Wednesday, March 27, 2013

Exercise to become smarter!

The value of mental-training games may be speculative, as Dan Hurley writes in his article on the quest to make ourselves smarter, but there is another, easy-to-achieve, scientifically proven way to make yourself smarter. Go for a walk or a swim. For more than a decade, neuroscientists and physiologists have been gathering evidence of the beneficial relationship between exercise and brainpower. But the newest findings make it clear that this isn’t just a relationship; it is the relationship. Using sophisticated technologies to examine the workings of individual neurons — and the makeup of brain matter itself — scientists in just the past few months have discovered that exercise appears to build a brain that resists physical shrinkage and enhance cognitive flexibility. Exercise, the latest neuroscience suggests, does more to bolster thinking than thinking does.
The most persuasive evidence comes from several new studies of lab animals living in busy, exciting cages. It has long been known that so-called “enriched” environments — homes filled with toys and engaging, novel tasks — lead to improvements in the brainpower of lab animals. In most instances, such environmental enrichment also includes a running wheel, because mice and rats generally enjoy running. Until recently, there was little research done to tease out the particular effects of running versus those of playing with new toys or engaging the mind in other ways that don’t increase the heart rate.
So, last year a team of researchers led by Justin S. Rhodes, a psychology professor at the Beckman Institute for Advanced Science and Technology at the University of Illinois, gathered four groups of mice and set them into four distinct living arrangements. One group lived in a world of sensual and gustatory plenty, dining on nuts, fruits and cheeses, their food occasionally dusted with cinnamon, all of it washed down with variously flavored waters. Their “beds” were colorful plastic igloos occupying one corner of the cage. Neon-hued balls, plastic tunnels, nibble-able blocks, mirrors and seesaws filled other parts of the cage. Group 2 had access to all of these pleasures, plus they had small disc-shaped running wheels in their cages. A third group’s cages held no embellishments, and they received standard, dull kibble. And the fourth group’s homes contained the running wheels but no other toys or treats.
All the animals completed a series of cognitive tests at the start of the study and were injected with a substance that allows scientists to track changes in their brain structures. Then they ran, played or, if their environment was unenriched, lolled about in their cages for several months.
Afterward, Rhodes’s team put the mice through the same cognitive tests and examined brain tissues. It turned out that the toys and tastes, no matter how stimulating, had not improved the animals’ brains.
“Only one thing had mattered,” Rhodes says, “and that’s whether they had a running wheel.” Animals that exercised, whether or not they had any other enrichments in their cages, had healthier brains and performed significantly better on cognitive tests than the other mice. Animals that didn’t run, no matter how enriched their world was otherwise, did not improve their brainpower in the complex, lasting ways that Rhodes’s team was studying. “They loved the toys,” Rhodes says, and the mice rarely ventured into the empty, quieter portions of their cages. But unless they also exercised, they did not become smarter.
Why would exercise build brainpower in ways that thinking might not? The brain, like all muscles and organs, is a tissue, and its function declines with underuse and age. Beginning in our late 20s, most of us will lose about 1 percent annually of the volume of the hippocampus, a key portion of the brain related to memory and certain types of learning.
Exercise though seems to slow or reverse the brain’s physical decay, much as it does with muscles. Although scientists thought until recently that humans were born with a certain number of brain cells and would never generate more, they now know better. In the 1990s, using a technique that marks newborn cells, researchers determined during autopsies that adult human brains contained quite a few new neurons. Fresh cells were especially prevalent in the hippocampus, indicating that neurogenesis — or the creation of new brain cells — was primarily occurring there. Even more heartening, scientists found that exercise jump-starts neurogenesis. Mice and rats that ran for a few weeks generally had about twice as many new neurons in their hippocampi as sedentary animals. Their brains, like other muscles, were bulking up.
But it was the ineffable effect that exercise had on the functioning of the newly formed neurons that was most startling. Brain cells can improve intellect only if they join the existing neural network, and many do not, instead rattling aimlessly around in the brain for a while before dying.
One way to pull neurons into the network, however, is to learn something. In a 2007 study, new brain cells in mice became looped into the animals’ neural networks if the mice learned to navigate a water maze, a task that is cognitively but not physically taxing. But these brain cells were very limited in what they could do. When the researchers studied brain activity afterward, they found that the newly wired cells fired only when the animals navigated the maze again, not when they practiced other cognitive tasks. The learning encoded in those cells did not transfer to other types of rodent thinking.
Exercise, on the other hand, seems to make neurons nimble. When researchers in a separate study had mice run, the animals’ brains readily wired many new neurons into the neural network. But those neurons didn’t fire later only during running. They also lighted up when the animals practiced cognitive skills, like exploring unfamiliar environments. In the mice, running, unlike learning, had created brain cells that could multitask.
Just how exercise remakes minds on a molecular level is not yet fully understood, but research suggests that exercise prompts increases in something called brain-derived neurotropic factor, or B.D.N.F., a substance that strengthens cells and axons, fortifies the connections among neurons and sparks neurogenesis. Scientists can’t directly study similar effects in human brains, but they have found that after workouts, most people display higher B.D.N.F. levels in their bloodstreams.
Few if any researchers think that more B.D.N.F. explains all of the brain changes associated with exercise. The full process almost certainly involves multiple complex biochemical and genetic cascades. A recent study of the brains of elderly mice, for instance, found 117 genes that were expressed differently in the brains of animals that began a program of running, compared with those that remained sedentary, and the scientists were looking at only a small portion of the many genes that might be expressed differently in the brain by exercise.
Whether any type of exercise will produce these desirable effects is another unanswered and intriguing issue. “It’s not clear if the activity has to be endurance exercise,” says the psychologist and neuroscientist Arthur F. Kramer, director of the Beckman Institute at the University of Illinois and a pre-eminent expert on exercise and the brain. A limited number of studies in the past several years have found cognitive benefits among older people who lifted weights for a year and did not otherwise exercise. But most studies to date, and all animal experiments, have involved running or other aerobic activities.
Whatever the activity, though, an emerging message from the most recent science is that exercise needn’t be exhausting to be effective for the brain. When a group of 120 older men and women were assigned to walking or stretching programs for a major 2011 study, the walkers wound up with larger hippocampi after a year. Meanwhile, the stretchers lost volume to normal atrophy. The walkers also displayed higher levels of B.D.N.F. in their bloodstreams than the stretching group and performed better on cognitive tests.
In effect, the researchers concluded, the walkers had regained two years or more of hippocampal youth. Sixty-five-year-olds had achieved the brains of 63-year-olds simply by walking, which is encouraging news for anyone worried that what we’re all facing as we move into our later years is a life of slow (or not so slow) mental decline.

Thursday, March 21, 2013

Trying to lose weight? Sleep more!

Lost Sleep Can Lead to Weight Gain

Stuart Bradford

For years researchers have known that
 adults who sleep less than five or six hours a night are at higher risk of being overweight. Among children, sleeping less than 10 hours a night is associated with weight gain.The best path to a healthy weight may be a good night’s sleep.
Now a fascinating new study suggests that the link may be even more insidious than previously thought. Losing just a few hours of sleep a few nights in a row can lead to almost immediate weight gain.
Sleep researchers from the University of Colorado recruited 16 healthy men and women for a two-week experiment tracking sleep, metabolism and eating habits. Nothing was left to chance: the subjects stayed in a special room that allowed researchers to track their metabolism by measuring the amount of oxygen they used and carbon dioxide they produced. Every bite of food was recorded, and strict sleep schedules were imposed.
The goal was to determine how inadequate sleep over just one week — similar to what might occur when students cram for exams or when office workers stay up late to meet a looming deadline — affects a person’s weight, behavior and physiology.
During the first week of the study, half the people were allowed to sleep nine hours a night while the other half stayed up until about midnight and then could sleep up to five hours. Everyone was given unlimited access to food. In the second week, the nine-hour sleepers were then restricted to five hours of sleep a night, while the sleep-deprived participants were allowed an extra four hours.
Notably, the researchers found that staying up late and getting just five hours of sleep increased a person’s metabolism. Sleep-deprived participants actually burned an extra 111 calories a day, according to the findings published last week in The Proceedings of the National Academy of Sciences.
But even though we burn more calories when we stay awake, losing sleep is not a good way to lose weight. The light sleepers ended up eating far more than those who got nine hours of sleep, and by the end of the first week the sleep-deprived subjects had gained an average of about two pounds.
During the second week, members of the group that had originally slept nine hours also gained weight when they were restricted to just five hours. And the other group began to lose some (but not all) of the weight gained in that first sleep-deprived week.
Kenneth Wrightdirector of the university’s sleep and chronobiology laboratory, said part of the change was behavioral. Staying up late and skimping on sleep led to not only more eating, but a shift in the type of foods a person consumed.
“We found that when people weren’t getting enough sleep they overatecarbohydrates,” he said. “They ate more food, and when they ate food also changed. They ate a smaller breakfast and they ate a lot more after dinner.”
In fact, sleep-deprived eaters ended up eating more calories during after-dinner snacking than in any other meal during the day. Over all, people consumed 6 percent more calories when they got too little sleep. Once they started sleeping more, they began eating more healthfully, consuming fewer carbohydrates and fats. Dr. Wright noted that the effect of sleep deprivation on weight would likely be similar in the real world although it might not be as pronounced as in the controlled environment. The researchers found that insufficient sleep changed the timing of a person’s internal clock, and that in turn appeared to influence the changes in eating habits. “They were awake three hours before their internal nighttime had ended,” Dr. Wright said. “Being awakened during their biological night is probably why they ate smaller breakfasts.”
The effect was similar to the jet lag that occurs when a person travels from California to New York.
Last fall, The Annals of Internal Medicine reported on a study by University of Chicago researchers, who found that lack of sleep alters the biology of fat cells. In the small study — just seven healthy volunteers — the researchers tracked the changes that occurred when subjects moved from 8.5 hours of sleep to just 4.5 hours. After four nights of less sleep, their fat cells were less sensitive to insulin, a metabolic change associated with both diabetes and obesity.
“Metabolically, lack of sleep aged fat cells about 20 years,” said Matthew Brady, an associate professor of medicine at the University of Chicago and the senior author on the study.
“These subjects were in their low 20s but it’s as if they were now middle-aged in terms of their response. We were surprised how profound the effects were.”
Both Drs. Wright and Brady noted that because their studies lasted only days, it was not clear how long-term sleep deprivation affects weight, and whether the body adjusts to less sleep.
Dr. Brady said that while better sleep would not solve the obesity problem, paying more attention to sleep habits could help individuals better manage their weight.
In the future he hopes to study whether a focus on better sleep could improve the health of people in middle age who are overweight or prediabetic.
“Telling someone they need to sleep more as a way to improve their metabolic health, we think would be more palatable,” said Dr. Brady. “We think sleep is very underappreciated.”
A version of this article appeared in print on 03/19/2013, on page D4 of the NewYork edition with the headline: Lost Sleep Can Lead to Weight Gain.

Wednesday, December 19, 2012

Diabetes increases risk of breast cancer and physical activity reduces the risk

Diabetes confers 27% increase in breast cancer risk

By: BRUCE JANCIN, Ob.Gyn. News Digital Network
SAN ANTONIO – Diabetes is independently associated with a 27% increased risk of breast cancer, but this elevated risk is confined to postmenopausal type 2 diabetic patients, a large meta-analysis has shown.

The meta-analysis, which included 40 published studies and 56,111 women with breast cancer, found no association between risk of the malignancy and circulating serum insulin level, insulin growth factor–1 level, fasting blood glucose level, or C-peptide concentration.

These findings suggest that the hyperinsulinemic theory of the pathogenesis of breast cancer may need to be reevaluated in order to account for the increased risk being confined to postmenopausal patients and unrelated to indices of metabolic control, Dr. Peter Boyle said at the annual San Antonio Breast Cancer Symposium.

The key risk factors for breast cancer that emerged from the meta-analysis were adiposity and lack of physical activity. Both are also well established as risk factors for diabetes.

Based on the findings from this meta-analysis, efforts to avoid overweight and increase physical activity should form the basis of a common public health strategy simultaneously aimed at preventing diabetes and breast cancer, according to Dr. Boyle of the International Prevention Research Institute in Lyon, France.

High levels of physical activity, whether occupational or recreational, were independently associated with a 17% reduction in the relative risk of being diagnosed with breast cancer in premenopausal women and a 12% decrease in the postmenopausal population.

The relationship between adiposity and breast cancer was less straightforward. Premenopausal women who were overweight or obese had a significantly lower breast cancer risk than did leaner women, while breast cancer risk was increased in adipose postmenopausal women. More specifically, a 5-U increase in body mass index – equivalent to an extra 14.5 kg in a woman 1.7 m tall – was associated with an 11% increased risk of breast cancer in postmenopausal women but a 10% reduction in risk in premenopausal women.

Dr. Boyle and coworkers also presented a related meta-analysis looking at breast cancer risk in women using insulin glargine (Lantus). The study was prompted by recent evidence linking pioglitazone to a possible increase in bladder cancer, liraglutide and pancreatic cancer, insulin use and lung cancer, and exenatide and pancreatic cancer.

This meta-analysis included 18 epidemiologic studies published within the past 3 years. Collectively the studies involved 4,080 cases of breast cancer in 903,675 patients followed for 2.7 million person-years.

The meta-analysis demonstrated no increase in breast cancer risk in insulin glargine users, compared with users of other insulins. Indeed, the risk of all forms of cancer was 9% lower in insulin glargine users, a statistically significant reduction. This was driven by a 14% reduction in the relative risk of colorectal cancer.

Another reassuring finding was that breast cancer risk did not increase with longer use of insulin glargine, as would be expected if a causal relationship existed, he added.

Both meta-analyses were funded by Sanofi-Aventis, which markets glargine. Dr. Boyle reported having no relevant financial conflicts, although several of his coinvestigators have served on advisory boards for Sanofi-Aventis and other insulin manufacturers.

Thursday, December 13, 2012

Why Afternoon May Be the Best Time to Exercise

Original Article

Does exercise influence the body’s internal clock? Few of us may be conscious of it, but our bodies, and in turn our health, are ruled by rhythms. “The heart, the liver, the brain — all are controlled by an endogenous circadian rhythm,” says Christopher Colwell, a professor of psychiatry at the University of California, Los Angeles’s Brain Research Institute, who led a series of new experiments on how exercise affects the body’s internal clock. The studies were conducted in mice, but the findings suggest that exercise does affect our circadian rhythms, and the effect may be most beneficial if the exercise is undertaken midday.
For the study, which appears in the December Journal of Physiology, the researchers gathered several types of mice. Most of the animals were young and healthy. But some had been bred to have a malfunctioning internal clock, or pacemaker, which involves, among other body parts, a cluster of cells inside the brain “whose job it is to tell the time of day,” Dr. Colwell says.
These pacemaker cells receive signals from light sources or darkness that set off a cascade of molecular effects. Certain genes fire, expressing proteins, which are released into the body, where they migrate to the heart, neurons, liver and elsewhere, choreographing those organs to pulse in tune with the rest of the body. We sleep, wake and function physiologically according to the dictates of our body’s internal clock.
But, Dr. Colwell says, that clock can become discombobulated. It is easily confused, for instance, by viewing artificial light in the evening, he says, when the internal clock expects darkness. Aging also worsens the clock’s functioning, he says. “By middle age, most of us start to have trouble falling asleep and staying asleep,” he says. “Then we have trouble staying awake the next day.”
The consequences of clock disruptions extend beyond sleepiness. Recent research has linked out-of-sync circadian rhythm in people to an increased risk for diabetes, obesity, certain types of cancer, memory loss and mood disorders, including depression.
“We believe there are serious potential health consequences” to problems with circadian rhythm, Dr. Colwell says. Which is why he and his colleagues set out to determine whether exercise, which is so potent physiologically, might “fix” a broken clock, and if so, whether exercising in the morning or later in the day is more effective in terms of regulating circadian rhythm.
They began by letting healthy mice run, an activity the animals enjoy. Some of the mice ran whenever they wanted. Others were given access to running wheels only in the early portion of their waking time (mice are active at night) or in the later stages, the equivalent of the afternoon for us.
After several weeks of running, the exercising mice, no matter when they ran, were found to be producing more proteins in their internal-clock cells than the sedentary animals. But the difference was slight in these healthy animals, which all had normal circadian rhythms to start with.
So the scientists turned to mice unable to produce a critical internal clock protein. Signals from these animals’ internal clocks rarely reach the rest of the body.
But after several weeks of running, the animals’ internal clocks were sturdier. Messages now traveled to these animals’ hearts and livers far more frequently than in their sedentary counterparts.
The beneficial effect was especially pronounced in those animals that exercised in the afternoon (or mouse equivalent).
That finding, Dr. Colwell says, “was a pretty big surprise.” He and his colleagues had expected to see the greatest effects from morning exercise, a popular workout time for many athletes.
But the animals that ran later produced more clock proteins and pumped the protein more efficiently to the rest of the body than animals that ran early in their day.
What all of this means for people isn’t clear, Dr. Colwell says. “It is evident that exercise will help to regulate” our bodily clocks and circadian rhythms, he says, especially as we enter middle age.
But whether we should opt for an afternoon jog over one in the morning “is impossible to say yet,” he says.
Late-night exercise, meanwhile, is probably inadvisable, he continues. Unpublished results from his lab show that healthy mice running at the animal equivalent of 11 p.m. or so developed significant disruptions in their circadian rhythm. Among other effects, they slept poorly.
“What we know, right now,” he says, “is that exercise is a good idea” if you wish to sleep well and avoid the physical ailments associated with an aging or clumsy circadian rhythm. And it is possible, although not yet proven, that afternoon sessions may produce more robust results.
“But any exercise is likely to be better than none,” he concludes. “And if you like morning exercise, which I do, great. Keep it up.”

Friday, December 7, 2012

Fruits and Veggies!

Nutrients in Fruits, Vegetables May Help Prevent Breast Cancer: Study

THURSDAY Dec. 6, 2012 -- Women with higher levels of micronutrients found in many fruits and vegetables may be less likely to develop breast cancer, a new study finds.
Previous research has shown that the nutrients, called carotenoids, can inhibit tumor growth and reduce the spread of breast cancers.
"Carotenoids are found in carrots, spinach, kale, tomatoes, bell peppers, sweet potatoes and other vegetables," noted one expert not connected to the study, Dr. Stephanie Bernik.
"There has been some evidence in the past that these substances are helpful in reducing the risk of cancer," said Bernik, who is chief of surgical oncology at Lenox Hill Hospital in New York City.
In the new study, researchers led by A. Heather Eliassen of Brigham and Women's Hospital and Harvard Medical School, in Boston, analyzed data from thousands of women who took part in eight previous studies on carotenoid levels and breast cancer.
They found a statistically significant association between higher levels of carotenoids and reduced breast cancer risk, especially so-called ER-negative breast cancers -- tumors that aren't reliant on estrogen to fuel their growth. The findings highlight carotenoid levels as one of the first modifiable risk factors to be identified for ER-negative breast cancers, the team said.
While there is some evidence that carotenoids also inhibit the growth of ER-positive breast cancers (cancers that respond to estrogen), it's possible that this benefit is hidden by hormone-related associations that overpower other risk factors, the researchers added.
"A diet high in carotenoid-rich fruits and vegetables offers many health benefits, including a possible reduced risk of breast cancer," they concluded.
Bernik agreed. She said the researchers "have shown that there appears to be a real benefit to higher circulating levels of the micronutrients. The present study has more conclusively shown that there probably is some truth to what we tell patients regarding their diets ... the foods that your mother always told you are good for you, truly are good for you."
The study was published Dec. 6 in the Journal of the National Cancer Institute.
The study found a link between carotenoid levels and breast cancer risk, but it did not prove that the nutrients prevent the disease.

Saturday, November 10, 2012

Eating sweets and other high glycemic index is dangerous

Can Foods Affect Colon Cancer Survival?

Whole-grain foods and others with a low glycemic load may protect against colon cancer recurrence.Whole-grain foods and others with a low glycemic load may protect against colon cancer recurrence
The research is among the first to look at the impact that specific nutrients have on the likelihood of disease recurrence in people with colon cancer, one of the leading causes of cancer death in the United States. It found that people treated for Stage 3 disease, in which tumor cells have spread to lymph nodes, had greatly increased chances of dying of it or experiencing a recurrence if their diets were heavy in carbohydrate-rich foods that cause spikes in blood sugar and insulin.A new study suggests that what you eat may affect your chances of surviving colon cancer.
The patients who consumed the most carbohydrates and foods with high glycemic loads — a measure of the extent to which a serving of food will raise blood sugar — had an 80 percent greater chance of dying or having a recurrence during the roughly seven-year study period than those who had the lowest levels. Stage 3 colon cancer patients typically have a five-year survival rate of about 50 to 65 percent.
The study, however, was observational, meaning it could only highlight an association between carbohydrates and cancer outcomes without proving direct cause and effect. The researchers also obtained some of their data from food questionnaires that required patients to recall details about their diets, a method that can be unreliable.
Still, the researchers, who published their findings in The Journal of the National Cancer Institute, believe insulin may play a critical role in colon cancer recurrence. Chronically high insulin levels have been linked to cancer recurrence and mortality in previous research, and people with a history of Type 2 diabetes or elevated plasma C-peptide, a marker of long-term insulin production, have also been found to have an increased risk of colon cancer. One hypothesis is that insulin may fuel the growth of cancer cells and prevent cell death, or apoptosis, in cancer cells that have spread.
“It’s not simply that all carbs are bad or that you should avoid all sugar,” said Dr. Jeffrey A. Meyerhardt, the lead author of the study and an associate professor of medicine at the Dana-Farber Cancer Institute in Boston. It’s not as simple as ‘sugar causes cancer to grow.’”
He added: “Different carbs and sugar lead to different responses in your body. I think people should focus on a well-balanced diet” and substitute foods associated with lower glycemic loads or carbs for foods that have higher levels.
Earlier research published by Dr. Meyerhardt’s group showed that Stage 3 colon cancer patients who most closely followed a Western-style diet — with high intakes of meat, fat, refined grains and sugary desserts — had a threefold increase in recurrence and death from the disease compared with those who most strongly deviated from Western patterns of eating.
For this study, Dr. Meyerhardt and his team wanted to see to what extent carbohydrate intake could influence the progression of the disease, so they followed about 1,000 Stage 3 colon cancer patients taking part in a clinical trial sponsored by the National Cancer Institute. The patients, who had all had surgery and chemotherapy as part of their treatments, provided information on their diets and lifestyle habits. But the researchers went beyond just carbohydrate and sugar intake, taking into account glycemic measures.
The glycemic index, an increasingly popular nutritional measure, looks at the rate at which carbohydrate-containing foods raise a person’s fasting level of blood sugar and subsequent need for insulin. Sugary drinks, white bread and other highly processed carbohydrates rank higher on the index, while those that are digested more slowly, like brown rice, many vegetables, unrefined grains and legumes, have a lower index value.
Another barometer, however, is the glycemic load, which refers to the blood sugar effect of a standard serving of a food. A glycemic load of 10 or less for a food is generally considered low, while 20 or more is high. The latest study showed that glycemic load and total carbohydrate intake were the best predictors of cancer recurrence and mortality, and the link was strongest in people who were overweight or obese.
Dr. Meyerhardt said the findings suggest that colon cancer patients would be wise to keep glycemic load in mind while making food decisions, looking for ways to work into their diets foods that rank lower on the scale.
“So if you think about beverages, most juices and certainly sodas have a higher glycemic load than flavored waters and tomato juice and things like that,” he said. “Fruits like a date or raisins have very high glycemic loads, whereas fresh fruits like an apple, orange or cantaloupe all have sugar but have a very low glycemic load. Substitute brown rice for white, whole grains instead of white bread, and instead of having a starchy potato as your side dish, substitute beans and vegetables.”
One expert who was not involved in the research, Somdat Mahabir, a nutritional epidemiologist with the National Cancer Institute’s division of cancer control and population sciences, said the findings from the latest study must be borne out in further research. But in the meantime, making dietary changes that reduce glycemic load is a reasonable recommendation for colon cancer patients, he said, since it can only be helpful, not harmful.
“The results of the current study need to be confirmed, but the current indications are that diet is important to colon cancer survival,” Dr. Mahabir said.

Friday, November 9, 2012

Can Exercise Overcome Eating Fatty Foods?

Exercise and Eating Fatty Foods

Exercise Reduces Cognitive Decline Induced by Dietary Fat
Can Exercise Protect the Brain From Fatty Foods?
In recent years, some research has suggested that a high-fat diet may be bad for the brain, at least in lab animals. Can exercise protect against such damage? That question may have particular relevance now, with the butter-and cream-laden holidays fast approaching. And it has prompted several new and important studies.
The most captivating of these, presented last month at the annual meeting of the Society for Neuroscience in New Orleans, began with scientists at the University of Minnesota teaching a group of rats to scamper from one chamber to another when they heard a musical tone, an accepted measure of the animals’ ability to learn and remember.
For the next four months, half of the rats ate normal chow. The others happily consumed a much greasier diet, consisting of at least 40 percent fat. Total calories were the same in both diets.
After four months, the animals repeated the memory test. Those on a normal diet performed about the same as they had before; their cognitive ability was the same. The high-fat eaters, though, did much worse.
Then, half of the animals in each group were given access to running wheels. Their diets didn’t change. So, some of the rats on the high-fat diet were now exercising. Some were not. Ditto for the animals eating the normal diet.
For the next seven weeks, the memory test was repeated weekly in all of the groups. During that time, the performance of the rats eating a high-fat diet continued to decline so long as they didn’t exercise.
But those animals that were running, even if they were eating lots of fat, showed notable improvements in their ability to think and remember.
After seven weeks, the animals on the high-fat diet that exercised were scoring as well on the memory test as they had at the start of the experiment.
Exercise, in other words, had “reversed the high-fat diet-induced cognitive decline,” the study’s authors concluded.
That finding echoes those of another study presented last month at the Society for Neuroscience meeting. In it, researchers at Kyoto University in Japan gathered a group of mice bred to have a predisposition to developing a rodent version of Alzheimer’s disease and its profound memory loss.
Earlier studies by the same scientists had shown that a high-fat diet exacerbated the animals’ progression to full-blown dementia, and that both a low-fat diet and exercise slowed the animals’ mental decline.
But it hadn’t been clear in these earlier experiments which was more effective at halting the loss of memory, a leaner diet or regular rodent workouts.
So the scientists set out now to tease out the effects of each intervention by first feeding all of their mice a high-fat diet for 10 weeks, then switching some of them to low-fat kibble, while moving others to cages equipped with running wheels.
A third group began both a low-fat diet and an exercise routine, while the remainder of the mice continued to eat the high-fat diet and didn’t exercise.
After an additional 10 weeks, this last group, the animals that ate lots of fat and lounged around their cages, had developed far more deposits of the particular brain plaques associated with Alzheimer’s disease than the other mice. They also performed much more poorly on memory tests.
The mice that had been switched to a low-fat diet had fewer plaques and better memories than the control group.
But the mice that were exercising had even healthier brains and better memory scores than the low-fat group — even if they had remained on a high-fat diet. In other words, exercise was “more effective than diet control in preventing high-fat diet-induced Alzheimer’s disease development,” the authors write.
Just why high-fat diets might affect the brain and how exercise undoes the damage is not yet clear. “Our research suggests that free fatty acids” from high-fat foods may actually infiltrate the brain, says Vijayakumar Mavanji, a research scientist at the Minnesota VA Medical Center at the University of Minnesota, who, with his colleagues Catherine M. Kotz, Dr. Charles J. Billington, and Dr. Chuan Feng Wang, conducted the rat study. The fatty acids may then jump-start a process that leads to cellular damage in portions of the brain that control memory and learning, he says.
Exercise, on the other hand, seems to stimulate the production of specific biochemical substances in the brain that fight that process, he says.
In the Japanese study, for instance, the brains of the exercised animals teemed with high levels of an enzyme that is known to degrade the plaques associated with Alzheimer’s disease.
Of course, lab animals are not people, Dr. Mavanji cautions, and it’s not known if exercise might protect our brains in the same manner as it does in mice and rats.
Still, he says, there’s enough accumulating evidence about the potential cognitive risks of high-fat foods and the countervailing benefits from physical activity to recommend that “people exercise moderately,” he says, particularly during periods of repeated exposure to alluring, fatty holiday buffets.
The amount of exercise required to potentially protect our brains from the possible depredations of marbled beef and cheesecake isn’t excessive, after all, he continues. His rats were running for the human equivalent of about a daily 30-minute jog. So if you can’t walk away from the buffet table, be sure to at least take a walk afterward.