Category: Ageing

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Good Hydration may be Key to Healthy Ageing

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Adults who stay well-hydrated appear to be healthier, develop fewer chronic conditions, such as heart and lung disease, and live longer than those who may not get sufficient fluids, according to a study published in eBioMedicine.

Using health data gathered from 11 255 adults over a 30-year period, researchers analysed links between serum sodium levels (which increase with reduced fluid intake) and various indicators of health. They found that adults with serum sodium levels at the higher end of a normal range were more likely to develop chronic conditions and show signs of advanced biological aging than those with serum sodium levels in the medium ranges. Adults with higher levels were also more likely to die at a younger age.

“The results suggest that proper hydration may slow down aging and prolong a disease-free life,” said Natalia Dmitrieva, PhD, a study author and researcher at the National Heart, Lung, and Blood Institute (NHLBI).

The study expands on previous research from the scientists, which found links between high-normal serum sodium levels and increased risks for heart failure. Both findings came from the Atherosclerosis Risk in Communities (ARIC) study, which started in 1987.

For this latest analysis, researchers assessed information study participants shared during five medical visits – the first two when they were in their 50s, and the last between ages 70–90. Adults who had high levels of serum sodium at baseline check-ins or with underlying conditions, like obesity, that could affect serum sodium levels, were excluded.

The researchers then evaluated how serum sodium levels correlated with biological ageing, which was assessed through 15 health markers such as systolic blood pressure, cholesterol, and blood sugar. These provided insight about how well each person’s cardiovascular, respiratory, metabolic, renal, and immune system was functioning. They also adjusted for factors, like age, race, biological sex, smoking status, and hypertension.

They found that adults with higher levels of normal serum sodium, normallu between 135–146 milliequivalents per litre (mEq/L), were more likely to show signs of faster biological ageing. This was based on indictors like metabolic and cardiovascular health, lung function, and inflammation. For example, adults with serum sodium levels above 142mEq/L had a 10-15% associated increased odds of being biologically older than their chronological age compared to ranges between 137–142mEq/L, while levels above 144mEq/L correlated with a 50% increase. Likewise, levels of 144.5–146 mEq/L were associated with a 21% increased risk of premature death compared to ranges between 137–142mEq/L.

Similarly, adults with serum sodium levels above 142mEq/L had up to a 64% increased associated risk for developing chronic diseases like heart failure, stroke, atrial fibrillation and peripheral artery disease, as well as chronic lung disease, diabetes, and dementia. Conversely, adults with serum sodium levels between 138–140 mEq/L had the lowest risk of developing chronic disease.

The researchers caution that randomised, controlled trials are needed to prove an association between fluid intake and signs of ageing.

“People whose serum sodium is 142mEq/L or higher would benefit from evaluation of their fluid intake,” Dmitrieva said. She noted that most people can safely increase their fluid intake to meet recommended levels, which can be done with water as well as other fluids, like juices, or vegetables and fruits with a high water content. The National Academies of Medicine, for example, suggest that most women consume around 6-9 cups (1.5–2.2 litres) of fluids daily and for men, 8-12 cups (2–3 litres).

Others may need medical guidance due to underlying health conditions. “The goal is to ensure patients are taking in enough fluids, while assessing factors, like medications, that may lead to fluid loss,” said study author Manfred Boehm, MD, director of the Laboratory of Cardiovascular Regenerative Medicine at NHLBI. “Doctors may also need to defer to a patient’s current treatment plan, such as limiting fluid intake for heart failure.”

The authors also cited research that finds about half of people worldwide don’t meet recommendations for daily total water intake, which often starts at 6 cups (1.5 litres).

“On the global level, this can have a big impact,” Dmitrieva said. “Decreased body water content is the most common factor that increases serum sodium, which is why the results suggest that staying well hydrated may slow down the aging process and prevent or delay chronic disease.”

Source: NIH/National Heart, Lung and Blood Institute

Categories : AgeingTags :

Longevity Treatments Fail to Turn Back the Clock

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In a new study published in the journal Nature Communications, researchers have taken a close look at three treatment approaches that have been widely believed to slow the ageing process. However, when tested in mice, these treatments proved largely ineffective in their supposed impact on ageing.

“There is no internal clock of ageing that you can regulate with a simple switch – at least not in the form of the treatments studied here,” concludes Dr Dan Ehninger of the German Centre for Neurodegenerative Diseases (DZNE), the initiator of the study. The team has developed a new analytical approach to make influences on ageing processes measurable.

“We chose three regulators for our interventions that many experts believe slow down aging,” explains Prof Martin Hrab de Angelis, who also drove the project with his team. One of them is intermittent fasting, in which the calories consumed are reduced. Number two targets a central node of cell metabolism (mTOR), which is also the target of the supposed “anti-ageing drug” rapamycin. Number three, in turn, interferes with the release of growth hormone. Similar treatments are also used by humans, although their efficacy with regard to ageing has not been sufficiently proven.

For the assessment in mice, the scientists developed a new answer to the question of how to measure ageing. “Many researchers in recent decades have used lifespan as an indirect measure of ageing,” explains Dan Ehninger, who is a senior scientist at DZNE. So, for example, how old do mice get – and how can that lifespan be extended? “It is often assumed that if they just live longer, they will also age more slowly. But the problem is that mice, like many other organisms, do not die from general old age, but from very specific diseases,” says Ehninger. For example, up to 90 percent of mice die from tumors that form in their bodies at an advanced age. “So, if you were to look at the whole genome for factors that make mice become long-lived, you would like find many genes that suppress tumor development – and not necessarily genes that play a general role in aging.”

For their study, the scientists therefore chose an approach that does not emphasize lifespan, but rather focused on a comprehensive investigation of age-related changes in a wide range of bodily functions. “You can think of it as a complete health status survey,” says Martin Hrab de Angelis: “The health check results in a compendium of hundreds of factors covering many areas of physiology” – an exact description of the state of the animal at the moment of examination. That’s exactly the approach the researchers applied to the animals subjected to one of the three treatment approaches that supposedly slow ageing. Across different life stages, they were analysed and compared: How much does each parameter typically change at a given stage of life? And, do parameters change more slowly when the mice are given one of the three treatments? This study design makes it possible to determine precisely whether the natural aging process can be slowed, and with it the deterioration of important physiological functions.

The results were unambiguous: Although the researchers were able to identify individual cases in which old mice looked younger than they actually were, it was clear that “this effect was not due to slowing down aging, but rather due to age-independent factors,” says Dan Ehninger. “The fact that a treatment already has its effect in young mice – prior to the appearance of age-dependent change in health measures – proves that these are compensatory, general health-promoting effects, not a targeting of aging mechanisms.”

The DZNE and Helmholtz Diabetes Center teams have now set their sights on the next goal: They want to investigate other treatment approaches that experts believe can slow aging. The researchers hope that the new research method will provide a more comprehensive picture of possible treatment approaches and their effectiveness.

Source: DZNE – German Center for Neurodegenerative Diseases

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Areas with Age Bias Associated with Greater Longevity

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Older adults living in areas with greater age bias had better health outcomes than those in areas with less bias, according to a study published in Social Science & Medicine. These findings came as a surprise to the researchers, who were expecting the reverse.

“Quite the opposite of what we expected emerged,” says senior author Allecia Reid, associate professor of social psychology and senior author of the paper published in the journal . “Rather than dying earlier in counties with more negative attitudes toward older adults, we found in fact that older adults were living longer in counties with more negative attitudes towards older adults.”

University of Massachusetts Amherst researcher Reid and colleagues had based their hypothesis on earlier research showing that minority groups, such as African Americans and sexual minorities, have worse health outcomes in counties with more negative attitudes toward their group.

“We were thinking, similar to those findings, that in counties with more negative attitudes towards older adults, we would see them being likely to die earlier than in counties with more positive attitudes toward residents 65 and older,” Reid says. “Contrary to what we thought, something positive is happening in these ageist communities that is helping them live longer, healthier lives.”

The only other study examining community-level age bias and older adults’ health found that explicit age bias was linked to positive health behaviours among older adults, while implicit bias was linked to negative health behaviours among older adults.

The UMass Amherst researchers analysed data on more than one million Americans who reported their explicit bias and taken an implicit bias test between 2003 and 2018

Based on that data, the team developed aggregate estimates at the county level about how much residents like older adults. Then they linked that with the county’s death rates for individuals age 65+. Counties with higher explicit age bias had lower mortality, or 87.67 fewer deaths per 100 000 residents. In contrast, implicit bias was not associated with mortality outcomes.

“The explicit age bias-mortality association was only evident in communities with younger populations but did not depend on community ethnic composition,” the paper states.

The researchers looked at ways that the more ageist communities might be doing things that helped maintain the health of older adults. They found that greater explicit age bias also was associated with lower death rates among young and middle-aged adults in those counties, suggesting that any health benefits of living in ageist communities may begin to accrue in earlier life.

In addition, “communities with higher explicit age bias also had higher rates of exercise…, better general health…, and more days of good mental health,” the paper states. These findings point to potential pathways through which ageist communities may promote health. However, the researchers also note that factors they were unable to examine, such as better medical care and more green spaces, may also explain associations of community age bias with better health.

Reid says the surprising findings point to more areas of examination which may lead to improved longevity for all communities.

“Can we figure out what is happening in these more ageist communities that seems to be potentially promoting both better mental health and better longevity,” she says. “And if we can pinpoint those things, then that’s a flag for all communities to think about.”

Source: University of Massachusetts Amherst

Categories : AgeingTags :

Macrophages Explain Vulnerability to Influenza in Old Age

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After being suppressed during the COVID pandemic, influenza is again circulating and threatening the health of over 65s. But why are older people so more susceptible to the flu? A new study from the University of Michigan, published in Nature Communications, offers clues.

The study, led by first author Judy Chen, a PhD candidate, senior author Professor Daniel Goldstein, MD, and their team investigates why cells called alveolar macrophages, the first line of defence in the lungs, appear to be compromised with age.

Macrophages attack pathogens like the flu virus and reside in alveoli. Importantly, these cells appear to be lost with ageing.

Previous research by another group showed that when macrophages from an old mouse were put into a young mouse, and cells looked young again. “This drove us to believe that something in the environment of the lungs is contributing to this,” said Chen.

Signs pointed to a lipid immune modulator known as prostaglandin E2 (PGE2) with wide ranging effects, from labour induction in pregnancy to inflammation with arthritis. The study team discovered there is more PGE2 in the lungs with age. This increase in PGE2, Chen explained, acts on the macrophages in the lung, limiting their overall health and ability to generate.

The team suspects that the buildup of PGE2 is yet another marker of a biological process called senescence, which is often seen with age. Senescence serves as insurance against the runaway division of damaged cells; cells that are senescent are no longer able to replicate.

“One of the interesting things about these cells is they secrete a lot of inflammatory factors,” said Chen.

The study showed that with age, the cells lining the air sacs in the lungs become senescent, and these cells lead to increased production of PGE2 and suppression of the immune response.

To test the link between PGE2 and increased susceptibility to influenza, they treated older mice with a drug that blocks a PGE2 receptor. “The old mice that got that drug actually ended up having more alveolar macrophages and had better survival from influenza infection than older mice that did not get the drug,” said Chen.

The team plans to next investigate the various ways PGE2 affects lung macrophages as well as its potential role in inflammation throughout the body. “As we get older, we become more susceptible not only to influenza, but to other infections, cancers, autoimmune diseases as well.”

Source: Michigan Medicine – University of Michigan

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Hormone Discovery could Predict Longevity of Men

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Researchers have discovered that a certain hormone, that develops in males during puberty, could be predictive of the risk of developing age-related disease in later life.

The novel insulin-like peptide hormone, called INSL3, was found by researchers to be consistent over long periods of time and is an important early biomarker for prediction of age-linked disease. Their latest findings have been published today in Frontiers in Endocrinology.

INSL3 is produced in the testes by Leydig cells, which also make testosterone, but unlike testosterone which fluctuates over a man’s life, INSL3 remains consistent, with the level at puberty staying about the same throughout life, decreasing only slightly into old age. This makes it the first clear and reliable predictive biomarker of age-related morbidity as compared to any other measurable parameters.

Blood levels of INSL3 were associated with a range of age-related illnesses, such as bone weakness, sexual dysfunction, diabetes, and cardiovascular disease.

Since the hormone is so consistent, a young man with high INSL3 would still have high INSL3 when he is older. But low levels of INSL3 when young will stay low when older, making a man more likely to acquire typical age-related illnesses. This opens up exciting possibilities for predicting age-related illnesses and finding ways to prevent the onset of these diseases with early intervention.

This study from University of Nottingham was led by Professors Ravinder Anand-Ivell and Richard Ivell and is the latest of three recent studies into this hormone. Prof Anand-Ivell explains: “The holy grail of ageing research is to reduce the fitness gap that appears as people age. Understanding why some people are more likely to develop disability and disease as they age is vital so that interventions can be found to ensure people not only live a long life but also a healthy life as they age. Our hormone discovery is an important step in understanding this and will pave the way for not only helping people individually but also helping to ease the care crisis we face as a society.”

The team analysed blood samples from 3000 men, with two samples taken four years apart and found that unlike testosterone, INSL3 remains at consistent.

The study also showed that there is an almost 10-fold variation in INSL3 levels in the normal male population, even among the young and healthy.

Prof Ivell adds: “Now we know the important role this hormone plays in predicting disease and how it varies amongst men we are turning our attention to finding out what factors have the most influence on the level of INSL3 in the blood. Preliminary work suggests early life nutrition may play a role, but many other factors such as genetics or exposure to some environmental endocrine disruptors may play a part.”

Source: University of Nottingham

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Friendly ‘Zombie’ Cells Help Promote Tissue Repair

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While most senescent cells may be harmful “zombies” spewing toxic compounds and should be targeted to reduce the risk of age-related disease, not all of them are like this. In fact, according to new research in Science, some of them embedded in young, healthy tissues seem to help repair damage.

Scientists have now seen these cells in action in lung tissue, as well as other organs that serve as barriers in the body, such as the small intestine, colon and skin. When they used drugs called senolytics to kill these cells, injuries to lung tissues healed more slowly.

“Senescent cells can occupy niches with privileged positions as ‘sentinels’ that monitor tissue for injury and respond by stimulating nearby stem cells to grow and initiate repair,” said Tien Peng, MD, associate professor of pulmonary, critical care, allergy and sleep medicine, and senior author of the study.

Ageing cells can both damage and heal

A/Prof Peng said it was understandable that scientists at first viewed senescent cells as purely detrimental. As people age, senescent cells – often termed “zombie cells” – accumulate that have characteristics of old, worn-out cells, including the inability to make new cells. Instead of dying like normal aged cells, they to live on, spewing a cocktail of inflammatory compounds that form the senescence associated secretory phenotype (SASP). These factors are linked to Alzheimer’s disease, arthritis, and other age-related maladies including cancer.

Using senolytics that selectively kill “zombie cells,” researchers made the exciting discovery that clearing senescent cells from animals thwarted or diminished age-related disease and extended the lifespan of the animals. Thereafter, a boom of activity ensued in research labs and pharmaceutical companies focused on discovering and refining more powerful versions of these drugs.

But killing off senescent cells has dangers, A/Prof Peng said. For one thing, this current study showed that senescent cells also possess the ability to promote normal healing through activation of stem cell repair. “Our study suggests that senolytics could adversely affect normal repair, but they also have the potential to target diseases where senescent cells drive pathologic stem cell behaviour,” said A/Prof Peng.

Lighting up senescent cells

One major challenge to studying senescent cells is that biomarkers of senescence (such as the gene p16) are often quite sparse, making it difficult to detect the cells. In early experiments, researchers extracted cells called fibroblasts into culture dishes, allowing them to grow and produce enough cells to experiment with, and then stressed the cells with chemicals that induced them to become senescent. But in living organisms, cells interact with tissues around them, strongly affecting the cells’ gene activity. This means that the characteristics of cells growing isolated in a glass dish could be quite different from that of cells in their natural environment.

To create a more powerful tool for their studies, the researchers improved on a common technique of fusing a relevant gene – in this case, the p16 gene, which is overly active in senescent cells –with green fluorescent protein (GFP) as a marker that can reveal the location of the cells under ultraviolet light. By enhancing the quantity and stability of green fluorescent protein in these senescent cells, the fluorescent signal was greatly amplified, finally enabling the researchers to see senescent cells in their natural habitat of living tissues.

“Zombies” stimulate stem cells shortly after birth

Using this highly sensitive tool, the researchers found that senescent cells exist in young and healthy tissues to a greater extent than previously thought, and actually begin appearing shortly after birth. The scientists also identified specific growth factors that senescent cells secrete to stimulate stem cells to grow and repair tissues. Relevant to aging and tissue injury is the discovery that cells of the immune system such as macrophages and monocytes can activate senescent cells, suggesting that inflammation seen in aged or damaged tissue is a critical modifier of senescent cell activity and regeneration.

In their studies of lung tissue, A/Prof Peng’s team observed green glowing senescent cells lying next to stem cells on the basement membrane that serves as a barrier preventing foreign cells and harmful chemicals from entering the body and also allows oxygen to diffuse from air in the lungs into underlying tissues. Damage can occur at this dynamic interface. The team saw senescent cells in similar positions in other barrier organs such as small intestine, colon, and skin, and their experiments confirmed that if senescent cells were killed with senolytics, lung stem cells were not able to properly repair the barrier surface.

Source: EurekAlert!

Categories : Ageing Diet and NutritionTags :

A Mediterranean Diet Doesn’t Keep Dementia at Bay

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It has been suggested in a number of studies that eating a healthy diet may reduce a person’s risk of dementia. A new study published in the journal Neurology has found, however, that both the conventionally recommended diet and the Mediterranean diet are not linked to a reduced risk of dementia.

The Mediterranean diet features a high intake of vegetables, legumes, fruits, fish and healthy fats such as olive oil, and a low intake of dairy products, meats and saturated fatty acids. “Previous studies on the effects of diet on dementia risk have had mixed results,” said study author Isabelle Glans, MD, of Lund University. “While our study does not rule out a possible association between diet and dementia, we did not find a link in our study, which had a long follow-up period, included younger participants than some other studies and did not require people to remember what foods they had eaten regularly years before.”

For the study, researchers identified 28 000 people from Sweden. Participants had an average age of 58 and did not have dementia at the start of the study. They were followed over a 20-year period. During the study, participants filled out a seven-day food diary, a detailed food frequency questionnaire and completed an interview. By the end of the study, 1943 people, or 6.9%, were diagnosed with dementia, including Alzheimer’s disease and vascular dementia.

Researchers examined how closely participants’ diets aligned with conventional dietary recommendations and the Mediterranean diet. After adjusting for age, gender, and education, researchers did not find a link between following either a conventional diet or the Mediterranean diet and a reduced risk of dementia. Dr Glans noted that further research is needed to confirm the findings.

Nils Peters, MD, of the University of Basel in Switzerland, who wrote an editorial accompanying the study, said, “Diet on its own may not have a strong enough effect on memory and thinking, but is likely one factor among others that influence the course of cognitive function. Dietary strategies will still potentially be needed along with other measures to control risk factors.” A limitation of the study was the risk of participants misreporting their own dietary and lifestyle habits.

Source: American Academy of Neurology

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The Emerging Link between Polypharmacy and Dementia

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According to new research published in the journal Aging and Disease, people with dementia are likely to have taken more than three medications for other health conditions in the five years directly before their diagnosis.

The study is the first to provide an in-depth exploration of the links between evolving polypharmacy and a dementia diagnosis. Researchers analysed the records of more than 33 000 dementia patients in Wales between 1990 to 2015.

Experts in e-health used machine learning techniques to identify potentially damaging patterns in a patient’s medicine usage, and how these patterns evolve in the run-up to diagnosis.

They found that in the 20 years leading up to them being diagnosed, the proportion of patients taking three or more medications rose from 5.5% (for the period 16 to 20 years prior to diagnosis) to 82.16% among those less than five years from a diagnosis.

Researchers also found that as the development towards dementia progressed, the patterns of polypharmacy shifted from being clearly distinct to being more closely associated with particular medical conditions.

And of those closest to their diagnosis, almost two-thirds (66.55%) were found to be taking multiple medicines for a combination of respiratory or urinary infections, arthropathies and rheumatism, and cardio-vascular disease. A further 22% of patients were found to be taking medicines for infections, arthropathies and rheumatism, cardio-metabolic disease and depression.

The study was supported by the Health Data Research UK and conducted by an international team of researchers from the University of Plymouth, Aptuit (an Evotec company), Swansea University Medical School, and the University of Oxford.

Study leader Professor Shangming Zhou at the University of Plymouth said: “Given the rise in dementia cases internationally, the need to understand how patterns of polypharmacy evolve before and after a dementia diagnosis are important for devising a safe treatment programme for each patient. Our aim in this study was to help doctors find ways to prescribe multiple items of dementia medication safely and without reducing their effectiveness. The use of machine learning has been vital in helping us understand how these patterns develop, and our hope is we can now use this knowledge to treat patients.”

It has previously been established that when multiple types of preventative medication are being prescribed, the benefits of the drugs may be reduced and the chances of harm from drug interaction and side effects increased.

Those requiring hospital treatment who are taking multiple medications are also known to have a higher likelihood of re-admission within three months after being discharged.

Source: EurekAlert!

Categories : Ageing GeneticsTags :

Genes that Influence Longevity Differ Between the Sexes

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There is an elaborate interplay between genes, sex, the environment during growth, and age and how they influence variation in longevity, according to a study published in the journal Science. These findings are an important step in understanding why some people live longer than others and provide a basis for future studies to improve a healthy lifespan.

Robert Williams, PhD, at the University of Tennessee Health Science Center (UTHSC), along with Johan Auwerx, MD, PhD, at the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland, began a program in 2016 to define genetic factors involved in agieng and lifespan. “Finding common molecular pathways that control differences in rate of aging is critical to our understanding of how individuals differ in their health and lifespan,” Dr Williams said. “Such insights may help us work out ways to intervene rationally.”

Drs Williams and Auwerx received DNA of over 12 000 mice from the National Institute of Aging. Each of the 27 574 genetically heterogeneous mice studied is a full sibling, sharing half its genetic inheritance with each other mouse in the programme, and each has a known lifespan, making them an ideal system to study.

The research team analysed the genes of over 3 000 mice, all of them genetic brothers or sisters which were allowed to live until their natural death. Comparing their DNA to lifespan, the researchers defined stretches of DNA in genomes that affect longevity. The results show the DNA segments, or loci, associated with longevity are largely sex-specific, with females having a region in chromosome 3 that affects lifespan. When the males who died early due to non-aging-related reasons were removed from the analysis, additional genetic signals started to emerge, suggesting some genetic variations only affect lifespan after a certain age.

In addition to finding genetic determinants of longevity, the researchers explored other contributors. In general, bigger mice die younger. The researchers found that some, but not all, of the genetic effects on longevity are through effects on growth. One of the non-genetic effects may be how early access to food affects growth. They observed that mice from smaller litters tended to be heavier adults and live shorter lives. Mice from larger litters that had to share their mother’s milk with more siblings, grew more slowly and lived longer on average. The researchers corroborated these trends of early growth versus longevity in large human datasets with hundreds of thousands of participants.

Beyond characterising how longevity is affected, the researchers worked to find genes most likely to play a role in longevity determination. They measured the effect of DNA variation on how genes are expressed and compared their analyses with multiple human and non-human databases. From this they nominated a few genes likely to modulate aging rates. They then tested the effects of manipulating these genes in roundworms and found that a subset of gene perturbations did in fact affect the lifespan. The results of this study will be a rich resource of aging genes that will hopefully guide the design of therapies that not only extend lifespan, but also healthspan.

Source: University of Tennessee Health Science Center

Categories : Ageing Metabolic DisordersTags :

Resilient Mindset Helps Older People with Type 2 Diabetes

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New research suggests that psychological resilience, ie having attitudes and behaviours that help people bounce back after stressful challenges, may help older individuals with type 2 diabetes to experience fewer hospitalisations and have better physical functioning, lower disability, better mental quality of life, and a lower likelihood of becoming frail.

The study, published in published in the Journal of the American Geriatrics Society, recruited 3199 participants, average age 72.2 years, 61% female, 61% white, and followed them for 14 years. The association of resilience with some metrics (grip strength and self-reported disability) varied based on recent hospitalisation history, and results suggested that some associations may differ based on race/ethnicity.

“This study suggests that individuals who report being psychologically resilient also report fewer aging-related concerns,” said lead author KayLoni L. Olson, PhD, of the Warren Alpert Medical School of Brown University. “This study is preliminary but points to the potential role of psychological resilience in helping individuals feel better mentally and physically, which can ultimately enhance their later years of life.”

Source: Wiley