Posts Tagged ‘aging’

by Bob Yirka

A team of researchers from several institutions in Iceland and the U.S. has conducted a unique blood serum investigation and discovered multiple protein networks that are involved in the aging process. In their paper published in the journal Science, the group describes their study and what they found.

Prior research has shown that when older mice have their blood systems connected to younger mice, the older mice experience improvements in age-related organ deterioration. This finding has led scientists to suspect that aging might be caused by something in the blood. In this new effort, the researchers sought to test this idea by studying proteins in the circulatory system.

The study consisted of analyzing blood samples from 5,457 people living in Iceland, all of whom were over the age of 65 and who were participants in an ongoing study called Age, Gene/Environment Susceptibility. The volunteers had also been chosen specifically to represent a cross section of the people living in Iceland. The major part of the blood analysis involved creating a panel of DNA aptamers (short sequences that bind to proteins) that could be used to recognize proteins, both known and unknown. Blood serum from the volunteers was then compared against the panels and the results were analyzed by a computer looking for patterns.

The researchers report that they discovered 27 networks that showed evidence of coordinated pattern expression. These networks, or modules, as the researchers call them, were different from one another in size and form and were made of proteins from both tissue and organs. They also report that many of the modules had expression patterns that have in the past been associated with age-related diseases such as heart disease and metabolic syndrome—and there were some that were also associated with mortality in the years after the samples were taken from the volunteers. The group suggests their findings offer more evidence of the role blood serum plays in the aging process.

The researchers report that they also looked for the means by which the networks they discovered are regulated and found that approximately 60 percent of mechanisms involved are unknown.

More information: Valur Emilsson et al. Co-regulatory networks of human serum proteins link genetics to disease, Science (2018). DOI: 10.1126/science.aaq1327

https://m.medicalxpress.com/news/2018-08-blood-serum-reveals-networks-proteins.html

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by Elie Dolgin

There might be no natural limit to how long humans can live — at least not one yet in sight — contrary to the claims of some demographers and biologists.

That’s according to a statistical analysis published Thursday in Science1 on the survival probabilities of nearly 4,000 ‘super-elderly’ people in Italy, all aged 105 and older.

A team led by Sapienza University demographer Elisabetta Barbi and University of Roma Tre statistician Francesco Lagona, both based in Rome, found that the risk of death — which, throughout most of life, seems to increase as people age — levels off after age 105, creating a ‘mortality plateau’. At that point, the researchers say, the odds of someone dying from one birthday to the next are roughly 50:50 (see ‘Longevity unlimited’).

“If there is a mortality plateau, then there is no limit to human longevity,” says Jean-Marie Robine, a demographer at the French Institute of Health and Medical Research in Montpellier, who was not involved in the study.

That would mean that someone like Chiyo Miyako, the Japanese great-great-great-grandmother who, at 117, is the world’s oldest known person, could live for years to come — or even forever, at least hypothetically.

Researchers have long debated whether humans have an upper age limit. The consensus holds that the risk of death steadily increases in adulthood, up to about age 80 or so. But there’s vehement disagreement about what happens as people enter their 90s and 100s.

Some scientists have examined demographic data and concluded that there is a fixed, natural ‘shelf-life’ for our species and that mortality rates keep increasing. Others have looked at the same data and concluded that the death risk flattens out in one’s ultra-golden years, and therefore that human lifespan does not have an upper threshold.

Age rage

In 2016, geneticist Jan Vijg and his colleagues at Albert Einstein College of Medicine in New York City rekindled the debate when they analysed the reported ages at death for the world’s oldest individuals over a half-century. They estimated that human longevity hit a ceiling at about 115 years — 125 tops.

Vijg and his team argued2 that with few, if any, gains in maximum lifespan since the mid-1990s, human ageing had reached its natural limit. The longest known lifespan belongs to Jeanne Calment, a French super-centenarian who died in 1997 at age 122.

Experts challenged the statistical methods in the 2016 study, setting off a firestorm into which now step Barbi and Lagona. Working with colleagues at the Italian National Institute of Statistics, the researchers collected records on every Italian aged 105 years and older between 2009 and 2015 — gathering certificates of death, birth and survival in an effort to minimize the chances of ‘age exaggeration’, a common problem among the oldest old.

They also tracked individual survival trajectories from one year to the next, rather than lump people into age intervals as previous studies that combine data sets have done. And by focusing just on Italy, which has one of the highest rates of centenarians per capita in the world, they avoided the issue of variation in data collection among different jurisdictions.

As such, says Kenneth Howse, a health-policy researcher at the Oxford Institute of Population Ageing in the United Kingdom, “these data provide the best evidence to date of extreme-age mortality plateaus in humans”.

Ken Wachter, a mathematical demographer at the University of California, Berkeley, and an author of the latest study, suspects that prior disputes over the patterns of late-life mortality have largely stemmed from bad records and statistics. “We have the advantage of better data,” he says. “If we can get data of this quality for other countries, I expect we’re going to see much the same pattern.”

Robine is not so sure. He says that unpublished data from France, Japan and Canada suggest that evidence for a mortality plateau is “not as clear cut”. A global analysis is still needed to determine whether the findings from Italy reflect a universal feature of human ageing, he says.

Off limits

The world is home to around 500,000 people aged 100 and up — a number that’s predicted to nearly double with each coming decade. Even if the risk of late-life mortality remains constant at 50:50, the swelling global membership in the 100-plus club should translate into a creep upwards in the oldest person alive by about one year per decade, says Joop de Beer, a longevity researcher at the Netherlands Interdisciplinary Demographic Institute in The Hague.

Many researchers say they hope to better understand what’s behind the levelling off of mortality rates in later life. Siegfried Hekimi, a geneticist at McGill University in Montreal, Canada, speculates that the body’s cells eventually reach a point where repair mechanisms can offset further damage to keep mortality rates level.

“Why this plateaus out and what it means about the process of ageing — I don’t think we have any idea,” Hekimi says.

For James Kirkland, a geriatrician at the Mayo Clinic in Rochester, Minnesota, the strong evidence for a mortality plateau points to the possibility of forestalling death at any age. Some experts think that the very frail are beyond repair. But if the odds of dying don’t increase over time, he says, interventions that slow ageing are likely to make a difference, even in the extremely old.

Not everyone buys that argument — or the conclusions of the latest paper.

Brandon Milholland, a co-author of the 2016 Nature paper, says that the evidence for a mortality plateau is “marginal”, as the study included fewer than 100 people who lived to 110 or beyond. Leonid Gavrilov, a longevity researcher at the University of Chicago in Illinois, notes that even small inaccuracies in the Italian longevity records could lead to a spurious conclusion.

Others say the conclusions of the study are biologically implausible. “You run into basic limitations imposed by body design,” says Jay Olshansky, a bio-demographer at the University of Illinois at Chicago, noting that cells that do not replicate, such as neurons, will continue to wither and die as a person ages, placing upper boundaries on humans’ natural lifespan.

This study is thus unlikely to be the last word on the age-limit dispute, says Haim Cohen, a molecular biologist at Bar-Ilan University in Ramat-Gan, Israel. “I’m sure that the debate is going to continue.”

Psychologists at the University of Sussex have found a link between depression and an acceleration of the rate at which the brain ages. Although scientists have previously reported that people with depression or anxiety have an increased risk of dementia in later life, this is the first study that provides comprehensive evidence for the effect of depression on decline in overall cognitive function (also referred to as cognitive state), in a general population.

For the study, published today, Thursday 24 May 2018, in the journal Psychological Medicine, researchers conducted a robust systematic review of 34 longitudinal studies, with the focus on the link between depression or anxiety and decline in cognitive function over time. Evidence from more than 71,000 participants was combined and reviewed. Including people who presented with symptoms of depression as well as those that were diagnosed as clinically depressed, the study looked at the rate of decline of overall cognitive state – encompassing memory loss, executive function (such as decision making) and information processing speed – in older adults.

Importantly, any studies of participants who were diagnosed with dementia at the start of study were excluded from the analysis. This was done in order to assess more broadly the impact of depression on cognitive ageing in the general population. The study found that people with depression experienced a greater decline in cognitive state in older adulthood than those without depression. As there is a long pre-clinical period of several decades before dementia may be diagnosed, the findings are important for early interventions as currently there is no cure for the disease.

Lead authors of the paper, Dr Darya Gaysina and Amber John from the EDGE (Environment, Development, Genetics and Epigenetics in Psychology and Psychiatry) Lab at the University of Sussex, are calling for greater awareness of the importance of supporting mental health to protect brain health in later life.

Dr Gaysina, a Lecturer in Psychology and EDGE Lab Lead, comments: “This study is of great importance – our populations are ageing at a rapid rate and the number of people living with decreasing cognitive abilities and dementia is expected to grow substantially over the next thirty years.

“Our findings should give the government even more reason to take mental health issues seriously and to ensure that health provisions are properly resourced. We need to protect the mental wellbeing of our older adults and to provide robust support services to those experiencing depression and anxiety in order to safeguard brain function in later life.”

Researcher Amber John, who carried out this research for her PhD at the University of Sussex adds: “Depression is a common mental health problem – each year, at least 1 in 5 people in the UK experience symptoms. But people living with depression shouldn’t despair – it’s not inevitable that you will see a greater decline in cognitive abilities and taking preventative measures such as exercising, practicing mindfulness and undertaking recommended therapeutic treatments, such as Cognitive Behaviour Therapy, have all been shown to be helpful in supporting wellbeing, which in turn may help to protect cognitive health in older age.”

The research paper, ‘Affective problems and decline in cognitive state in older adults’ will be available at: https:// doi.org/10.1017/S0033291718001137 from Thursday 24 May 2018.

http://www.sussex.ac.uk/broadcast/read/44977

by MELISSA BREYER

If there’s a single way of eating that persists in laying claim as one of the healthiest, it’s the Mediterranean diet. Experts continue to sing the praises of eating plenty of olive oil, plant foods, fish and wine.

The latest research — following several years of headline-making studies — makes it hard to argue with them.

Following a Mediterranean diet can protect against the harmful effects of air pollution, according to a 2018 study conducted by New York University. The study analyzed about 550,000 people for 17 years and factored in their level of exposure to pollution. Those who followed the Mediterranean diet compared to those who didn’t had a lower risk of dying from cardiovascular disease and heart attacks.

“Air pollution is hypothesized to cause bad health effects through oxidative stress and inflammation, and the Mediterranean diet is really rich in foods that are anti-inflammatory and have antioxidants that might intervene through those avenues,” said study author Chris Lim on Time.com.

It’s worth noting that the diet doesn’t protect against ozone exposure. (Researchers believe that ozone exposure effects the cardiac system differently.)

Why the hits keep on coming

Researchers have been uncovering the benefits of this particular diet for years. In fact, the diet’s benefits for heart health were so clear in one 2013 study that researchers ended the study early, saying it was unethical to continue.

Research from 2014 added to the accolades. Scientists in Boston looked at the nutritional data from 4,676 women participating in the Harvard Nurses’ Health Study — the well-known ongoing prospective cohort analysis ­— and discovered that those whose food choices most closely followed a Mediterranean diet had longer telomeres. Telomeres are the protective buffers on the ends of chromosomes and can be used as a biomarker of aging; the longer they are, the better.

“We know that having shorter telomeres is associated with a lower life expectancy and a greater risk of cancer, heart disease and other diseases,” said study coauthor Immaculata De Vivo, an associate professor of medicine at Brigham and Women’s Hospital. “Certain lifestyle factors like obesity, sugary sodas, and smoking have been found to accelerate telomere shortening, and now our research suggests the Mediterranean diet can slow this shortening.”

The key is cell aging

The Mediterranean diet isn’t a specific diet plan per se, but rather eating in the traditional style of those living in Mediterranean countries. It’s characterized by consuming a lot of vegetables, fruits, nuts, legumes and unrefined grains. There is plenty of olive oil, but little saturated fat; a moderate intake of fish, but little dairy, meat and poultry. And while cookies and sugar are limited, a regular but moderate dose of wine is involved.

It’s thought that the antioxidants present in the favored foods protect against cell aging. While the researchers didn’t find that any specific food provided the silver bullet, they suggest that it was a combination of the components that predicted telomere length.

The researchers scored each woman’s diet according to how closely it adhered to Mediterranean components. What they found was that each one-point change in their grading system equated to an extra year and a half of life. A three-point change, the study notes, would correspond to an average 4.5 years of aging, which is comparable to the difference between smokers with non-smokers.

The researchers also concluded that women who may have veered slightly from the Mediterranean diet but who still ate a healthy diet — like eating chicken and low-fat dairy products in addition to the Mediterranean basics — also had longer telomeres than those who ate a standard American diet with red meat, saturated fats, sweets and empty calories. Those who followed the Mediterranean diet, however, had the longest telomeres on average.

https://www.mnn.com/food/healthy-eating/stories/mediterranean-diet-could-add-years-to-your-life

Brown University researchers studying the biology of aging have demonstrated a new strategy for stimulating autophagy, the process by which cells rebuild themselves by recycling their own worn-out parts.

In a study published in the journal Cell Reports, the researchers show that the approach increased the lifespans of worms and flies, and experiments in human cells hint that the strategy could be useful in future treatments for Alzheimer’s disease, ALS and other age-related neurodegenerative conditions.

“Autophagy dysfunction is present across a range of age-related diseases including neurodegeneration,” said Louis Lapierre, an assistant professor of molecular biology, cell biology and biochemistry at Brown who led the work. “We and others think that by learning how to influence this process pharmacologically, we might be able to affect the progression of these diseases. What we’ve shown here is a new and conserved entry point for stimulating autophagy.”

Autophagy has become a hot topic in recent years, earning its discoverer the Nobel Prize in Physiology and Medicine in 2016. The process involves the rounding up of misfolded proteins and obsolete organelles within a cell into vesicles called autophagosomes. The autophagosomes then fuse with a lysosome, an enzyme-containing organelle that breaks down those cellular macromolecules and converts it into components the cell can re-use.

Lapierre and his colleagues wanted to see if they could increase autophagy by manipulating a transcription factor (a protein that turns gene expression on and off) that regulates autophagic activity. In order for the transcription factor to switch autophagic activity on, it needs to be localized in the nucleus of a cell. So Lapierre and his team screened for genes that enhance the level of the autophagy transcription factor, known as TFEB, within nuclei.

Using the nematode C. elegans, the screen found that reducing the expression of a protein called XPO1, which transports proteins out of the nucleus, leads to nuclear accumulation of the nematode version of TFEB. That accumulation was associated with an increase in markers of autophagy, including increased autophagosome, autolysosomes as well as increased lysosome biogenesis. There was also a marked increase in lifespan among the treated nematodes of between about 15 and 45 percent.

“What we showed was that by blocking the escape of this transcription factor from the nucleus, we could not only influence autophagy but we could get an increase in lifespan as well,” Lapierre said.

The next step was to see if there were drugs that could mimic the effect of the gene inhibition used in the screening experiment. The researchers found that selective inhibitors of nuclear export (SINE), originally developed to inhibit XPO1 to treat cancers, had a similar effect — increasing markers of autophagy and significantly increasing lifespan in nematodes.

The researchers then tested SINE on a genetically modified fruit fly that serves as a model organism for the neurodegenerative disease ALS. Those experiments showed a small but significant increase in the lifespans of the treated flies. “Our data suggests that these compounds can alleviate some of the neurodegeneration in these flies,” Lapierre said.

As a final step, the researchers set out to see if XPO1 inhibition had similar effects on autophagy in human cells as it had in the nematodes. After treating a culture of human HeLa cells with SINE, the researchers found that, indeed, TFEB concentrations in nuclei increased, as did markers of autophagic activity and lysosomal biogenesis.

“Our study tells us that the regulation of the intracellular partitioning of TFEB is conserved from nematodes to humans and that SINE could stimulate autophagy in humans,” Lapierre said. “SINE have been recently shown in clinical trials for cancer to be tolerated, so the potential for using SINE to treat other age-related diseases is there.”

Future research, Lapierre said, will focus on testing these drugs in more clinically relevant models of neurodegenerative diseases. But this initial research is a proof of concept for this strategy as a means to increase autophagy and potentially treat age-related diseases.

Lapierre is a faculty member in the newly approved Center on the Biology of Aging within the Brown Institute for Translational Science. This center, led by Professor of Biology John Sedivy, studies the biological mechanisms of aging. The center’s mission is to expand biomedical research and education programs in the emerging discipline of biogerontology, and to bring forth scientific discoveries related to aging and associated disorders.

Want to prolong your life expectancy by more than a decade? A new study suggests that you can do just that by following these five healthy habits: never smoke, maintain a healthy body-mass index, keep up moderate to vigorous exercise, don’t drink too much alcohol, and eat a healthy diet.

Adhering to those five lifestyle factors at age 50, compared with not adhering to any of them, was associated with 14 additional years of life expectancy among women and 12.2 additional years among men in the study, published in the journal Circulation on Monday.

Each of those factors is significantly associated with a reduced risk of dying from the top two killers in the United States, cardiovascular disease and cancer, according to the study.
About 610,000 people die of heart disease in the US each year, which is about one in every four deaths, according to the US Centers for Disease Control and Prevention.
About 609,640 Americans are expected to die of cancer this year, according to the American Cancer Society.

“These are some of the leading causes of premature death, so by preventing or reducing the incidence of those diseases, it promotes longevity, and it also improves survival after diagnosis of those diseases,” said Dr. Meir Stampfer, a professor of medicine at Harvard Medical School and professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, who was a co-author of the study.

“We can do so much better for having a long healthy life by pretty simple minimal changes in our behavior, and only 8% of adults in our country are adhering to these,” he said. “The main take-home message is that there’s huge gains in health and longevity to be had just by simple changes in our behavior pattern, and as a country, I think we need to make it easier for ourselves to do this by promoting tobacco cessation, by providing better environments for physical activity and so on.”

Globally, the US ranks 43rd when it comes to life expectancy at birth, with an average life expectancy of 80, according to 2017 data from the Central Intelligence Agency’s World Factbook.
The three countries ranked highest for life expectancy at birth are Monaco, with 89.4 years; Japan, with 85.3 years; and Singapore, with 85.2 years, according to those data.

The countries with the lowest life expectancy at birth, based on that data, are Chad, with 50.6 years; Guinea-Bissau, with 51 years; and Afghanistan, with 51.7 years.

The ‘surprising’ impact of behaviors on longevity

For the new study, researchers measured the association between those five lifestyle factors and premature death using data from the national Nurses’ Health Study and the Health Professionals Follow-Up Study. The data came from 1980 to 2014 and included more than 122,000 people combined.

Then, the researchers used data from the National Health and Nutrition Examination Surveys to estimate the distribution of those modifiable lifestyle factors among adults in the United States. Those data, from 2013 to 2014, consisted of 2,128 adults, 50 to 80 years old.

The researchers also derived death rates of US adults using the CDC’s Wide-Ranging Online Data for Epidemiologic Research database.

After analyzing the data, the researchers found that, in 2014, the overall projected life expectancy at age 50 was to live 33.3 more years for women and 29.8 more years for men.

Yet among the adults who reported that they adopted all five healthy lifestyle factors, the researchers found, they lived 43.1 more years among women and 37.6 more years among men.

Among those adults who reported that they adhered to none of the five healthy lifestyle factors, the researchers found that they lived only 29 additional years among women and 25.5 additional years among men.

“To me, the surprising outcome was how strong it was: what a big impact these simple behaviors could have on life expectancy,” Stampfer said. “I was surprised that it was that pronounced.”

Among the women, on average, about 30.8% of the life expectancy at age 50 that they gained from adopting five, versus zero, of those lifestyle factors was attributed to a reduced risk of cardiovascular disease death; 21.2% was attributed to a reduced risk of cancer and 48% to other causes of death.

Among the men, those percentages were 34.1% attributed to a reduced risk of cardiovascular disease death, 22.8% attributed to a reduced risk of cancer and 43.1% to other causes.

The study had some limitations, including that the data on adherence to the five lifestyle factors were all self-reported, making outcome vulnerable to measurement errors.

Also, the data analysis did not include measures of certain health conditions that are risk factors for a shorter life expectancy, such as diabetes or high blood pressure.

That limitation, however, “is both a strength and a limitation, in a way … because what we’re estimating here is the prolongation of life expectancy just based on behaviors,” Stampfer said.
“Obviously, it’s much better to do these healthy behaviors from childhood, really, but if you’re beyond age 50, beyond age 60, beyond age 70, it’s not too late,” he added.

The factor that was seen as more ‘powerful’

The findings should encourage and motivate people to adopt a healthier lifestyle, said Dr. Douglas Vaughan, chairman of the department of medicine in Northwestern University’s Feinberg School of Medicine, who was not involved in the study.

Though the study highlighted how the combination of all five lifestyle factors could help prolong life expectancy, Vaughan pointed out how each individual factor also was tied to a reduced risk of premature death.

“It looks like cigarette smoking has a more powerful effect than the other lifestyle changes or behaviors. Certainly, maintaining a reasonable body-mass index is a great way to protect oneself against the development of diabetes,” Vaughan said.

Body-mass index, a calculation derived from a person’s weight and height, is used as a screening tool for body fatness. A normal or healthy body-mass index is typically said to be between 18.5 and 24.9.

“So, in aggregate, we see the effect on longevity, but you can imagine it’s largely through effects on cardiovascular risk and metabolic risk,” Vaughan said. “It suggests potentially at a defined point in life, say age 50, if you adhere to a healthy paradigm like this, you can have an impact on your longevity and on your health span.”

Dr. Jack Der-Sarkissian, a family medicine physician and assistant area medical director of Kaiser Permanente Los Angeles Medical Center, called smoking “the least-debated health risk factor.”

“Beyond cancer risk, smoking contributes to lung disease, heart disease and diabetes. The study shows that even minimal smoking — from one to 14 cigarettes a day — is associated with increased death due to cancer and heart disease,” said Der-Sarkissian, who was not involved in the new study.

As for some of the other lifestyle factors, “getting weight below a BMI of 30 appears to help considerably, according to the study. A higher body weight is linked to increased risk of diabetes and cancer, among other obesity-related conditions,” he said. “The study suggests physical activity of at least 30 minutes a day of moderate or vigorous activities, including brisk walking.”

https://www.cnn.com/2018/04/30/health/life-expectancy-habits-study/index.html


By Alex Horton

At 117, Nabi Tajima was older than modern-day Australia, and everyone else known to live on the planet.

Tajima, born Aug. 4, 1900, in Araki, Japan, and recognized as the world’s oldest person, has passed on that mantle. She died Saturday, having been hospitalized since January, the Associated Press reported, and was the last known person born in the 19th century.

She was living in the small island town of Kikai, the AP reported.

The title of “world’s oldest living person” is a remarkable, if fleeting, one. Tajima claimed the distinction in September, when fellow 117-year-old Violet Brown died in Jamaica. Brown was the oldest person in the world for about five months.

Tajima was in the exclusive group of supercentenarians, people who have crossed the 110-year threshold. The U.S.-based Gerontology Research Group, which tracks certified people who become supercentenarians, reports 36 worldwide. All but one of them are women, and 18 of them are Japanese. Good diets and supportive family structure have been linked to Japan’s world-leading life expectancy.

Tajima straddled the 19th, 20th and 21st centuries and is one of the few people who could recall a time before World War I. Two days after her 45th birthday, the United States dropped the first of two atomic bombs northeast of her home island.

Her legacy is similarly expansive; she had nine children and 160 descendants, including great-great-great grandchildren, the Gerontology Research Group said.

Tajima’s secret to longevity was “eating delicious things and sleeping well,” the group said. She danced with her hands at the sound of a samisen, a traditional three-string instrument.

Chiyo Miyako, also in Japan, has become the world’s oldest person, according to the group. At 116 years and 355 days, she has about nine months to reach her countrywoman’s mark of 117 years and 260 days.

Miyako would not have to travel far to visit her male compatriot. Japan’s Masazo Nonaka, at 112 years and 271 days old, was confirmed to be the world’s oldest man by Guinness World Records this month. The organization had been set to recognize Tajima before she died, the AP reported.