Researchers Uncover Link Between Mediterranean Diet, Aging
The benefits of the Mediterranean diet could be closely tied to telomeres, one of many biomarkers of aging, according to a recent study by researchers at the Harvard-affiliated Brigham and Women's Hospital.
By analyzing 4,676 disease-free women from the Nurses’ Health Study, researchers found that adherence to the Mediterranean diet—which has long been associated with longer life expectancy and a lower risk of heart disease—is linked to longer telomeres.
“We look at telomeres, which are the ends of chromosomes,” said Immaculata De Vivo, senior author of the study and an associate professor at the Medical School and the School of Public Health. “If you look at a shoelace, there’s a plastic part at the end that protects the shoestring. That’s what a telomere does. It keeps the chromosome from falling apart.”
This protective structure of chromosomes gets shorter each time a cell divides, and shorter telomeres are correlated with lower life expectancy and a higher risk of diseases related to aging.
Clifford W. Lo, an associate professor in the School of Public’s Health Department of Nutrition who was not a part of the study, said that the new study provides strong scientific evidence for the benefits of the Mediterranean diet.
“For many years, nutrition has concentrated on nutrients rather than food and diets, and most of the dietary suggestions by the U.S. government are not specifically tested in regard to mechanism,” Lo said.
The Mediterranean diet has drawn increased scientific support within the last decade, which could help persuade the public to adopt it, according to Lo.
Moreover, health benefits are not the only incentive for people to practice the Mediterranean diet. The dietary pattern, which consists of wine, olive oil, whole grain, fish, poultry, fruits, and vegetables, is “not only good for you, but also delicious,” De Vivo said.
While the researchers have found a correlation, scientists are still uncertain if the Mediterranean diet specifically results in longer telomeres. “Our study shows that the dietary pattern is effective only when all components are put together, so it should be the combined result of different substances,” said Marta Crous Bou, first author of the study and a postdoctoral research fellow.
According to De Vivo and Crous Bou, the next steps are to look for evidence of causation between these variables and also to test the effect of the Mediterranean diet on men.
—Crimson staff writer Tianxing V. Lan can be reached at tianxinglan@college.harvard.edu.
Sit Less, Live Longer?
If people need motivation to get up from their office chairs or couches and become less sedentary, two useful new studies could provide the impetus. One found that sitting less can slow the aging process within cells, and the other helpfully underscores that standing up — even if you are standing still — can be good for you as well.
For most of us nowadays, sitting is our most common waking activity, with many of us sitting for eight hours or more every day. Even people who exercise for an hour or so tend to spend most of the remaining hours of the day in a chair.
The health consequences of this sedentariness are well-documented. Past studies have found that the more hours that people spend sitting, the more likely they are to develop diabetes, heart disease and other conditions, and potentially to die prematurely — even if they exercise regularly.
But most of these studies were associational, meaning that they found a link between sitting and illness, but could not prove whether or how sitting actually causes ill health.
So for the most groundbreaking of the new studies, which waspublished this month in the British Journal of Sports Medicine, scientists in Sweden decided to mount an actual experiment, in which they would alter the amount of time that people spent exercising and sitting, and track certain physiological results. In particular, with this experiment, the scientists were interested in whether changes in sedentary time would affect people’s telomeres.
If you are unfamiliar with the componentry of your genes, telomeres are the tiny caps on the ends of DNA strands. They shorten and fray as a cell ages, although the process is not strictly chronological. Obesity, illness and other conditions can accelerate the shortening, causing cells to age prematurely, while some evidence suggests that healthy lifestyles may preserve telomere length, delaying cell aging.
For the new experiment, the Swedish scientists recruited a group of sedentary, overweight men and women, all aged 68, and drew blood, in order to measure the length of telomeres in the volunteers’ white blood cells. Then half of the volunteers began an individualized, moderate exercise program, designed to improve their general health. They also were advised to sit less.
The other volunteers were told to continue with their normal lives, although the scientists urged them to try to lose weight and be healthy, without offering any specific methods.
After six months, the volunteers all returned for a second blood draw and to complete questionnaires about their daily activities. These showed that those in the exercise group were, not surprisingly, exercising more than they had been previously. But they were also, for the most part, sitting substantially less than before.
And when the scientists compared telomeres, they found that the telomeres in the volunteers who were sitting the least had lengthened. Their cells seemed to be growing physiologically younger.
Meanwhile, in the control group telomeres generally were shorter than they had been six months before.
But perhaps most interesting, there was little correlation between exercise and telomere length. In fact, the volunteers in the exercise group who had worked out the most during the past six months tended now to have slightly less lengthening and even some shortening, compared to those who had exercised less but stood up more.
Reducing sedentary time had lengthened telomeres, the scientists concluded, while exercising had played little role.
Exactly what the volunteers did in lieu of sitting is impossible to say with precision, said Per Sjögren, a professor of public health at Uppsala University in Sweden, who led the study, because the researchers did not track their volunteers’ movement patterns with monitors. But “it’s most likely,” he said, that “sitting time was predominantly replaced with low-intensity activities,” and in particular with time spent standing up.
Which makes the second new study of sedentary behavior particularly relevant. Standing is not, after all, physically demanding for most people, and some scientists have questioned whether merely standing up — without also moving about and walking — is sufficiently healthy or if standing merely replaces one type of sedentariness with another.
If so, standing could be expected to increase health problems and premature death, as sitting has been shown to do.
To find out whether that situation held true, Peter Katzmarzyk, a professor of public health at the Pennington Biomedical Research Center in Baton Rouge, La., and an expert on sedentary behavior, turned to a large database of self-reported information about physical activity among Canadian adults. He noted the amount of time that the men and women had reported standing on most days over the course of a decade or more and crosschecked that data with death records, to see whether people who stood more died younger.
The results, published in May in Medicine & Science in Sports & Exercise, are soothing if predictable. Dr. Katzmarzyk found no link between standing and premature death. Rather, as he writes in the study, “mortality rates declined at higher levels of standing,” suggesting that standing is not sedentary or hazardous, a conclusion with which our telomeres would likely concur.
If you are unfamiliar with the componentry of your genes, telomeres are the tiny caps on the ends of DNA strands. They shorten and fray as a cell ages, although the process is not strictly chronological. Obesity, illness and other conditions can accelerate the shortening, causing cells to age prematurely, while some evidence suggests that healthy lifestyles may preserve telomere length, delaying cell aging.
Nobel prize for chromosome find
Chromosomes house genetic material
|
This year's Nobel prize for medicine goes to three US-based researchers who discovered how the body protects the chromosomes housing vital genetic code.
Elizabeth Blackburn, Carol Greider and Jack Szostak jointly share the award.Their work revealed how the chromosomes can be copied and has helped further our understanding on human ageing, cancer and stem cells.
The answer lies at the ends of the chromosomes - the telomeres - and in an enzyme that forms them - telomerase.
 |
FROM THE PM PROGRAMME
 |
The 46 chromosomes contain our genome written in the code of life - DNA.
When a cell is about to divide, the DNA molecules, housed on two strands, are copied.
But scientists had been baffled by an anomaly.
For one of the two DNA strands, a problem exists in that the very end of the strand cannot be copied.
Protecting the code of life
Therefore, the chromosomes should be shortened every time a cell divides - but in fact that is not usually the case.
If the telomeres did repeatedly shorten, cells would rapidly age.
|  The discoveries ... have added a new dimension to our understanding of the cell, shed light on disease mechanisms, and stimulated the development of potential new therapies
The Nobel Assembly
|
Conversely, if the telomere length is maintained, the cell would have eternal life, which could also be problematic. This happens in the case of cancer cells.
This year's prize winners solved the conundrum when they discovered how the telomere functions and found the enzyme that copies it.
Elizabeth Blackburn, of the University of California, San Francisco, and Jack Szostak, of Harvard Medical School, discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation.
Joined by Johns Hopkins University's Carol Greider, then a graduate student, Blackburn started to investigate how the teleomeres themselves were made and the pair went on to discover telomerase - the enzyme that enables DNA polymerases to copy the entire length of the chromosome without missing the very end portion.
Their research has led others to hunt for new ways to cure cancer.
It is hoped that cancer might be treated by eradicating telomerase. Several studies are under way in this area, including clinical trials evaluating vaccines directed against cells with elevated telomerase activity.
Some inherited diseases are now known to be caused by telomerase defects, including certain forms of anaemia in which there is insufficient cell divisions in the stem cells of the bone marrow.
The Nobel Assembly at Sweden's Karolinska Institute, which awarded the prize, said: "The discoveries... have added a new dimension to our understanding of the cell, shed light on disease mechanisms, and stimulated the development of potential new therapies."
Carol Greider, now 48, said she was phoned in the early hours with the news that she had won.
She said: "It's really very thrilling, it's something you can't expect."
Elizabeth Blackburn, now 60, shared her excitement, saying: "Prizes are always a nice thing. It doesn't change the research per se, of course, but it's lovely to have the recognition and share it with Carol Greider and Jack Szostak."
Professor Roger Reddel of the Children's Medical Research Institute in Sydney, Australia, said: "The telomerase story is an outstanding illustration of the value of basic research."
Sir Leszek Borysiewicz, chief executive of the Medical Research Council, said: "The Medical Research Council extends its congratulations to Blackburn, Greider and Szostak on winning the 2009 Nobel Prize.
"Their research on chromosomes helped lay the foundations of future work on cancer, stem cells and even human ageing, research areas that continue to be of huge importance to the scientists MRC funds and to the many people who will ultimately benefit from the discoveries they make."
telomere
Line breaks: telo|mere
Pronunciation: /ˈtiːlə(ʊ)mɪə, ˈtɛl-/
NOUN
GeneticsOrigin
1940s: from Greek telos 'end' + meros 'part'.
Derivatives
chromosome
Line breaks: chromo|some 染色體
Pronunciation: /ˈkrəʊməsəʊm
/
NOUN
Biology
Each chromosome consists of a DNA double helix bearing a linear sequence of genes, coiled and recoiled around aggregated proteins (histones). Their number varies from species to species: humans have 22 pairs plus the two sex chromosomes (two X chromosomes in females, one X and one Y in males). During cell division each DNA strand is duplicated, and the chromosomes condense to become visible as distinct pairs of chromatids joined at the centromere
Each chromosome consists of a DNA double helix bearing a linear sequence of genes, coiled and recoiled around aggregated proteins (histones). Their number varies from species to species: humans have 22 pairs plus the two sex chromosomes (two X chromosomes in females, one X and one Y in males). During cell division each DNA strand is duplicated, and the chromosomes condense to become visible as distinct pairs of chromatids joined at the centromere
Origin
late 19th century: coined in German from Greek khrōma'colour' + sōma 'body'.
late 19th century: coined in German from Greek khrōma'colour' + sōma 'body'.
age
Syllabification: (age)
Pronunciation: /āj/
Translate age | into French | into German | into Italian | into Spanish
沒有留言:
張貼留言