I've Decided to Live Years: The Ancient Secret to Longevity, Vitality, and Life Transformation . Learn how to be self-reliant for your health and happiness Let your long life be a blessing to yourself and others by doing good. Description. New York Times bestselling author and one of the most renowned meditation.
Table of contents
- Damage, Yes. But Aging?
- Chapter 5: The Last Chapter: Cell Aging and Death
- Error (Forbidden)
- Good news for human life spans — at age 105, death rates suddenly stop going up
Large-scale clinical studies are under way to examine the link between aging and antioxidants —compounds, such as vitamins E and C, found in fruits and vegetables as well as within our own bodies. Antioxidants are less potent than the enzymes that quash reactive oxygen species, but like the enzymes, they can disarm dangerous reactive oxygen compounds.
Many scientists speculate that another contributor to the aging process is the accumulation of cellular retirees. After cells divide about 50 times, they quit the hard work of dividing and enter a phase in which they no longer behave as they did in their youth.
Damage, Yes. But Aging?
How do our cells know when to retire? Do cellular clocks have a big hand and a little hand and go, "Tick, tock? It turns out that each cell has 92 internal clocks—one at each end of its 46 chromosomes. Before a cell divides, it copies its chromosomes so that each daughter cell will get a complete set. But because of how the copying is done, the very ends of our long, slender chromosomes don't get copied.
It's as if a photocopier cut off the first and last lines of each page. As a result, our chromosomes shorten with each cell division. Fortunately, the regions at the ends of our chromosomes—called telomeres —spell out the genetic equivalent of gibberish, so no harm comes from leaving parts of them behind. But once a cell's telomeres shrink to a critical minimum size, the cell takes notice and stops dividing.
In , scientists discovered telomerase. This enzyme extends telomeres, rebuilding them to their former lengths. In most of our cells, the enzyme is turned off before we're born and stays inactive throughout our lives. But theoretically, if turned back on, telomerase could pull cellular retirees back into the workforce.
Using genetic engineering, scientists reactivated the enzyme in human cells grown in the laboratory. As hoped, the cells multiplied with abandon, continuing well beyond the time when their telomerase-lacking counterparts had stopped. Mary was diagnosed with Werner syndrome at age 26, when she was referred to an ophthalmologist for cataracts in both eyes, a condition most commonly found in the elderly. She had developed normally until she'd reached her teens, at which point she failed to undergo the growth spurt typical of adolescents.
She remembers being of normal height in elementary school, but reports having been the shortest person in her high school graduating class, and she had slender limbs relative to the size of her trunk. In her early 20s, she noticed her hair graying and falling out, and her skin became unusually wrinkled for someone her age. Soon after the diagnosis, she developed diabetes. Although hypothetical, Mary's case is a classic example of Werner syndrome, a rare inherited disease that in many respects resembles premature aging.
People with Werner syndrome are particularly prone to cancer, cardiovascular disease, and diabetes, and they die at a young age—typically in their 40s. At a genetic level, their DNA is marked by many mutations.
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These characteristics support the theory that accumulating DNA mutations is a significant factor in normal human aging. The gene involved in Werner syndrome was identified in and was found to encode what appears to be an enzyme involved in DNA repair. This suggests that people with Werner syndrome accumulate excessive DNA mutations because this repair enzyme is either missing or not working properly. A few years after the discovery of the human Werner syndrome gene, scientists identified a corresponding gene in yeast.
Deleting the gene from yeast cells shortened their lifespan and led to other signs of accelerated aging. This supports a link between this gene and aging, and it provides scientists a model with which to study Werner syndrome and aging in general. Could reactivating telomerase in our cells extend the human lifespan? Unfortunately, the exact opposite—an untimely death from cancer—could occur.
Chapter 5: The Last Chapter: Cell Aging and Death
Cancer cells resurrect telomerase, and by maintaining the ends of the cell's chromosomes, the enzyme enables the runaway cell division that typifies cancer. It may, therefore, be a good thing that shrinking telomeres mark most of our cells for eventual retirement. Nonetheless, scientists still have high hopes for harnessing telomerase.
For instance, the enzyme could be used as a tool for diagnosing cancer, alerting doctors to the presence of a malignancy.
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Another possibility is to use chemicals that block telomerase to put the brakes on cell division in cancer cells. The search for such chemicals is on, and several candidates already have shown promise in preliminary studies. According to most scientists, aging is caused by the interplay of many factors, such as reactive oxygen species, DNA mutations, and cellular retirement. Unfortunately, as a result, there is probably no such thing as a simple anti-aging remedy. As you read this, millions of your cells are dying. Don't panic—you won't miss them.
Error (Forbidden)
Most of them are either superfluous or potentially harmful, so you're better off without them. In fact, your health depends on the judicious use of a certain kind of cell death— apoptosis. Apoptosis is so carefully planned out that it is often called programmed cell death. During apoptosis, the cell shrinks and pulls away from its neighbors.
Then, the surface of the cell appears to boil, with fragments breaking away and escaping like bubbles from a pot of boiling water. The DNA in the nucleus condenses and breaks into regular-sized fragments, and soon the nucleus itself, followed by the entire cell, disintegrates. A cellular cleanup crew rapidly mops up the remains. Cells come primed for apoptosis, equipped with the instructions and instruments necessary for their own self-destruction. They keep these tools carefully tucked away, like a set of sheathed knives, until some signal—either from within or outside the cell—triggers their release.
This initiates a cascade of carefully coordinated events that culminate in the efficient, pain-free excision of unneeded cells. There is another kind of cell death, called necrosis , that is unplanned. Necrosis can result from a sudden traumatic injury, infection, or exposure to a toxic chemical. During necrosis, the cell's outer membrane loses its ability to control the flow of liquid into and out of the cell.
The cell swells up and eventually bursts, releasing its contents into the surrounding tissue. A cleanup crew composed of immune cells then moves in and mops up the mess, but the chemicals the cells use cause the area to become inflamed and sensitive. Think of the redness and pain in your finger after you accidentally touch a hot stove. Many different kinds of injuries can cause cells to die via necrosis. It's what happens to heart cells during a heart attack, to cells in severely frostbitten fingers and toes, and to lung cells during a bout of pneumonia. Elizabeth Blackburn, a molecular biologist at the University of California, San Francisco, has been studying telomeres since the s.
She says that we can think of telomeres as the plastic caps at the ends of our shoelaces—the aglets of our genome. Her work has propelled our understanding of telomeres, in particular as they relate to aging and cancer.
Prior to her work, scientists knew telomeres existed but knew little else about them. Blackburn probed the genetic aglets through studies of a pond-dwelling microorganism called Tetrahymena. It may seem like a strange choice, but Tetrahymena has the distinct advantage of having roughly 20, chromosomes humans have 46 , so it's a rich source of telomeres.
Good news for human life spans — at age 105, death rates suddenly stop going up
In a paper, Blackburn described the structure of telomeres in detail for the first time. Even his critics say he funds some good science. Although funding pledges have been low compared to early hopes, billionaires — not just from the technology industry — have long supported research into the biology of ageing. Whereas much biomedical research concentrates on trying to cure individual diseases, say cancer, scientists in this small field hunt something larger.
They investigate the details of the ageing process with a view to finding ways to prevent it at its root, thereby fending off the whole slew of diseases that come along with ageing. Life expectancy has risen in developed countries from about 47 in to about 80 today, largely due to advances in curing childhood diseases. But those longer lives come with their share of misery. The standard medical approach — curing one disease at a time — only makes that worse, says Jay Olshansky, a sociologist at the University of Chicago School of Public Health who runs a project called the Longevity Dividend Initiative, which makes the case for funding ageing research to increase healthspan on health and economic grounds.
By tackling ageing at the root they could be dealt with as one, reducing frailty and disability by lowering all age-related disease risks simultaneously, says Olshansky. Evidence is now building that this bolder, age-delaying approach could work. Scientists have already successfully intervened in ageing in a variety of animal species and researchers say there is reason to believe it could be achieved in people. Reason for optimism comes after several different approaches have yielded promising results. Some existing drugs, such as the diabetes drug metformin, have serendipitously turned out to display age-defying effects, for example.
Several drugs are in development that mimic the mechanisms that cause lab animals fed carefully calorie-restricted diets to live longer. Others copy the effects of genes that occur in long-lived people. One drug already in clinical trials is rapamycin, which is normally used to aid organ transplants and treat rare cancers. Other drugs set to be tested in humans are compounds inspired by resveratrol, a compound found in red wine.
In , Sinclair published evidence that high doses of resveratrol extend the healthy lives of yeast cells. Although development has proved more complicated than first thought , GSK is planning a large clinical trial this year, says Sinclair. He is now working on another drug that has a different way of activating the same pathway. One of the more unusual approaches being tested is using blood from the young to reinvigorate the old. The idea was borne out in experiments which showed blood plasma from young mice restored mental capabilities of old mice.
Tony Wyss-Coray, a researcher at Stanford leading the work, says that if it works he hopes to isolate factors in the blood that drive the effect and then try to make a drug that does a similar thing. James Kirkland, a researcher who studies ageing at the Mayo Clinic, says he knows of about 20 drugs now — more than six of which had been written up in scientific journals — that extended the lifespan or healthspan of mice. The aim is to begin tests in humans, but clinical studies of ageing are difficult because of the length of our lives, though there are ways around this such as testing the drugs against single conditions in elderly patients and looking for signs of improvements in other conditions at the same time.
Quite what the first drug will be, and what it will do, is unclear. Ideally, you might take a single pill that would delay ageing in every part of your body. Led by Elisabetta Barbi at the Sapienza University of Rome and experts at the Italian National Institute of Statistics, the new research tracked everyone in Italy born between and who lived to or beyond. The data included 3, people, of whom 3, were women and were men. The national Italian registry, which requires yearly updates from citizens, provides more-accurate information than U.
Using similar longevity data from Japan and Western countries collected by the Max Planck Institute for Demographic Research, Rootzen rejected the notion of a hard limit to human life in research published in December in the journal Extremes. He predicted it would be possible in the next quarter-century for someone to reach the age of Two years ago, researchers at the Albert Einstein College of Medicine argued in Nature , based on longevity data from 40 countries, for a maximum limit at around , as The Washington Post reported.
He agreed that the Gompertz law must end, because mortality rates cannot double beyond percent. But this study has not convinced him that mortality rates stop increasing at around 50 percent. Rootzen disputed the conclusions of the Nature paper estimating a limit on life span, saying the authors had made a statistical error: Yes, the odds of living beyond are low, but that does not mean a limit exists, he said. He used the example of throwing darts at a dartboard. You might not get a bull's eye in 10 throws. Toss thousands of darts at a dartboard, though, and maybe you will.
The numbers of the very old are growing. In Italy, for example, four people born in lived to or beyond.
More than people born in lived as long. Between and , infant mortality in Italy lessened, Wachter said. In later decades, the care of and year-olds improved, too, welcoming more people into the centenarian ranks.