Research
Sitting still for long periods increases mortality risk, says study
Sitting for long hours without breaks can increase risk mortality risk in older women, a new study shows.
The research, published in the Journal of the American Heart Association (JAHA), has data showing that older women who sat for 11.7 hours or more per day increased their risk of death by 30 percent, regardless of whether they exercised vigorously.
The study examined measurements of sitting and daily activity collected from hip devices worn for up to seven days by 6,489 women, aged 63 to 99, who were followed for eight years for mortality outcomes.
This data was collected as part of a long-term national project known as the Women’s Health Initiative (WHI), which began in 1991 and is ongoing, led by Andrea LaCroix, Ph.D., M.P.H., Distinguished Professor at the Herbert Wertheim School of Public Health.
The paper is the first to apply a novel and validated machine-learned algorithm called CHAP to examine total sitting time and length of sitting bouts in relation to the risk of death.
Study co-author Steve Nguyen, PhD., M.P.H., a postdoctoral fellow at the University of California San Diego Herbert Wertheim School of Public Health and Human Longevity Science, said: “Sedentary behaviour is defined as any waking behaviour involving sitting or reclining with low energy expenditure.
“Previous techniques for calculating sedentary behaviour used cut points that identified low or absent movement. The CHAP algorithm was developed using machine-learning, a type of artificial intelligence, that enhanced its ability to accurately distinguish between standing and sitting.”
Fine-tuning “sitting” enabled Nguyen to parse total sitting time and usual sitting bout durations.
Sedentary behaviour is a health risk because it reduces muscle contractions, blood flow and glucose metabolism.
Exercise cannot undo these negative effects, according to the study, whether women participated in low or high amounts of moderate-to-vigorous intensity physical activity, they showed the same heightened risk if they sat for long hours.
LaCroix explained: “When you’re sitting, the blood flow throughout your body slows down, decreasing glucose uptake. Your muscles aren’t contracting as much, so anything that requires oxygen consumption to move the muscles diminishes, and your pulse rate is low.
“If I take a brisk long walk for an hour but sit the rest of the day, I’m still accruing all the negative effects on my metabolism.”
Based on the research, LaCroix makes the following recommendation: “The risk starts climbing when you’re sitting about 11 hours per day, combined with the longer you sit in a single session. For example, sitting more than 30 minutes at a time is associated with higher risk than sitting only 10 minutes at a time. Most people aren’t going to get up six times an hour, but maybe people could get up once an hour, or every 20 minutes or so. They don’t have to go anywhere, they can just stand for a little while.”
However, Nguyen points out that not all sitting is the same.
“Looking beyond conditions like cardiovascular disease, we start thinking about cognitive outcomes, including dementia,” he said.
“There are cognitively stimulating activities that can result in sedentary behavior, like sitting while studying a new language. Is sedentary behavior in that context overall bad for a person? I think it’s hard to say.” Nguyen has recently received a National Institute of General Medical Sciences K99 award for 12 months of mentored research to look at protein signatures of physical activity and how they relate to dementia.
LaCroix added: “We’ve created this world in which it’s so fascinating to sit and do things. You can be engrossed by TV or scroll on your Instagram for hours. But sitting all the time isn’t the way we were meant to be as humans, and we could reverse all of that culturally just by not being so attracted to all the things that we do while sitting.”
Shingles vaccination may slow biological ageing in older adults, research suggests.
The study examined more than 3,800 people aged 70 and older and found that those who received the vaccine showed slower biological ageing on average than unvaccinated individuals.
The study used data from a nationally representative US survey to assess how shingles vaccination related to several measures of biological ageing.
Even when controlling for other sociodemographic and health variables, vaccinated individuals had lower inflammation measurements, slower epigenetic ageing (changes in how genes are switched on or off) and slower transcriptomic ageing (changes in how genes are transcribed into RNA used to create proteins).
The research was carried out at the USC Leonard Davis School of Gerontology, using data from the US Health and Retirement Study.
Shingles, also called herpes zoster, is a painful, blistering skin rash caused by reactivation of the chickenpox virus. Anyone who has had chickenpox is at risk of shingles. While shingles can occur at younger ages, risk is higher for those 50 and older and for immunocompromised people. Vaccination offers protection from shingles and lowers the chance of postherpetic neuralgia, or long-term pain after infection.
While vaccines are designed to protect against acute infection, recent research has highlighted a possible link between adult vaccines, including those for shingles and influenza, and lower risks of dementia and other neurodegenerative disorders, said research associate professor of gerontology Jung Ki Kim, the study’s first author.
“This study adds to emerging evidence that vaccines could play a role in promoting healthy ageing by modulating biological systems beyond infection prevention.”
Biological ageing refers to how the body changes over time, including how well organs and systems are working, unlike chronological ageing, which is simply time passing. Two people who are both 65 years old may look very different inside: one may have the biological profile of someone younger, while another may show signs of ageing earlier.
Kim and coauthor Eileen Crimmins, USC university professor and AARP professor of gerontology, measured seven aspects of biological ageing: inflammation, innate immunity (the body’s general defences against infection), adaptive immunity (responses to specific pathogens after exposure or vaccination), cardiovascular haemodynamics (blood flow), neurodegeneration, epigenetic ageing and transcriptomic ageing. The team also used the measures collectively to record a composite biological ageing score.
Chronic, low-level inflammation is a contributor to many age-related conditions, including heart disease, frailty and cognitive decline. This phenomenon is known as inflammaging, Kim said.
“By helping to reduce this background inflammation, possibly by preventing reactivation of the virus that causes shingles, the vaccine may play a role in supporting healthier ageing. While the exact biological mechanisms remain to be understood, the potential for vaccination to reduce inflammation makes it a promising addition to broader strategies aimed at promoting resilience and slowing age-related decline.”
The effect may persist. When analysing how time since vaccination related to results, Kim and Crimmins found that participants who received their vaccine four or more years before providing their blood sample still showed slower epigenetic, transcriptomic and overall biological ageing on average than unvaccinated participants.
“These findings indicate that shingles vaccination influences key domains linked to the ageing process. While further research is needed to replicate and extend these findings, especially using longitudinal and experimental designs, our study adds to a growing body of work suggesting that vaccines may play a role in healthy ageing strategies beyond solely preventing acute illness.
The work was supported by the National Institute on Aging at the National Institutes of Health. The Health and Retirement Study is supported by the National Institute on Aging.
Sharp rises in blood sugar after meals may raise Alzheimer’s risk, according to genetic analysis of more than 350,000 adults.
The findings point to after-meal glucose, rather than overall blood sugar, as a possible factor in long-term brain health.
Researchers examined genetic and health data from over 350,000 UK Biobank participants aged 40 to 69, focusing on fasting glucose, insulin, and blood sugar measured two hours after eating.
The team used Mendelian randomisation, a genetic method that helps test whether biological traits may play a direct role in disease risk.
People with higher after-meal glucose had a 69 per cent higher risk of Alzheimer’s disease.
This pattern, known as postprandial hyperglycaemia (elevated blood sugar after eating), stood out as a key factor.
The increased risk was not explained by overall brain shrinkage (atrophy) or white matter damage, suggesting after-meal glucose may affect the brain through other pathways not yet fully understood.
Dr Andrew Mason, lead author, said: “This finding could help shape future prevention strategies, highlighting the importance of managing blood sugar not just overall, but specifically after meals.”
Dr Vicky Garfield, senior author, added: “We first need to replicate these results in other populations and ancestries to confirm the link and better understand the underlying biology.
“If validated, the study could pave the way for new approaches to reduce dementia risk in people with diabetes.”
A recent international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age.
The findings show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer’s-associated genes like APOE ε4.
This suggests that brain ageing is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology.
Alvaro Pascual-Leone, MD, PhD is senior scientist at the Hinda and Arthur Marcus Institute for Aging Research and medical director at the Deanna and Sidney Wolk Center for Memory Health.
The researcher said: “By integrating data across dozens of research cohorts, we now have the most detailed picture yet of how structural changes in the brain unfold with age and how they relate to memory.”
The study found that structural brain change associated with memory decline is widespread, rather than confined to a single region.
While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships.
This suggests that cognitive decline in ageing reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions.
The pattern across regions formed a gradient, with the hippocampus at the high end and progressively smaller but still meaningful effects across large portions of the brain.
Importantly, the relationship between regional brain atrophy and memory decline was not only variable across individuals but also highly nonlinear.
Individuals with above-average rates of structural loss experienced disproportionately greater declines in memory, suggesting that once brain shrinkage reaches higher levels, cognitive consequences accelerate rather than progress evenly.
This nonlinear pattern was consistent across multiple brain regions, reinforcing the conclusion that memory decline in cognitively healthy ageing is linked to global and network-level structural changes, with the hippocampus playing a particularly sensitive role but not acting alone.
Pascual-Leone said: “Cognitive decline and memory loss are not simply the consequence of ageing, but manifestations of individual predispositions and age-related processes enabling neurodegenerative processes and diseases.
“These results suggest that memory decline in ageing is not just about one region or one gene — it reflects a broad biological vulnerability in brain structure that accumulates over decades.
“Understanding this can help researchers identify individuals at risk early, and develop more precise and personalized interventions that support cognitive health across the lifespan and prevent cognitive disability.”
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