Category: Ageing

Categories : Ageing NeurologyTags :

Brain Ages at Different Paces According to Social and Physical Environments

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An international study employing advanced measurements of brain ageing on a wide range of participants found that people from more disadvantaged countries and backgrounds had older biological ages for their brains compared to chronological ages. The results are published in Nature Medicine.

The pace at which the brain ages can vary significantly among individuals.  This difference between biological and chronological ages may be affected by environmental factors like pollution and social factors like income or health inequalities, especially in older people and those with dementia. Until now, it was unclear how these combined factors could either accelerate or delay brain ageing across diverse geographical populations. 

The study used advanced brain clocks based on deep learning of brain networks, involved a diverse dataset of 5306 participants from 15 countries. By analysing data from functional magnetic resonance imaging (fMRI) and electroencephalography (EEG), the researchers quantified brain age gaps in healthy individuals and those with neurodegenerative conditions such as mild cognitive impairment (MCI), Alzheimer’s disease, and frontotemporal lobe degeneration (FTLD). 

Participants with a diagnosis of dementia, particularly Alzheimer’s disease, exhibited the most critical brain age gaps. The research also highlighted sex differences in brain ageing, with women in Latin American and Caribbean countries showing greater brain age gaps, particularly in those with Alzheimer’s disease. These differences were linked to biological sex and gender disparities in health and social conditions. Variations in signal quality, demographics, or acquisition methods did not explain the results. These findings underscore the role of environmental and social factors in brain health disparities. 

The findings of this study have profound implications for neuroscience and brain health, particularly in understanding the interaction between macro factors (exposome) and the mechanisms that underlie brain ageing across diverse populations in healthy ageing and dementia. The study’s approach, which integrates multiple dimensions of diversity into brain health research, offers a new framework for personalised medicine. This framework could be crucial for identifying individuals at risk of neurodegenerative diseases and developing targeted interventions to mitigate these risks. Moreover, the study’s results highlight the importance of considering the biological embedding of environmental and social factors in public health policies. Policymakers can reduce brain age gaps and promote healthier ageing across populations by addressing issues such as socioeconomic inequality and environmental pollution. 

Source: University of Surrey

Categories : Ageing Metabolic DisordersTags :

Reconsidering Dialysis for Chronic Kidney Failure in the Elderly

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Chronic kidney disease (CKD). Credit: Scientific Animations CC4.0

Whether dialysis is the best option for kidney failure and, if so, when to start, may deserve more careful consideration, according to a new study published in Annals of Internal Medicine.

For older adults who were not healthy enough for a kidney transplant, starting dialysis when their kidney function fell below a certain threshold, rather than waiting, afforded them roughly one more week of life, Stanford Medicine researchers and their colleagues found.

More critically, perhaps, they spent an average of two more weeks in hospitals or care facilities, in addition to the time spent undergoing dialysis.

“Is that really what a 75- or 80-year-old patient wants to be doing?” asked lead author Maria Montez Rath, PhD, a senior research engineer. Manjula Tamura, MD, a professor of nephrology, is the senior author.

“For all patients, but particularly for older adults, understanding the trade-offs is really essential,” Tamura said. “They and their physicians should carefully consider whether and when to proceed with dialysis.”

Patients with kidney failure who are healthy enough for transplantation may receive a donated kidney, which will rid their blood of toxins and excess fluid. But that option is unavailable to many older adults who have additional health conditions such as heart or lung disease or cancer.

For those patients, physicians often recommend dialysis when patients progress to kidney failure – when estimated glomerular filtration rate (eGFR), a measure of renal function, falls below 15.

Patients and their family members sometimes assume that dialysis is their only option, or that it will prolong life significantly, Montez Rath said. “They often say yes to dialysis, without really understanding what that means.”

But patients can take medications in lieu of dialysis to manage symptoms of kidney failure such as fluid retention, itchiness and nausea, Tamura said. She added that dialysis has side effects, such as cramping and fatigue, and typically requires a three- to four-hour visit to a clinic three times a week.

“It’s a pretty intensive therapy that entails a major lifestyle change,” she said.

Lifespan and time at home

The researchers conducted the study to quantify what dialysis entails for older adults who are ineligible for a transplant: whether and how much it prolongs life, along with the relative number of days spent in an inpatient facility such as a hospital, nursing home or rehabilitation center.

The team evaluated the health records, from 2010 to 2018, of 20 440 patients (98% of them men) from the U.S. Department of Veterans Affairs. The patients were 65 and older, had chronic kidney failure, were not undergoing evaluation for transplant and had an eGFR below 12.

Simulating a randomised clinical trial with electronic health records, they divided patients into groups: those who started dialysis immediately, and those who waited at least a month. Over three years, about half of the patients in the group who waited never started dialysis.

Patients who started dialysis immediately lived on average nine days longer than those who waited, but they spent 13 more in an inpatient facility. Age made a difference: Patients 65 to 79 who started dialysis immediately on average lived 17 fewer days while spending 14 more days in an inpatient facility; patients 80 and older who started dialysis immediately on average lived 60 more days but spent 13 more days in an inpatient facility.

Patients who never underwent dialysis on average died 77 days earlier than those who started dialysis immediately, but they spent 14 more days at home.

“The study shows us that if you start dialysis right away, you might survive longer, but you’re going to be spending a lot of time on dialysis, and you’re more likely to need hospitalization,” Montez Rath said.

Tamura noted that physicians sometimes recommend dialysis because they want to offer patients hope or because the downsides of the treatment haven’t always been clear. But the study indicates physicians and patients may want to wait until the eGFR drops further, Tamura said, and should consider symptoms along with personal preferences before starting dialysis.

“Different patients will have different goals,” she said. “For some it’s a blessing to have this option of dialysis, and for others it might be a burden.”

It may be helpful, she added, if clinicians portray dialysis for frail, older adults as a palliative treatment – primarily intended to alleviate symptoms.

“Currently, dialysis is often framed to patients as a choice between life and death,” she said. “When it’s presented in this way, patients don’t have room to consider whether the treatment aligns with their goals, and they tend to overestimate the benefits and well-being they might experience. But when treatment is framed as symptom-alleviating, patients can more readily understand that there are trade-offs.”

Source: Stanford Medicine

Categories : AgeingTags :

The Ageing Process Makes Big Jumps in Our 40s and 60s

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Photo by LOGAN WEAVER | @LGNWVR on Unsplash

If it’s ever felt like everything in your body is breaking down at once, that might not be your imagination. A new Stanford Medicine study shows that many of our molecules and microorganisms dramatically rise or fall in number during our 40s and 60s.

Researchers assessed many thousands of different molecules in people from age 25 to 75, as well as their microbiomes – the bacteria, viruses and fungi that live inside us and on our skin – and found that the abundance of most molecules and microbes do not shift in a gradual, chronological fashion. Rather, we undergo two periods of rapid change during our life span, averaging around age 44 and age 60. A paper describing these findings was published in the journal Nature Aging.

“We’re not just changing gradually over time; there are some really dramatic changes,” said Michael Snyder, PhD, professor of genetics and the study’s senior author. “It turns out the mid-40s is a time of dramatic change, as is the early 60s. And that’s true no matter what class of molecules you look at.”

Xiaotao Shen, PhD, a former Stanford Medicine postdoctoral scholar, was the first author of the study. Shen is now an assistant professor at Nanyang Technological University Singapore.

These big changes likely impact our health – the number of molecules related to cardiovascular disease showed significant changes at both time points, and those related to immune function changed in people in their early 60s.

Abrupt changes in number

Snyder, the Stanford W. Ascherman, MD, FACS Professor in Genetics, and his colleagues were inspired to look at the rate of molecular and microbial shifts by the observation that the risk of developing many age-linked diseases does not rise incrementally along with years. For example, risks for Alzheimer’s disease and cardiovascular disease rise sharply in older age, compared with a gradual increase in risk for those under 60.

The researchers used data from 108 people they’ve been following to better understand the biology of aging. Past insights from this same group of study volunteers include the discovery of four distinct “ageotypes,” showing that people’s kidneys, livers, metabolism and immune system age at different rates in different people.

The new study analysed participants who donated blood and other biological samples every few months over the span of several years; the scientists tracked many different kinds of molecules in these samples, including RNA, proteins and metabolites, as well as shifts in the participants’ microbiomes. The researchers tracked age-related changes in more than 135 000 different molecules and microbes, for a total of nearly 250 billion distinct data points.

They found that thousands of molecules and microbes undergo shifts in their abundance, either increasing or decreasing – around 81% of all the molecules they studied showed non-linear fluctuations in number, meaning that they changed more at certain ages than other times. When they looked for clusters of molecules with the largest changes in amount, they found these transformations occurred the most in two time periods: when people were in their mid-40s, and when they were in their early 60s.

Although much research has focused on how different molecules increase or decrease as we age and how biological age may differ from chronological age, very few have looked at the rate of biological aging. That so many dramatic changes happen in the early 60s is perhaps not surprising, Snyder said, as many age-related disease risks and other age-related phenomena are known to increase at that point in life.

The large cluster of changes in the mid-40s was somewhat surprising to the scientists. At first, they assumed that menopause or perimenopause was driving large changes in the women in their study, skewing the whole group. But when they broke out the study group by sex, they found the shift was happening in men in their mid-40s, too.

“This suggests that while menopause or perimenopause may contribute to the changes observed in women in their mid-40s, there are likely other, more significant factors influencing these changes in both men and women. Identifying and studying these factors should be a priority for future research,” Shen said.

Changes may influence health and disease risk

In people in their 40s, significant changes were seen in the number of molecules related to alcohol, caffeine and lipid metabolism; cardiovascular disease; and skin and muscle. In those in their 60s, changes were related to carbohydrate and caffeine metabolism, immune regulation, kidney function, cardiovascular disease, and skin and muscle.

It’s possible some of these changes could be tied to lifestyle or behavioural factors that cluster at these age groups, rather than being driven by biological factors, Snyder said. For example, dysfunction in alcohol metabolism could result from an uptick in alcohol consumption in people’s mid-40s, often a stressful period of life.

The team plans to explore the drivers of these clusters of change. But whatever their causes, the existence of these clusters points to the need for people to pay attention to their health, especially in their 40s and 60s, the researchers said. That could look like increasing exercise to protect your heart and maintain muscle mass at both ages or decreasing alcohol consumption in your 40s as your ability to metabolise alcohol slows.

“I’m a big believer that we should try to adjust our lifestyles while we’re still healthy,” Snyder said.

Source: Stanford Medicine

Categories : AgeingTags :

Turning off Pro-inflammatory Cytokine IL-11 Extends Healthy Lifespan in Mice

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Credit: MRC LMS, Duke-NUS Medical School

Scientists have discovered that ‘turning off’ the cytokine IL-11 can significantly increase the healthy lifespan of mice by almost 25%.

The scientists, at the Medical Research Council Laboratory of Medical Science (MRC LMS), Imperial College London and Duke-NUS Medical School in Singapore, tested the effects of IL-11 by creating mice with the gene for IL-11 (interleukin 11) deleted. This extended the lives of the mice by over 20% on average. The cytokine has for years been misidentified as an anti-inflammatory and anti-fibrotic.

They also treated 75-week-old mice, equivalent to the age of about 55 years in humans, with an injection of an anti-IL-11 antibody, a drug that stops the effects of the IL-11 in the body.

Median lifespan extended

The results, published in Nature, were dramatic, with mice given the anti-IL-11 drug from 75 weeks of age until death having their median lifespan extended by 22.4% in males and 25% in females. The mice lived for an average of 155 weeks, compared with 120 weeks in untreated mice.

The treatment largely reduced deaths from cancer in the animals, as well as reducing the many diseases caused by fibrosis, chronic inflammation and poor metabolism, which are hallmarks of ageing. There were very few side effects observed.

Fewer cancers and free from the usual signs of ageing and frailty

Professor Stuart Cook, who was co-corresponding author, from MRC LMS, Imperial College London and Duke-NUS Medical School in Singapore, said:

These findings are very exciting. The treated mice had fewer cancers, and were free from the usual signs of ageing and frailty, but we also saw reduced muscle wasting and improvement in muscle strength. In other words, the old mice receiving anti-IL11 were healthier.

Previously proposed life-extending drugs and treatments have either had poor side-effect profiles, or don’t work in both sexes, or could extend life, but not healthy life, however this does not appear to be the case for IL-11.

While these findings are only in mice, it raises the tantalising possibility that the drugs could have a similar effect in elderly humans. Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially providing exciting opportunities to study its effects in ageing humans in the future.

The researchers have been investigating IL-11 for many years and in 2018 they were the first to show that IL-11 is a pro-fibrotic and pro-inflammatory protein, overturning years of incorrect characterisation as anti-fibrotic and anti-inflammatory.

Levels of IL-11 increases with age

Assistant Professor Anissa Widjaja, who was co-corresponding author, from Duke-NUS Medical School, Singapore, said:

This project started back in 2017 when a collaborator of ours sent us some tissue samples for another project. Out of curiosity, I ran some experiments to check for IL-11 levels. From the readings, we could clearly see that the levels of IL-11 increased with age and that’s when we got really excited!

We found these rising levels contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although our work was done in mice, we hope that these findings will be highly relevant to human health, given that we have seen similar effects in studies of human cells and tissues.

This research is an important step toward better understanding ageing and we have demonstrated, in mice, a therapy that could potentially extend healthy ageing, by reducing frailty and the physiological manifestations of ageing.

Previously, scientists have posited that IL-11 is an evolutionary hangover in humans, as while it is vital for limb regeneration in some animal species, it is thought to be largely redundant in humans.

IL-11 linked to chronic inflammation and frailty

However, after about the age of 55 in humans, more IL-11 is produced and past research has linked this to chronic inflammation, fibrosis in organs, disorders of metabolism, muscle wasting (sarcopaenia), frailty, and cardiac fibrosis. These conditions are many of the signs we associate with ageing.

When two or more such conditions occur in an individual, it is known as multimorbidity, which encompasses a range of conditions including lung disease, cardiovascular disease, diabetes, vision and hearing decline and a host of other conditions.

Professor Cook said:

The IL-11 gene activity increases in all tissues in the mouse with age. When it gets turned on it causes multimorbidity, which is diseases of ageing and loss of function across the whole body, ranging from eyesight to hearing, from muscle to hair, and from the pump function of the heart to the kidneys.

Multimorbidity among biggest global healthcare challenges

Multimorbidity and frailty are acknowledged to be among the biggest global healthcare challenges of the 21st century, according to many leading health bodies, including the NHS and the World Health Organization.

Currently, no treatment for multimorbidity is available, other than to try to treat the separate multiple underlying causes individually.

The scientists caution that the results in this study were in mice and the safety and effectiveness of these treatments in humans need further establishing in clinical trials before people consider using anti-IL-11 drugs for this purpose.

Source: UK Research & Innovation

Categories : Ageing Diet and NutritionTags :

Greater Attention Needs to be Paid to Malnutrition in the Sick and Elderly

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Photo by JD Mason on Unsplash

As many as half of all patients admitted to hospital, other healthcare facilities are malnourished. This has serious consequences for the individual in terms of poorer quality of life and mortality. Providing nutrients can alleviate these problems, but not enough attention is paid to this knowledge, write researchers from Uppsala University and the University of Gothenburg published in the NEJM.

“Far too few patients are diagnosed with malnutrition. Underdiagnosis and undertreatment of the condition remains a problem in healthcare and elderly care, not only in Sweden but worldwide. However, by using fairly simple methods, patients and older adults could be made to feel much better,” says Tommy Cederholm, professor of clinical nutrition at Uppsala University.

Together with Ingvar Bosaeus, a consultant at Sahlgrenska University Hospital, Cederholm is coauthor of a review article on undernourishment published in the New England Journal of Medicine. The article summarises the global state of knowledge over the last 50 years, with the emphasis on developments over the last 5 years, concluding that the healthcare sector needs to make much greater use of the experience and knowledge revealed in the research.

It is estimated that between 5 and 10% of all older adults in Sweden are malnourished. This figure rises to up to 50% of patients being cared for in hospitals, nursing homes or similar facilities. Weight loss and malnutrition have traditionally been viewed as a natural expression of disease or aging, and something about which nothing can be done. It is now recognised that the most common cause is an underlying disease that causes the individual to eat less, leading to the breakdown of bodily organs and tissues.

People suffering from malnutrition will lose weight and the lack of nutrients may lead to muscle atrophy, making it difficult to cope with everyday life. They may also be more susceptible to infection and require more care, possibly involving long periods of hospitalisation and increased mortality.

Great strides have been made in knowledge about malnutrition and how to treat it over recent years. There is now global consensus among researchers and clinicians on the criteria for diagnosing malnutrition: weight loss, low body mass index, and reduced muscle mass in an individual with poor appetite, either with or without an underlying disease.

Recent large-scale clinical studies clearly show that malnutrition can be reversed. Counselling and treatment offered in collaboration with dietitians and the use of nutritional drinks can slow weight loss and reduce mortality.

“These are simple measures that are ignored every day. We now know that, with the exception of those in the advanced stages of terminal illnesses such as metastatic cancer, the vast majority of patients can be treated. In Sweden, for example, we have been working on this for many years, but we need to be even better,” says Ingvar Bosaeus, a consultant at Sahlgrenska University Hospital.

The researchers propose concrete measures to reduce suffering among older adults.

“It is crucial to register risk factors for malnutrition at an early stage and to be alert to weight loss and loss of appetite. One also needs to recommend nutrient-dense foods at an early stage and begin nutritional therapy in good time with, for example, nutritional drinks. This knowledge must become a much more explicit component of both basic and specialist training for doctors and nurses,” says Tommy Cederholm.

Source: Uppsala University

Categories : Ageing GeneticsTags :

Genetic Variants may Predict X Chromosome Loss in Older Women

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Photo by Loren Joseph on Unsplash

Researchers have identified inherited genetic variants that may predict the loss of one copy of a woman’s two X chromosomes as she ages, a phenomenon known as mosaic loss of chromosome X, or mLOX. These genetic variants may play a role in promoting abnormal blood cells (that have only a single copy of chromosome X) to multiply, which may lead to several health conditions, including cancer. The study, co-led by researchers at the National Cancer Institute, part of the National Institutes of Health, was published in Nature.

To better understand the causes and effects of mLOX, researchers analysed circulating white blood cells from nearly 900 000 women across eight biobanks, of whom 12% had the condition. The researchers identified 56 common genetic variants – located near genes associated with autoimmune diseases and cancer susceptibility – that influenced whether mLOX developed. In addition, rare variants in a gene known as FBXO10 were associated with a doubling in the risk of mLOX.

In women with mLOX, the investigators also identified a set of inherited genetic variants on the X chromosome that were more frequently observed on the retained X chromosome than on the one that was lost. These variants could one day be used to predict which copy of the X chromosome is retained when mLOX occurs. This is important because the copy of the X chromosome with these variants may have a growth advantage that could elevate the woman’s risk for blood cancer.

The researchers also looked for associations of mLOX with more than 1,200 diseases and confirmed previous findings of an association with increased risk of leukemia and susceptibility to infections that cause pneumonia.

The scientists suggest that future research should focus on how mLOX interacts with other types of genetic variation and age-related changes to potentially alter disease risk.

Source: NIH/National Cancer Institute

Categories : Ageing Diet and NutritionTags :

Less of a Specific Amino Acid Extends Lifespan and Health in Mice

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New research in mice has demonstrated that not having too much of a certain amino acid – present in many foods commonly eaten by overweight or obese individuals – extends their lifespan and reduces the incidence of diseases such as cancers.

“We like to say a calorie is not just a calorie,” says Dudley Lamming, a professor and metabolism researcher at the University of Wisconsin School of Medicine and Public Health. “Different components of your diet have value and impact beyond their function as a calorie, and we’ve been digging in on one component that many people may be eating too much of.”

Lamming is the lead author of a new study in mice, published recently in the journal Cell Metabolism showing that cutting down the amount of a single amino acid called isoleucine can, among other benefits, extend their lifespan, make them leaner and less frail as they age and reduce cancer and prostate problems, all while the mice ate more calories.

Amino acids are the molecular building blocks of proteins, and Lamming and his colleagues are interested in their connection to healthy aging.

In earlier research, data from UW–Madison’s Survey of the Health of Wisconsin showed the scientists that Wisconsinites with higher body mass index measurements tend to consume more isoleucine, an essential amino acid. Isoleucine is plentiful in foods including eggs, dairy, soy protein and many kinds of meat.

To better understand its health effects, Lamming and collaborators from across disciplines at UW–Madison fed genetically diverse mice either a balanced control diet, a version of the balanced diet that was low in a group of about 20 amino acids, or a diet formulated to cut out two-thirds of the diet’s isoleucine. The mice, which began the study at about six months of age (equivalent to a 30-year-old person) got to eat as much as they wanted.

“Very quickly, we saw the mice on the reduced isoleucine diet lose adiposity – their bodies got leaner, they lost fat,” says Lamming, while the bodies of the mice on the low-amino-acid diet also got leaner to start, but eventually regained weight and fat.

Mice on the low-isoleucine diet lived longer – on average 33% longer for males and 7% longer for females. And, based on 26 measures of health, including assessments ranging from muscle strength and endurance to tail use and even hair loss, the low-isoleucine mice were in much better shape during their extended lives.

“Previous research has shown lifespan increase with low-calorie and low-protein or low-amino-acid diets starting in very young mice,” says Lamming, whose work is supported by the National Institutes of Health. “We started with mice that were already getting older. It’s interesting and encouraging to think a dietary change could still make such a big difference in lifespan and what we call ‘healthspan,’ even when it started closer to mid-life.”

The mice on the low-isoleucine diets chowed down, eating significantly more calories than their study counterparts – probably to try to make up for getting less isoleucine, according to Lamming. But they also burned far more calories, losing and then maintaining leaner body weights simply through adjustments in metabolism, not by getting more exercise.

At the same time, Lamming says, they maintained steadier blood sugar levels and male mice experienced less age-related prostate enlargement. And while cancer is the leading cause of death for the diverse strain of mice in the study, the low-isoleucine males were less likely to develop a tumour.

Dietary amino acids are linked to a gene called mTOR that appears to be a lever on the aging process in mice and other animals as well as to a hormone that manages the body’s response to cold and has been considered a potential diabetes drug candidate for human patients. But the mechanism behind the stark benefits of low-isoleucine intake is not well understood. Lamming thinks the new study’s results may help future research pick apart causes.

“That we see less benefit for female mice than male mice is something we may be able to use to get to that mechanism,” he says.

While the results are promising, humans do need isoleucine to live, and reducing isoleucine from a diet that hasn’t been preformulated by a mouse chow company is not an easy task.

“We can’t just switch everyone to a low-isoleucine diet,” Lamming says. “But narrowing these benefits down to a single amino acid gets us closer to understanding the biological processes and maybe potential interventions for humans, like an isoleucine-blocking drug.”

The Survey of the Health of Wisconsin showed that people vary in isoleucine intake, with leaner participants tending to eat a diet lower in isoleucine. Other data from Lamming’s lab suggest that overweight and obese Americans may be eating significantly more isoleucine than they need.

“It could be that by choosing healthier foods and healthier eating in general, we might be able to lower isoleucine enough to make a difference,” Lamming says.

Source: University of Wisconsin-Madison

Categories : Ageing ExerciseTags :

New Insights into How Exercise Slows Age-related Cognitive Decline

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New research published in Aging Cell provides insights into how exercise may help to prevent or slow cognitive decline during aging.

For the study, investigators assessed the expression of genes in individual cells in the brains of mice. The team found that exercise has a significant impact on gene expression in microglia, the immune cells of the central nervous system that support brain function. Specifically, the group found that exercise reverts the gene expression patterns of aged microglia to patterns seen in young microglia.

Treatments that depleted microglia revealed that these cells are required for the stimulatory effects of exercise on the formation of new neurons in the brain’s hippocampus, a region involved in memory, learning, and emotion.

The scientists also found that allowing mice access to a running wheel prevented and/or reduced the presence of T cells in the hippocampus during aging. These immune cells are not typically found in the brain during youth, but they increase with age.

“We were both surprised and excited about the extent to which physical activity rejuvenates and transforms the composition of immune cells within the brain, in particular the way in which it was able to reverse the negative impacts of aging,” said co–corresponding author Jana Vukovic, PhD, of The University of Queensland, in Australia. “It highlights the importance of normalising and facilitating access to tailored exercise programs. Our findings should help different industries to design interventions for elderly individuals who are looking to maintain or improve both their physical and mental capabilities.”

Source: Wiley

Categories : AgeingTags :

Increase in Global Life Expectancy of Nearly 5 Years by 2050

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The latest findings from the Global Burden of Disease Study (GBD) 2021, published in The Lancet, forecast that global life expectancy will increase by 4.9 years in males and 4.2 years in females between 2022 and 2050.

The largest increases are expected in countries where life expectancy is lower, such as in sub-Saharan Africa, contributing to a convergence of increased life expectancy across geographies. The trend is largely driven by public health measures that have prevented and improved survival rates from cardiovascular diseases, COVID, and a range of communicable, maternal, neonatal, and nutritional diseases (CMNNs).

This study indicates that the ongoing shift in disease burden to non-communicable diseases (NCDs) like cardiovascular diseases and cancer, and exposure to NCD-associated risk factors, such as obesity and smoking, will have the greatest impact on disease burden of the next generation.

Longer lives, but more years of poor health

As the disease burden continues to shift from CMNNs to NCDs and from years of life lost (YLLs) to years lived with disability (YLDs), more people are expected to live longer, but with more years spent in poor health. Global life expectancy is forecasted to increase from 73.6 years of age in 2022 to 78.1 years of age in 2050 (a 4.5-year increase). Global healthy life expectancy (HALE) – the average number of years a person can expect to live in good health – will increase from 64.8 years in 2022 to 67.4 years in 2050 (a 2.6-year increase).

To come to these conclusions, the study forecasts cause-specific mortality; YLLs; YLDs; disability-adjusted life years (DALYs, or lost years of healthy life due to poor health and early death); life expectancy; and HALE from 2022 through 2050 for 204 countries and territories.

“In addition to an increase in life expectancy overall, we have found that the disparity in life expectancy across geographies will lessen,” said Dr Chris Murray, Chair of Health Metrics Sciences at the University of Washington and Director of the Institute for Health Metrics and Evaluation (IHME). “This is an indicator that while health inequalities between the highest- and lowest-income regions will remain, the gaps are shrinking, with the biggest increases anticipated in sub-Saharan Africa.”

Dr Murray added that the biggest opportunity to speed up reductions in the global disease burden is through policy interventions aimed to prevent and mitigate behavioural and metabolic risk factors.

These findings build upon the results of the GBD 2021 risk factors study, also released today in The Lancet. This accompanying study found that the total number of years lost due to poor health and early death (measured in DALYs) attributable to metabolic risk factors has increased by 50% since 2000. Read more on the risk factors report at https://bit.ly/GBDRisks2021.

Alternative scenarios for 2050

The study also puts forth various alternative scenarios to compare the potential health outcomes if different public health interventions could eliminate exposure to several key risk factor groups by 2050.

“We forecast large differences in global DALY burden between different alternative scenarios to see what is the most impactful on our overall life expectancy data and DALY forecasts,” said Dr Stein Emil Vollset, first author of the study who leads the GBD Collaborating Unit at the Norwegian Institute of Public Health. “Globally, the forecasted effects are strongest for the ‘Improved Behavioural and Metabolic Risks’ scenario, with a 13.3% reduction in disease burden (number of DALYs) in 2050 compared with the ‘Reference’ (most likely) scenario.”

The authors also ran two more scenarios: one focused on safer environments and another on improved childhood nutrition and vaccination.

“Though the largest effects in global DALY burden were seen from the ‘Improved Behavioural and Metabolic Risk’ scenario, we also forecasted reductions in disease burden from the ‘Safer Environment’ and ‘Improved Childhood Nutrition and Vaccination’ scenarios beyond our reference forecast, said Amanda E. Smith, Assistant Director of Forecasting at IHME. “This demonstrates the need for continued progress and resources in these areas and the potential to accelerate progress through 2050.”

“There is immense opportunity ahead for us to influence the future of global health by getting ahead of these rising metabolic and dietary risk factors, particularly those related to behavioural and lifestyle factors like high blood sugar, high body mass index, and high blood pressure,” continued Dr Murray.

Source: Institute for Health Metrics and Evaluation

Categories : Ageing Cardiovascular DiseaseTags :

Age-related Brain Changes Affect Stroke Recovery, Study Finds

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A new study by a global team of researchers has revealed that areas of age-related damage in the brain relate to motor outcomes after a stroke – a potentially under-recognised phenomenon in stroke research. The study was published in Neurology.

A stroke often leads to motor impairment, which is traditionally linked to the extent of damage to the corticospinal tract (CST), a crucial brain pathway for motor control. Signaling along the CST is involved in a variety of movements, including walking, reaching, and fine finger movements like writing and typing. However, stroke recovery outcomes aren’t fully predicted by damage to the CST, suggesting other factors are at play.

The new observational from the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Stroke Recovery working group. It examines how one such factor could be white matter hyperintensities (WMHs) – areas of age-related damage in the brain’s white matter, which represent vascular dysfunction and are known to impact cognitive functions. The goal of the ENIGMA Stroke Recovery working group is to understand how changes in the brain after stroke relate to functional outcomes and recovery. ENIGMA Stroke Recovery has data from over 2100 stroke patients collected across 65 research studies and 10 countries, comprising the most extensive multisite retrospective stroke data collaboration to date.

Study leader Sook-Lei Liew, PhD, said: “We are grateful for our many collaborators around the world who lead independent stroke research programs and who are willing to come together and enable large-scale investigations into these critical questions about the role of overall brain health in stroke recovery and rehabilitation.” Dr Liew is an associate professor at the Keck School of Medicine of USC.

The study analysed data from 223 stroke patients across four countries and found that larger WMH volumes were associated with more severe motor impairment after a stroke (e.g., difficulty moving or using their arm for daily tasks), independent of CST damage. WMHs are related to chronic hypertension, diabetes, high cholesterol, and smoking, among other factors and conditions, and have been strongly related to cognitive impairment, but not extensively studied in the context of motor impairment. Interestingly, the relationship between CST damage and motor impairment varied based on WMH severity. Patients with mild WMHs showed a typical relationship between CST damage and motor impairment, while patients with moderate to severe WMHs did not have this relationship. Instead, motor impairment was related to WMH volume, not CST damage.

These findings suggest that WMHs, indicative of cerebrovascular damage from a variety of sources, could provide additional context to understand an individual’s potential for recovery post-stroke. Therefore, assessing WMH volume could improve predictive models for stroke recovery.

“WMHs are related to overall cardiovascular and brain health as we age. By integrating assessments of age-related brain health, we may be better able to predict stroke recovery and tailor rehabilitation to individual needs. This personalised approach could open avenues to improve outcomes after stroke,” says lead author Jennifer K. Ferris, PhD, of Simon Fraser University.

The researchers’ next step is to pursue longitudinal studies to confirm their findings. This insight lays the groundwork for developing more accurate markers for recovery, which could transform post-stroke care and rehabilitation.

Source: Keck School of Medicine of USC