Category: Ageing

Categories : AgeingTags :

Fame Itself May Be Critical Factor in Shortening Singers’ Lives

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Effects of fame comparable to certain other health risks, suggest the researchers

Freddie Mercury performing with Queen in 1977. Source: Wikimedia Commons

Fame itself may be a critical factor in shortening singers’ lives beyond the hazards of the job—at least those in the UK/Europe and North America – suggests research published online in the Journal of Epidemiology & Community Health.

These stars seem to die around four years earlier, on average, than their peers who haven’t achieved celebrity status, and the effects of fame are on a par with certain other health risks, suggest the researchers.

Previously published research indicates that famous singers tend to die earlier than the general public. But it’s far from clear whether it’s fame itself, the demands of the music industry, or the lifestyle associated with being a musician, which contribute to this heightened risk, explain the researchers.

To shed more light on this conundrum, they retrospectively compared the risk of death in 648 singers, half of whom had achieved celebrity status and half of whom hadn’t.

Each of the 324 stars was matched for birth year, gender, nationality, ethnicity, music genre and solo/lead singer in a band status with their lesser known peers.

Most (83.5%) were male, and the average year of birth was 1949, but ranged from 1910 to 1975. Over half (61%) the singers were from North America, with the remainder from Europe/the UK. And most were White (77%), with only 19% being of Black and 4% of other or mixed ethnicities.

Most singers were in the Rock genre (65%), followed by R&B (14%), Pop (9%), New-Wave (6%), Rap (4%), and Electronica (2%). Over half (59%) the singers were in a band; 29% were solo artists; and 12% performed both solo and in a band.

The sample of famous singers was drawn from the Top 2000 Artists of All Time on acclaimedmusic.net, a database that aggregates global rankings based on published lists from music critics, journalists, and industry professionals, but not audience polls or sales data.

Only artists active after 1950 and before 1990 were included to gather sufficient tracking information on the risk of death by the end of December 2023.

Analysis of the data showed that, on average, famous singers survived until they were 75; less famous singers survived until they were 79.

While band membership was associated with a 26% lower risk of death compared with going it alone, the inclusion of this variable didn’t influence the overall effect of fame, as famous singers were still 33% more likely to die earlier than their less well known counterparts.

Only two (0.6%) of the stars achieved fame posthumously, and the heightened risk of death started only once fame had been achieved and remained significantly associated throughout the period of fame.

This suggests that the heightened risk of death isn’t attributable to baseline differences or to reverse causation, whereby earlier death contributes to fame, but that this risk emerges specifically after the attainment of fame, say the researchers.

“Together, the analyses indicate that an elevated risk emerges specifically after achieving fame, which highlights fame as a potential temporal turning point for health risks including mortality. Beyond occupational explanations, our findings suggest that fame adds further vulnerability within an already at-risk group,” they explain.

The heightened risk associated with fame is comparable to other known health risks, such as occasional smoking, which confers a heightened risk of death of 34%, they add.

This is an observational study, and as such, no firm conclusions can be drawn about cause and effect. And the researchers acknowledge that their study sample wasn’t global and was confined to singers, meaning that their observations might not apply to other regions of the world or to other domains of fame, such as acting or sport.

But a possible explanation for the findings may lie in “the unique psychosocial stress that accompanies fame, such as intense public scrutiny, performance pressure, and loss of privacy,” they suggest.

“These stressors may fuel psychological distress and harmful coping behaviours, making fame a chronic burden that amplifies existing occupational risk,” they add.

Fame brings with it significant financial security, a factor that is frequently associated with healthy ageing, while wealth is usually associated with a lower risk of premature death, they point out.

But they conclude: “Being famous appears so detrimental that it overrides any potential benefits associated with high socioeconomic status. Again, this highlights the increased vulnerability of famous individuals, suggesting a need for targeted protection and support for this population.”

Source: BMJ Group

Categories : AgeingTags :

Muscle Wasting Reversed in Patients with Rheumatoid Arthritis

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Photo by Towfiqu barbhuiya

Patients with rheumatoid arthritis increased their leg muscle volume when treated with an anti-rheumatic drug, offering new hope for improved muscle health.

Publishing in the prestigious journal, The Lancet Rheumatology, a team from Newcastle University and The Newcastle upon Tyne Hospitals NHS Foundation Trust describe how 15 patients were given Tofacitinib, a Janus kinase (JAK) inhibitor used to treat RA, as part of an experimental medicine study. After six months, their leg muscles increased in size, particularly in the thigh.  

Sarcopenia is a progressive, age-related musculoskeletal disease characterized by the loss of muscle mass, strength, and physical performance, increasing the risk of falls, fractures, physical disability, and mortality. Currently there are no medicines approved to reverse this muscle-wasting disease. It is commonly seen in patients with rheumatoid arthritis where chronic inflammation contributes to the loss of muscle mass and strength.

The Rheumatoid Arthritis and MUScle (RAMUS) study

In this study, the leg muscles of 15 patients were measured by MRI scans at one month and at six months. After 6 months, participants’ muscle volume had increased by 4% for the whole leg, equating to an average increase of 242 cm3, and by 5% for the thigh.

Alongside the increase in muscle volume, the RAMUS study also reported changes in the gene expression in muscle tissue with treatment, which were opposite to changes seen in ageing muscle.

Dr Joshua Bennett, NIHR Clinical Lecturer at Newcastle University and Paediatric Rheumatology Registrar within the Newcastle Upon Tyne Hospitals NHS Trust and lead author of the paper said: “This small study is the first to show that JAK inhibitor drugs may be able to reverse sarcopenia in rheumatoid arthritis. We know that sarcopenia is also seen in many other diseases and in old age, but no drugs have been approved to reverse it. Larger studies are now needed to test our findings, but it is exciting to think of the potential for these drugs to treat muscle wasting.”

13 patients experienced adverse events, the majority of which were mild. The team say a larger,  follow up study is needed which would include a control group.

Supports growing evidence

Professor John Isaacs, Professor of Clinical Rheumatology, Newcastle University, Director of Research at Newcastle Hospitals and Deputy Director of the National Institute for Health and Care Research (NIHR) Newcastle Biomedical Research Centre (BRC) who led the study added: “Our findings support growing evidence that inflammation, as evidenced by pro-inflammatory cytokines, may contribute to muscle loss.

“Tofacitinib treatment led to increased muscle volume in patients and triggered changes in muscle gene activity that run counter to the patterns typically seen in age-related muscle decline, suggesting a distinct biological effect.

“While this research did not demonstrate improved muscle strength, patients with arthritis often struggle to perform strength tests due to joint pain and so this does not diminish the potential benefits of reversing sarcopenia as we know it increases the risk of falls, fractures, physical disability, and mortality.”

The primary study funding was by Pfizer, with The BMA Foundation, the JGW Patterson Foundation and the Newcastle Hospitals Charity also contributing. RAMUS was also supported by the NIHR Newcastle Biomedical Research Centre (BRC) and Clinical Research Facility.

Source: Newcastle University

Categories : Ageing PaediatricsTags :

Longevity Gene from Supercentenarians Offers Hope for Rapid Ageing Disease in Children

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A new breakthrough in a rare genetic disease which causes children to age rapidly has been discovered using ‘longevity genes’ found in people who live exceptionally long lives – over 100 years old. The research, by the University of Bristol and IRCCS MultiMedica, found these genes which helps keep the heart and blood vessels healthy during ageing could reverse the damage caused by this life-limiting disease.

This is the first study, published in Signal Transduction and Targeted Therapy, to show that a gene from long-lived people can slow down heart ageing in a progeria model. Also known as Hutchinson-Gilford Progeria Syndrome (HGPS), Progeria is a rare, fatal genetic condition of “rapid-ageing” in children.

HGPS is caused by a mutation in the LMNA gene, which leads to the production of a toxic protein called progerin. Most affected individuals die in their teens due to heart problems, although a few, like Sammy Basso, the oldest known person with progeria, have lived longer.  Sadly, late last year (24 October) at the age of 28 Sammy passed away.

Progerin damages cells by disrupting the structure of their nucleus leading to early signs of ageing, especially in the heart and blood vessels.

Currently, the only United States Food and Drug Administration (FDA)-approved treatment is a drug called lonafarnib, which helps reduce the build-up of progerin. A newer clinical trial is now testing lonafarnib in combination with another drug called Progerinin to see if the combination works better.

In this study, researchers from Bristol Heart Institute, Dr Yan Qiu and Professor Paolo Madeddu, in collaboration with Professor Annibale Puca’s team at IRCCS MultiMedica in Italy, sought to explore whether genes from supercentenarians could help protect children with Progeria from the damaging effects of progerin.

The team focused on a ‘longevity gene’ found in centenarians, called LAV-BPIFB4. Previous research has showed that this gene helps keep the heart and blood vessels healthy during ageing.

Using mouse models genetically engineered to have Progeria, the research team were able to show early heart problems like those seen in children with the disease. The team found that a single injection of the longevity gene helped to improve heart function, specifically diastolic function.

It reduced heart tissue fibrosis and decreased the number of ‘aged’ cells in the heart. The gene also boosted the growth of new small blood vessels, which could help keep heart tissue healthy.

The team then tested the effect of the longevity gene in human cells from Progeria patients. Their findings showed adding the longevity gene to these cells reduced signs of ageing and fibrosis, without changing progerin levels directly. This suggests the gene helps protect cells from the effects of progerin, rather than removing it.  Importantly, the treatment doesn’t try to eliminate progerin but instead helps the body cope with its toxic effects.

Dr Yan Qiu, Honorary Research Fellow in the Bristol Heart Institute at the University of Bristol, said: “Our research has identified a protective effect of a “supercentenarian longevity gene” against progeria heart dysfunction in both animal and cell models.

“The results offer hope to a new type of therapy for Progeria; one based on the natural biology of healthy ageing rather than blocking the faulty protein. This approach, in time, could also help fight normal age-related heart disease.

“Our research brings new hope in the fight against Progeria and suggests the genetics of supercentenarians could lead to new treatments for premature or accelerated cardiac ageing, which might help us all live longer, healthier lives.”

Professor Annibale Puca, Research Group Leader at IRCCS MultiMedica and Dean of the Faculty of Medicine at the University of Salerno, added: “This is the first study to indicate that a longevity-associated gene can counteract the cardiovascular damage caused by progeria.

“The results pave the way for new treatment strategies for this rare disease, which urgently requires innovative cardiovascular drugs capable of improving both long-term survival and patient quality of life. Looking ahead, the administration of the LAV-BPIFB4 gene through gene therapy could be replaced and/or complemented by new protein- or RNA-based delivery methods.

“We are currently conducting numerous studies to investigate the potential of LAV-BPIFB4 in counteracting the deterioration of the cardiovascular and immune systems in various pathological conditions, with the goal of translating these experimental findings into a new biologic drug.”

Source: University of Bristol

Categories : AgeingTags :

1st-generation Antihistamines Linked to Delirium Risk in Older Hospitalised Patients

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An analysis in the Journal of the American Geriatrics Society reveals that older inpatients admitted to physicians who prescribe higher amounts of first-generation antihistamines face an elevated risk of delirium while in the hospital.

First-generation antihistamines, such as diphenhydramine, are among the leading causes of medication-related harms in older adults, and although these medications are indicated for histamine-related conditions such as hives and anaphylaxis, they may be prescribed inappropriately.

When investigators analysed data on 328 140 patients aged 65 years and older who were admitted by 755 attending physicians to 17 hospitals in Ontario, Canada in 2015–2022, they found that the overall prevalence of delirium was 34.8%. Patients admitted to physicians who more commonly prescribed first-generation antihistamines had 41% increased odds of experiencing delirium compared with patients admitted to physicians who rarely prescribed first-generation antihistamines.

“We hope our study raises awareness among hospitalists that sedating antihistamines can be harmful, and should be prescribed with caution,” said corresponding author Aaron M. Drucker, MD, of the University of Toronto and Women’s College Hospital.

Source: Wiley

Categories : Ageing VaccinesTags :

How Age Affects Vaccine Responses – and How to Make Them Better

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Age-related shifts in T cells weaken vaccine response in older adults, but new findings pave the way for next generation of vaccines

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Allen Institute scientists are learning why vaccines can trigger a weaker response in older adults, around age 65, and what can be done to improve them. These insights open the door to designing more effective vaccines.  

In the largest study of its kind, published in Nature, scientists discovered that T cells undergo profound and specific changes as we age. These changes, far from being random or a byproduct of chronic disease and inflammation, are a fundamental feature of healthy aging and will happen to all of us as we get older.  

“We were surprised that inflammation is not driving healthy aging. We think inflammation is driven by something independent from just the age of a person,” said Claire Gustafson, PhD, assistant investigator at the Allen Institute and one of the lead authors of the study. “This is important because there’s been research showing similar findings that inflammation and aging don’t go hand in hand, and your immune system is just changing with age.”  

The changes also point to why vaccines, including the annual flu shot and COVID-19 boosters, tend to be less effective in older adults.

The changes scientists discovered

T cells are a critical part of our immune system that help “train” B cells, to produce antibodies in response to viruses and vaccines. But this study found that memory T cells in older adults undergo a dramatic shift toward what is known as a “Th2-like” state, which is a change in gene expression that fundamentally alters how these cells respond to threats. Researchers found this shift directly affects B cells’ ability to generate strong antibody responses. In other words, the flu shot might still deliver the right viral components, but if the memory T cells aren’t functioning properly, the body struggles to respond effectively.  

How this could lead to better vaccines 

With this insight, doctors may be able to use a person’s immune profile to predict how well they’ll respond to a vaccine. Now that scientists can pinpoint how T cells become less effective with age, they can also start designing new vaccine formulas or immune-boosting treatments to address these issues.  

Since T cells in older adults function differently, scientists could reformulate vaccines to compensate specifically for age-related cellular changes rather than using a one-size-fits-all approach. Gene-editing tools like CRISPR could also be used to reprogram a person’s T cells before vaccination, essentially re-programming older immune cells to make them respond to vaccines like younger cells do—like CAR-T cell therapy that reprograms immune cells to fight cancer.  

Researchers say this work goes beyond just vaccines and reveals how our immune systems change in all of us as we get older and how our bodies fight age-related disease and viruses. It also opens the door to interventions like new therapies to restore key immune cells.  

How researchers made the discovery

Scientists tracked more than 96 healthy adults ages 25–65 for over two years in collaboration with Benaroya Research Institute. The researchers then used cutting-edge techniques like single-cell RNA sequencing, proteomics, and spectral flow cytometry to profile the immune system of these individuals over time. The scientists then used this data on the immune system to create a detailed Human Immune Health Atlas, an online resource mapping 71 different immune cell types and how they change over time, and why those changes matter. Then, they applied this Atlas to study over 16 million individual immune cells from healthy adults 25–90+ years of age, offering an unprecedented tool for researchers worldwide to better understand, and support, the aging immune system. This online resource is the largest of its kind and freely available to researchers worldwide.  

“This research illustrates how working collaboratively can make a significant impact on our understanding of the immune system, both now and in the future,” said Jane Buckner, MD, president of the Benaroya Research Institute. “It was made possible through the combined efforts of several Seattle-based research institutions, dedicated scientists, clinicians and research coordinators, as well as the individuals who generously volunteered their time, samples, and health information.”  

The significance of this work extends beyond aging research and provides a roadmap for understanding how immune dysfunction develops over time, offering concrete targets for intervention and potentially transforming how we approach immune health across the entire human lifespan.  

“There’s so much more information to be gained by looking at this dataset we’ve produced,” said Gustafson. “My hope is that it will be used for a long time to enable other researchers to look more deeply and find more insights into human immunity.” 

Source: Allen Institute

Categories : AgeingTags :

New Research Reveals Longevity Gains Slowing, Life Expectancy of 100 Unlikely

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A new study co-authored by a University of Wisconsin-Madison professor finds that life expectancy gains made by high-income countries in the first half of the 20th century have slowed significantly, and that none of the generations born after 1939 will reach 100 years of age on average.

Published in the journal Proceedings of the National Academy of Sciences, the study by Héctor Pifarré i Arolas of the La Follette School of Public Affairs, José Andrade of the Max Planck Institute for Demographic Research, and Carlo Giovanni Camarda of the Institut national d’études démographiques analysed life expectancy for 23 high-income and low-mortality countries using data from the Human Mortality Database and six different mortality forecasting methods.

“The unprecedented increase in life expectancy we achieved in the first half of the 20th century appears to be a phenomenon we are unlikely to achieve again in the foreseeable future,” according to Pifarré i Arolas. “In the absence of any major breakthroughs that significantly extend human life, life expectancy would still not match the rapid increases seen in the early 20th century even if adult survival improved twice as fast as we predict.”

From 1900 to 1938, life expectancy rose by about five and a half months with each new generation. The life expectancy for an individual born in a high-income country in 1900 was an average of 62 years. For someone born just 38 years later in similar conditions, life expectancy had jumped to 80 years on average.

For those born between 1939 and 2000, the increase slowed to roughly two and a half to three and a half months per generation, depending on the forecasting method. Mortality forecasting methods are statistical techniques that make informed predictions about future lifespans based on past and current mortality information. These models enabled the research team to estimate how life expectancy will develop under a variety of plausible future scenarios.

“We forecast that those born in 1980 will not live to be 100 on average, and none of the cohorts in our study will reach this milestone. This decline is largely due to the fact that past surges in longevity were driven by remarkable improvements in survival at very young ages,” according to corresponding author Andrade.

At the beginning of the 20th century, infant mortality fell rapidly due to medical advances and other improvements in quality of life for high-income countries. This contributed significantly to the rapid increase in life expectancy. However, infant and child mortality are now so low that the forecasted improvements in mortality in older age groups will not be enough to sustain the previous pace of longevity gains.

While mortality forecasts can never be certain as the future may unfold in unexpected ways – by way of pandemics, new medical treatments or other unforeseen societal changes – this study provides critical insight for governments looking to anticipate the needs of their healthcare systems, pension planning and social policies.

Although a population-level analysis, this research also has implications for individuals, as life expectancy influences personal decisions about saving, retirement and long-term planning. If life expectancy increases more slowly as this study shows is likely, both governments and individuals may need to recalibrate their expectations for the future.

Source: La Follette School of Public Affairs

Categories : Ageing ExerciseTags :

Number of Steps Matters More for Older Women’s Health than the Frequency

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4000 steps once/twice weekly is associated with 26% lower risk of death rising to 40% if done on 3 days of the week – but it’s daily step count rather than number of days that matters, findings suggest 

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Clocking up at least 4000 daily steps on just 1 or 2 days per week is linked to a lower risk of death and cardiovascular disease among older women, according to research published online in the British Journal of Sports Medicine.

This large prospective study examined not only how many steps older women take but how often they reach their step targets across the week, addressing a key gap in current physical activity guidelines.

Researchers found that achieving at least 4000 steps per day on 1-2 days per week was associated with a significantly lower risk of death and lower risk of cardiovascular disease (CVD), compared with not reaching this level on any day.

A large body of evidence shows that lifelong physical activity is important for improving the healthspan, say the researchers. But it’s not entirely clear how much physical activity people should do as they age to reap appreciable health benefits, particularly in respect of step counts which are yet to make it into physical activity guideline recommendations, they add.

To explore this further, they set out to look at the associations between daily step counts of between 4000 and 7000 and death from all causes and from cardiovascular disease in older women.

They also wanted to find out if the total number of daily steps might drive any observed associations, rather than the frequency of achieving step count thresholds, with a view to informing future guidelines–in particular the US Physical Activity Guidelines, the next edition of which is planned for 2028.

The study followed 13547 women (average age 71) from the US Women’s Health Study who wore accelerometers (activity trackers) for seven consecutive days between 2011–2015 and were tracked for nearly 11 years. The women were free of cardiovascular disease or cancer at the start of the study.

During the monitoring period of nearly 11 years up to the end of 2024, 1765 women (13%) died and 781 (5%) developed cardiovascular disease.

Clocking up at least 4000 steps/day on 1–2 days of the week was associated with a 26% lower risk of death from all causes and a 27% lower risk of a cardiovascular disease death compared with not reaching this threshold on any day of the week.

For those achieving this step count on at least 3 days of the week, the lower risk of death from any cause increased to 40%, but remained at 27% for the risk of cardiovascular death.

But while higher daily step counts of 5000 to 7000 on 3 or more days of the week were associated with a further fall in all-cause mortality risk (32%) they were associated with a levelling out in cardiovascular disease mortality risk (16%).

When the findings were adjusted to take account of average daily steps, previously observed associations weakened, suggesting that [average] steps is the key driver of the protective effect, suggest the researchers.

This is an observational study, and as such, no firm conclusions can be drawn about cause and effect. The researchers also acknowledge that physical activity was assessed only for 1 week, and therefore couldn’t account for variations in behaviour over longer periods, nor did they have information on dietary patterns.

Nevertheless, they suggest: “The present study….suggests that frequency of meeting daily step thresholds is not critical (even 1–2 days/week of ≥4000 steps/day was related to lower mortality and CVD), and that step volume is more important than the frequency of meeting daily step thresholds in the older population.”

And they go on to explain: “An important translational implication of these findings is that since step volume is the important driver of the inverse associations, there is no ‘better’ or ‘best’ pattern to take steps; individuals can undertake [physical activity] in any preferred pattern (eg, ‘slow and steady’ vs ‘bunched patterns’) for lower mortality and CVD risk, at least among older women.”

They conclude: “These findings provide additional evidence for considering including step metrics in the next [physical activity] guidelines, and that ‘bunching’ steps is a viable option for health.”

Source: BMJ Group

Categories : AgeingTags :

New Evidence that Stress Alters Metabolic Hormone with Health Consequences

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A new biomarker for mental health called FGF21 offers a window into aging and disease risk

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A long-studied metabolic hormone, FGF21, also acts as a stress hormone – a discovery that helps explain how psychological stress causes metabolic dysregulation and drive physical disease, according to a new study published in Nature Metabolism.

FGF21 (fibroblast growth factor 21) has been researched for over two decades for its role in metabolism, glucose regulation, and diabetes. 

The new findings, from researchers at Columbia University Mailman School of Public Health, Vagelos College of Physicians and Surgeons, and the Butler Columbia Aging Center, show for the first time that psychological stress acutely alters FGF21 levels in the bloodstream, highlighting the hormone’s potential to link mental states to metabolic responses and ultimately affect overall health and biological aging.

“This is the first human evidence that FGF21 responds to mental stress, acting as a hormonal bridge between body and mind,” said senior author Martin Picard, PhD, associate professor of behavioural medicine at Columbia and co-director of the Columbia Science of Health programme. “It integrates psychosocial experiences with systemic metabolic signalling – expanding the neuroendocrine framework beyond traditional stress hormones.”

The study tracked hormonal changes following acute psychological stress in both healthy individuals and patients with mitochondrial disease, a group of genetic disorders that impair cellular energy transformation. In healthy participants, FGF21 levels on average dropped immediately after exposure to a standardised stressor, returning to baseline within 90 minutes – demonstrating a tightly regulated, dynamic hormonal pattern.

In contrast, participants with mitochondria that cannot transform energy normally showed a different pattern: FGF21 levels rose following stress and peaked at 90 minutes, indicating a fundamentally different stress response, likely regulated by mitochondrial biology.

“These results reveal a new axis of vulnerability,” said Mangesh Kurade, lead author on the study at Columbia. “The way our social environment and psychological experiences interact with mitochondrial health may directly shape metabolic outcomes and long-term disease risk.”

To validate their findings, the team analysed data from more than 20 000 participants in the UK Biobank and also drew on data from their ongoing MiSBIE study (Mitochondrial Stress and Biomarkers in Emotion), which investigates how psychosocial variables map onto biological processes.

The results showed that loneliness, childhood neglect, or recent relationship breakdowns including marital separation was linked to higher FGF21, while individuals with stronger social ties and emotional well-being – including frequent social interactions and high couple satisfaction and social support, were associated with lower levels – providing population-level evidence that FGF21 tracks with psychosocial conditions.

“Our findings suggest that the stress hormone and mitochondrial disease biomarker FGF21 signals not just acute stress, but also reflects a person’s social and emotional life over time,” said co-author Michio Hirano, MD, professor of Neurology at Columbia University Irving Medical Center who led the clinical portion of the study.

This cross-validation strengthens the case for FGF21 as a reliable biomarker of how psychological and social environments shape metabolic biology and perhaps also the clinical trajectory of mitochondrial diseases. By identifying FGF21 as both a biological mediator and potential biomarker of psychological stress, the study opens new avenues for research and clinical monitoring.

“This study bridges traditionally separate fields – metabolism and stress biology – suggesting that future precision mental health strategies may benefit from incorporating FGF21 and other biomarkers to monitor metabolic stress vulnerability and therapeutic responses,” said Kurade.

As a hormone once studied strictly within metabolic disease contexts, FGF21 now appears to straddle the boundary between mind and body, offering biological insight into how we age, adapt, and break down under pressure.

“This is about more than a single hormone,” said Picard, who is also associate professor at the Columbia Butler Aging Center. “It’s about understanding how our lived experience – our relationships, our stress, our resilience – gets translated into biology. A more accurate, holistic picture of human health is emerging. It’s an exciting time for science and medicine.”

Source: Columbia Mailman School of Public Health

Categories : Ageing NeurologyTags :

Quitting Smoking Late in Life May Still Slow Cognitive Decline

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Quitting smoking in middle age or later is linked to slower age-related cognitive decline over the long term, according to a new study by UCL researchers.

The study, published in The Lancet Healthy Longevity, looked at data from 9436 people aged 40 or over (average age: 58) in 12 countries, comparing cognitive test results among people who quit smoking with those of a matched control group who kept smoking.

The research team found that the cognitive scores of those who had quit smoking declined significantly less than their smoking counterparts in the six years after they quit. For verbal fluency, the rate of decline roughly halved, while for memory it slowed by 20%.

Since slower cognitive decline is related to reduced dementia risk, their findings add to a growing body of evidence suggesting quitting smoking might be a preventative strategy for the disease. Still, more research is needed to confirm this.

Lead author Dr Mikaela Bloomberg (UCL Institute of Epidemiology & Health Care) said: “Our study suggests that quitting smoking may help people to maintain better cognitive health over the long term even when we are in our 50s or older when we quit.

“We already know that quitting smoking, even later in life, is often followed by improvements in physical health and well-being. It seems that, for our cognitive health too, it is never too late to quit.

“This finding is especially important because middle-aged and older smokers are less likely to try to quit than younger groups, yet they disproportionately experience the harms of smoking. Evidence that quitting may support cognitive health could offer new compelling motivation for this group to try and quit smoking.

“Also, as policymakers wrestle with the challenges of an ageing population, these findings provide another reason to invest in tobacco control.”

Smoking is thought to harm brain health in part because it affects cardiovascular health – smoking causes damage to blood vessels that supply oxygen to the brain. Smoking is also thought to affect cognitive health by causing chronic inflammation and directly damaging brain cells through oxidative stress (due to the creation of unstable molecules called free radicals).

Co-author Professor Andrew Steptoe (UCL Institute of Epidemiology & Health Care) said: “Slower cognitive decline is linked to lower dementia risk. These findings add to evidence suggesting that quitting smoking might be a preventative strategy for the disease. However, further research will be needed that specifically examines dementia to confirm this.”

Previous studies, the researchers noted, had found a short-term improvement in cognitive function after people stopped smoking. But whether this improvement was sustained over the longer term – particularly when people quit smoking later in life – was not known.

To answer this question the research team looked at data from three ongoing studies* where a nationally representative group of participants answered survey questions every two years. The studies covered England, the US, and 10 other European countries.

More than 4,700 participants who quit smoking were compared with an equal number of people who carried on smoking. The two groups were matched in terms of their initial cognitive scores and other factors such as age, sex, education level, and country of birth.

The research team found that the two groups’ scores in memory and verbal fluency tests declined at a similar rate in the six years prior to participants of one group quitting smoking. These trajectories then diverged in the six years following smoking cessation.

For the smokers who quit, the rate of decline was about 20% slower for memory and 50% slower for verbal fluency. In practical terms, this meant that with each year of ageing, people who quit experienced three to four months less memory decline and six months less fluency decline than those who continued smoking.

This was an observational analysis, so unmeasured differences between smokers who quit and continuing smokers could remain; while the trends before quitting were similar, the study cannot prove cause and effect.

However, the research team noted their findings were consistent with earlier studies showing that adults aged over 65 who quit smoking during early- or mid-life have comparable cognitive scores to never smokers, and that former and never smokers have a similar risk of dementia a decade or longer after quitting.

*The longitudinal studies were the English Longitudinal Study of Ageing (ELSA), the Survey of Health, Ageing and Retirement in Europe (SHARE), and the Health and Retirement Study (HRS).

Source: University College London

Categories : Ageing Diet and Nutrition NeurologyTags :

Link Between Calcium Supplements and Dementia Debunked by New Research

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New research has found no evidence that calcium monotherapy increases the long-term risk for dementia.

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New research from Edith Cowan University (ECU), Curtin University and the University of Western Australia has found no evidence that calcium monotherapy increases the long-term risk for dementia, helping to dispel previous concerns about its potential negative effects on brain health in older women.

This study, which leveraged outcomes from prior research that provided calcium supplements or a placebo to 1460 older women over a five-year period, found that the supplement did not increase the long-term risk of dementia.

“Calcium supplements are often recommended to prevent or manage osteoporosis,” said ECU PhD student Ms Negar Ghasemifard.

Around 20 per cent of women over the age of 70 are affected by osteoporosis and calcium supplementation is widely recommended as a preventative measure against fracture.

“Previous research has raised concerns around the impacts that calcium supplements could have on cognitive health, particularly dementia. Results from our study provides reassurance to patients and clinicians regarding the safety of calcium supplements in the context of dementia risk for older women,” Ms Ghasemifard said.

ECU Senior Research Fellow Dr Marc Sim noted that when the analysis was adjusted for supplement compliance, a range of lifestyle factors, including dietary calcium intake and genetic risk, the results remained unchanged.

“Previous research suggesting potential links between calcium supplement use and the risk for dementia was purely observational in nature. Our research, in comparison, consisted of a post-hoc analysis from a 5-year double-blind, placebo controlled randomised clinical trial on calcium supplements to prevent fracture. Whilst our study is still epidemiology, its design does reduce the likelihood of unmeasured confounding”

“Some 730 older women were given calcium supplements over five years, and a further 730 were given placebo. This study design offers more accurate data on dosage and duration, and we had a long follow-up period of 14.5 years, which strengthens our results,” Dr Sim said.

While these findings may alleviate concerns regarding calcium supplementation and all-cause dementia risk in older women, particularly after the age of 80 years, Professor Simon Laws, Director of ECU’s Centre for Precision Health, said further research was required.

“Whether this extrapolates to other demographics, such as men or even women commencing supplementation earlier in life, remains unknown. To confirm the current findings, particularly regarding brain health, and to address these population gaps, future clinical trials of calcium supplements, with or without vitamin D, would need to be undertaken. These should include specific and robust assessments of brain health as the primary outcome measures.”

Curtin University’s Professor Blossom Stephan, Director of the Dementia Centre of Excellence and a Dementia Australia Honorary Medical Advisor said the research highlighted a very important finding that provides reassurance to clinicians and patients about the long-term safety of calcium supplementation.

“Given calcium’s critical role in multiple physiological functions, including bone health, these results provide reassurance that long-term calcium supplementation did not increase dementia risk in older women,” she said.

Source: Edith Cowan University