevin Ma and his colleagues, all based at Harvard University in Cambridge, Massachusetts, describe their design today inScience1.

The tiny components, some of which are just micrometres across, are extremely difficult to make using conventional manufacturing technologies, so the researchers came up with a folding process similar to that used in a pop-up book. They created layers of flat, bendable materials with flexible hinges that enabled the three-dimensional structure to emerge in one fell swoop. “It is easier to make two-dimensional structures and fold them into three dimensions than it is to make three dimensional structures directly,” explains Ma.

Manufacturing marvel

“The ability to manufacture these little flexure joints is going to have implications for a lot of aspects of robotics that have nothing to do with making a robotic fly,” notes Michael Dickinson, a neuroscientist at the University of Washington in Seattle.

The work “will also lead to better understanding of insect flapping wing aerodynamics and control strategies” because it uses an engineering system “that can be more easily modified or controlled than an animal”, Fearing adds.

Weighing in at just 80 milligrams, the tiny drone cannot carry its own power source, so has to stay tethered to the ground. It also relies on a computer to monitor its motion and adjust its attitude. Still, it is the first robot to deploy a fly’s full range of aerial motion, including hovering.

The biggest technical obstacle to independent flight is building a battery that is small enough to be carried by the robotic fly, says Fearing. At present, the smallest batteries with enough power weigh about half a gram — ten times more than what the robotic fly can support. Ma says he believes that the battery obstacle might be overcome in 5-10 years.

If researchers can come up with such a battery, and with lightweight onboard sensors, Ma says that the robots could be useful in applications such as search and rescue missions in collapsed buildings, or as ways to pollinate crops amid dwindling bee populations.

Source: Nature