Category: Ageing

Categories : Ageing ExerciseTags :

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

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in Mayo Clinic Proceedings.

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

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

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

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

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

Categories : Ageing Skeletal SystemTags :

Intermittent Corticosteroid Use is Less Likely to Need Fracture Prevention Care

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Photo by Mehmet Turgut Kirkgoz on Unsplash

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

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

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

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

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

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

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

Source: London School of Hygiene & Tropical Medicine

Categories : AgeingTags :

Inflammation Discovery Could Lead to a Way to Slow Aging

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Colourised electron micrograph image of a macrophage. Credit: NIH

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

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

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

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

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

The inflammation of aging – ‘Inflammaging’

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

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

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

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

Next steps

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

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

Source: University of Virginia Health System

Categories : AgeingTags :

Joining Circulatory Systems of Old and Young Mice Slows Aging

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Photo by Kanashi ZD on Unsplash

By surgically joining together the circulatory systems of a young and old mouse, scientists were able to slow the aging process at the cellular level and lengthens the lifespan of the older animal by up to 10%. Published in Nature Aging, the Duke Health-led team also found that that the longer the animals shared circulation, the longer the anti-aging benefits lasted once the two were separated.

The findings suggest a cocktail of components and chemicals in the blood of the young contributes to vitality, and these factors could potentially be isolated as therapies to speed healing, rejuvenate the body and add years to an older individual’s life. (Joining up the circulatory systems of young and old humans should hopefully remain the stuff of dystopian science fiction novels).

“This is the first evidence that the process, called heterochronic parabiosis, can slow the pace of aging, which is coupled with the extension in lifespan and health,” said senior author James White, PhD, assistant professor at Duke University School of Medicine.

White and colleagues set out to determine whether the benefits of heterochronic parabiosis, surgically fusing two animals of different ages to enable a shared circulatory system, were fleeting, or more long-lasting.

Earlier studies at Duke and elsewhere documented anti-aging benefits in tissues and cells of the older mice after three weeks of parabiosis. These studies found that the older mice became more active and animated, and their tissue showed evidence of rejuvenation.

“Our thought was, if we see these anti-aging effects in three weeks of parabiosis, what happens if you bring that out to 12 weeks,” White said. “That’s about 10% of a mouse’s lifespan of three years.”

White said the ages of the mice were also important, with the young mouse aged four months, and the older mouse aged two years.

With follow-up during a two-month detachment period, the older animals exhibited improved physiological abilities and lived 10% longer than animals that had not undergone the procedure.

At the cellular level, parabiosis drastically reduced the epigenetic age of blood and liver tissue, and showed gene expression changes opposite to aging, but akin to several lifespan-extending interventions such as calorie restriction.

The rejuvenation effect persisted even after two months of detachment.

In human terms, the parabiosis exposure would be the equivalent of pairing a 50 year-old with an 18-year-old for about eight years, with the effects adding eight years to the person’s lifespan.

White said the experiment was designed to study if long-term exposure of young blood will cause lasting effects in the old mouse. Pairing humans for heterochronic parabiosis is obviously not practical or even ethical, he said. He also noted that other anti-aging strategies, such as calorie restriction, work better to extend longevity in mice.

“Our work points to a need to explore what factors in the circulation of youthful blood cause this anti-aging phenomenon” White said. “We have demonstrated that this shared circulation extends life and health for the older mouse, and the longer the exposure, the more permanent the changes.

“The elements that are driving this are what’s important, and they are not yet known,” White said. “Are they proteins or metabolites? Is it new cells that the young mouse is providing, or does the young mouse simply buffer the old, pro-aging blood? This is what we hope to learn next.”

Source: Duke University Medical Center

Categories : Ageing Metabolic DisordersTags :

Metformin Also Seems to Protect Against Muscle Atrophy and Fibrosis

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Photo by Barbara Olsen on Pexels

Diabetes and muscle function might seem like they don’t have much to do with each other. But University of Utah Health researchers have discovered that metformin can also prevent muscle atrophy and muscular fibrosis – which can help the elderly bounce back faster from injury or illness. Their findings were published in the journal Aging Cell.

Metformin, the researchers found, actually has surprising applications on a cellular level. It can target senescent cells which impact muscle function. Senescent cells secrete factors associated with inflammation that may underlie fibrotic tissue, a hardening or scarring of tissues. They also discovered that metformin also reduces muscle atrophy.

“We’re interested in clinical application of this research,” says Micah Drummond, PhD, senior author of the study and professor of physical therapy and athletic training at the College of Health. “For example, knee surgeries in the elderly are notoriously hard to recover from. If we give a metformin-type agent during the recovery period, could we help the muscles get back to normal faster?”

Reinvigorating muscle recovery

Ageing comes with the risks of falls, hospitalisation, or developing chronic disease, which are more likely with muscle disuse. The research team wanted to find a therapeutic solution that could properly target both disuse atrophy and muscle recovery.

There’s an optimal level of senescent cells that are beneficial, no matter your age. In younger, healthier people, short-term senescence is required for a proper recovery from injury, and completely blocking the senescent effect impedes the body’s efforts to heal. Typically, a younger person can bounce back more easily after muscle disuse without the use of an intervention such as Metformin.

“In the case of aging, we know that there’s immune dysfunction,” says Drummond. “As you get older, it becomes harder for your body to clear senescent cells and they accumulate. That’s one reason recovery is much slower for the elderly after periods of disuse.”

Metformin’s anti-senescent properties have been demonstrated through pre-clinical studies. To test the intervention in humans, the team recruited 20 healthy male and female older adults for a multi-week study. They had participants undergo a muscle biopsy and MRI before the intervention, which involved five days of bed rest. One group of 10 received metformin and the other 10 received placebo pills during a two-week run-in period, then each group continued the placebo or metformin treatment during bed rest.

After the bed rest, participants received another muscle biopsy and MRI, then ceased treatments. All patients completed a seven-day re-ambulation period followed by a final muscle biopsy.

“We saw two things in our study,” Drummond says. “When participants took Metformin during a bed rest, they had less muscle atrophy. During the recovery period, their muscles also had less fibrosis or excessive collagen. That build-up can make it harder for the muscle to properly function.”

Tying these results to senescence, the research team examined muscle biopsies from study participants. They found that the participants who took Metformin had fewer markers of cellular senescence.

“This is the first paper that has made the direct connection between a therapy targeting cellular senescence and improved muscle recovery following disuse in aging,” says lead author Jonathan Petrocelli, PhD He explains that metformin helps muscle cells better remodel and repair tissue during periods of recovery after inactivity.

“Our real goal is to have patients maintain their muscle mass and function as they age, because atrophy and weakness are some of the strongest predictors of disease development and death,” he says.

Drummond’s team is following up on these findings by examining combining the drug with leucine, an amino acid that promotes growth and could accelerate recovery even further. They’ve already demonstrated the potency of this combination in preclinical animal studies.

“Metformin is cheap, effective and quite safe, so it’s exciting to see that we can use it to accelerate recovery for older individuals,” adds Drummond.

Source: University of Utah Health

Categories : Ageing Cardiovascular DiseaseTags :

Rethink Preventative Aspirin for Older Adults, Researchers Say

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Photo by cottonbro studio: https://www.pexels.com/photo/person-holding-white-round-medication-pill-4661296/

Low-dose aspirin is used as primary prevention for ischaemic stroke, but its protective effect weighed against the increased risk of bleeding events is controversial. A new secondary analysis of daily aspirin in older people found that, in this population, aspirin failed to reduce the risk for ischaemic stroke but increased it for intracranial bleeding. The findings were presented in JAMA Network Open.

The researchers analysed data from the ASPREE randomised clinical trial, the first large-scale trial to study the risks and benefits of 100mg daily aspirin in an older population, where increased bleeding risk may alter the balance of risks and benefits of aspirin. This is particularly relevant to intracerebral events because intracranial haemorrhage is harder to treat than ischaemic events and more frequently fatal or disabling. With previous aspirin trials in mostly younger participants, excess intracerebral haemorrhagic events was seen, though usually few in number and non-significant.

Cloud et al. performed a secondary analysis of the ASPREE trial, which included 19 114 older adults, and found a statistically significant 38% increase in intracranial bleeding resulting from a combination of haemorrhagic stroke and other causes of intracerebral haemorrhage among individuals randomised to aspirin. The difference in incidence of ischaemic stroke was not statistically significant.

While aspirin did not cause a statistically significant reduction in ischaemic stroke (hazard ratio [HR], 0.89), there was a a statistically significant 38% increase in intracranial bleeding. Rates of intracranial bleeding from those assigned to aspirin (1.1%) were higher than placebo (0.8%). This came from an increase in a combination of subdural, extradural, and subarachnoid bleeding with aspirin (0.6%) compared with placebo (0.4%). Haemorrhagic stroke was recorded in 0.5% of those assigned to aspirin compared with 0.4% for placebo.

Absolute numbers of haemorrhagic and non-haemorrhagic events were small. Among 1000 individuals taking 100mg/day of low-dose aspirin over five years, there were 2.5 fewer ischaemic strokes at the expense of 3.5 cases of intracranial haemorrhage, but not statistically significant. No difference would be expected for overall stroke incidence or stroke mortality, but haemorrhagic stroke was associated with a mortality rate of nearly a third, compared to 7.7% for ischaemic stroke. Major extracranial haemorrhage was driven by the increased risk of upper gastrointestinal bleeding with aspirin compared with placebo, as previously found (Hazard Ratio, 1.87).

The researchers concluded that “there was no statistically significant benefit from aspirin in preventing stroke or any conventional stroke etiological subtype. However, aspirin significantly increased the overall risk of intracranial bleeding.”

Categories : AgeingTags :

Black Adults Experience Less Cognitive Decline after Retirement

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A study published in the Journal of the American Geriatrics Society found that immediately after retirement, white adults tended to experience a significant decline in cognitive function, whereas Black adults experienced minimal cognitive decline. White men showed the steepest post-retirement cognitive decline across sex/race combinations, whereas Black women showed the least decline.

White women performed better cognitively at retirement than other race/sex subgroups, and after retirement, their cognitive functioning declined at a rate that was slightly less than the average for this study. Results were adjusted for sociodemographics and physical and mental health indicators.

The study, which included 2226 US participants followed for up to 10 years, revealed greater post-retirement cognitive decline among individuals who attended college compared with those who did not.

“The results seem to point to the possibility that better job opportunities could lead to greater cognitive losses after retirement whereas exposure to lifelong structural inequalities may actually ease transition to retirement with respect to cognitive aging,” said lead author Ross Andel, PhD, of Arizona State University’s Edson College of Nursing and Health Innovation.

Source: Wiley

Categories : AgeingTags :

Scientists Discover That a Key Protein Boosts Cell Repair and Healthy Ageing

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Researchers have found an anti-ageing function in a protein deep within human cells. They discovered that a protein called ATSF-1 controls a fine balance between the creation of new mitochondria and the repair of damaged mitochondria. Their findings were published in Nature Cell Biology.

Mitochondria create toxic by-products during their energy production process, which contributes to the rate at which the cell ages.

Associate Professor Steven Zuryn and Dr Michael Dai at the Queensland Brain Institute made the discovery of a key repair protein. “In conditions of stress, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritises repair which promotes cellular health and longevity,” Dr Zuryn said.

As an analogy, Dr Zuryn likened the relationship to a race car needing a pitstop.

“ATSF-1 makes the call that a pitstop is needed for the cell when mitochondria need repairs,” he said.

“We studied ATFS-1 in C. elegans, or round worms and saw that enhancing its function promoted cellular health, meaning the worms became more agile for longer. They didn’t live longer, but they were healthier as they aged.”

“Mitochondrial dysfunction lies at the core of many human diseases, including common age-related diseases such as dementias and Parkinson’s. Our finding could have exciting implications for healthy ageing and for people with inherited mitochondrial diseases.”

Understanding how cells promote repair is an important step towards identifying possible interventions to prevent mitochondrial damage.

“Our goal is to prolong the tissue and organ functions that typically decline during ageing by understanding how deteriorating mitochondria contribute to this process,” Dr Dai said. “We may ultimately design interventions that keep mitochondrial DNA healthier for longer, improving our quality of life.”

Source: University of Queensland

Categories : Ageing Metabolic DisordersTags :

Mouse Study Highlights Potential Therapeutic for Metabolic Syndrome

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Photo by Diana Polekhina on Unsplash

Mopping up free radicals with antioxidants was a major health fad in the 1970s. In an effort to supposedly blunt the effects of aging and stave off chronic disease, people took huge amounts of antioxidants in the form of minerals and vitamins. Not only was this ineffective, it sometimes caused harm because untargeted antioxidants also compromised beneficial cellular signalling pathways. As theories of mitochondrial causes of disease fell out of favour, this health fad disappeared along with bell bottoms and disco.

Now, research recently published in Free Radical Biology and Medicine suggests a new way of dealing with free radicals: rather than mop them up, take a pill that selectively keeps them from being produced in the first place. Building on this work, collaborative research between the Buck and Calico Labs shows that specifically inhibiting free radical production at a particular mitochondrial site prevents and treats metabolic syndrome in mice, by preventing and reversing insulin resistance.

“We think that mitochondrial radical production drives many chronic diseases of aging, and that blocking the production of free radicals is a viable disease-treating and anti-aging intervention,” said Martin Brand, PhD, Buck Professor Emeritus and senior investigator of the study. “We’ve found a way to selectively keep problematic free radicals in check without compromising normal energy production in the mitochondria. These compounds act like a cork in a wine bottle. They plug a specific site so that it doesn’t produce free radicals, without hindering the mitochondria’s critical function of energy metabolism. We look forward to continuing this groundbreaking area of research.”

The orally bioavailable compound that has been developed, S1QEL1.719 (a new “S1QEL” – Suppressor of site IQ Electron Leak), was given both prophylactically and therapeutically to mice fed a high-fat diet that causes metabolic syndrome. Treatment decreased fat accumulation, strongly protected against decreased glucose tolerance and prevented or reversed the increase in fasting insulin levels by protecting against the development of insulin resistance.

Acting on mitochondrial complex I highlights potential interventions for other conditions

S1QEL1s act on site IQin mitochondrial complex I. (The mitochondrial electron transport chain consists of four protein complexes integrated into the inner mitochondrial membrane. Together they carry out a multi-step process, oxidative phosphorylation, through which cells derive 90% of their energy.)

First author and Buck staff scientist Mark Watson, Ph.D., says current literature strongly implicates complex I in a number of different diseases, from metabolic syndrome to Alzheimer’s, fatty liver disease, and noise-induced hearing loss, as well as the underlying aging process itself.

“S1QELs don’t sequester oxidants or radicals. Rather, they specifically inhibit radical production at the IQ site on complex I without interfering with other sites,” Watson said. “So the normal redox signaling that we require in our cells will continue. S1QELs just modulate that one site. They are very clean, very specific, and do not disrupt mitochondrial functioning like inhibitors of mitochondria do.”

Brand says the data shows that free radical production from complex I is an essential driver of insulin resistance and metabolic syndrome, a major disease of poor lifestyle choices and of aging. He says this feature is a strong reason to revisit the mitochondrial theory of aging. “These compounds fine-tune mitochondrial production of free radicals,” he said. “And it’s really interesting; just inhibiting this specific site improves the whole redox environment and prevents metabolic disease, and that is amazing.”

Source: Buck Institute for Research on Aging

Categories : Ageing Mental HealthTags :

SA Retirement Home Study Reveals the Mental Health Benefits for Residents Interacting with Children

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A small South African study published in the open-access journal PLOS ONE suggests that programmes promoting interaction between retirement home residents and children may provide quality of life improvements and could help manage residents’ anxiety and depression.

Among retirement home residents, previous research has shown that common mental health conditions often go undetected and untreated. These conditions, which include anxiety and depression, are typically treated with a combination of drugs and non-pharmacological interventions.

One intervention is the Eden Alternative, which identifies loneliness, helplessness and boredom as key challenges to overcome provide a higher quality of life. Evidence suggests that programmes that enable older adults to regularly interact with children may improve mental health, but these have mostly been done outside of retirement homes and few have looked at such programmes in South Africa.

To deepen the understanding of potential benefits of intergenerational interactions, Elizabeth Jane Earl and Debbie Marais of Stellenbosch University, South Africa, conducted a study at a retirement home in South Africa. Residents were able to regularly interact with children who attend an onsite preschool. Activities include playing games, doing puzzles, reading, or singing with the children.

Ten female residents were recruited and invited to complete a questionnaire evaluating their anxiety and depression levels, as well as asking them to describe their experiences with the children. Four of the participants were screened as possible having anxiety, depression, or both. The participants all took part in the same interactions, though to varying degrees of participation.

Generally, the participants reported positive experiences with the children. Analysing their responses, the researchers found that the interactions fostered a sense of purpose and belonging, fond reminiscences of their own childhood and a positive influence on mood and emotions. Recollections of childhood also sparked a sense of playfulness and positive self-evaluation. They noted that the participants differed in their preconceptions of children, which might have affected their experiences.

The authors wrote that, “Interactions with children promote a sense of belonging and purpose, evoke reminiscence, and positively influence the mental well-being of older persons.”

Based on their findings, Earl and Marais concluded that intergenerational interaction programmes may help manage the mental health conditions that are common for retirement home residents. They suggest that trained staff facilitate the interaction, preparing the children and residents, and should be voluntary, which helps preserve the residents’ agency. Running the interaction as a regular programme should help build bonds and give the residents something to look forward to. Additionally, there should be an educational aspect for the children, giving the residents a sense of purpose.

Looking to the future, they wrote that larger studies would be able to better outline the benefits of such programmes.