How To Post Natal Yoga: Breathing Exercise
Mayo Clinic researchers say interval training may have anti-aging benefits at the cellular level.
HIIT—or high intensity interval training—has been the buzzy sweat method for a while now. These fast-paced workouts alternate short bursts of exercise with quick recovery periods, and torch more calories in less time than traditional steady-state training sessions. HIIT has been shown to boost metabolism, melt fat, build muscle, and more—and now, Mayo Clinic researchers have discovered yet another benefit: it can reverse signs of aging at the cellular level.
Look at a photo of yourself as a teenager and, mistaken fashion choices aside, it’s likely you see traces of the same person with the same personality quirks as you are today. But whether or not you truly are the same person over a lifetime—and what that notion of personhood even means—is the subject of ongoing philosophical and psychology debate.
There’s a multi-billion-dollar industry devoted to products that fight signs of aging, but moisturizers only go skin deep.
Aging occurs deeper — at a cellular level — and scientists have found that eating less can slow this cellular process.
Recent research published in Molecular & Cellular Proteomics offers one glimpse into how cutting calories impacts aging inside a cell.
The researchers found that when ribosomes — the cell’s protein makers — slow down, the aging process slows too. The decreased speed lowers production but gives ribosomes extra time to repair themselves.
“The ribosome is a very complex machine, sort of like your car, and it periodically needs maintenance to replace the parts that wear out the fastest,” said Brigham Young University biochemistry professor and senior author John Price.
“When tires wear out, you don’t throw the whole car away and buy new ones. It’s cheaper to replace the tires.”
So what causes ribosome production to slow down in the first place? At least for mice: reduced calorie consumption.
Price and his fellow researchers observed two groups of mice. One group had unlimited access to food while the other was restricted to consume 35 percent fewer calories, though still receiving all the necessary nutrients for survival.
“When you restrict calorie consumption, there’s almost a linear increase in lifespan,” Price said. “We inferred that the restriction caused real biochemical changes that slowed down the rate of aging.”
Price’s team isn’t the first to make the connection between cut calories and lifespan, but they were the first to show that general protein synthesis slows down and to recognize the ribosome’s role in facilitating those youth-extending biochemical changes.
“The calorie-restricted mice are more energetic and suffered fewer diseases,” Price said. “And it’s not just that they’re living longer, but because they’re better at maintaining their bodies, they’re younger for longer as well.”
Ribosomes, like cars, are expensive and important — they use 10-20 percent of the cell’s total energy to build all the proteins necessary for the cell to operate.
Because of this, it’s impractical to destroy an entire ribosome when it starts to malfunction. But repairing individual parts of the ribosome on a regular basis enables ribosomes to continue producing high-quality proteins for longer than they would otherwise.
This top-quality production in turn keeps cells and the entire body functioning well.
Despite this study’s observed connection between consuming fewer calories and improved lifespan, Price assured that people shouldn’t start counting calories and expect to stay forever young.
Calorie restriction has not been tested in humans as an anti-aging strategy, and the essential message is understanding the importance of taking care of our bodies.
“Food isn’t just material to be burned — it’s a signal that tells our body and cells how to respond,” Price said. “We’re getting down to the mechanisms of aging, which may help us make more educated decisions about what we eat.”
New research suggests it is possible to slow or even reverse aging, at least in mice, by undoing changes in gene activity—the same kinds of changes that are caused by decades of life in humans.
By tweaking genes that turn adult cells back into embryoniclike ones, researchers at the Salk Institute for Biological Studies reversed the aging of mouse and human cells in vitro, extended the life of a mouse with an accelerated-aging condition and successfully promoted recovery from an injury in a middle-aged mouse, according to a study published Thursday in Cell.
Molecular biologist Elizabeth Blackburn shared a Nobel Prize for her research on telomeres—structures at the tips of chromosomes that play a key role in cellular aging. But she was frustrated that important health implications of her work weren’t reaching beyond academia.
So along with psychologist Elissa Epel, she has published her findings in a new book aimed at a general audience—laying out a scientific case that may give readers motivation to keep their new year’s resolutions to not smoke, eat well, sleep enough, exercise regularly, and cut down on stress.
The main message of “The Telomere Effect,” being published Tuesday, is that you have more control over your own aging than you may imagine. You can actually lengthen your telomeres—and perhaps your life—by following sound health advice, the authors argue, based on a review of thousands of studies.
“Telomeres listen to you, they listen to your behaviors, they listen to your state of mind,” said Blackburn, president of the Salk Institute for Biological Studies in La Jolla, Calif.
Telomeres sit at the end of strands of DNA, like the protective caps on shoelaces. Stress from a rough lifestyle will shorten those caps, making it more likely that cells will stop dividing and essentially die.
Too many of these senescent cells accelerates human aging, the pair say. This doesn’t cause any particular disease, but research suggests that it hastens the time when whatever your genes have in store will occur—so if you’re vulnerable to heart disease, you’re more likely to get it younger if your telomeres are shorter, said Epel, director of the University of California, San Francisco’s Aging, Metabolism and Emotions Center.
“We can provide a new level of specificity and tell people more precisely with clues emerging from telomere science, what exactly about exercise is related to long telomeres, what exact foods are related to long telomeres, what aspects of sleep are more related to long telomeres,” Epel added.
Other researchers in the field praised Blackburn and Epel’s efforts to make telomere research relevant to the general public, though several warned that it risked oversimplifying the science.
“I think it’s a very difficult thing to prove conclusively” that lifestyle can affect telomere length and therefore lifespan, said Harvard geneticist and anti-aging researcher David Sinclair. “To get cause-effect in humans is impossible, so it’s based on associations.”
Judith Campisi, an expert on cellular aging at the Buck Institute for Research on Aging in Novato, Calif., said the underlying research is solid. “If you have a terrible diet and you smoke, you’re definitely shortening your life, and shortening your telomeres,” she said.
Short telomeres increase the likelihood of cells becoming senescent and producing molecules that lead to inflammation, which she said is a huge risk factor for every age-related disease. “So there is a link there,” Campisi said, “it’s just not this exclusive magic bullet, that’s all.”
Cells can age in different ways, so someone could have lots of aging cells but normal-looking telomeres. “If all aging was due to telomeres, we would have solved the aging problem a long time ago,” she said.
In a telephone interview from her publisher’s office in New York, Blackburn said the best part of the telomere research is that it’s quantifiable, giving people more specific direction than the advice your mother may have given you to get off the couch and exercise.
“Your mother didn’t tell you if you had to run marathons every week, or if three to four times a week is enough,” she said. Telomere research suggests that extreme exercise isn’t necessary to live healthier longer.
Also, Blackburn said, her research suggests that lengthening telomeres with medications could be dangerous—that lifestyle changes are far safer than a pill.
One surprise from the research: You don’t actually need a full eight hours of sleep to benefit your telomeres. Seven is enough, as long as you feel well-rested. “That’s something quite useful, so people won’t lie awake fretting that they’re not getting eight hours,” Blackburn said.
One of the challenges with telomere research is that most studies measure the length of telomeres in blood cells. But it may be that the liver is aging faster or slower than the blood—we’re not all one age throughout, Campisi said.
By measuring telomere length in the blood, “what you’re really reporting on is the capacity of immune stem cells to function well,” said Matt Kaeberlein, who studies the molecular basis of aging at the University of Washington. “What this may be really telling us is the immune system may be particularly sensitive to lifestyle and environmental factors.”
Kaeberlein said he’s only at the periphery of telomere research, but is skeptical about the predictive value of shorter versus longer telomeres.
“It’s not at all clear whether the methods are quantitative enough or of high enough resolution to really make those kinds of arguments,” Kaeberlein said. “I think it has the potential to be a biomarker predicting health outcomes, but I don’t know that I would feel comfortable saying people should make lifestyle changes based on a measure of their telomere length,” he said.
Sara Gottfried did. A Harvard-trained gynecologist in Berkeley, Calif., she said a test of her telomere length put her 20 years beyond her biological age, and shocked her into action.
“It was an interesting anecdotal experiment,” said Gottfried, whose examination led to a book, due out in March, called “Younger: A Breakthrough Program to Reset Your Genes, Reverse Aging, and Turn Back the Clock 10 Years.” “It organized my thinking around the levers of health span—food, sleep, exercise, lean body mass, stress—how so many of us are in a failure state, which I think accelerates aging.”
Much of human health hinges on how well the body manufactures and uses energy. For reasons that remain unclear, cells’ ability to produce energy declines with age, prompting scientists to suspect that the steady loss of efficiency in the body’s energy supply chain is a key driver of the aging process. Now, scientists at Washington University School of Medicine in St. Louis have shown that supplementing healthy mice with a natural compound called NMN can compensate for this loss of energy production, reducing typical signs of aging such as gradual weight gain, loss of insulin sensitivity and declines in physical activity. Credit: Michael Worful
More than 40 million people worldwide suffer from Alzheimer’s disease, and that number is expected to increase drastically in the coming years. But no real progress has been made in the fight against the disease since its classification more than 100 years ago. Scientist Samuel Cohen shares a new breakthrough in Alzheimer’s research from his lab as well as a message of hope. “Alzheimer’s is a disease,” Cohen says, “and we can cure it.”
People who have reached their later years may think it’s primarily a time to relax, not to increase their physical activity. Not so. Previous research has suggested that exercise can improve memory and reverse muscle loss in older adults, among other benefits. And a study out Monday finds that a regular program of physical activity reduces the time spent with mobility-limiting disability.
Researchers took more than 1,600 sedentary people between 70 and 89 years old who had some functional limitations, but who could walk about a quarter of a mile in 15 minutes or less, unassisted by another person or a walker. (Canes were OK.)
Half of the participants got a health education program involving regular in-person sessions and some stretching exercises, while the other group was told to aim for 150 minutes of aerobic activity as well as strength, flexibility and balance training both at the study’s facilities and at home. “Walking was the cornerstone of the program,” says Thomas Gill, a professor of geriatrics at the Yale School of Medicine and an author of the study, which appears in Annals of Internal Medicine.
The study followed participants for about 2.7 years, and found that the physical activity program cut the amount of time that people spent with a “major mobility disability” — defined as being unable to walk a quarter mile — by 25 percent compared to the education program. Previous findings from the same study showed that the exercise program lowered the risk of becoming disabled in the first place; this one showed that it sped recovery from an episode of disability and lowered the risk of subsequent episodes.
“They’ve done a really nice job of showing the incredible power of physical activity,” says Bradley Cardinal, a professor of kinesiology at Oregon State University who wasn’t involved with the study. “It’s the secret ingredient to successful aging in terms of quality of life.” An editorial accompanying the study, by the University of California, San Francisco’s Patricia Katz and the University of South Carolina’s Russell Pate, also noted that people who engage in physical activity have a lower risk for heart disease, diabetes, certain cancers, depression, cognitive impairment and functional decline.
The exercise program pretty closely followed thegovernment’s recommendations for all adults, including older ones: 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity exercise per week, plus two strength sessions that hit all the major muscle groups.
But most Americans don’t get that much exercise, and that becomes increasingly true as people age. According to statistics from the Centers for Disease Control and Prevention, just 28 percent of those 75 and up meet the recommendation for aerobic activity, and only 8 percent also did the suggested amount of strength training.
Cardinal says older adults need to realize that exercise can greatly improve their quality of life by maximizing function as long as possible. But he says that many believe that older age is for relaxing and that physical activity is somehow dangerous or unnatural. That belief “is pervasive among older adults,” he says, even though for many of them, meeting the minimum requirements “is doable.”
Semantics can help. “We try to frame this as more physical activity than exercise,” says Gill. “We talk with older folks and many say, ‘I can’t exercise, but maybe I can become more physically active.’ ” Study participants were advised to “start low and go slow,” and some were even able to get rid of their canes after six months of exercise, which Gill says they found particularly rewarding.
Physicians can also help. “Prescribing exercise may be just as important as prescribing medications — perhaps even more important in some cases,” the editorial said. The authors called on medical schools to “start preparing students to prescribe exercise as effectively as they prescribe statins, and for health systems to support physicians in addressing inactivity just as they provide support in addressing other health risks.” (The American College of Sports Medicine has an “Exercise is Medicine” initiative to help physicians integrate exercise recommendations into their treatment plans.)
There are also some basic behavioral strategies for getting yourself to get moving, no matter your age, including giving yourself an incentive to change and engineering your environment to encourage the activity.
Link original: http://www.npr.org/sections/health-shots/2016/09/26/495477531/walking-fends-off-disability-and-its-not-too-late-to-start