Some researchers believe that they will soon be able to slow down or even stop the body clock - at least for a short time
Most older Americans spend their later years with one or two chronic illnesses, such as rheumatism, diabetes, heart disease, or the effects of a stroke. The longer their body clock ticks, the more disease they are exposed to. Doctors and pharmaceutical companies tend to treat these age-related diseases only when they appear. But a small group of scientists began to advance a bold new approach. They believe that it is possible to stop or even turn back the clock so that these diseases start later or not at all.
Studies on people over a hundred years old show that the task is possible. Most of these people live for many years because they somehow avoided the diseases that plague other people in their 70s and 80s, says Nir Barzilai, director of the Institute for Aging Research at Yeshiva University's Albert Einstein College of Medicine in New York. The longevity of people over a hundred also does not cause a longer than usual decline towards the end of life. In fact, says Barzilai, a study of hundreds of "super-elderly" suggests exactly the opposite. Their illnesses often start later and closer to the end. "They live, live, live and then one day they die," he says.
Researchers have already developed various methods to extend the lifespan of yeast, worms, flies, rats and possibly monkeys. The next logical step is to adapt these methods to humans. "There's starting to be a consensus that it's time to take what we've learned from aging research and start translating it to help people," says Brian Kennedy, CEO and president of the Beck Institute for the Study of Aging, an independent research group in Novoto, California.
Delaying the aging process even by a few years can provide enormous social benefits due to the continued aging of populations worldwide. The US Bureau of Statistics estimates that one in five Americans will be over the age of 65 by 2030, compared to one in seven in 2014. In 2013, approximately 44 million people worldwide suffered from dementia. This number is expected to jump to 76 million in 2030 and 135 million in 2050, without having enough young people to care for them.
Of the handful of approaches that the researchers are examining, three stand out. But it is still unclear whether the possible benefits outweigh the risks involved in the treatments.
Evidence
Of course, to clearly determine that the treatment is effective, researchers need to define aging and find a way to quantify the process. Both things are missing. If a kidney cell divided yesterday, is it one day old or was it discovered as the age of the person in which it resides? And yet, studies in the last decade have provided clues that it is possible to delay the harmful aspects of aging, let's define it as we will.
In a study published in 2005, Thomas Rando, director of the Paul P. Glenn Center for the Biology of Aging at Stanford University, showed that an elderly mouse whose bloodstream was surgically connected to that of a young mouse regained the recovery capacity of the young. Somehow, the older rodent's stem cells, which are responsible for replacing old or damaged cells, became more efficient at creating new tissue. Biologist Amy Wagers of Harvard University, who worked as a postdoctoral fellow with Rando at Stanford, later discovered a protein, called GDF11, found in the blood that may have contributed to the faster recovery.
Her experiments, published in the journal Science in 2014, showed that the protein is more common in young mice than in old ones. Wagers showed that when GDF11 is injected into aged mice, it restores the muscle structure, genetic integrity and strength of young muscles.
A second approach involves testing about 20 medications and supplements available today, at a level of detail not previously possible to see their true effect on the aging process. For example, researchers at Cardiff University in Wales and their colleagues reported in 2014 that the lives of type 2 diabetics who took the drug metformin were extended by an average of 15% compared to the lives of healthy controls, who did not suffer from the metabolic disease but were similar in every respect Almost another. Scientists hypothesize that metformin interferes with one of the normal aging processes, called glycation, in which glucose binds to proteins and other important molecules, impairing their normal activity. The finding related to metformin is particularly impressive because people with diabetes, even if it is under control, often have a slightly shorter life expectancy than healthy people.
At the same time, in a study of 218 adults published last year in the journal Science Translational Medicine, researchers at the drug company Novartis showed that a compound called everolimus, which is chemically similar to the drug rapamycin, used to prevent kidney rejection after a transplant, improved the effectiveness of flu shots. In people over 65 years of age.
As people age, their immune system's antibody response to the deadly virus is weaker than that of younger people. Because of this, they may get sick if they get infected with a real flu virus after the vaccine. Tests showed that study subjects who received everolimus had a higher concentration of virus-fighting antibodies in their blood than subjects who were not treated with the drug. Researchers interpreted this finding as a sign that the young drug, in some way, affected the immune system of the subjects.
As with any drug, the side effects caused difficulties. People in the treatment group were more likely to develop mouth ulcers, which may limit the use of the drug if used to treat aging. And Cheryl also consider the price. Everolimus, which has been approved by the US Food and Drug Administration for its ability to fight cancer, costs more than $7,000 a month in the doses effective for cancer. It is not clear how much the drug will cost and how long it will be necessary to take it as an anti-aging drug.
Nevertheless, the results indicate that it is possible to slow down aging. Indeed, everolimus and other drugs similar to rapamycin significantly extended the life span of mice, prevented diseases such as cancer and reversed the changes that occur with age in the blood, liver, metabolism and immune system.
A third, completely different approach involves nutrition. It has been known for a long time that restricting calorie intake extends the life of mice. The effect of limiting food consumption (without causing malnutrition) on humans is still unclear. First, very few people can or want to adhere to such a low-calorie diet for the decades required to prove without a doubt that this approach works. But such drastic measures may not be necessary. Walter Longo, director of the Longevity Institute at the University of Southern California, has shown that he can extend the life span of mice even by limiting food intake to once every two days or by limiting the amount of protein they consume. Such intermittent fasting may be more acceptable for people, although its benefits have not yet been proven.
Disadvantages
Longevity may have a price. If old cells are made to become young again, they start dividing again. Controlled cell division equates to youth, but uncontrolled cell division equates to cancer. Right now scientists aren't sure they can cause one without the other.
It is also difficult to understand when is the right time to start treatment. If the goal is to prevent a variety of aging diseases, do you start antiaging treatment when the first disease starts? the second? "Once we break down, it is very difficult to fix us. It's easier to keep people healthy," says Kennedy. So it probably makes more sense to start treatment years earlier, during healthy middle age. But studies that prove the assumption will take many decades.
If it is possible to postpone many diseases, the obvious question is for how long. James Kirkland, director of the Robert and Arlene Kogood Center on Aging at the Mayo Clinic in Rochester, Minnesota, says it will take at least 20 years of research to answer the question. Scientists have managed to extend the life span of worms eightfold and added one year of life to three-year-old laboratory mice. Can these successes be translated into adding five or six hundred years to 80-year-olds? 30 more years? Or will they only win one more year? Life extension in humans is likely to be more modest than in yeast, worms, flies or mice, Rando says. Previous research suggests that simpler creatures benefit more from life extension experiments. Yeast, for example, are more responsive to calorie restriction experiments than mammals. "The closer you get to humans, the less the effect" on life expectancy, he says. And what is the rate of profit required to justify taking such treatment and paying for it? "Do you take the drug for life in the hope of extending life by 4% or 7%?" Rando asks.
What, if anything, are aging researchers doing to slow their own aging? The half-dozen scientists interviewed for this article all said they are making efforts aimed at extending their lifespans. One is happy to be diagnosed as pre-diabetic, which means a legal prescription for metformin. The studies are becoming so reliable, Kennedy says, that he has trouble convincing himself not to take the drugs.
All the experts say that they try to live a healthy life, apart from the burden of stressful work. They try to sleep about eight hours a night, eat moderate amounts of nutritious food and exercise a lot. None of them smokes. Most Americans, unfortunately, do not lead such healthy lives. The greatest irony would be to discover that the pill is not, in the end, more effective than the healthy habits we ignore today.
on the notebook
Karen Weintraub is a freelance health and science reporter in Cambridge, Massachusetts. She writes regularly for the Boston Globe, USA Today and the New York Times.
The article was published with the permission of Scientific American Israel
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