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JULY 3, 2013, 12:01 AM
How Exercise Can Calm Anxiety
By GRETCHEN REYNOLDS

In an eye-opening demonstration of nature’s ingenuity, researchers at Princeton University recently discovered that exercise creates vibrant new brain cells — and then shuts them down when they shouldn’t be in action.
For some time, scientists studying exercise have been puzzled by physical activity’s two seemingly incompatible effects on the brain. On the one hand, exercise is known to prompt the creation of new and very excitable brain cells. At the same time, exercise can induce an overall pattern of calm in certain parts of the brain.
Most of us probably don’t realize that neurons are born with certain predispositions. Some, often the younger ones, are by nature easily excited. They fire with almost any provocation, which is laudable if you wish to speed thinking and memory formation.
But that feature is less desirable during times of everyday stress. If a stressor does not involve a life-or-death decision and require immediate physical action, then having lots of excitable neurons firing all at once can be counterproductive, inducing anxiety.
Studies in animals have shown that physical exercise creates excitable neurons in abundance, especially in the hippocampus, a portion of the brain known to be involved in thinking and emotional responses.
But exercise also has been found to reduce anxiety in both people and animals.
How can an activity simultaneously create ideal neurological conditions for anxiety and leave practitioners with a deep-rooted calm, the Princeton researchers wondered?
So they gathered adult mice, injected them with a substance that marks newborn cells in the brain, and for six weeks, allowed half of them to run at will on little wheels, while the others sat quietly in their cages.
Afterward, the scientists determined each group’s baseline nervousness. Given access to cages with open, well-lighted areas, as well as shadowy corners, the running mice were more willing to cautiously explore and spend time in open areas, an indication that they were more confident and less anxious than the sedentary animals.
The researchers also checked the brains of some of the runners and the sedentary mice to determine how many and what varieties of new neurons they contained.
As expected, the runners’ brains teemed with many new, excitable neurons. The sedentary mice’s brains also contained similar, volatile newborn cells, but not in such profusion.
The runners’ brains, however, also had a notable number of new neurons specifically designed to release the neurotransmitter GABA, which inhibits brain activity, keeping other neurons from firing easily. In effect, these are nanny neurons, designed to shush and quiet activity in the brain.
In the runners’ brains, there were large new populations of these cells in a portion of the hippocampus, the ventral region, associated with the processing of emotions. (The rest of the hippocampus, the dorsal region, is more involved with thinking and memory.)
What role these nanny neurons were playing in the animals’ brains and subsequent behavior was not altogether clear.
So the scientists next gently placed the remaining mice in ice-cold water for five minutes. Mice do not enjoy cold water. They find immersion stressful and anxiety-inducing, although it is not life-threatening.
Then the scientists checked these animals’ brains. They were looking for markers, known as immediate early genes, that indicate a neuron has recently fired.
They found them, in profusion. In both the physically fit and the sedentary mice, large numbers of the excitable cells had fired in response to the cold bath. Emotionally, the animals had become fired up by the stress.
But with the runners, it didn’t last long. Their brains, unlike those of the sedentary animals, showed evidence that the shushing neurons also had been activated in large numbers, releasing GABA, calming the excitable neurons’ activity and presumably keeping unnecessary anxiety at bay.
In effect, the runners’ brains had responded to the relatively minor stress of a cold bath with a quick rush of worry and a concomitant, overarching calm.
What all of this suggests, says Elizabeth Gould, director of the Gould Lab at Princeton, who wrote the paper with her graduate student Timothy Schoenfeld, now at the National Institute of Mental Health, and others, “is that the hippocampus of runners is vastly different from that of sedentary animals. Not only are there more excitatory neurons and more excitatory synapses, but the inhibitory neurons are more likely to become activated, presumably to dampen the excitatory neurons, in response to stress.” The findings were published in The Journal of Neuroscience.
It’s important to note, she adds, that this study examined long-term training responses. The runners’ wheels had been locked for 24 hours before their cold bath, so they would gain no acute calming effect from exercise. Instead, the difference in stress response between the runners and the sedentary animals reflected fundamental remodeling of their brains.
Of course, as we all know, mice are not men or women. But, Dr. Gould says, other studies “show that physical exercise reduces anxiety in humans,” suggesting that similar remodeling takes place in the brains of people who work out.
“I think it’s not a huge stretch,” she concludes, “to suggest that the hippocampi of active people might be less susceptible to certain undesirable aspects of stress than those of sedentary people.”
JULY 3, 2013, 12:01 AM

How Exercise Can Calm Anxiety

By GRETCHEN REYNOLDS

In an eye-opening demonstration of nature’s ingenuity, researchers at Princeton University recently discovered that exercise creates vibrant new brain cells — and then shuts them down when they shouldn’t be in action.

For some time, scientists studying exercise have been puzzled by physical activity’s two seemingly incompatible effects on the brain. On the one hand, exercise is known to prompt the creation of new and very excitable brain cells. At the same time, exercise can induce an overall pattern of calm in certain parts of the brain.

Most of us probably don’t realize that neurons are born with certain predispositions. Some, often the younger ones, are by nature easily excited. They fire with almost any provocation, which is laudable if you wish to speed thinking and memory formation.

But that feature is less desirable during times of everyday stress. If a stressor does not involve a life-or-death decision and require immediate physical action, then having lots of excitable neurons firing all at once can be counterproductive, inducing anxiety.

Studies in animals have shown that physical exercise creates excitable neurons in abundance, especially in the hippocampus, a portion of the brain known to be involved in thinking and emotional responses.

But exercise also has been found to reduce anxiety in both people and animals.

How can an activity simultaneously create ideal neurological conditions for anxiety and leave practitioners with a deep-rooted calm, the Princeton researchers wondered?

So they gathered adult mice, injected them with a substance that marks newborn cells in the brain, and for six weeks, allowed half of them to run at will on little wheels, while the others sat quietly in their cages.

Afterward, the scientists determined each group’s baseline nervousness. Given access to cages with open, well-lighted areas, as well as shadowy corners, the running mice were more willing to cautiously explore and spend time in open areas, an indication that they were more confident and less anxious than the sedentary animals.

The researchers also checked the brains of some of the runners and the sedentary mice to determine how many and what varieties of new neurons they contained.

As expected, the runners’ brains teemed with many new, excitable neurons. The sedentary mice’s brains also contained similar, volatile newborn cells, but not in such profusion.

The runners’ brains, however, also had a notable number of new neurons specifically designed to release the neurotransmitter GABA, which inhibits brain activity, keeping other neurons from firing easily. In effect, these are nanny neurons, designed to shush and quiet activity in the brain.

In the runners’ brains, there were large new populations of these cells in a portion of the hippocampus, the ventral region, associated with the processing of emotions. (The rest of the hippocampus, the dorsal region, is more involved with thinking and memory.)

What role these nanny neurons were playing in the animals’ brains and subsequent behavior was not altogether clear.

So the scientists next gently placed the remaining mice in ice-cold water for five minutes. Mice do not enjoy cold water. They find immersion stressful and anxiety-inducing, although it is not life-threatening.

Then the scientists checked these animals’ brains. They were looking for markers, known as immediate early genes, that indicate a neuron has recently fired.

They found them, in profusion. In both the physically fit and the sedentary mice, large numbers of the excitable cells had fired in response to the cold bath. Emotionally, the animals had become fired up by the stress.

But with the runners, it didn’t last long. Their brains, unlike those of the sedentary animals, showed evidence that the shushing neurons also had been activated in large numbers, releasing GABA, calming the excitable neurons’ activity and presumably keeping unnecessary anxiety at bay.

In effect, the runners’ brains had responded to the relatively minor stress of a cold bath with a quick rush of worry and a concomitant, overarching calm.

What all of this suggests, says Elizabeth Gould, director of the Gould Lab at Princeton, who wrote the paper with her graduate student Timothy Schoenfeld, now at the National Institute of Mental Health, and others, “is that the hippocampus of runners is vastly different from that of sedentary animals. Not only are there more excitatory neurons and more excitatory synapses, but the inhibitory neurons are more likely to become activated, presumably to dampen the excitatory neurons, in response to stress.” The findings were published in The Journal of Neuroscience.

It’s important to note, she adds, that this study examined long-term training responses. The runners’ wheels had been locked for 24 hours before their cold bath, so they would gain no acute calming effect from exercise. Instead, the difference in stress response between the runners and the sedentary animals reflected fundamental remodeling of their brains.

Of course, as we all know, mice are not men or women. But, Dr. Gould says, other studies “show that physical exercise reduces anxiety in humans,” suggesting that similar remodeling takes place in the brains of people who work out.

“I think it’s not a huge stretch,” she concludes, “to suggest that the hippocampi of active people might be less susceptible to certain undesirable aspects of stress than those of sedentary people.”

Posted on Monday, July 8th 2013

 Source The New York Times

Find time to challenge yourself everyday!

Find time to challenge yourself everyday!

Posted on Monday, July 8th 2013

 Source

 You can get stronger and fitter exercising just 2 hours per week.  Permanently changing your body requires you to make some good nutritional choices the other 166 hours remaining.  You can never out exercise a bad diet!

You can get stronger and fitter exercising just 2 hours per week. Permanently changing your body requires you to make some good nutritional choices the other 166 hours remaining. You can never out exercise a bad diet!

Posted on Monday, July 8th 2013

This reminds me of what the typical “low-fat” diet has done to the country.  Generally low-fat translates as high carb and high sodium.

This reminds me of what the typical “low-fat” diet has done to the country.  Generally low-fat translates as high carb and high sodium.

Posted on Monday, July 8th 2013

Exercise reorganizes the brain to be more resilient to stress

Posted July 3, 2013; 02:30 p.m.
by Morgan Kelly, Office of Communications
Physical activity reorganizes the brain so that its response to stress is reduced and anxiety is less likely to interfere with normal brain function, according to a research team based at Princeton University.
The researchers report in the Journal of Neuroscience that when mice allowed to exercise regularly experienced a stressor — exposure to cold water — their brains exhibited a spike in the activity of neurons that shut off excitement in the ventral hippocampus, a brain region shown to regulate anxiety.


A research team based at Princeton University found that physical activity reorganizes the brain so that its response to stress is reduced and anxiety is less likely to interfere with normal brain function. Running produced a large increase in the number of new neurons in the hippocampus — a brain region shown to regulate anxiety — of a mouse that ran for six weeks (above). The brown cells are new neurons, which are more numerous in active mice than sedentary mice, and the blue cells are mature neurons. (Photo courtesy of the Gould laboratory)


These findings potentially resolve a discrepancy in research related to the effect of exercise on the brain — namely that exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus. Because these young neurons are typically more excitable than their more mature counterparts, exercise should result in more anxiety, not less. The Princeton-led researchers, however, found that exercise also strengthens the mechanisms that prevent these brain cells from firing.
The impact of physical activity on the ventral hippocampus specifically has not been deeply explored, said senior author Elizabeth Gould, Princeton’s Dorman T. Warren Professor of Psychology. By doing so, members of Gould’s laboratory pinpointed brain cells and regions important to anxiety regulation that may help scientists better understand and treat human anxiety disorders, she said.
From an evolutionary standpoint, the research also shows that the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings, Gould said. A higher likelihood of anxious behavior may have an adaptive advantage for less physically fit creatures. Anxiety often manifests itself in avoidant behavior and avoiding potentially dangerous situations would increase the likelihood of survival, particularly for those less capable of responding with a “fight or flight” reaction, she said.
"Understanding how the brain regulates anxious behavior gives us potential clues about helping people with anxiety disorders. It also tells us something about how the brain modifies itself to respond optimally to its own environment," said Gould, who also is a professor in the Princeton Neuroscience Institute. 

The researchers found that running prevents the activation of new neurons in response to stress. In sedentary mice, stress activated new neurons in the hippocampus (red and green cell above), but after 6 weeks of running, the stress-induced activation of both new and mature neurons disappeared. The red cells are new neurons and the green cells are activated mature neurons.(Photo courtesy of the Gould laboratory)


The research was part of the graduate dissertation for first author Timothy Schoenfeld, now a postdoctoral fellow at the National Institute of Mental Health, as well as part of the senior thesis project of co-author Brian Hsueh, now an MD/Ph.D. student at Stanford University. The project also included co-authors Pedro Rada and Pedro Pieruzzini, both from the University of Los Andes in Venezuela.
For the experiments, one group of mice was given unlimited access to a running wheel and a second group had no running wheel. Natural runners, mice will dash up to 4 kilometers (about 2.5 miles) a night when given access to a running wheel, Gould said. After six weeks, the mice were exposed to cold water for a brief period of time.
The brains of active and sedentary mice behaved differently almost as soon as the stressor occurred, an analysis showed. In the neurons of sedentary mice only, the cold water spurred an increase in “immediate early genes,” or short-lived genes that are rapidly turned on when a neuron fires. The lack of these genes in the neurons of active mice suggested that their brain cells did not immediately leap into an excited state in response to the stressor.
Instead, the brain in a runner mouse showed every sign of controlling its reaction to an extent not observed in the brain of a sedentary mouse. There was a boost of activity in inhibitory neurons that are known to keep excitable neurons in check. At the same time, neurons in these mice released more of the neurotransmitter gamma-aminobutyric acid, or GABA, which tamps down neural excitement. The protein that packages GABA into little travel pods known as vesicles for release into the synapse also was present in higher amounts in runners.
The anxiety-reducing effect of exercise was canceled out when the researchers blocked the GABA receptor that calms neuron activity in the ventral hippocampus. The researchers used the chemical bicuculine, which is used in medical research to block GABA receptors and simulate the cellular activity underlying epilepsy. In this case, when applied to the ventral hippocampus, the chemical blocked the mollifying effects of GABA in active mice.

The paper, “Physical Exercise Prevents Stress-Induced Activation of Granule Neurons and Enhances Local Inhibitory Mechanisms in the Dentate Gyrus,” was published May 1 in the Journal of Neuroscience. This research was supported by National Institute of Mental Health grant MH091567.

Exercise reorganizes the brain to be more resilient to stress

Physical activity reorganizes the brain so that its response to stress is reduced and anxiety is less likely to interfere with normal brain function, according to a research team based at Princeton University.

The researchers report in the Journal of Neuroscience that when mice allowed to exercise regularly experienced a stressor — exposure to cold water — their brains exhibited a spike in the activity of neurons that shut off excitement in the ventral hippocampus, a brain region shown to regulate anxiety.

A research team based at Princeton University found that physical activity reorganizes the brain so that its response to stress is reduced and anxiety is less likely to interfere with normal brain function. Running produced a large increase in the number of new neurons in the hippocampus — a brain region shown to regulate anxiety — of a mouse that ran for six weeks (above). The brown cells are new neurons, which are more numerous in active mice than sedentary mice, and the blue cells are mature neurons. (Photo courtesy of the Gould laboratory)

These findings potentially resolve a discrepancy in research related to the effect of exercise on the brain — namely that exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus. Because these young neurons are typically more excitable than their more mature counterparts, exercise should result in more anxiety, not less. The Princeton-led researchers, however, found that exercise also strengthens the mechanisms that prevent these brain cells from firing.

The impact of physical activity on the ventral hippocampus specifically has not been deeply explored, said senior author Elizabeth Gould, Princeton’s Dorman T. Warren Professor of Psychology. By doing so, members of Gould’s laboratory pinpointed brain cells and regions important to anxiety regulation that may help scientists better understand and treat human anxiety disorders, she said.

From an evolutionary standpoint, the research also shows that the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings, Gould said. A higher likelihood of anxious behavior may have an adaptive advantage for less physically fit creatures. Anxiety often manifests itself in avoidant behavior and avoiding potentially dangerous situations would increase the likelihood of survival, particularly for those less capable of responding with a “fight or flight” reaction, she said.

"Understanding how the brain regulates anxious behavior gives us potential clues about helping people with anxiety disorders. It also tells us something about how the brain modifies itself to respond optimally to its own environment," said Gould, who also is a professor in the Princeton Neuroscience Institute. 

Running stress

The researchers found that running prevents the activation of new neurons in response to stress. In sedentary mice, stress activated new neurons in the hippocampus (red and green cell above), but after 6 weeks of running, the stress-induced activation of both new and mature neurons disappeared. The red cells are new neurons and the green cells are activated mature neurons.(Photo courtesy of the Gould laboratory)

The research was part of the graduate dissertation for first author Timothy Schoenfeld, now a postdoctoral fellow at the National Institute of Mental Health, as well as part of the senior thesis project of co-author Brian Hsueh, now an MD/Ph.D. student at Stanford University. The project also included co-authors Pedro Rada and Pedro Pieruzzini, both from the University of Los Andes in Venezuela.

For the experiments, one group of mice was given unlimited access to a running wheel and a second group had no running wheel. Natural runners, mice will dash up to 4 kilometers (about 2.5 miles) a night when given access to a running wheel, Gould said. After six weeks, the mice were exposed to cold water for a brief period of time.

The brains of active and sedentary mice behaved differently almost as soon as the stressor occurred, an analysis showed. In the neurons of sedentary mice only, the cold water spurred an increase in “immediate early genes,” or short-lived genes that are rapidly turned on when a neuron fires. The lack of these genes in the neurons of active mice suggested that their brain cells did not immediately leap into an excited state in response to the stressor.

Instead, the brain in a runner mouse showed every sign of controlling its reaction to an extent not observed in the brain of a sedentary mouse. There was a boost of activity in inhibitory neurons that are known to keep excitable neurons in check. At the same time, neurons in these mice released more of the neurotransmitter gamma-aminobutyric acid, or GABA, which tamps down neural excitement. The protein that packages GABA into little travel pods known as vesicles for release into the synapse also was present in higher amounts in runners.

The anxiety-reducing effect of exercise was canceled out when the researchers blocked the GABA receptor that calms neuron activity in the ventral hippocampus. The researchers used the chemical bicuculine, which is used in medical research to block GABA receptors and simulate the cellular activity underlying epilepsy. In this case, when applied to the ventral hippocampus, the chemical blocked the mollifying effects of GABA in active mice.

The paper, “Physical Exercise Prevents Stress-Induced Activation of Granule Neurons and Enhances Local Inhibitory Mechanisms in the Dentate Gyrus,” was published May 1 in the Journal of Neuroscience. This research was supported by National Institute of Mental Health grant MH091567.

Posted on Monday, July 8th 2013

Tags fitness

 Source princeton.edu


Are Happy Gut Bacteria Key to Weight Loss?
Imbalances in the microbial community in your intestines may lead to metabolic syndrome, obesity, and diabetes. What does science say about how to reset our bodies?
By Moises Velasquez-Manoff | Mon Apr. 22, 2013 3:00 AM PDT








A few years before Super Size Me hit theaters in 2004, Dr. Paresh Dandona [1], a diabetes specialist in Buffalo, New York, set out to measure the body’s response to McDonald’s [2]—specifically breakfast. Over several mornings, he fed nine normal-weight volunteers an egg sandwich with cheese and ham, a sausage muffin sandwich, and two hash brown patties.
Dandona is a professor at the State University of New York-Buffalo who also heads the Diabetes-Endocrinology Center of Western New York, and what he observed has informed his research ever since. Levels of a C-reactive protein, an indicator of systemic inflammation, shot up “within literally minutes.” “I was shocked,” he recalls, that “a simple McDonald’s meal that seems harmless enough”—the sort of high-fat, high-carbohydrate meal that 1 in 4 Americans eats regularly—would have such a dramatic effect. And it lasted for hours.
Inflammation comes in many forms. The swelling of a sprained ankle indicates repairing torn muscle and tendon. The redness and pain around an infected cut signifies the body’s repulsion of microbes. The fever, aches, and pains that accompany the flu represent a body-wide seek-and-destroy mission directed against an invading virus. They’re all essential to survival, the body’s response to a perceived threat or injury. But inflammation can also cause collateral damage, especially when the response is overwhelming—like in septic shock—or when it goes on too long.






Chronic, low-grade inflammation has long been recognized as a feature of metabolic syndrome [10], a cluster of dysfunctions that tends to precede full-blown diabetes and that also increases the risk of heart disease, stroke, certain cancers, and even dementia—the top killers of the developed world. The syndrome includes a combination of elevated blood sugar and high blood pressure, low “good” cholesterol, and an abdominal cavity filled with fat, often indicated by a “beer belly.” But recently, doctors have begun to question whether chronic inflammation is more than just a symptom of metabolic syndrome: Could it, in fact, be a major cause?
For Dandona, who’s given to waxing grandiloquent about the joys of a beer on the porch in his native Delhi, or the superb ice wines from the Buffalo region, the results presented a quandary. Food was a great pleasure in life. Why would Nature be so cruel, he wondered, and punish us just for eating?
Over the next decade he tested the effects of various foods on the immune system. A fast-food breakfast inflamed, he found, but a high-fiber breakfast with lots of fruit did not. A breakthrough came in 2007 [11] when he discovered that while sugar water, a stand-in for soda, caused inflammation, orange juice—even though it contains plenty of sugar—didn’t.
DIAGRAM: Meet the complex bacterial ecosystems instrumental to a healthy body. [4]

The Florida Department of Citrus, a state agency, was so excited it underwrote a subsequent study, and had fresh-squeezed orange juice flown in for it. This time, along with their two-sandwich, two-hash-brown, 910-calorie breakfast, one-third of his volunteers—10 in total—quaffed a glass of fresh OJ. The non-juice drinkers, half of whom drank sugar water, and the other half plain water, had the expected response—inflammation and elevated blood sugar. But the OJ drinkers had neither elevated blood sugar nor inflammation. The juice seemed to shield their metabolism. “It just switched off the whole damn thing,” Dandona says. Other scientists have since confirmed that OJ has a strong anti-inflammatory effect.
Orange juice is rich in antioxidants like vitamin C, beneficial flavonoids, and small amounts of fiber, all of which may be directly anti-inflammatory. But what caught Dandona’s attention was another substance. Those subjects who ate just the McDonald’s breakfast had increased blood levels of a molecule called endotoxin. This molecule comes from the outer walls of certain bacteria. If endotoxin levels rise, our immune system perceives a threat and responds with inflammation.
If theories about the interplay of food and intestinal microbes pan out, it could help cure obesity and revolutionize the $66 billion weight loss industry.
Where had the endotoxin come from? One possibility was the food itself. But there was another possibility. We all carry a few pounds’ worth of microbes in our gut, a complex ecosystem collectively called the microbiota. The endotoxin, Dandona suspected, originated in this native colony of microbes. Somehow, a greasy meal full of refined carbohydrates ushered it from the gut, where it was always present but didn’t necessarily cause harm, into the bloodstream, where it did. But orange juice stopped that translocation cold.
Dandona’s ongoing experiments—and others like it—could upend much of we thought we knew about the causes of obesity, or just that extra pesky 10 pounds of flab. If what some scientists now suspect about the interplay of food and intestinal microbes pans out, it could revolutionize the $66 billion weight loss industry—and help control the soaring $2.7 trillion we spend on health care yearly. “What matters is not how much you eat,” Dandona says, “but what you eat.” 
EVER SINCE THE DUTCH DRAPER Antonie van Leeuwenhoek first scrutinized his own plaque [12] with a homemade microscope more than three centuries ago and discovered “little living animalcules, very prettily a-moving,” we’ve known that we’re covered in microbes. But as new and cheaper methods for studying these microbes have become available recently, their importance to our health has grown increasingly evident. Scientists now suspect that our microbial communities contribute to a number of diseases, from allergic disorders like asthma and hay fever, to inflammatory conditions like Crohn’s disease, to cancer, heart disease, and obesity.
We are, numerically speaking, 10 percent human, and 90 percent microbe. 
As newborns, we encounter our first microbes as we pass through the birth canal. Until that moment, we are 100 percent human. Thereafter, we are, numerically speaking, 10 percent human, and 90 percent microbe. Our microbiome contains at least 150 times more genes, collectively, than our human genome. Think of it as a hulking instruction manual compared to a single page to-do list.
As we mature, we pick up more microbes from breast milk, food, water, animals, soil, and other people. Sometime in childhood, the bustling community of between 500 and 1,000 species stabilizes. Some species are native only to humans, and may have been passed down within the family like heirlooms. Others are generalists—maybe they’ve hopped aboard from pets, livestock, and other animal sources.


A cluster of Enterobacter cloacae bacteria Eye of Science / Science Source

Most of our microbes inhabit the colon, the final loop of intestine, where they help us break down fibers, harvest calories, and protect us from micro-marauders. But they also do much, much more. Animals raised without microbes essentially lack a functioning immune system. Entire repertoires of white blood cells remain dormant; their intestines don’t develop the proper creases and crypts; their hearts are shrunken; genes in the brain that should be in the “off” position remain stuck “on.” Without their microbes, animals aren’t really “normal.”
What do we do for our microbes in return? Some scientists argue that mammals are really just mobile digestion chambers for bacteria. After all, your stool is roughly half living bacteria by weight. Every day, food goes in one end and microbes come out the other. The human gut is roughly 26 feet in length. Hammered flat, it would have a surface area of a tennis court. Seventy percent of our immune activity occurs there. The gut has its own nervous system; it contains as many neurons as the spinal cord. About 95 percent of the body’s serotonin, a neurotransmitter usually discussed in the context of depression, is produced in the gut.
Children raised in microbially rich environments—with pets, on farms, or attending day care—are at lower risk of allergic diseases.
So the gut isn’t just where we absorb nutrients. It’s also an immune hub and a second brain. And it’s crawling with microbes. They don’t often cross the walls of the intestines into the blood stream, but they nevertheless change how the immune, endocrine, and nervous systems all work on the other side of the intestine wall.
Science isn’t always consistent about what, exactly, goes wrong with our microbes in disease situations. But a recurrent theme is that loss of diversity correlates with the emergence of illness. Children in the developing world have many more types of microbes than kids in Europe or North America, and yet generally develop allergies and asthma at lower rates than those in industrialized nations. In the developed world, children raised in microbially rich environments—with pets, on farms, or attending day care—have a lower risk of allergic disease than kids raised in more sterile environments.
—By Sarah Zhang [13]

Those who study human microbial communities fret that they are undergoing an extinction crisis similar to the one afflicting the biosphere at large—and that modern medicine may be partly to blame. Some studies find that babies born by C-section, deprived of their mother’s vaginal microbes at birth, have a higher risk of celiac disease, Type 1 diabetes, and obesity. Early-life use of antibiotics—which tear through our microbial ecosystems like a forest fire—has also been linked to allergic disease, inflammatory bowel disease, and obesity.
Which brings us to the question more and more scientists are asking: If our microbiota plays a role in keeping us healthy, then how about attacking disease by treating the microbiota? After all, our community of microbes is quite plastic. New members can arrive and take up residence. Old members can get flushed out. Member ratios can shift. The human genome, meanwhile, is comparatively stiff and unresponsive. So the microbiota represents a huge potential leverage point in our quest to treat, and prevent, chronic disease. In particular, the “forgotten organ,” as some call the microbiota, may hold the key to addressing our single greatest health threat: obesity. 
PARESH DANDONA LEFT INDIA in 1966 for a Rhodes Scholarship at Oxford University. He became “the first colored guy,” he says, to head his unit at the University of London hospital. His bearing—heels together, back stiff, and an orator’s care with words delivered in a deep, sonorous voice—recalls a bygone era. He moved to Buffalo in 1991.
During those decades, the number of Americans considered obese nearly tripled. One-third of Americans are now considered overweight, and another third obese. Worldwide, one-fourth of humanity is too heavy, according to the World Health Organization. In 2011, the United Nations announced that for the first time ever, chronic diseases, most of which are linked to obesity, killed more people than infectious diseases. In the United States, obesity accounts for 20 percent of health care costs, according to Cornell University economists.
And the problems aren’t limited to the obese themselves: Children born to obese mothers have hardened arteries at birth, a risk factor for cardiovascular disease. They have a greater risk of asthma. Some studies suggest they’re more likely to suffer from attention deficit disorders and autism.
Why are we increasingly prone to obesity? The long-dominant explanation is simply that too little exercise and too many calories equals too much stored fat. The solution: more exercise and a lot more willpower. But there’s a problem with this theory: In the developed world, most of us consume more calories than we really need, but we don’t gain weight proportionally.
A pound of body fat contains roughly 3,500 calories. If you run a daily surplus of just 500 calories—the amount in a bagel with a generous serving of cream cheese—you should, judging by the strict calorie-in-must-equal-calorie-out model, gain a pound of fat per week. Most of us do run a surplus in that range, or even higher, but we either gain weight much more slowly, or don’t gain weight at all.
Some corpulent people, meanwhile, have metabolisms that work fine. Their insulin and blood sugar levels are within normal range. Their livers are healthy, not marbled with fat. And some thin people have metabolic syndrome, often signaled by a beer gut. They suffer from fatty liver, insulin resistance, elevated blood sugar, high blood pressure, and low-grade, systemic inflammation. From a public health perspective, these symptoms are where the real problem lies—not necessarily how well we fit into our jeans.
Inflammation might not be a symptom of metabolic syndrome: It could be a cause.
Here’s the traditional understanding of metabolic syndrome: You ate too much refined food sopped in grease. Calories flooded your body. Usually, a hormone called insulin would help your cells absorb these calories for use. But the sheer overabundance of energy in this case overwhelms your cells. They stop responding to insulin. To compensate, your pancreas begins cranking out more insulin. When the pancreas finally collapses from exhaustion, you have diabetes. In addition, you develop resistance to another hormone called leptin, which signals satiety, or fullness. So you tend to overeat. Meanwhile, fat cells, which have become bloated and stressed as they try to store the excess calories,begin emitting a danger signal—low-grade inflammation.
But new research suggest another scenario: Inflammation might not be a symptom, it could be a cause. According to this theory, it is the immune activation caused by lousy food that prompts insulin and leptin resistance. Sugar builds up in your blood. Insulin increases. Your liver and pancreas strain to keep up. All because the loudly blaring danger signal—the inflammation—hampers your cells’ ability to respond to hormonal signals. Maybe the most dramatic evidence in support of this idea comes from experiments where scientists quash inflammation in animals. If you simply increase the number of white blood cells that alleviate inflammation—called regulatory T-cells—in obese mice with metabolic syndrome, the whole syndrome fades away. Deal with the inflammation, it seems, and you halt the dysfunction.


Now, on the face of it, it seems odd that a little inflammation should have such a great impact on energy regulation. But consider: This is about apportioning a limited resource exactly where it’s needed, when it’s needed. When not under threat, the body uses energy for housekeeping and maintenance—and, if you’re lucky, procreation, an optimistic, future-oriented activity. But when a threat arrives—a measles virus, say—you reprioritize. All that hormone-regulated activity declines to a bare minimum. Your body institutes a version of World War II rationing: troops (white blood cells) and resources (calories) are redirected toward the threat. Nonessential tasks, including the production of testosterone, shut down. Forget tomorrow. The priority is to preserve the self today.
This, some think, is the evolutionary reason for insulin resistance. Cells in the body stop absorbing sugar because the fuel is required—requisitioned, really—by armies of white blood cells. The problems arise when that emergency response, crucial to repelling pillagers in the short term, drags on indefinitely. Imagine it this way. Your dinner is cooking on the stove. You’re paying bills. You smell smoke. You jump up, leaving those tasks half-done, and search for the fire before it burns down your house. Normally, once you put the fire out, you’d return to your tasks and then eat dinner.
Junk food may not kill us directly, but rather by prompting the collapse of an ancient and mutually beneficial symbiosis.
But now imagine that you never find the fire, and you never stop smelling the smoke. You remain in a perpetual state of alarm. Your bills never get paid. You never eat your dinner. Your house smolders. Your life falls into disarray.
That’s metabolic syndrome. Normal function ceases. Aging accelerates. Diabetes develops. Heart attacks strike. The brain degenerates. Life ends early. And it’s all driven, in this understanding, by chronic, low-grade inflammation.
Where does the perceived threat come from—all that inflammation? Some ingested fats are directly inflammatory. And dumping a huge amount of calories into the bloodstream from any source, be it fat or sugar, may overwhelm and inflame cells. But another source of inflammation is hidden in plain sight, the 100 trillion microbes inhabiting your gut. Junk food, it turns out, may not kill us entirely directly, but rather by prompting the collapse of an ancient and mutually beneficial symbiosis, and turning a once cooperative relationship adversarial.
We’re already familiar with a version of this dynamic [14]: cavities. Tooth decay is as old as teeth, but it intensified with increased consumption of refined carbohydrates, like sugar, just before and during the industrial revolution. Before cheap sugar became widely available, plaque microbes probably occupied the warm and inviting ecological niche of your mouth more peaceably. But dump a load of sugar on them, and certain species expand exponentially. Their by-product—acid—which, in normal amounts, protects you from foreign bacteria—now corrodes your teeth. A once cooperative relationship becomes antagonistic.
Something similar may occur with our gut microbes when they’re exposed to the highly refined, sweet, and greasy junk-food diet. They may turn against us.
A DECADE AGO, microbiologists at Washington University in St. Louis noticed that mice raised without any microbes, in plastic bubbles with positive air pressure, could gorge on food without developing metabolic syndrome [15] or growing obese. But when colonized with their native microbes, these mice quickly became insulin resistant and grew fat, all while eating less food than their germ-free counterparts.
The researchers surmised that the microbes helped the rodents harvest energy from food. The mice, which then had more calories than they needed, stored the surplus as fat. But across the Atlantic, Patrice Cani [16] at the Catholic University of Louvain in Brussels, Belgium, suspected that inflammation contributed, and that the inflammation emanated from native microbes.
To prove the principle, he gave mice a low dose of endotoxin [17], that molecule that resides in the outer walls of certain bacteria. The mice’s livers became insulin resistant; the mice became obese and developed diabetes. A high-fat diet alone produced the same result: Endotoxin leaked into circulation; inflammation took hold; the mice grew fat and diabetic. Then came the bombshell. The mere addition of soluble plant fibers [18] called oligosaccharides, found in things like bananas, garlic, and asparagus, prevented the entire cascade—no endotoxin, no inflammation, and no diabetes.
"If we take care of our gut microbiota, it will take care of our health," says one researcher. "I like to finish my talks with one sentence: ‘In gut we trust.’"
Oligosaccharides are one form of what’s known as a “prebiotic”: fibers that, because they make it all the way to the colon intact, feed, as it were, the bacteria that live there. One reason we’ve evolved to house microbes at all is because they “digest” these fibers by fermenting them, breaking them down and allowing us to utilize their healthful byproducts, like acetic acid, butyric acid, B vitamins, and vitamin K.
Cani had essentially arrived at the same place as Dandona with his freshly squeezed orange juice. Only his controlled animal experiments allowed a clearer understanding of the mechanisms. Junk food caused nasty microbes to bloom, and friendly bugs to decline. Permeability of the gut also increased, meaning that microbial byproducts—like that endotoxin—could more easily leak into circulation, and spur inflammation. Simply adding prebiotics enjoyed by a select group of microbes—in this case, Bifidobacteria—kept the gut tightly sealed, preventing the entire cascade. The fortified bacteria acted like crowd-control police, keeping the rest of the microbial mob from storming the barrier.
"If we take care of our gut microbiota, it will take care of our health," Cani says. "I like to finish my talks with one sentence: ‘In gut we trust.’"
So our sweet and greasy diet—almost certainly without evolutionary precedent—doesn’t just kill us directly: It also changes gut permeability and alters the makeup of our microbial organ. Our “friendly” community of microbes becomes unfriendly, even downright pathogenic, leaking noxious byproducts where they don’t belong. H.G. Wells would be proud of this story—the mighty Homo sapiens felled by microscopic life turned toxic by junk food. It’s nothing personal; the bugs that bloom with an energy-dense diet may act in their own self-interest. They want more of that food sweet, fatty food on which they thrive.
AROUND THE TIME when Paresh Dandona began puzzling over the immune response to a fast-food breakfast, a Chinese microbiologist named Liping Zhao was realizing that he needed to change how he ate, or he might drop dead. He was 44 pounds overweight, his blood pressure was elevated, and his “bad” cholesterol was high.
He caught wind of the studies at Washington University in St. Louis suggesting that microbes were central to obesity. The research jibed with ancient precepts in Chinese medicine that viewed the gut as central to health. So Zhao decided on a hybridized approach—some 21st-century microbiology topped with traditional Chinese medicine.
He changed his diet to whole grains, rich in those prebiotic fibers important for beneficial bacteria. And he began regularly consuming two traditional medicinal foods thought to have such properties: bitter melon and Chinese yam.
Zhao’s blood pressure began normalizing and his “bad” cholesterol declined. Over the course of two years, he lost 44 pounds. He sampled his microbes throughout. As his metabolism normalized, quantities of a bacterium called Faecalibacterium prausnitzii increased in his gut. Was its appearance cause or consequence? Others have observed that this bacterium is absent in people suffering from inflammatory diseases, such as Crohn’s disease, as well as Type 2 diabetes. Scientists at the University of Tokyo have shown that colonizing mice with this bacterium and its relatives—called “Clostridium clusters”—protects them against colitis. But still, evidence of causation was lacking.
Then one day in 2008, a morbidly obese man walked into Zhao’s lab in China [19]. The 26-year-old was diabetic, inflamed, had high bad cholesterol, and elevated blood sugar. No one in his immediate family was heavy, but he weighed 385 pounds.
Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man.
Zhao noticed something odd about the man’s microbes. Thirty-five percent belonged to a single, endotoxin-producing species called Enterobacter cloacae. So he put the man on a version of his own regimen—whole grains supplemented with other prebiotics. As treatment progressed, the Enterobacter cloacae declined, as did circulating endotoxin and markers of inflammation.
After 23 weeks, the man had lost 113 pounds. That bacterial bloom had receded to the point of being undetectable. Counts of anti-inflammatory bacteria—microbes that specialize in fermenting nondigestible fibers—had increased. But could Zhao prove that these microbial changes caused anything? After all, the regimen may have simply contained far fewer calories than the patient’s previous diet.
So Zhao introduced the Enterobacter into mice. They developed endotoxemia, fattened up and became diabetic—but only when eating a high fat diet. Mice colonized with bifidobacteria and fed a high fat diet, meanwhile, remained lean, as did germ-free mice. The enterobacter was evidently unique, an opportunist. Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man.
Zhao, who related his own story to Science [20] last year, has repeated a version of this regimen in at least 90 subjects, achieved similar improvements, and has more than 1,000 patients in ongoing trials. He declined to be interviewed for this article, saying that the response to his research, both by press and individuals seeking advice, had been overwhelming. “I receive too many emails to ask for help but I can not provide much,” he wrote in an email. “I feel very bad about this and would like to concentrate on my research.”
There’s a flood of what you might call “fecoprospectors” seeking to catalog and preserve microbial diversity before it is lost in the extinction wave sweeping the globe.
Other researchers have tried an even more radical approach to treating the microbiome: the fecal transplant. It was originally developed to treat the potentially life-threatening gut infection caused by the bacterium Clostridium difficile. Studies so far suggest that it’s 95 percent effective in ousting C. diff. and has no major side effects. “Fecal engraftment” is now being considered a method for rebooting microbiota generally. Scientists at the Academic Medical Center in Amsterdam mixed stool from lean donors with saline solution and, via a tube that passed through the nose, down the throat and past the stomach, introduced the mixture to the small intestine of nine patients with metabolic syndrome. Control subjects received infusions of their own feces.
Those who received “lean” microbes saw improvements in insulin sensitivity [21], though they didn’t lose weight and saw the improvements disappear within a year. But Max Nieuwdorp, senior author on the study, aims to conduct the procedure repeatedly to see if the “lean” microbes will stick. And when he’s identified which are important, he hopes to create an anti-obesity “probiotic”to be taken orally.
Probiotics are just bacteria thought to be beneficial, like the lactobacilli and other bacteria in some yogurts. In the future probiotics might be bacteria derived from those found in Amazonian Indians, rural Africans, even the Amish—people, in other words, who retain a microbial diversity that the rest of us may have lost. Already, the literature suggests that a gold rush has begun—a flood of what you might call “fecoprospectors” seeking to catalog and preserve the diversity and richness of the ancestral microbiota before it is lost in the extinction wave sweeping the globe.
Ultimately, the strongest evidence to support microbial involvement in obesity may come from a procedure that, on the face of it, has nothing to do with microbes: gastric bypass surgery. The surgery, which involves creating a detour around the stomach, is the most effective intervention for morbid obesity—far more effective than dieting.


Originally, scientists thought it worked by limiting food consumption. But it’s increasingly obvious that’s not how the procedure works. The surgery somehow changes expression of thousands of genes in organs throughout the body, resetting the entire metabolism. In March, Lee Kaplan [22], director of the Massachusetts General Hospital Weight Center in Boston, published a study in Science Translational Medicine showing a substantial microbial contribution to that resetting [23].
He began with three sets obese mice, all on a high-fat diet. The first set received a sham operation—an incision in the intestine that didn’t really change much, but was meant to control for the possibility that trauma alone could cause weight loss. These mice then resumed their high fat diet. A second set also received a sham operation, but was put on a calorically restricted diet. The third group received gastric bypass surgery, but was then allowed to eat as it pleased.
As expected, both the bypass mice and dieted mice lost weight.But only the bypass mice showed normalization of insulin and glucose levels. Without that normalization, says Kaplan, mice and people alike inevitably regain lost weight.
"I won’t argue that all the effects of the gastric bypass can be transferred by the microbiota. What we’ve found is the first evidence that any can."
To test the microbial contribution to these outcomes, Kaplan transplanted the microbiota from each set to germ-free mice. Only rodents colonized with microbes from the bypass mice lost weight, while actually eating more than mice colonized with microbes from the other groups.
In humans, some studies show a rebound of anti-inflammatory bacteria after gastric-bypass surgery. Dandona has also noted a decline in circulating endotoxin after the procedure. “I would never argue, and won’t argue, that all the effects of the gastric bypass can be transferred by the microbiota,” says Kaplan. “What we’ve found is the first evidence that any can. And these ‘any’ are pretty impressive.” If we understand the mechanism by which the microbiota shifts, he says, perhaps we can induce the changes without surgery. 
NOW, NOT EVERYONE ACCEPTS that inflammation drives metabolic syndrome and obesity. And even among the idea’s proponents, no one claims that all inflammation emanates from the microbiota. Moreover, if you accept that inflammation contributes to obesity, then you’re obligated to consider all the many ways to become inflamed. The odd thing is, many of them are already implicated in obesity.
Particulate pollution from tailpipes and factories, linked to asthma, heart disease, and obesity, is known to be a cause of inflammation. So is chronic stress. And risk factors may interact with each other: In macaque troops, the high-ranking females, which experience less stress, can eat more junk food without developing metabolic syndrome than the more stressed, lower-ranking females. Epidemiologists have made similar observations in humans. Poorer people suffer the consequences of lousy dietary habits more than do those who are wealthier. The scientists who study this phenomenon call it “status syndrome.”
Exercise, meanwhile, is anti-inflammatory, which may explain why a brisk walk can immediately improve insulin sensitivity. Exercise may also fortify healthy brown fat, which burns off calories rather than storing them, like white fat does. This relationship may explain how physical activity really helps us lose weight. Yes, exercise burns calories, but the amount is often trivial. Just compensating for that bagel you ate for breakfast—roughly 290 calories—requires a 20-minute jog. And that’s not counting any cream cheese. Sleep deprivation may have the opposite effect, favoring white fat over brown, and altering the metabolism.
Brain inflammation precedes weight gain, suggesting that the injury might cause, or at least contribute to, obesity.
Then there’s the brain. Michael Schwartz [24], director of the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle, has found that the appetite regulation center of the brain—the hypothalamus—is often inflamed and damaged in obese people [25]. He can reproduce this damage by feeding mice a high-fat diet; chronic consumption of junk food, it seems, injures this region of the brain. Crucially, the brain inflammation precedes weight gain, suggesting that the injury might cause, or at least contribute to, obesity. In other words, by melting down our appetite control centers, junk food may accelerate its own consumption, sending us into a kind of vicious cycle where we consume more of the poison wreaking havoc on our physiology.
Of course there’s a genetic contribution to obesity. But even here, inflammation rears its head. Some studies suggest that gene variants that increase aspects of immune firepower are over-represented among obese individuals. In past environments, these genes probably helped us fight off infections. In the context of today’s diet, however, they may increase the risk of metabolic syndrome.
Whether inflammation drives obesity or just contributes, how much of it emanates from our microbiota, or even whether it causes weight gain, or results from it—these are still somewhat open questions. But it is clear that chronic, low-grade inflammation, wherever it comes from, is unhealthy. And as Dandona discovered all those years ago, food can be either pro- or anti-inflammatory. Which brings us back to the question: What should we eat? 
FIFTY YEARS AGO, due to the perceived link with heart disease, nutritionists cautioned against consuming animal fats and recommended hydrogenated vegetable oils, such as margarine, instead. Alas, it turned out that these fats may encourage the formation of arterial plaques, while some fats that were discarded—in fish and olive oil, for example—seem to prevent cardiovascular disease and obesity.
As people unwittingly cut out healthy fats, they compensated by consuming more sugar and other refined carbohydrates. But a high-sugar diet can produce endotoxemia, fatty liver, and metabolic syndrome in animals. So that’s yet another reason to avoid refined, sugary foods.
What about popular weight loss regimes, like the Atkins diet, that emphasize protein? In a 2011 study [26] by scientists at the University of Aberdeen, in Scotland, 17 obese men were given a high-protein, low-carb diet. It prompted a decline of anti-inflammatory microbes, whose fermentation byproducts are critical to colonic health, and produced a microbial profile associated with colon cancer. So although it may prompt rapid weight loss, a high-protein, low-carb diet may predispose people to colon cancer. In the rodent version of this experiment, the addition of a prebiotic starch blunted the carcinogenic effect. Again, it’s not only what’s present in your diet that matters, but also what’s absent.
So, should we sprinkle a packet of fiber on our cheeseburger? Dandona has looked at this possibility and says that though this study has not yet been published, he’s found that packeted fiber does, when eaten with a fast-food meal, soften the food’s inflammatory effects. Fast-food companies could, in theory, pack their buns full of prebiotics, shielding their customers somewhat from metabolic syndrome.
But that’s not really what Dandona or anyone else is advocating. The pill approach—the idea that we can capture a cure in a gel cap—may be part of what got us in trouble to begin with. Natural variety and complexity have their own value, both for our own bodies and for our microbes. This may explain why orange juice, which contains plenty of sugur, doesn’t have inflammatory effects while a calorically equivalent quantity of sugar water does. Flavonoids, other phytochemicals, vitamins, the small amount of fiber it carries, and other things we have yet to quantify may all be protective.
Fast-food companies could, in theory, pack their buns full of prebiotics, shielding their customers somewhat from metabolic syndrome.
To that end, consider a study by Jens Walter [27] (PDF), a scientist at the University of Nebraska-Lincoln. He supplemented the diet of 28 volunteers with either brown rice, barley, or both. Otherwise, they continued eating their usual fare. After four weeks, those who consumed both grains saw increased counts of anti-inflammatory bacteria, improved insulin sensitivity, and reduced inflammation—more so than subjects who just had one grain. Walter doesn’t think it’s an accident that those who ate both barley and brown rice saw the greatest improvement. The combination likely presented microbes with the largest array of fermentable fibers.
Scientists are also intensely interested in concocting “synbiotics,” a mixture of probiotic bacteria and the prebiotic fibers that feed them. This type of combination may already exist in staple dishes and garnishes, from sauerkraut to kefir, in traditional cuisines the world over.  In theory, such unpasteurized, fermented foods that retain their microbial communities are a health-producing triple whammy, containing prebiotic fibers, probiotic bacteria, and healthful fermentation byproducts like vitimins B and K. A smattering of recent studies suggest that embracing such grub could protect against metabolic syndrome. In one monthlong trial on 22 overweight South Koreans [28], unpasteurized fermented kimchi, which is made from cabbage, improved markers of inflammation and caused very minor decreases in body fat. Fresh, unfermented kimchi also helped, but not as much. In another double-blind, placebo-controlled study on 30 South Koreans [29], a pill of fermented soybean paste eaten daily for 12 weeks decreased that deadly visceral fat by 5 percent. Triglycerides, a risk factor for heart attacks, also declined. An epidemiological study, meanwhile, found that consumption of rice and kimchi cut the odds of metabolic syndrome. It all hints at a future where sauerkraut, kimchi, sour pickles, and other fermented foods that contain live microbial cultures do double duty as anti-obesity medicine.
So what else to eat? Onions and garlic are especially rich in the prebiotic fiber inulin, which selectively feeds good bacteria within. Potatoes, bananas, and yams carry loads of digestion-resistant starches. Apples and oranges carry a healthy serving of polysaccharides (another form of prebiotic). Nuts and whole grains do as well. Don’t forget your cruciferous vegetables (cabbage, broccoli, and cauliflower) and legumes. There’s no magic vegetable. Yes, some plant products are extra rich in prebiotics—the Jerusalem artichoke, for example—but really, these fibers abound in plants generally, and for a simple reason: Plants store energy in them. That’s why they’re resistant to degradation. They’re designed to last. (For more on what foods to eat, see “Should I Take A Probiotic? [30]”)
The very qualities that improve palatability and lengthen shelf life—high sugar content, fats that resist turning rancid, and a lack of organic complexity—make refined foods toxic to your key microbes. Biologically simple, processed foods may cultivate a toxic microbial community, not unlike the algal blooms that result in oceanic “dead zones.”
In fact, scientists really do observe a dead zone of sorts when they peer into the obese microbiota. Microbes naturally form communities. In obese people, not only are anti-inflammatory microbes relatively scarce, diversity in general is depleted, and community structure degraded. Microbes that, in ecological parlance, we might call weedy species—the rats and cockroaches of your inner world—scurry around unimpeded. What’s the lesson? Junk food may produce a kind of microbial anarchy. Opportunists flourish as the greater structure collapses. Cooperative members get pushed aside. And you, who both contain and depend on the entire ecosystem, pay the price.







Source URL: http://www.motherjones.com/environment/2013/04/gut-microbiome-bacteria-weight-loss

Links:[1] http://medicine.buffalo.edu/faculty/profile.html?ubit=dandona[2] http://ajcn.nutrition.org/content/79/4/682.long[3] http://www.motherjones.com/environment/2013/04/gut-microbiome-bacteria-weight-loss[4] http://www.motherjones.com/environment/2013/04/bacteria-in-human-body[5] http://www.motherjones.com/environment/2013/04/should-you-take-probiotics-supplement[6] http://www.motherjones.com/environment/2012/10/what-is-fecal-transplant-difficile-bacteria[7] http://www.motherjones.com/environment/2013/12/can-antibiotics-make-you-fat[8] http://www.motherjones.com/environment/2013/02/can-antibiotics-cure-hunger[9] http://www.motherjones.com/environment/2013/04/sinus-infections-antibiotics-resistance[10] http://www.nhlbi.nih.gov/health/health-topics/topics/ms/[11] http://ajcn.nutrition.org/content/91/4/940.full[12] http://www.ucmp.berkeley.edu/history/leeuwenhoek.html[13] http://www.motherjones.com/authors/sarah-zhang[14] http://www.nature.com/ng/journal/v45/n4/full/ng.2536.html[15] http://www.pnas.org/content/101/44/15718[16] http://www.uclouvain.be/patrice.cani&langue=fr[17] http://diabetes.diabetesjournals.org/content/56/7/1761[18] http://dx.doi.org/10.1007/s00125-007-0791-0[19] http://www.nature.com/ismej/journal/v7/n4/abs/ismej2012153a.html[20] http://www.sciencemag.org/content/336/6086/1248[21] http://dx.doi.org/10.1053/j.gastro.2012.06.031[22] http://www.massgeneral.org/doctors/doctor.aspx?id=16686[23] http://stm.sciencemag.org/content/5/178/178ra41[24] http://www.diabetes-obesity-center.org/?q=faculty/schwartz-md[25] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248304/[26] http://ajcn.nutrition.org/content/93/5/1062.long[27] http://www.glnc.org.au/wp-content/uploads/2011/12/Martinez-ISME-2012-Gut-microbiome-composition-is-linked-to-WG-induced-immunological-improvements.pdf[28] http://www.sciencedirect.com/science/article/pii/S027153171100114X[29] http://www.nutritionandmetabolism.com/content/pdf/1743-7075-10-24.pdf[30] http://www.motherjones.com/environment/2013/04/probiotics-supplements-fermentation-lactobacillus-marketing

Mother Jones

Are Happy Gut Bacteria Key to Weight Loss?

Imbalances in the microbial community in your intestines may lead to metabolic syndrome, obesity, and diabetes. What does science say about how to reset our bodies?


Posted on Thursday, July 4th 2013

Tags fitness fat loss

 Source Mother Jones

Study: Foam Roller Lessens Soreness After Hard Workout | Runner's World & Running Times

Published
June 25, 2013
2012_FoamRoller_Glutes

Last year we reported on a study that showed that using a foam roller before a workout increased range of motion without decreasing power, suggesting that foam rolling could substitute for pre-run static stretching. Now there’s evidence a post-workout roll might also be a good idea.

In a study that will be published in Medicine & Science in Sports & Exercise, 20 men did a workout of ten sets of 10 squats, with each squat at 60% of their one-rep max. Afterward, half of them did 20 minutes of foam rolling on their legs, and the other half followed their usual post-workout routine.

Researchers measured things like muscle soreness, range of motion, and vertical leap 24, 48, and 72 hours after the hard workout.

By all measures, the foam-roller group fared better in the days after their hard workout. They not only had less soreness at all times, but their soreness peaked 24 hours after the workout, while muscle soreness peaked 48 hours after the workout in those who didn’t foam roll. The foam-roller group also performed better in tests of vertical leap, range of motion, and muscle contraction.

All of these findings suggest that the post-workout foam rolling helped to speed recovery. In theory, this should allow a higher level of training.

Posted on Wednesday, June 26th 2013

Tags fitness

Changing gut bacteria through diet affects brain function, UCLA study shows

By Rachel Champeau May 28, 2013

Dr. Kirsten Tillisch

UCLA researchers now have the first evidence that bacteria ingested in food can affect brain function in humans. In an early proof-of-concept study of healthy women, they found that women who regularly consumed beneficial bacteria known as probiotics through yogurt showed altered brain function, both while in a resting state and in response to an emotion-recognition task.
 
The study, conducted by scientists with the Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, part of the UCLA Division of Digestive Diseases, and the Ahmanson–Lovelace Brain Mapping Center at UCLA, appears in the current online edition of the peer-reviewed journal Gastroenterology.
 
The discovery that changing the bacterial environment, or microbiota, in the gut can affect the brain carries significant implications for future research that could point the way toward dietary or drug interventions to improve brain function, the researchers said.
 
"Many of us have a container of yogurt in our refrigerator that we may eat for enjoyment, for calcium or because we think it might help our health in other ways," said Dr. Kirsten Tillisch, an associate professor of medicine in the digestive diseases division at UCLA’s David Geffen School of Medicine and lead author of the study. "Our findings indicate that some of the contents of yogurt may actually change the way our brain responds to the environment. When we consider the implications of this work, the old sayings ‘you are what you eat’ and ‘gut feelings’ take on new meaning."
 
Researchers have known that the brain sends signals to the gut, which is why stress and other emotions can contribute to gastrointestinal symptoms. This study shows what has been suspected but until now had been proved only in animal studies: that signals travel the opposite way as well.
 
"Time and time again, we hear from patients that they never felt depressed or anxious until they started experiencing problems with their gut," Tillisch said. "Our study shows that the gut–brain connection is a two-way street."
 
The small study involved 36 women between the ages of 18 and 55. Researchers divided the women into three groups: one group ate a specific yogurt containing a mix of several probiotics — bacteria thought to have a positive effect on the intestines — twice a day for four weeks; another group consumed a dairy product that looked and tasted like the yogurt but contained no probiotics; and a third group ate no product at all.
 
Functional magnetic resonance imaging (fMRI) scans conducted both before and after the four-week study period looked at the women’s brains in a state of rest and in response to an emotion-recognition task in which they viewed a series of pictures of people with angry or frightened faces and matched them to other faces showing the same emotions. This task, designed to measure the engagement of affective and cognitive brain regions in response to a visual stimulus, was chosen because previous research in animals had linked changes in gut flora to changes in affective behaviors.
 
The researchers found that, compared with the women who didn’t consume the probiotic yogurt, those who did showed a decrease in activity in both the insula — which processes and integrates internal body sensations, like those from the gut — and the somatosensory cortex during the emotional reactivity task. 
 
Further, in response to the task, these women had a decrease in the engagement of a widespread network in the brain that includes emotion-, cognition- and sensory-related areas. The women in the other two groups showed a stable or increased activity in this network.
 
During the resting brain scan, the women consuming probiotics showed greater connectivity between a key brainstem region known as the periaqueductal grey and cognition-associated areas of the prefrontal cortex. The women who ate no product at all, on the other hand, showed greater connectivity of the periaqueductal grey to emotion- and sensation-related regions, while the group consuming the non-probiotic dairy product showed results in between. 
 
The researchers were surprised to find that the brain effects could be seen in many areas, including those involved in sensory processing and not merely those associated with emotion, Tillisch said.
 
The knowledge that signals are sent from the intestine to the brain and that they can be modulated by a dietary change is likely to lead to an expansion of research aimed at finding new strategies to prevent or treat digestive, mental and neurological disorders, said Dr. Emeran Mayer, a professor of medicine (digestive diseases), physiology and psychiatry at the David Geffen School of Medicine at UCLA and the study’s senior author.
 
"There are studies showing that what we eat can alter the composition and products of the gut flora — in particular, that people with high-vegetable, fiber-based diets have a different composition of their microbiota, or gut environment, than people who eat the more typical Western diet that is high in fat and carbohydrates," Mayer said. "Now we know that this has an effect not only on the metabolism but also affects brain function."
 
The UCLA researchers are seeking to pinpoint particular chemicals produced by gut bacteria that may be triggering the signals to the brain. They also plan to study whether people with gastrointestinal symptoms such as bloating, abdominal pain and altered bowel movements have improvements in their digestive symptoms which correlate with changes in brain response.
 
Meanwhile, Mayer notes that other researchers are studying the potential benefits of certain probiotics in yogurts on mood symptoms such as anxiety. He said that other nutritional strategies may also be found to be beneficial.
 
By demonstrating the brain effects of probiotics, the study also raises the question of whether repeated courses of antibiotics can affect the brain, as some have speculated. Antibiotics are used extensively in neonatal intensive care units and in childhood respiratory tract infections, and such suppression of the normal microbiota may have long-term consequences on brain development.
 
Finally, as the complexity of the gut flora and its effect on the brain is better understood, researchers may find ways to manipulate the intestinal contents to treat chronic pain conditions or other brain related diseases, including, potentially, Parkinson’s disease, Alzheimer’s disease and autism.
 
Answers will be easier to come by in the near future as the declining cost of profiling a person’s microbiota renders such tests more routine, Mayer said.
 
The study was funded by Danone Research. Mayer has served on the company’s scientific advisory board. Three of the study authors (Denis Guyonnet, Sophie Legrain-Raspaud and Beatrice Trotin) are employed by Danone Research and were involved in the planning and execution of the study (providing the products) but had no role in the analysis or interpretation of the results.
 
UCLA’s Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, part of the UCLA Division of Digestive Diseases, is an NIH-funded multidisciplinary, translational research program partially supported by philanthropy. Its mission is to identify the role of the brain in health and medical disease.  The Center is comprised of several research programs which focus on the interactions of the brain with the digestive, cardiovascular and urological systems, chronic pain and mind brain body interactions.
 
For more news, visit the UCLA Newsroom and follow us on Twitter.

© 2013 UC Regents

Changing gut bacteria through diet affects brain function, UCLA study shows

Kirsten Tillisch
Dr. Kirsten Tillisch
UCLA researchers now have the first evidence that bacteria ingested in food can affect brain function in humans. In an early proof-of-concept study of healthy women, they found that women who regularly consumed beneficial bacteria known as probiotics through yogurt showed altered brain function, both while in a resting state and in response to an emotion-recognition task.
 
The study, conducted by scientists with the Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, part of the UCLA Division of Digestive Diseases, and the Ahmanson–Lovelace Brain Mapping Center at UCLA, appears in the current online edition of the peer-reviewed journal Gastroenterology.
 
The discovery that changing the bacterial environment, or microbiota, in the gut can affect the brain carries significant implications for future research that could point the way toward dietary or drug interventions to improve brain function, the researchers said.
 
"Many of us have a container of yogurt in our refrigerator that we may eat for enjoyment, for calcium or because we think it might help our health in other ways," said Dr. Kirsten Tillisch, an associate professor of medicine in the digestive diseases division at UCLA’s David Geffen School of Medicine and lead author of the study. "Our findings indicate that some of the contents of yogurt may actually change the way our brain responds to the environment. When we consider the implications of this work, the old sayings ‘you are what you eat’ and ‘gut feelings’ take on new meaning."
 
Researchers have known that the brain sends signals to the gut, which is why stress and other emotions can contribute to gastrointestinal symptoms. This study shows what has been suspected but until now had been proved only in animal studies: that signals travel the opposite way as well.
 
"Time and time again, we hear from patients that they never felt depressed or anxious until they started experiencing problems with their gut," Tillisch said. "Our study shows that the gut–brain connection is a two-way street."
 
The small study involved 36 women between the ages of 18 and 55. Researchers divided the women into three groups: one group ate a specific yogurt containing a mix of several probiotics — bacteria thought to have a positive effect on the intestines — twice a day for four weeks; another group consumed a dairy product that looked and tasted like the yogurt but contained no probiotics; and a third group ate no product at all.
 
Functional magnetic resonance imaging (fMRI) scans conducted both before and after the four-week study period looked at the women’s brains in a state of rest and in response to an emotion-recognition task in which they viewed a series of pictures of people with angry or frightened faces and matched them to other faces showing the same emotions. This task, designed to measure the engagement of affective and cognitive brain regions in response to a visual stimulus, was chosen because previous research in animals had linked changes in gut flora to changes in affective behaviors.
 
The researchers found that, compared with the women who didn’t consume the probiotic yogurt, those who did showed a decrease in activity in both the insula — which processes and integrates internal body sensations, like those from the gut — and the somatosensory cortex during the emotional reactivity task. 
 
Further, in response to the task, these women had a decrease in the engagement of a widespread network in the brain that includes emotion-, cognition- and sensory-related areas. The women in the other two groups showed a stable or increased activity in this network.
 
During the resting brain scan, the women consuming probiotics showed greater connectivity between a key brainstem region known as the periaqueductal grey and cognition-associated areas of the prefrontal cortex. The women who ate no product at all, on the other hand, showed greater connectivity of the periaqueductal grey to emotion- and sensation-related regions, while the group consuming the non-probiotic dairy product showed results in between. 
 
The researchers were surprised to find that the brain effects could be seen in many areas, including those involved in sensory processing and not merely those associated with emotion, Tillisch said.
 
The knowledge that signals are sent from the intestine to the brain and that they can be modulated by a dietary change is likely to lead to an expansion of research aimed at finding new strategies to prevent or treat digestive, mental and neurological disorders, said Dr. Emeran Mayer, a professor of medicine (digestive diseases), physiology and psychiatry at the David Geffen School of Medicine at UCLA and the study’s senior author.
 
"There are studies showing that what we eat can alter the composition and products of the gut flora — in particular, that people with high-vegetable, fiber-based diets have a different composition of their microbiota, or gut environment, than people who eat the more typical Western diet that is high in fat and carbohydrates," Mayer said. "Now we know that this has an effect not only on the metabolism but also affects brain function."
 
The UCLA researchers are seeking to pinpoint particular chemicals produced by gut bacteria that may be triggering the signals to the brain. They also plan to study whether people with gastrointestinal symptoms such as bloating, abdominal pain and altered bowel movements have improvements in their digestive symptoms which correlate with changes in brain response.
 
Meanwhile, Mayer notes that other researchers are studying the potential benefits of certain probiotics in yogurts on mood symptoms such as anxiety. He said that other nutritional strategies may also be found to be beneficial.
 
By demonstrating the brain effects of probiotics, the study also raises the question of whether repeated courses of antibiotics can affect the brain, as some have speculated. Antibiotics are used extensively in neonatal intensive care units and in childhood respiratory tract infections, and such suppression of the normal microbiota may have long-term consequences on brain development.
 
Finally, as the complexity of the gut flora and its effect on the brain is better understood, researchers may find ways to manipulate the intestinal contents to treat chronic pain conditions or other brain related diseases, including, potentially, Parkinson’s disease, Alzheimer’s disease and autism.
 
Answers will be easier to come by in the near future as the declining cost of profiling a person’s microbiota renders such tests more routine, Mayer said.
 
The study was funded by Danone Research. Mayer has served on the company’s scientific advisory board. Three of the study authors (Denis Guyonnet, Sophie Legrain-Raspaud and Beatrice Trotin) are employed by Danone Research and were involved in the planning and execution of the study (providing the products) but had no role in the analysis or interpretation of the results.
 
UCLA’s Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, part of the UCLA Division of Digestive Diseases, is an NIH-funded multidisciplinary, translational research program partially supported by philanthropy. Its mission is to identify the role of the brain in health and medical disease.  The Center is comprised of several research programs which focus on the interactions of the brain with the digestive, cardiovascular and urological systems, chronic pain and mind brain body interactions.
 
For more news, visit the UCLA Newsroom and follow us on Twitter.

© 2013 UC Regents

Posted on Monday, June 24th 2013

Tags fitness nutrition

The many ways a common spice can save lives
The many healing properties of curcumin are some of the most exciting discoveries in the field of functional medicine. Curcumin counters inflammation, detoxifies excess estrogen, supports the body’s antioxidant system, helps deal with abnormal blood fat ratios (dyslipidemia) and offers protection against colds and flu. What’s more, I came across one study published in 2010 reporting the successful use of curcumin in West Bengal, India, to deal with DNA damage associated with arsenic toxicity that is common in that region. In fact, I would go so far as to say that if you can afford five supplements only, one of them should be curcumin.Although it has many powerful healing properties, you should understand that curcumin is not a prescription drug, nor is it considered an over-the-counter medication. Far from it. It’s simply a nutrient found in the herb turmeric; it’s used as a spice in cooking and is commonly found in mustard and cheese. It has been used for over 4,000 years to treat many medical conditions; in Chinese medicine specifically, curcumin has been used to treat wounds, skin diseases and digestive disorders.Particularly interesting is that curcumin has been extensively researched in the area of preventing and treating many types of cancers, although the news has yet to appear much in mainstream media.In a paper published in the August 2008 issue of the medical journal Cancer Letters, the authors found that curcumin could target cancers affecting such areas as the the lungs, colon, breasts, stomach, ovaries, genitals and colon. Because cancer is often associated with old age, the authors concluded that one of the best ways to fight an “old-age disease such as cancer” was with an “‘age-old’ treatment” in the form of curcumin.Especially exciting are the effects of curcumin on breast cancer, as it targets cancer cells without affecting healthy breast tissue. One study on breast cancer patients published in the January 2010 issue of Cancer Biology and Therapy recommended dosages as high as 6,000 mg/day for seven consecutive days and concluded that the maximal tolerated dose could be as high as 8,000 mg/day. As a comparison, a typical dosage recommendation for healthy individuals would be about 900 mg/day.For men in the US and Western Europe, the second leading cause of cancer death is prostate cancer. When a cancer spreads to other parts of the body (metastasizes), the results are often lethal. A study on prostate cancer published in 2012 in the journal Carcinogenesis found that curcumin may disrupt the chronic inflammation that is associated with the “development and metastatic progression of prostate cancer.”The Inflammation ResponseChronic inflammation is associated with many other life threatening diseases besides cancer – and the word is getting out. A 2012 cover story in Time magazine was about inflammation, which the magazine named “The Secret Killer.” The cover line described the article content as “the surprising link between inflammation and heart attacks, cancer, Alzheimer’s and other diseases.”The takeaway points of the Time magazine article were about lifestyle behaviors and promising drugs available that can be used to fight inflammation, but we can’t ignore the fact that drugs, no matter how “promising,” often have serious side effects.An estimated 30 million Americans take drugs to deal with inflammation. Specifically, the types of drugs I’m referring to are called nonsteroidal anti-inflammatory drugs, or NSAIDs.There are three general types of NSAIDs. These are salicylates such as aspirin, traditional NSAIDs (common brand names include Advil and Aleve), and Cox-2 inhibitors, which have the most serious side effects and as such require a prescription. How serious are these side effects?According to the Food and Drug Administration (FDA), more than 2,700 deaths in the US were attributed to the use of NSAIDs during the first three months of 2008! Among the common side effects of NSAIDs are stomach and liver problems, blood disorders and problems with vision and hearing. One Cox-2 inhibitor, Bextra, was voluntarily withdrawn from the market in 2005 at the request of the FDA due to its possible link to serious cardiovascular complications.Although NSAIDs have their place in medicine, the fact is that NSAIDs interfere with the healing process. One study published in the Archives of Internal Medicine found that NSAIDs wiped out entire acute phase healing in 0-4 days. Further, important nutrients such as co-enzyme Q10 (which, by the way, is one of my top five supplements) may not function properly when used with NSAIDs.Here’s where curcumin is so useful. With its powerful ability to fight inflammation, curcumin can often be an effective substitute for NSAIDs because it doesn’t have the side effects associated with these drugs. It is even available now in topical form, so it can be applied directly to an inflamed area.Now, the most exciting news about curcumin are about how it affects brain health. Strong evidence now shows that curcumin can reverse hep brain plaque, which is essentially one of the main causative factors associated with Alzheimer’s and senile dementia.Regarding dosages, very broad recommendations can be found. However, most practitioners will agree that 4 to 6 capsules a day of 350 mg, in divided dosages, will provide the fastest results. For example, for elevated oxidized LDL levels, a drop of 30 percent in 8 weeks can be seen in patients using 1,800  to 2,400 daily of a standardized extract.In the bestselling novel . by Frank Herbert, the most important product in the galactic empire was a “spice” that offered the promise of extending life. While no one is suggesting that the spice curcumin can do that, it is a nutrient that has untapped potential for keeping us healthy. Sometimes, and this certainly appears to be the case with curcumin, science fiction becomes science fact.
 

The many ways a common spice can save lives


The many healing properties of curcumin are some of the most exciting discoveries in the field of functional medicine. Curcumin counters inflammation, detoxifies excess estrogen, supports the body’s antioxidant system, helps deal with abnormal blood fat ratios (dyslipidemia) and offers protection against colds and flu. What’s more, I came across one study published in 2010 reporting the successful use of curcumin in West Bengal, India, to deal with DNA damage associated with arsenic toxicity that is common in that region. In fact, I would go so far as to say that if you can afford five supplements only, one of them should be curcumin.

Although it has many powerful healing properties, you should understand that curcumin is not a prescription drug, nor is it considered an over-the-counter medication. Far from it. It’s simply a nutrient found in the herb turmeric; it’s used as a spice in cooking and is commonly found in mustard and cheese. It has been used for over 4,000 years to treat many medical conditions; in Chinese medicine specifically, curcumin has been used to treat wounds, skin diseases and digestive disorders.

Particularly interesting is that curcumin has been extensively researched in the area of preventing and treating many types of cancers, although the news has yet to appear much in mainstream media.

In a paper published in the August 2008 issue of the medical journal Cancer Letters, the authors found that curcumin could target cancers affecting such areas as the the lungs, colon, breasts, stomach, ovaries, genitals and colon. Because cancer is often associated with old age, the authors concluded that one of the best ways to fight an “old-age disease such as cancer” was with an “‘age-old’ treatment” in the form of curcumin.

Especially exciting are the effects of curcumin on breast cancer, as it targets cancer cells without affecting healthy breast tissue. One study on breast cancer patients published in the January 2010 issue of Cancer Biology and Therapy recommended dosages as high as 6,000 mg/day for seven consecutive days and concluded that the maximal tolerated dose could be as high as 8,000 mg/day. As a comparison, a typical dosage recommendation for healthy individuals would be about 900 mg/day.

For men in the US and Western Europe, the second leading cause of cancer death is prostate cancer. When a cancer spreads to other parts of the body (metastasizes), the results are often lethal. A study on prostate cancer published in 2012 in the journal Carcinogenesis found that curcumin may disrupt the chronic inflammation that is associated with the “development and metastatic progression of prostate cancer.”

The Inflammation Response
Chronic inflammation is associated with many other life threatening diseases besides cancer – and the word is getting out. A 2012 cover story in Time magazine was about inflammation, which the magazine named “The Secret Killer.” The cover line described the article content as “the surprising link between inflammation and heart attacks, cancer, Alzheimer’s and other diseases.”

The takeaway points of the Time magazine article were about lifestyle behaviors and promising drugs available that can be used to fight inflammation, but we can’t ignore the fact that drugs, no matter how “promising,” often have serious side effects.

An estimated 30 million Americans take drugs to deal with inflammation. Specifically, the types of drugs I’m referring to are called nonsteroidal anti-inflammatory drugs, or NSAIDs.

There are three general types of NSAIDs. These are salicylates such as aspirin, traditional NSAIDs (common brand names include Advil and Aleve), and Cox-2 inhibitors, which have the most serious side effects and as such require a prescription. How serious are these side effects?

According to the Food and Drug Administration (FDA), more than 2,700 deaths in the US were attributed to the use of NSAIDs during the first three months of 2008! Among the common side effects of NSAIDs are stomach and liver problems, blood disorders and problems with vision and hearing. One Cox-2 inhibitor, Bextra, was voluntarily withdrawn from the market in 2005 at the request of the FDA due to its possible link to serious cardiovascular complications.

Although NSAIDs have their place in medicine, the fact is that NSAIDs interfere with the healing process. One study published in the Archives of Internal Medicine found that NSAIDs wiped out entire acute phase healing in 0-4 days. Further, important nutrients such as co-enzyme Q10 (which, by the way, is one of my top five supplements) may not function properly when used with NSAIDs.

Here’s where curcumin is so useful. With its powerful ability to fight inflammation, curcumin can often be an effective substitute for NSAIDs because it doesn’t have the side effects associated with these drugs. It is even available now in topical form, so it can be applied directly to an inflamed area.

Now, the most exciting news about curcumin are about how it affects brain health. Strong evidence now shows that curcumin can reverse hep brain plaque, which is essentially one of the main causative factors associated with Alzheimer’s and senile dementia.

Regarding dosages, very broad recommendations can be found. However, most practitioners will agree that 4 to 6 capsules a day of 350 mg, in divided dosages, will provide the fastest results. For example, for elevated oxidized LDL levels, a drop of 30 percent in 8 weeks can be seen in patients using 1,800  to 2,400 daily of a standardized extract.

In the bestselling novel . by Frank Herbert, the most important product in the galactic empire was a “spice” that offered the promise of extending life. While no one is suggesting that the spice curcumin can do that, it is a nutrient that has untapped potential for keeping us healthy. Sometimes, and this certainly appears to be the case with curcumin, science fiction becomes science fact.
 

Posted on Saturday, June 15th 2013

Tags fitness

An interesting interview with an evolutionary biologist on running

Exercise confers huge health benefits, so why does it often feel like such a chore? Evolutionary biologist Daniel Lieberman explains the paradox

Why did you start to study the evolution of running and exercise?

I got interested in how we hold our heads still when we run. It began when my colleagues and I were doing some experiments with pigs as models. It is very uncomfortable to watch a pig run: its head bobs all over the place. But animals that are good at running, like us, are extremely good at keeping the head still, because it is important for gaze stabilisation. We started thinking about humans and chimps, and came up with hypotheses about how we evolved head stabilisation to run.

Why do you think head stabilisation evolved for running, and not another form of movement?

If you watch someone with a ponytail running, the ponytail bobs up and down. That’s because of the pitching forces acting on the head. The head itself stays very stable. There are special mechanisms – the semicircular canals in human heads are greatly enlarged relative to apes, for instance – that give us a much greater ability to perceive and react to rapid accelerations of the head.
Walking does not create such accelerations. And I don’t think our ancestors were jumping on trampolines or hitting each other on the head so much. The only explanation we can come up with is running.


Being able to run is one thing – how did we then go on to become endurance athletes?

We evolved from very non-active creatures. A typical chimp will walk 2 to 3 kilometres a day, run about 100 metres and climb a tree or two. Your average hunter-gatherer walks or runs 9 to 15 kilometres per day, and we have all these features in our bodies, literally from our heads down to our toes, that make us really good at long-distance walking and running.
I and my colleagues at the University of Utah, Dennis Bramble and David Carrier, think the key advantage for humans was persistence hunting, whereby you run very long distances to chase animals in the heat and run them into heat stroke. We can run for very long distances, marathons in fact, at speeds at which other animals have to gallop. That’s not an endurance gait for quadrupeds, because they cool by panting – short shallow breaths. You can’t pant and gallop at the same time. If you make an animal gallop in the heat for 15 minutes or so, on a hot day, you’ll kill it.


But we have adaptations for this kind of endurance running?


Yes. Our bodies are loaded with all kinds of features: short toes that require less energy to stabilise and generate less shock when running; the Achilles tendon that stores and releases energy appropriately as we run; the large gluteus maximus muscles that steady the trunk; and stabilisation of the head. I’m a middle-aged professor, I’m not a great specimen of an athlete, but I can easily run a marathon at a speed that would cause a dog my size to gallop.

What’s your best marathon time?


[Laughs] 3 hours and 34 minutes. There are guys who can run almost twice as fast as me.
Still, if you made an animal run that far at your speed, you would… I’d have dinner.

Why, in spite of our adaptations, have we gone from endurance athletes to couch potatoes?


It was incredibly recently in history that a large number of humans have been freed from having to do physical activity. My argument, from an evolutionary perspective, would be that not having regular physical activity every day is pathological and abnormal. In a lot of medical studies, we compare people who are sick with controls. But who are those controls? They are relatively sedentary Westerners. I’d argue that we are comparing people who are sick to people who are abnormal and semi-pathological.


If being inactive is pathological and abnormal, then how come we hate exercise so much?


There was never any evolutionary selection pressure to make us like exercise. If you are a Neanderthal or Homo erectus or an early modern human, you didn’t think, “Gee, I’m going to go for a run so that I’m not going to get depressed”. They had to go long distances every day in order to survive. Not exercising was never an option, so there was never any selection pressure to make people like exercise. On the contrary, there was probably selection to help people avoid needless exercise when they could. Some hunter-gatherers had diets of about 2200 calories a day. When your energy intake is that low, you can’t afford to go for a jog just for fun.

So evolution selected for traits that made us relax or be lazy?

Of course. Just like any time you crave sugary, fatty foods – that would have been advantageous for early humans. It’s only now that they have become maladaptive.
When you walk into a train station and there is a staircase and an escalator, your brain always tells you to take the escalator. Given a choice between a piece of cake and a carrot, we always go for the cake. It’s not in your best interest, but it’s probably a very deeply rooted evolutionary instinct.

What are the consequences of the modern sedentary lifestyle?

It’s hard to think of one disease that is not affected by physical activity. Take the two major killers: heart disease and cancer. The heart requires exercise to grow properly. Exercise increases the peripheral arteries and decreases your cholesterol levels, it decreases your risk of heart disease by at least half.
Breast cancers and many other reproductive tissue cancers also respond strongly to exercise. Other factors being constant, women who have engaged in regular vigorous exercise have significantly lower cancer rates than women who have not. Colon cancer has been shown to be reduced by up to 30 per cent by exercise. There are also benefits for mental health – depression, anxiety, the list is incredibly long.


What can we do about our maladaptive traits?


If we want to practice preventive medicine, that means we have to eat foods that we might not prefer, and exercise when we don’t want to. The only way to do that is through some form of socially acceptable coercion. There is a reason why we require good food and exercise in school – otherwise the kids won’t get enough of it. Right now we are dropping those requirements around the world.
If we are going to solve these health problems, we have to push ourselves to act in our own self-interest. As a society, as a culture, we have to somehow agree that it’s necessary or face the consequence – which is billions of unfit, overweight people.


Has evolution given us any instincts that promote exercise?

Yes. It’s important to recognise that the body isn’t adapted only in one way or another. There are multiple competing adaptations. While it’s true that many of our instincts are to not like exercise, we also have other adaptations that make us enjoy exercise. The most obvious example is the runner’s high.

What’s the evolutionary advantage of the runner’s high?


Imagine you are chasing an animal, and you have to keep going. When you are chasing, you are usually also tracking, which is all about observation. You are looking for clues in the environment. What does a runner’s high do? It makes everything more intense. It stimulates your perception and your sensory awareness.
I can give you an example: I ran the London marathon a few years ago, and as I was nearing the finish I remember running by Big Ben and thinking, “Wow, Big Ben is really big.” And then I remember thinking to myself, “Oh, I must be high.”

From New Scientist
Daniel Lieberman is a professor of human evolutionary biology at Harvard University. He specialises in research on human movement and endurance running, and is a keen long-distance runner*

Posted on Thursday, June 13th 2013

Tags athletics fitness blog