Category: Ageing

Categories : Ageing GenderTags :

Women Who Reach Their 90s Tend to Have Maintained Stable Weight

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Reaching the age of 90, 95 or 100, known as exceptional longevity, was more likely for women who maintained their body weight after age 60, according to a multi-institutional study led by University of California San Diego. Older women who sustained a stable weight were 1.2 to 2 times more likely to achieve longevity compared to those who lost 5% of their weight or more.

In this study published in the Journal of Gerontology: Medical Sciences, researchers investigated the link between weight changes later in life with exceptional longevity among 54 437 women who enrolled in the Women’s Health Initiative, a prospective study investigating causes of chronic diseases among postmenopausal women. Throughout the follow up period, 30 647 (56%) of the participants survived to the age of 90 or beyond.

Women who lost at least 5% weight were less likely to achieve longevity compared to those who achieved stable weight. For example, women who unintentionally lost weight were 51% less likely to survive to the age of 90. However, gaining 5% or more weight, compared to stable weight, was not associated with exceptional longevity.

“It is very common for older women in the United States to experience overweight or obesity with a body mass index range of 25 to 35. Our findings support stable weight as a goal for longevity in older women,” said first author Aladdin H. Shadyab, PhD, MPH, associate professor at UC San Diego.

“If aging women find themselves losing weight when they are not trying to lose weight, this could be a warning sign of ill health and a predictor of decreased longevity.”

The findings suggest that general recommendations for weight loss in older women may not help them live longer. Nevertheless, the authors caution that women should heed medical advice if moderate weight loss is recommended to improve their health or quality of life.

The data adds to research connecting weight change and mortality and is notably the first large study to examine weight change later in life and its relation to exceptional longevity.

Source: University of California – San Diego

Categories : Ageing Cardiovascular DiseaseTags :

Stressful Life Events Contribute to Atrial Fibrillation Risk in Postmenopausal Women

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An estimated 1 in 4 postmenopausal women may develop atrial fibrillation in their lifetime, with stressful life events and insomnia being major contributing factors, according to new research published in the Journal of the American Heart Association.

Atrial fibrillation may lead to blood clots, stroke, heart failure or other cardiovascular complications. It primarily affects older adults.

“In my general cardiology practice, I see many postmenopausal women with picture perfect physical health who struggle with poor sleep and negative psychological emotional feelings or experience, which we now know may put them at risk for developing atrial fibrillation,” said lead study author Susan X. Zhao, M.D., a cardiologist at Santa Clara Valley Medical Center in California. “I strongly believe that in addition to age, genetic and other heart-health related risk factors, psychosocial factors are the missing piece to the puzzle of the genesis of atrial fibrillation.“

Researchers reviewed data from more than 83 000 questionnaires by women ages 50-79 from the Women’s Health Initiative, a major US study. Participants were asked a series of questions in key categories: stressful life events, their sense of optimism, social support and insomnia. Questions about stressful life events addressed topics such as loss of a loved one; illness; divorce; financial pressure; and domestic, verbal, physical or sexual abuse. Questions about sleeping habits focused on if participants had trouble falling asleep, wake up several times during the night and  overall sleep quality, for example. Questions about participants’ outlook on life and social supports addressed having friends to talk with during and about difficult or stressful situations; a sense of optimism such as believing good things are on the horizon; and having help with daily chores.

During approximately a decade of follow-up, the study found:

  • About 25% or 23 954 women developed atrial fibrillation.
  • A two-cluster system (the stress cluster and the strain cluster).
  • For each additional point on the insomnia scale, there is a 4% higher likelihood of developing atrial fibrillation. Similarly, for each additional point on the stressful life event scale, there is a 2% higher likelihood of having atrial fibrillation.

“The heart and brain connection has been long established in many conditions,” Zhao said. “Atrial fibrillation is a disease of the electrical conduction system and is prone to hormonal changes stemming from stress and poor sleep. These common pathways likely underpin the association between stress and insomnia with atrial fibrillation.”

Researchers noted that stressful life events, poor sleep and feelings, such as depression, anxiety or feeling overwhelmed by one’s circumstances, are often interrelated. It’s difficult to know whether these factors accumulate gradually over the years to increase the risk of atrial fibrillation as women age.

Chronic stress has not been consistently associated with atrial fibrillation, and the researchers note that a limitation of their study is that it relied on patient questionnaires from the start of the study. Stressful life events, however, though significant and traumatic, may not be long lasting, Zhao notes. Further research is needed to confirm these associations and evaluate whether customised stress-relieving interventions may modify atrial fibrillation risk.

Source: EurekAlert!

Categories : Ageing Diet and NutritionTags :

Yeast Studies Suggest that Early Diet may be Key for Lifelong Health

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Researchers at the Babraham Institute are proposing an alternative link between diet and ageing based on studies in yeast. In a study using yeast, a useful model organism to study ageing, researchers showed that a ‘healthier’ galactose diet in early life led to reduced senescence in those cells. The findings, published in PLOS Biology, suggest that dietary makeup at a young age may have a long-lasting impact on health throughout the lifespan.

Dr Jon Houseley and his team have published their experiments, showing that healthy ageing is achievable through dietary change without restriction by potentially optimising diet, and that ill-health is not an inevitable part of the ageing process.

Scientists have long known that caloric restriction improves health in later life and may even extend life. However, studies in mice show that caloric restriction really needs to be maintained throughout life to achieve this impact, and the health benefits disappear when a normal diet is resumed. Dr Houseley’s new research conducted in yeast suggests an alternative to calorie restriction can lead to improved health through the lifecycle.

“We show that diet in early life can switch yeast onto a healthier trajectory. By giving yeast a different diet without restricting calories we were able to suppress senescence, when cells no longer divide, and loss of fitness in aged cells.” Said Dr Dorottya Horkai, lead researcher on the study.

Rather than growing yeast on their usual glucose-rich diet, the researchers swapped their diet to galactose and observed that many molecular changes which normally accompany ageing did not occur. The cells grown on galactose remained just as fit as young cells even late in life, despite not living any longer, showing that the period of ill-health towards the end of life was dramatically reduced.

“Crucially, the dietary change only works when cells are young, and actually diet makes little difference in old yeast. It is hard to translate what youth means between yeast and humans, but all these studies point to the same trend – to live a long and healthy life, a healthy diet from an early age makes a difference.” explains Dr Houseley.

Yeast are good model organisms for studying ageing as they share many of the same cellular machinery as animals and humans. This avenue of research in yeast helps us to seek a more achievable way to improve healthy ageing though diet compared to sustained and severe calorie restriction, although more research is needed.

Source: Babraham Institute

Categories : Ageing GeneticsTags :

Mice Live Longer when Given a Longevity Gene from Naked Mole Rats

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CRISPR-Cas9 is a customisable tool that lets scientists cut and insert small pieces of DNA at precise areas along a DNA strand. This lets scientists study our genes in a specific, targeted way. Credit: Ernesto del Aguila III, National Human Genome Research Institute, NIH

In a ground-breaking advance in aging research, scientists have successfully transferred a longevity gene from naked mole rats to mice, resulting in improved health and an extension of the mouse’s lifespan.

Naked mole rats are known for their long lifespans and exceptional resistance to age-related diseases. By introducing a specific gene responsible for enhanced cellular repair and protection into mice, the researchers have opened exciting possibilities for unlocking the secrets of aging and extending human lifespan.

“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, professor at Rochester University. Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, report in a study published in Nature that they successfully transferred a gene responsible for making high molecular weight hyaluronic acid (HMW-HA) from a naked mole rat to mice. This led to improved health and an approximate 4.4 percent increase in median lifespan for the mice.

A unique mechanism for cancer resistance

Naked mole rats are mouse-sized rodents that have exceptional longevity for rodents of their size; they can live up to 41 years, nearly ten times as long as similar-size rodents. Unlike many other species, naked mole rats do not often contract age-related diseases such neurodegeneration, cardiovascular disease, arthritis, and cancer. Gorbunova and Seluanov have devoted decades of research to understanding the unique mechanisms that naked mole rats use to protect themselves against aging and diseases.

The researchers previously discovered that HMW-HA is one mechanism responsible for naked mole rats’ unusual resistance to cancer. Compared to mice and humans, naked mole rats have about ten times more HMW-HA in their bodies. When the researchers removed HMW-HA from naked mole rat cells, the cells were more likely to form tumours.

Gorbunova, Seluanov, and their colleagues wanted to see if the positive effects of HMW-HA could also be reproduced in other animals.

Transferring an HMW-HA-producing gene

The team genetically modified a mouse model to produce the naked mole rat version of the hyaluronan synthase 2 gene, which is the gene responsible for making a protein that produces HMW-HA. While all mammals have the hyaluronan synthase 2 gene, the naked mole rat version seems to be enhanced to drive stronger gene expression.

The researchers found that the mice that had the naked mole rat version of the gene had better protection against both spontaneous tumors and chemically induced skin cancer. The mice also had improved overall health and lived longer compared to regular mice. As the mice with the naked mole rat version of the gene aged, they had less inflammation in different parts of their bodies — inflammation being a hallmark of aging — and maintained a healthier gut.

While more research is needed on exactly why HMW-HA has such beneficial effects, the researchers believe it is due to HMW-HA’s ability to directly regulate the immune system.

A fountain of youth for humans?

“It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice,” Gorbunova says. “Our next goal is to transfer this benefit to humans.”

They believe they can accomplish this through two routes: either by slowing down degradation of HMW-HA or by enhancing HMW-HA synthesis.

“We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials,” Seluanov says. “We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health.”

Source: University of Rochester

Categories : Ageing Metabolic DisordersTags :

In Animal Studies, Metformin Extends Lifespan

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Researchers have discovered that the common antidiabetic drug metformin not only lowers blood sugar levels but has revealed to extend lifespan in C. Elegans, an animal model that shares similar metabolic systems with humans and are often used to model human diseases.

This study, led by investigators at Massachusetts General Hospital (MGH), reveals that metformin promotes longevity by stimulating the body’s production of ether lipids, a major structural component of cell membranes.

The findings, which are published in eLife, suggest that boosting production of ether lipids in humans may support healthy aging and reduce the impact of aging-related diseases.

To identify the genes required to enable lifespan extension in response to metformin and its sister drug phenformin (drugs called biguanides), the scientists silenced individual genes in the roundworm Caenorhabditis elegans (which shares over 80% of its proteins with humans and has an average lifespan of about two weeks) and examined what happens to the altered worms after exposure to the medications.

The experiments reveal that genes that increase production of ether lipids are required to extend lifespan in response to the biguanides. Inactivation of the genes that encode for these enzymes completely prevented the longevity-promoting effects of biguanides. Importantly, inactivation of these genes prevented lifespan extension in a variety of situations that are also known to promote longevity, including dietary restriction.

The team also found that increasing ether lipid synthesis alone (by overexpressing a single, key ether lipid biosynthetic enzyme called fard-1) was sufficient to extend C. elegans’ lifespan, orchestrating a metabolic stress defense response through a factor called SKN-1, which is the worm counterpart to the mammalian protein Nrf. This response altered metabolism to promote a longer lifespan.

“Our study implicates promotion of ether lipid biosynthesis as a novel therapeutic target to promote healthy aging. This suggests that dietary or pharmacologic intervention to promote ether lipid synthesis might one day represent a strategy to treat aging and aging-related diseases,” says senior author Alexander A. Soukas, MD, PhD, an Associate Professor at Harvard Medical School.

“Because our studies focused solely on interventions in C. elegans, further studies in mammalian models (such as human cells and mice), epidemiological observation, and rigorous clinical trials are required to determine the viability of promoting ether lipid synthesis to promote human health-span and lifespan.”

Source: Massachusetts General Hospital

Categories : Ageing NeurologyTags :

Social Isolation Linked to Reduced Brain Volume in Older People

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A study of nearly 9000 older people in Japan found that those who have little social contact with others may be more likely to have reduction of overall brain volume, and in areas of the brain affected by dementia, compared with those who have more frequent social contact. The study results were published in Neurology.

“Social isolation is a growing problem for older adults,” said study author Toshiharu Ninomiya, MD, PhD, of Kyushu University in Fukuoka, Japan. “These results suggest that providing support for people to help them start and maintain their connections to others may be beneficial for preventing brain atrophy and the development of dementia.”

The study involved 8896 people without dementia, average age 73. They had MRI brain scans and health exams, and were asked how often they were in contact with friends or relatives that did not live with them.

The people with the lowest amount of social contact had overall brain volume that was significantly lower than those with the most social contact. The total brain volume, or the sum of white and grey matter, as a percentage of the total intracranial volume, or the volume within the cranium, including the brain, meninges, and cerebrospinal fluid, was 67.3% in the lowest contact group compared to 67.8% in the highest contact group. They also had lower volumes in areas of the brain such as the hippocampus and amygdala that play a role in memory and are affected by dementia.

The researchers took into account other factors that could affect brain volume, such as age, diabetes, smoking and exercise.

The socially isolated people also had more small areas of damage in the brain, called white matter lesions, than the people with frequent social contact. The percentage of intracranial volume made up of white matter lesions was 0.30 for the socially isolated group, compared to 0.26 for the most socially connected group.

The researchers found that symptoms of depression partly explained the relationship between social isolation and brain volumes. However, symptoms of depression accounted for only 15% to 29% of the association.

“While this study is a snapshot in time and does not determine that social isolation causes brain atrophy, some studies have shown that exposing older people to socially stimulating groups stopped or even reversed declines in brain volume and improved thinking and memory skills, so it’s possible that interventions to improve people’s social isolation could prevent brain volume loss and the dementia that often follows,” Ninomiya said.

Since the study involved only older Japanese people, a limitation is that the findings may not be generalisable to people of other ethnicities and younger people.

Source: American Academy of Neurology

Categories : Ageing Skeletal SystemTags :

Does Low Bone Density Predict an Increased Risk of Dementia?

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People who have low bone density may have an increased risk of developing dementia compared to people who have higher bone density, according to a study of over 3500 people published in Neurology. As an observational study, it only shows an association and cannot prove that low bone density causes dementia.

“Low bone density and dementia are two conditions that commonly affect older people simultaneously, especially as bone loss often increases due to physical inactivity and poor nutrition during dementia,” said study author Mohammad Arfan Ikram, MD, PhD, of the Erasmus University Medical Center in Rotterdam, Netherlands. “However, little is known about bone loss that occurs in the period leading up to dementia. Our study found that bone loss indeed already occurs before dementia and thus is linked to a higher risk of dementia.”

The study involved 3651 people in the Netherlands with an average age of 72 who did not have dementia at the start of the study. Over an average of 11 years of follow-up, 688 people or 19% developed dementia.

X-rays were used to identify bone density, and participants were interviewed every four to five years and completed physical tests such as bone scans and tests for dementia.

Of the 1211 people with the lowest total body bone density, 90 people developed dementia within 10 years, compared to 57 of the 1211 people with the highest bone density.

After adjusting for factors such as age, sex, education, other illnesses and medication use, and a family history of dementia, researchers found that within 10 years, people with the lowest total body bone density were 42% more likely to develop dementia than people in the highest group.

“Previous research has found factors like diet and exercise may impact bones differently as well as the risk of dementia,” Ikram added. “Our research has found a link between bone loss and dementia, but further studies are needed to better understand this connection between bone density and memory loss. It’s possible that bone loss may occur already in the earliest phases of dementia, years before any clinical symptoms manifest themselves. If that were the case, bone loss could be an indicator of risk for dementia and people with bone loss could be targeted for screening and improved care.”

A limitation of the study is that participants were primarily of European origin and age 70 or older at the start of the study, so these findings may vary in different races, ethnicities, and younger age groups.

Source: American Academy of Neurology

Categories : Ageing ExerciseTags :

Mediterranean Lifestyle Linked to Lower Risk of All-cause and Cancer Mortality

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in Mayo Clinic Proceedings.

People who adhere to a Mediterranean lifestyle, which involves a plant-rich diet, adequate rest, physical activity and socialisation, have a lower risk of all-cause and cancer mortality, according to a new study in Mayo Clinic Proceedings. People who adhered to the lifestyle’s emphasis on rest, exercise, and socialising with friends had a lower risk of cardiovascular disease mortality.

While many studies have established the health benefits of a Mediterranean diet and lifestyle, there are few studies on the diet outside of its region of origin. “This study suggests that it’s possible for non-Mediterranean populations to adopt the Mediterranean diet using locally available products and to adopt the overall Mediterranean lifestyle within their own cultural contexts,” said lead author Mercedes Sotos Prieto, Ramon y Cajal research fellow at La Universidad Autónoma de Madrid and adjunct assistant professor of environmental health at Harvard Chan School. “We’re seeing the transferability of the lifestyle and its positive effects on health.”

Led by La Universidad Autónoma de Madrid and Harvard T.H. Chan School of Public Health, the study analysed the habits of 110,799 members of the UK Biobank cohort, a population-based study across England, Wales, and Scotland using the Mediterranean Lifestyle (MEDLIFE) index, which is derived from a lifestyle questionnaire and diet assessments. Participants, who were between the ages of 40 and 75, provided information about their lifestyle according to the three categories the index measures: “Mediterranean food consumption” (intake of foods part of the Mediterranean diet such as fruits and whole grains); “Mediterranean dietary habits” (adherence to habits and practices around meals, including limiting salt and drinking healthy beverages); and “physical activity, rest, and social habits and conviviality” (adherence to lifestyle habits including taking regular naps, exercising, and spending time with friends). Each item within the three categories was then scored, with higher total scores indicating higher adherence to the Mediterranean lifestyle.

The researchers followed up nine years later to examine participants’ health outcomes. Among the study population, 4247 died from all causes; 2401 from cancer; and 731 from cardiovascular disease. Analysing these results alongside MEDLIFE scores, the researchers observed an inverse association between adherence to the Mediterranean lifestyle and risk of mortality. Participants with higher MEDLIFE scores were found to have a 29% lower risk of all-cause mortality and a 28% lower risk of cancer mortality compared to those with lower MEDLIFE scores. Adherence to each MEDLIFE category independently was associated with lower all-cause and cancer mortality risk. The “physical activity, rest, and social habits and conviviality” category was most strongly associated with these lowered risks, and additionally was associated with a lower risk of cardiovascular disease mortality.

Source: Harvard T.H. Chan School of Public Health

Categories : Ageing Skeletal SystemTags :

Intermittent Corticosteroid Use is Less Likely to Need Fracture Prevention Care

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Prolonged use of corticosteroids, such as prednisolone, has been shown to cause osteoporosis increase fracture risk. The damage can increase the more corticosteroids are taken. But an analysis of prescribing data showed that for those taking intermittent doses of corticosteroids, there was less fracture risk.

Fracture preventive measures are recommended in cases of prolonged corticosteroid use, especially in older age. These can include referrals to specialist osteoporosis clinics or prescribing bisphosphonates.

In a study published in JAMA Dermatology, a team of researchers analysed data to determine whether corticosteroid prescription patterns may affect the likelihood that fracture prevention is considered. The authors, including researchers from the London School of Hygiene & Tropical Medicine (LSHTM), looked at data from across the UK and Ontario, Canada.

Dr Julian Matthewman, lead study author and Research Fellow at LSHTM, said, “Despite well understood benefits of fracture preventive care, including the use of bisphosphonates, previous research suggests that it is under-prescribed. One reason for this could be that doctors are not made aware when some patients have been prescribed an amount of corticosteroids that can damage the bones, such as when they are prescribed gradually or intermittently over multiple prescriptions, potentially even by several doctors.

“In our study, we focused on people aged 66 or older that were prescribed corticosteroids at a level where fracture preventive care should be considered. We used data from GP practices and hospitals across the UK and Ontario, Canada, including information on both corticosteroid and bisphosphonate prescriptions.

“We found that patients prescribed gradual or intermittent corticosteroids were indeed less likely to receive fracture preventive care as compared to patients prescribed corticosteroids in fewer but higher doses or longer-lasting prescriptions. In the UK, the former were about half as likely to receive fracture preventive care. In Ontario, they are about one third less likely.

“Fractures in older age can be dangerous, even deadly, cause disability and incur high costs for health care systems. Hip fractures alone cost the UK around £2 billion, and account for 1.8 million days spent in hospitals each year, according to the Office of Health Improvement & Disparities. Better recognizing patients who can benefit from proactive care has the potential to prevent fractures and their consequences.”

Source: London School of Hygiene & Tropical Medicine

Categories : AgeingTags :

Inflammation Discovery Could Lead to a Way to Slow Aging

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Colourised electron micrograph image of a macrophage. Credit: NIH

University of Virginia School of Medicine researchers have discovered a key driver of chronic inflammation that accelerates aging. This could lead to treatments that let people live longer, healthier lives, and prevent age-related conditions such as cardiovascular disease and devastating brain disorders.

Improper calcium signalling in the mitochondria of certain immune cells seems to be the culprit behind this chronic age-related inflammation. Mitochondria rely heavily on calcium signalling, and they are the powerhouses of cells.

The UVA Health researchers, led by Bimal N. Desai, PhD, found that in macrophages, mitochondria lose their ability to take up and use calcium with age. This, the researchers show, leads to chronic inflammation responsible for many of the ailments that afflict our later years.

The researchers believe that increasing calcium uptake by the mitochondrial macrophages could prevent the harmful inflammation and its terrible effects. Because macrophages reside in all organs of our bodies, including the brain, targeting such “tissue-resident macrophages” with appropriate drugs may allow us to slow age-associated neurodegenerative diseases.

“I think we have made a key conceptual breakthrough in understanding the molecular underpinnings of age-associated inflammation,” said Desai, of UVA’s Department of Pharmacology and UVA’s Carter Immunology Center. “This discovery illuminates new therapeutic strategies to interdict the inflammatory cascades that lie at the heart of many cardiometabolic and neurodegenerative diseases.”

The inflammation of aging – ‘Inflammaging’

Macrophages swallow up dead or dying cells, removing cellular debris, and patrol for pathogens and other foreign invaders. In this latter role, they act as important sentries for our immune systems, calling for help from other immune cells as needed.

Scientists have known that macrophages become less effective with age, but it has been unclear why. Desai’s new discovery suggests answers.

Desai and his team say their research has identified a “keystone” mechanism responsible for age-related changes in the macrophages. These changes, the scientists believe, make the macrophages prone to chronic, low-grade inflammation at the best of times. And when the immune cells are confronted by an invader or tissue damage, they can become hyperactive. This drives what is known as “inflammaging” – chronic inflammation that drives aging.

Further, the UVA Health scientists suspect that the mechanism they have discovered will hold true not just for macrophages but for many other related immune cells generated in the bone marrow. That means we may be able to stimulate the proper functioning of those cells as well, potentially giving our immune systems a big boost in old age, when we become more susceptible to disease.

Next steps

Fixing “inflammaging” won’t be as simple as taking a calcium supplement. The problem isn’t a shortage of calcium so much as the macrophages’ inability to use it properly. But Desai’s new discovery has pinpointed the precise molecular machinery involved in this process, so we should be able to discover ways to stimulate this machinery in aging cells.

“This highly interdisciplinary research effort, at the interface of computational biology, immunology, cell biology and biophysics, wouldn’t have been possible without the determination of Phil Seegren, the graduate student who spearheaded this ambitious project,” Desai said. “Now, moving forward, we need an equally ambitious effort to figure out the wiring that controls this mitochondrial process in different types of macrophages and then manipulate that wiring in creative ways for biomedical impact.”

Source: University of Virginia Health System