Translation carried out by the project Newочем.
Probably, in scientific circles, the most ardent opponent of the death due to old age is Aubrey de grey, a British biologist with a doctoral degree from Cambridge University and long-long hair that he ties in a ponytail. In his view, aging is an unhealthy process — a kind of collection of undesirable side effects that we live in. He draws an analogy between old age and malaria, because the latter also kills a lot of people. If you had the ability to cure her, would you not have done?
“Every day my success in the fight against aging save 100 of thousands of lives. Hundred of thousands of lives — that’s 30 World trade centers,” he said in 2014.
A group of qualified scientists studying the significant increase in life expectancy, continues to grow: geneticist Craig Venter, one of the first sequenced the human genome; biochemist Cynthia Kenyon, who discovered that a mutation in just one gene doubled the lifespan of the worm (now Kenyon is the Vice — President research project on aging in Calico, a subsidiary of Google); biologist bill Andrews, who stood at the head of the team that discovered the human gene for telomerase, the enzyme which is essential in the aging process.
Among their promises — health 90-year-old to 50-year-old (as stated by the Foundation of Methuselah), life up to 150 years (according to Andrews) and the eternal biological age of 25 years (says grey).
We were taught that death is natural and that attempts to avoid it — the slave’s dream-madness. However, these researchers have made real discoveries. They published their work in highly respected journals and has attracted significant funding. When these scientists claim that it is possible to live longer or even forever, they want to believe.
In the end, we have already doubled the life expectancy in the early twentieth century. Who can with certainty say that we can’t do it now, when we know so much about aging? Maybe the idea of preventing death is not really so insane?
What is aging
In December last year, a study at the Salk Institute, alarmed the media. Scientists experimented on mice with progeria — a disease that causes premature aging. The researchers were able to genetically modify mice so that the ability to “include” four of a gene associated with aging that exposing the mice to the action of the antibiotic. Mice with progeria lived 30 percent longer. As it turned out, healthy mice after treatment rejuvenated and recovered faster. “Our study shows that aging does not have to flow in one direction,” explained lead researcher.
Every few months scientists say about the next discovery, which demonstrates how very specific set of changes has slowed down some aspects of aging in animals. Of course, each study becomes more informative when presented as a part of a single process study of aging.
To assess the achievements of researchers in studying this field, you need to understand what it means to “aging” in a scientific context. In particular, the aging is called associated with the passage of time the deterioration or destruction of vital body functions — “the gradual depletion of the integrity of all systems of bodies,” said Dan Belke, associate Professor of medicine, chair of geriatrics at the Medical school of Duke University. We know that diseases such as Alzheimer’s, diabetes, cardiovascular disease and cancer, are caused at least partly by the aging.
As we age, our body there are intracellular changes which influence not only the heart and lungs, but also the muscles and nervous system. “These changes affect various systems of the body. And each of these systems individually is starting to run a little worse as we get older, and gradually it contributes to the development of dysfunction that lead to disease, disability and eventually to death,” concludes BelCCI.
We now understand that biological age does not always match chronological. Imagine twins, one drinks a lot, malnourished, sleep deprived and never exercises and the other doing the opposite. The first of this pair is likely to grow old before, and it will develop ageing-related diseases.
What is happening with our bodies depend on cells, so the biggest breakthrough in our knowledge about aging, perhaps, was the understanding of some of the pathways that affect aging at the cellular level.
The key lies in the process, which scientists call a signal — by means of cells communicate between themselves to adjust the simplest functions like cell repair or immune response. While errors in cell signaling can cause autoimmune diseases, diabetes and cancer, it turns out that the modification of the signaling paths can also slow down the aging process, at least in animals.
Researchers have identified two age-related signaling pathway: insulin-like growth factor (IGF-1), which is associated with growth and metabolism, and Target Rapamycin, or TOR (Target of Rapamycin), which, in addition to growth, regulates the movement and replication of cells. The more we delve into the science of rejuvenation, the often will meet these reductions.
It is assumed that if we can slow down the biological clock sufficiently, you can delay the onset of old age and come with her disease. Wrestlers with death like Peter Thiel, Larry Ellison, and Larry page are funding research on rejuvenation and I believe that such an opening in conjunction with drugs will turn into a combined solution and prolong life, perhaps forever.
Starvation, gene hacking and other interference
Today Cynthia Kenyon directs aging research at Calico. In 1993, she worked at the University of California in San Francisco, where he first thought about the fact that different animals have different life expectancy. Cynthia began to search for the genetic basis of longevity, delving into the genetic code of one species of round worm called C. elegans.
Although in most cases we see in round worms, parasites (e.g., heart worms that live in dogs), C. elegans, according to Kenyon, do not exceed the size of a comma in this sentence and parasites are not. Kenyon chose this view for two reasons. First, the average duration of life is 2-3 weeks, which facilitates its measurement. Secondly, before the study found a mutated strain of C. elegans, which mysteriously lived longer than the others.
Kenyon and a group of researchers in her laboratory began to modify genes in the individuals of C. elegans at random to see if they can make worms live longer. Over time, they found that damage to a single gene, called daf-2 doubles the lifespan of C. elegans. And modified worms are not just living longer, but aging slower. A two-week modified C. elegans was moving faster and was much more nimble than its natural counterpart. Kenyon found that a modified worm takes two days to age as much as in one day the normal worm aging.
Discovery was not limited to the worm C. elegans. When the researchers modified the same gene in flies and mice, they also lived longer. Most interesting is that in worms, the daf-2 gene modifies the hormone receptor, which is very similar to the human receptor of IGF-1. Centenarians who were able to live 100 years or longer are more likely than dying before, have mutations that reduce the activity of receptors of IGF-1.
At the same time, similar studies of yeast have shown that if genetically altered signaling pathways TOR to communication constraints, the yeast also live longer. Overall, the study suggests that finding ways to stop all the transmission signals have a chance to slow down the aging process.
The genetic modification of people represents a number of ethical and practical problems, therefore, most of the immediate focus of the science of rejuvenation is aimed at suppression of the signaling pathways TOR and IGF-1 without changes in genes.
One of the ways of suppressing signal paths TOR, you won’t like it if you love to eat. Studies have shown that mice that were fed 65% less, lived on 60% longer. Fortunately, scientists have discovered other ways to intervene that are similar. Rapamycin — a drug used anti-rejection in renal transplantation — increased the lifespan of mice by 14%; low dose aspirin prolongs life of the worm by 23%.
The authors of the theory of rejuvenation enthusiasm for chemical intervention, including the use of vitamin D, Metformin, and acarbose, which function in IGF-path open through the experiments Kenyon. Vitamin D has extended the life of worms by 31%, and created for the treatment of type II diabetes Metformin and acarbose have extended the life of mice by 5%. A separate British study found that patients with diabetes who were treated with Metformin lived longer with diabetes, although had to die on average 8 years earlier. If the drug were treating their diabetes, then they had to die around the same age as healthy people, not to live longer than them.
A national clinical study called “Treatment of aging Metformin,” or TAME (Targeting Aging with Metformin), which aims to test anti-ageing effects of Metformin on humans was approved by Management on sanitary inspection behind quality of food and medicines. “We want to show that the delay of aging is the best way to delay the disease”, explains the journal Nature, Dr. NIR Barzilai, one of the researchers in the project.
There is another strategy that does not affect the signal path.
If you ever wondered about why it seems that children have the energy just over the edge, while you barely survive to the end of the day, at least part of the difference lies in the mitochondria. Their mitochondria — cellular power plants — productive your. When we grow older, yet for unknown reasons the mitochondria stop working well, causing changes that slowly accumulate on the level of organs.
In the last few years at the forefront sirtuins as well, the types of proteins that control host cellular processes, including mitochondrial processes related to ageing. Although the role of sirtuins are still controversial, researchers have found that sirtuins fuelling the body can not only slow aging, but reverse it. Mice which were fed activators sirtuin, lived in 16-20% longer. This year in Japan started the first clinical trial of nicotinamide mononucleotide (NMD).
All of the above: lifestyle, medical and genetic intervention — excavation allowed the worms to live 10 times longer, and mice by 15-20%. This does not mean that any of these interventions will work in people, but it gives scientists a starting point.
“Ten years ago it would be difficult to think of anything but physical activity and diet. We now have about 10-15 different interventions that can work,” concludes Brian Kennedy, Professor of the Institute of the Tank for the study of aging, addressing the issue for more than 20 years.
In theory, if we can discover which of these interventions work in the human body better than others, and attach some cloned organs is completely worn, it will allow you to develop an effective set of measures, which if not would do away with aging, or at least significantly slow it down. Unfortunately, today such a prospect is backed by more a dream than real science.
The rise and fall of the popularity of the resveratrol extract, often contained in grape plants — a cautionary tale.
In many studies on animals have discovered that resveratrol extends the life of yeast by 70 per cent and fish by 59 percent. Another study showed that resveratrol improves health and prolongs the lives of mice on high-calorie diet — which probably explains the French paradox (the French kept a low level of cardiovascular disease despite a diet high in fat content). Well with him with the cake, I thought it let him drink the wine. The sale of dietary supplements with resveratrol have soared to $30 million dollars a year.
Unfortunately, the effects in humans have not been confirmed. Research 2014, published in JAMA, which studied the lives of the elderly of the famous Chianti wine area in Italy showed that people with higher levels of resveratrol do not live any longer. Earlier studies on the subject of whether resveratrol can help prevent or treat cancer have shown mixed results. “Nutritional support with resveratrol in modeling cancer in animals led to positive, neutral, and negative outcomes depending on the route of administration of resveratrol, dose, tumor type, species and other factors,” write the authors of the report 2014.
One of the problems of experiments with ageing is that people live too long. A mouse lives about two years; the extension of its life by 20 percent extends it by about five months. It’s pretty easy to learn and repeat in a controlled environment. Much harder to repeat such experiments on humans.
Scientists had to wait until their patients die, together with their own mortality becomes a problem. To properly conduct an experiment, you may need generations of scientists to study the life cycle of patients.
Researchers are struggling with aging, can adapt to work with the elderly, but it will make impossible the testing of preventive technologies. At the same time, the manipulation of young people represent an ethical issue. Test, for example, gene therapy for a healthy young man can be potentially risky.
The best solution would be to find a way to measure biological aging without the need to wait until the patient is actually old. For this, the researchers looking for a marker that reflects biological age.
For this role there are several promising candidates, for example, telomeres — the spikes at the ends of chromosomes that shorten as we age. Scientists are also looking for epigenetic mutilazioni watch. Our DNA or genes are mostly unchanged, but a manifestation of parts of genes changes over time depending on environmental factors. Epigenetics studies changes. If genetics would have been recorded on the note sheet, the DNA would be notes, as epigenetics set of instructions — clock size, pace, which would indicate us how to play these notes. Epigenetic changes occur through the methylation, or adding methyl groups to nuclear DNA, but as we age, DNA methylation slows down. Epigenetic mutilazioni watch will help to relate what we know about methylation and epigenetics and to compare it with the biological age.
Among other potentially promising timers are profiles of inflammatory cytokines that characterize the properties of cytokines, proteins that are included in an alarm system in the cells that are associated with metabolic markers and markers of aging. They are like the fingerprints that retain cellular processes, such as aging.
Until you find a suitable metric, we do not know what measures for the prevention of aging will work, if at all possible.
Death is at all natural?
Our knowledge about aging is similar to knowledge about sleep. This is a fundamental sign of life, but we don’t know how it works. We see how people age, and begin to understand how to discern the markers of aging, but don’t quite understand why we age. Human aging is a bug or a feature?
This year, scientists from the University of albert Einstein has published a study based on existing data about the course of life. His conclusion is that the natural life cycle lasts for about 115 years. While most of us live to be 70, the number lived to 100 incredibly small. “We wanted to see what kind of progress we have achieved or not achieved in terms of human longevity,” wrote Brandon Millholland, lead author of the study.
The reason, as the researchers claim, is not that death is the ultimate goal, but rather in the fact that aging is a byproduct of genetic codes which define our lives — development, birth, growth, reproduction. Codes that give us life, have imperfections, leading to death. And although scientists may try to extend the life further natural limits, we still end up with them will be limited, as if trying to build a skyscraper on the Foundation of a country house. Not that no one could live longer 115 — Millholland says that live to 125 on average one in ten thousand is just statistically unbelievable.
It may seem that it’s not consistent with the history of mankind. The life expectancy of Americans increased from 47 years in the early twentieth century, to 78.7 years in our day, which you can make the assumption that the cycle of human life is easily changed. But it is not. The increase in life expectancy, which is the average meaning of all life cycles, to a great extent obliged to reduce infant mortality as public health, hygiene and medicine have dramatically reduced the number of children not surviving to their fifth birthday. People who lived to adulthood, he could have lived to 40, 50 or even 60 years, and sometimes longer. Thomas Jefferson died at age 83, Ben Franklin at 84, and John Adams lived to be 90. Jeanne Louise calment from France who died at 122 years and which holds the record for the longest confirmed lifespan, was born in 1875. “Her record will probably not be beaten for a very long time,” — said Millholland.
Meanwhile, the growing lobby against aging little doubling of life expectancy. They are attracted by the eternal life — longer than 4000 years of black coral or 2000-year-old sponges, or Cream pie, 38-year-old cat. At the moment there was not a single study on the establishment of an eternal organism in the wild there is also not found. Ichnogenus the only living creature known to man, this is a cancer cell, but it kills its host.
Most aging researchers do not do their job because tend to eternal life. Kennedy first started to watch the yeast from a purely scientific curiosity, and continued the research after I realized that aging is a major risk factor for many chronic diseases. Bielski in his work focuses on health inequalities — in particular, on why people with low earnings are more likely to suffer from chronic diseases. One reason: their so-called “biological aging” faster than others.
None of gerontologists with whom I spoke talked about eternal life — it is closer to slowing aging and improving health. Even de grey, the phrase “eternal life” does not like — he calls it “religious.”
One famous quote usually attributed to Ralph Waldo Emerson: “Why eternity to someone who does not know how to spend a half hour?” For most of us the goal is not in life expectancy and its quality. And if all this attention to eternal life will lead to funding true research, our life can become longer, and health is strong.