Posts Tagged ‘aging’

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

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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.


by Diana Kwon

Findings from a randomized, controlled trial finds that reducing food intake decreases metabolism and reduces oxidative damage to tissues and cells.

Studies in various animals, including rodents and monkeys, have reported that caloric restriction can extend their lifespans. Findings from a two-year, randomized, controlled trial with human participants, published last week (March 22) in Cell Metabolism, suggest that cutting down on calories may also be able to prolong the lives of people.

To investigate the effects of reducing food intake, Leanne Redman, an endocrinologist at the Pennington Biomedical Research Center at Louisiana State University, and her colleagues enrolled 53 healthy men and women between the ages of 21 and 50 and split them into two groups—one group reduced their caloric intake by 15 percent over two years, and the other remained on a regular diet.

The team found that the people who ate a restricted diet lost an average of around 9 kilograms and experienced a 10-percent drop in their resting metabolic rates. When the researchers examined the participants’ blood, they also found a reduction in markers of oxidative stress in those who cut down on calories. “After two years, the lower rate of metabolism and level of calorie restriction was linked to a reduction in oxidative damage to cells and tissues,” Redman tells Wired.

“[I]f by-products of metabolism accelerate aging processes, calorie restriction sustained over several years may help to decrease risk for chronic disease and prolong life,” Redman says in a statement.

This study was part of a larger, multi-center investigation of caloric restriction in humans, the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy (CALERIE) trial. Luigi Fontana, an internist who ran a CALERIE investigation at Washington University in St. Louis, says that a slower metabolism and reduced oxidative stress will not necessarily lead to a longer life. “You can have a low resting metabolic rate because you’re dying of starvation,” he tells Wired. “Does that make it a biomarker of longevity? No. You can be calorie restricted by eating half a hamburger and a few fries each day but will you live longer? No, you will die of malnutrition.”

https://www.the-scientist.com/?articles.view/articleNo/52141/title/Caloric-Restriction-Slows-Signs-of-Aging-in-Humans/

A group of genes and genetic switches involved in age-related brain deterioration have been identified by scientists at the Babraham Institute, Cambridge and Sapienza University, Rome. The research, published online today (5th March) in Aging Cell, found that changes to one of these genes, called Dbx2, could prematurely age brain stem cells, causing them to grow more slowly. The study was led jointly by Giuseppe Lupo and Emanuele Cacci in Italy and Peter Rugg-Gunn in the UK.

Cells in the brain are constantly dying and being replaced with new ones produced by brain stem cells. As we age, it becomes harder for these stem cells to produce new brain cells and so the brain slowly deteriorates. By comparing the genetic activity in brain cells from old and young mice, the scientists identified over 250 genes that changed their level of activity with age. Older cells turn some genes, including Dbx2, on and they turn other genes off.

By increasing the activity of Dbx2 in young brain stem cells, the team were able to make them behave more like older cells. Changes to the activity of this one gene slowed the growth of brain stem cells. These prematurely aged stem cells are not the same as old stem cells but have many key similarities. This means that many of the genes identified in this study are likely to have important roles in brain ageing.

The research also identified changes in several epigenetic marks – a type of genetic switch – in the older stem cells that might contribute to their deterioration with age. Epigenetic marks are chemical tags attached to the genome that affect the activity of certain genes. The placement of these marks in the genome change as we age and this alters how the cells behave. The researchers think that some of these changes that happen in the brain may alter causing brain stem cells to grow more slowly.

First author on the paper, Dr Giuseppe Lupo, Assistant Professor at Sapienza University said: “The genes and gene regulators that we identified are corrupted in neural stem cells from older mice. By studying the Dbx2 gene we have shown that these changes may contribute to ageing in the brain by slowing the growth of brain stem cells and by switching on the activity of other age-associated genes.”

Co-lead scientist Dr Peter Rugg-Gunn at the Babraham Institute said: “Ageing ultimately affects all of us and the societal and healthcare burden of neurodegenerative diseases is enormous. By understanding how ageing affects the brain, at least in mice, we hope to identify ways to spot neural stem cell decline. Eventually, we may find ways to slow or even reverse brain deterioration – potentially by resetting the epigenetic switches – helping more of us to stay mentally agile for longer into old age.”

Co-lead scientist Dr Emanuele Cacci at Sapienza University said: “We hope this research will lead to benefits for human health. We have succeeded in accelerating parts of the ageing process in neural stem cells. By studying these genes more closely, we now plan to try turning back the clock for older cells. If we can do this in mice, then the same thing could also be possible for humans.”

This article has been republished from materials provided by the Babraham Institute. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference: Lupo, G., Nisi, P. S., Esteve, P., Paul, Y.-L., Novo, C. L., Sidders, B., … Rugg-Gunn, P. J. (n.d.). Molecular profiling of aged neural progenitors identifies Dbx2 as a candidate regulator of age-associated neurogenic decline. Aging Cell, n/a-n/a. https://doi.org/10.1111/acel.12745

https://www.technologynetworks.com/genomics/news/these-genes-are-involved-in-age-linked-brain-deterioration-298221?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=61138279&_hsenc=p2ANqtz-_FeiFbqi-SP5EqlFOOosvK1dViRCt4fG_ztTzGnpct1WLd4sY0BUbdkcuE7-2clIdZwQsKU1fdtv-8HDaJoh76WD9KwA&_hsmi=61138279