In a Journal of the American Geriatrics Society analysis of nationally representative data from 6905 US adults aged 65 or older followed between 2011–2024, higher body mass index (BMI) was associated with lower mortality risk, whereas higher waist circumference, a marker of abdominal obesity, was independently associated with higher mortality risk after accounting for BMI.
Compared with normal weight, overweight males and males with class I and II obesity (BMI of 30 to less than 40 kg/m2) had 46% and 51% lower risks of mortality, respectively. Additionally, a high waist circumference was also associated with a 24% higher mortality risk in males. Similar patterns were observed in females.
When BMI and waist circumference were evaluated together, being overweight was associated with lower mortality risk regardless of waist circumference among males. Class I and II obesity also remined associated with lower mortality risk exclusively among males with elevated waist circumference. In contrast, being underweight, regardless of waist circumference, and having normal BMI with elevated waist circumference were both associated with higher mortality risk in both males and females.
“BMI and waist circumference provide complementary information about health risk in older adults,” said study co-author, Bryan Blissmer, PhD, of the University of Rhode Island. “Our findings suggest that considering both measures together, rather than relying on BMI alone, may improve mortality risk assessment and support more informed clinical decision-making.”
New Emory University research suggests that higher vitamin D supplement intake may be associated with better cognitive function in adults with an elevated risk of dementia.
In a study of 54 adults with sleep disturbances and mild cognitive impairments (MCI), two hallmarks of early dementia, participants taking at least 5000 IU of vitamin D daily showed better cognitive function compared to those who didn’t.
The study, recently published in Sleep Medicine, found that participants who reported taking 5000 IU or more of vitamin D daily scored more than 13% higher on the Montreal Cognitive Assessment (MoCA) than those who didn’t, even after accounting for other factors.A screening tool to detect risk of developing dementia, MoCA is widely used to assess memory and thinking skills. In this study, lower daily doses of vitamin D were not associated with higher cognitive scores.
The study also emphasises the significance of timing. MCI is an intermediate stage between normal cognitive aging and dementia.
“In older adults experiencing both sleep disturbance and mild cognitive impairment, this may represent a critical window for intervention, when cognitive changes are emerging, but opportunities to support brain health may remain,” says Victoria Pak, senior author of the study.
“Identifying accessible and modifiable factors, such as vitamin D supplement intake, during the earlier stages of cognitive decline may become increasingly important, particularly as rates of Alzheimer’s disease continue to rise,” adds Pak, associate professor at Emory University’s Nell Hodgson Woodruff School of Nursing.
In addition to the timing of the intervention, the study also found that cognitive performance did not differ based on the form of vitamin D – D2, typically derived from plants or fungi, or D3, produced after sun exposure or consuming animal-based foods.
Vitamin D, an essential nutrient, is not only necessary for muscle and nerve function, but also influences sleep quality and sleep-wake cycles. Additionally, 50% of those with moderate to severe Alzheimer’s disease report having sleep disturbances, indicating a bidirectional relationship between sleep deprivation and cognitive decline.
While vitamin D deficiencies have been implicated in sleep disorders, such as insomnia and more nighttime awakenings, this preliminary study is the first to assess the relationship between vitamin D supplement intake and cognitive function in a high-risk population with both MCI and sleep disturbances.
Use of hormone therapy later in life was associated with a lower risk of developing dementia, according to a study published August 12, 2026, in Neurology®, the medical journal of the American Academy of Neurology. The study does not prove that hormone therapy prevents dementia; it only shows an association.
“While these findings help us better understand the relationship between hormone therapy use and various markers of dementia, more research needs to be done before we can make recommendations to women about their use of these therapies in relation to their brain health,” said study author Jennifer Bruno, PhD, of Stanford Medicine in Stanford, California. “This study looked back at women who were using hormone therapy decades ago with the timing and type of use differing from what is current practice for most women today, so the results are informative, but they may not apply to today’s standards.”
For the study, researchers examined medical records from two large data sets. In total, the study reports data from 21 462 female participants from both groups who had clinical tests taken while they were living. A total of 728 participants from one data set completed brain scans or biomarker tests while they were living and 2959 participants from the other data set had autopsies after death, at an average age of 82, to look for signs of Alzheimer’s disease. Across both data sets, participants were followed for approximately three to five years, starting at an average age 71.
Of the total participants, 1953 participants took hormone therapy and 19 509 participants did not take hormone therapy. Those who used hormone therapy started using it when they were over age 70, on average. The researchers looked only at participants who took oestrogen-only therapy, since previous studies had indicated that oestrogen plus progestin combination therapy may increase the risk of dementia. In current standard practice, oestrogen-only therapy is prescribed only for those who have undergone a hysterectomy due to the risk of endometrial cancer.
Among the group with autopsy information available, participants who had taken hormone therapy were less likely to have signs of Alzheimer’s disease in their brains than those who had not taken hormone therapy. The autopsy assessment used a composite score that measures three hallmarks of Alzheimer’s disease: amyloid-beta plaques, tau tangles and neuritic plaques, which are amyloid plaques surrounded by damaged nerve cells.
Of those who had taken hormone therapy, 18% had no signs of Alzheimer’s disease in their brains at autopsy, compared to 10% of those who had not taken the therapy, and 40% of hormone therapy users had all three signs of Alzheimer’s disease, compared to 51% of those who had not taken the therapy. After adjusting for age, education, genetics, race and hypertension, researchers found that participants who took hormone therapy had 35% lower odds of signs of Alzheimer’s disease at autopsy when compared to those who did not take hormone therapy.
In a separate analysis using biomarker tests performed when women were living, those who used hormone therapy had levels of amyloid biomarkers in their blood and spinal fluid that indicated less amyloid buildup in the brain compared to women who did not take hormone therapy. Specifically, higher levels of amyloid-beta protein in blood and spinal fluid suggest that less of this protein was being deposited as plaques in the brain.
Finally, use of hormone therapy was also associated with 39% lower odds of receiving a clinical diagnosis of dementia and less risk of showing symptoms of memory problems or decline in functional abilities.
Bruno noted that the study participants who used hormone therapy had an average age of 70, which differs from current standard practice of starting hormone therapy usually in the late 40s to early 50s and stopping it before age 60.
“Despite these limitations, our findings provide evidence of an association between use of oestrogen-only hormone therapy during later life and better outcomes on dementia and brain health,” Bruno said.
Several tools are currently used to assess the health of older people and their risk of future health problems, but it is unclear which ones perform best. A new study published in BMC Medicine compares seven widely used geriatric assessment tools. The results show that a relatively simple tool developed by researchers at Karolinska Institutet – can be just as reliable as more advanced and comprehensive approaches.
As populations age, healthcare systems face growing challenges in identifying older adults at increased risk of declining health, care dependency, and other adverse outcomes. Although numerous assessment tools have been developed for this purpose, few studies have directly compared their ability to predict a broad range of health outcomes.
In the current study, researchers analysed data from 3108 people aged 60 years and over who participated in the Swedish National study on Aging and Care in Kungsholmen, SNAC-K. Participants were followed for up to six years.
The researchers compared seven different assessment tools commonly used in healthcare and research. They evaluated how well each tool predicted a broad range of outcomes, including formal care use, nursing home admission, hospitalisation, dementia, disability, injurious falls, quality of life, and death. The results showed that three tools – the Health Assessment Tool (HAT), Intrinsic Capacity (IC) and the Frailty Index – consistently performed best across outcomes.
The simpler tool, HAT, combines a small number of measures that are relatively easy to collect in clinical practice, including an individual’s ability to manage everyday activities, cognitive function, walking speed, and number of chronic conditions.
“Our findings suggest that relatively simple tools that capture multiple dimensions of health can effectively identify older people at increased risk of future health decline and support clinical decision-making,” says Amaia Calderón-Larrañaga, the study’s senior author and senior researcher at the Aging Research Centre, and director of the TraCeDem research centre at Karolinska Institutet.
The study also found that several widely used tools, which are often endorsed by guidelines, performed less well for certain outcomes compared to HAT, IC, and the Frailty Index.
The researchers note that the findings should be interpreted with some caution. Participants in the study were, on average, healthier and more highly educated than the general older population, which may influence how well the results generalise to other settings.
See the scientific article for information on funding and potential conflicts of interest.
People who don’t eat meat may be less likely than meat eaters to reach the age of 100, according to a recent study. But before you reconsider your plant-based diet, there’s more to these findings than meets the eye.
The research tracked over 5,000 Chinese adults aged 80 and older who participated in the Chinese Longitudinal Healthy Longevity Survey, a nationally representative study that began in 1998. By 2018, those following diets that don’t contain meat were less likely to become centenarians compared with meat eaters.
On the surface, this appears to contradict decades of research showing that plant-based diets are good for your health. Vegetarian diets, for example, have been consistently linked to lower risks of heart disease and stroke, type 2 diabetes and obesity. These benefits come partly from higher fibre intake and lower saturated fat consumption.
So what’s going on? Before drawing any firm conclusions, there are several important factors to consider.
Your body’s needs change as you age
This study focused on adults aged 80 and older, whose nutritional needs differ markedly from those of younger people. As we age, physiological changes alter both how much we eat and what nutrients we need. Energy expenditure drops, while muscle mass, bone density and appetite often decline. These shifts increase the risk of malnutrition and frailty.
Most evidence for the health benefits of diets that exclude meat comes from studies of younger adults rather than frail older populations. Some research suggests older non-meat eaters face a higher risk of fractures due to lower calcium and protein intake.
In later life, nutritional priorities shift. Rather than focusing on preventing long-term diseases, the goal becomes maintaining muscle mass, preventing weight loss and ensuring every mouthful delivers plenty of nutrients.
The study’s findings may, therefore, reflect the nutritional challenges of advanced age, rather than any inherent problems with plant-based diets. Crucially, this doesn’t diminish the well-established health benefits of these diets for younger and healthier adults.
Maintaining muscle mass in older age is important, and that requires protein. Photo by Barbara Olsen on Pexels
Here’s a crucial detail: the lower likelihood of reaching 100 among non-meat eaters was only observed in underweight participants. No such association was found in older adults of healthy weight.
Being underweight in older age is already strongly linked with increased risks of frailty and death. Body weight therefore appears to be a key factor in explaining these findings.
It’s also worth remembering that this was an observational study, meaning it shows associations rather than cause and effect. Just because two things occur together doesn’t mean one causes the other.
The findings also align with the so-called “obesity paradox” in ageing, where a slightly higher body weight is often linked to better survival in later life.
Notably, the reduced likelihood of reaching 100 observed among non-meat eaters was not evident in those who included fish, dairy or eggs in their diets. These foods provide nutrients that are essential for maintaining muscle and bone health, including high-quality protein, vitamin B12, calcium and vitamin D.
Older adults following these diets were just as likely to live to 100 as meat eaters. The researchers suggested that including modest amounts of animal-source foods may help prevent undernutrition and loss of lean muscle mass in very old age, compared with strictly plant-based diets.
What this means for healthy ageing
Rather than focusing on whether one diet is universally better than another, the key message is that nutrition should be tailored to your stage of life. Energy needs decline with age (due to decreased resting energy expenditure), but some nutrient requirements increase.
Older adults still require adequate protein, vitamin B12, calcium and vitamin D – especially to preserve muscle mass and prevent frailty. In older adulthood, preventing malnutrition and weight loss often becomes more important than long-term chronic disease prevention.
Plant-based diets can still be healthy choices, but they may require careful planning and, in some cases, supplementation to ensure nutritional adequacy, particularly in later life.
The bottom line is that our nutritional needs at 90 may look very different from those at 50, and dietary advice should reflect these changes across the lifespan. What works for you now might need adjusting as you age – and that’s perfectly normal.
By calming inflammation and reducing excess fat, semaglutide may postpone several molecular signs of aging, pointing to the potential of GLP‑1 receptor agonists to help prevent age‑related diseases.
Semaglutide slowed biological aging across multiple epigenetic clocks in a randomised, double-blind, placebo-controlled clinical trial. The strongest signals were seen in epigenetic measures linked to inflammation, brain, heart, blood, kidney, liver and metabolic health, suggesting that the drug may influence aging-related biology across multiple body systems. The findings offer early clinical evidence that GLP-1 receptor agonists may influence aging biology.
Glucagon-like peptide-1 (GLP-1) receptor agonist medications have gained widespread attention for effectively treating obesity, lowering blood sugar and decreasing the risk of cardiovascular disease. Some researchers have proposed that these drugs may also influence the biology of aging, but direct evidence in humans has remained limited. Now, a new study provides the first randomised, placebo-controlled clinical evidence that semaglutide, a widely used GLP-1 drug, slows down the accumulation of biological aging markers in the DNA of adults with HIV. The study is published in Nature Communications.
Researchers at the University of California San Diego and several partner institutions analysed data from a previously published clinical trial of 108 adults with HIV‑associated lipohypertrophy, a condition in which excess fat builds up around the abdomen. About half of the participants received weekly injections of semaglutide, with the rest receiving placebo injections.
The team used a set of biological “epigenetic clocks” to track cellular aging over the 32-week treatment period. These clocks detect DNA methylation, chemical marks on DNA that help regulate how genes are turned on or off without changing the genetic sequence itself. By measuring changes in these marks, the team could assess whether the treatment was associated with a slower or faster biological aging pattern.
People with HIV often experience accelerated aging, even if it is well-controlled with antiretroviral therapy, according to first author Michael Corley, PhD, associate professor at UC San Diego School of Medicine and the Stein Institute for Research on Aging. However, the study found compared to the placebo group:
Participants treated with semaglutide exhibited a broad pattern of slower biological aging across epigenetic clocks linked to inflammation and blood, brain, heart, kidney, liver and metabolic health.
The drug slowed the pace of biological aging by 9 %, as measured by the DunedinPACE epigenetic clock.
The drug significantly slowed biological processes associated with the risk of all‑cause mortality and age-related disease, as measured by the PCGrimAge epigenetic clock.
Research suggests there are several mechanisms by which semaglutide may influence biological aging. By reducing inflammation and metabolic stress, GLP-1 drugs decreased chronic immune activation, a primary driver of accelerated aging in people with HIV. They also reduce visceral and ectopic fat that accumulates around the abdomen and organs, which may help curb the inflammatory and metabolic signals that promote aging.
“Emerging data also suggest that GLP-1 drugs may reprogram certain cells in different organs, which could help explain why we see effects across multiple aging clocks,” said Corley.
While the study focused on people with HIV‑associated lipohypertrophy, Corley says it may also offer lessons for the wider population.
“Many of the biological processes we study in HIV are also central to aging in the general population,” he said. “Because these processes can emerge earlier or be more pronounced in people with HIV, this community can help us identify interventions that may improve healthspan more broadly.”
In a related pilot study published in npj Aging, Corley and another team of researchers found that taking semaglutide for 24 weeks:
Reduced the rate of biological aging for 42% of participants with HIV and metabolic dysfunction-associated steatotic liver disease (MASLD) as measured by the DunedinPACE epigenetic clock. Those participants also had a greater reduction in liver fat compared with participants whose pace of aging sped up.
Slowed aging associated with the risk of all‑cause mortality in 34% of participants as measured by the PCGrimAge epigenetic clock.
Increased the length of telomeres in nearly 49 % of participants as measured by the PCDNAmTL epigenetic clock. Those participants also tended to walk faster after treatment, suggesting better physical function.
Together, these studies add to growing evidence that GLP-1 drugs may influence pathways involved in biological aging.
“We are not saying that semaglutide reverses aging or makes people younger. What we are seeing is a signal that it may slow some of the biological processes associated with aging.”
— Michael Corley, PhD
“We are not saying that semaglutide reverses aging or makes people younger,” said Corley. “What we are seeing is a signal that it may slow some of the biological processes associated with aging. With newer GLP-1–based therapies now emerging, the field has an opportunity to test whether different drugs in this class have distinct effects on aging biology and to identify which patients may benefit most.”
Larger clinical trials are needed to confirm the findings, determine how long treatment effects last, and establish optimal dosing and treatment duration for both people with HIV and the broader population. Future studies will also be needed to test whether the effects of GLP-1 effects on aging biology are enhanced when combined with lifestyle interventions such as diet, exercise and sleep optimization.
The Stein Institute for Research on Aging plans to translate these results into individualized “aging dashboards” to track biological aging with epigenetic clocks, enabling clinicians to design personalised therapies that target the underlying mechanisms of aging and help prevent age‑related diseases.
High intensity interval training (HIIT) may be the optimal exercise for reducing body fat while maintaining muscle mass in older adults, according to new research led by Australian academics.
“We found that high, medium and low intensity exercises all led to modest fat loss but only HIIT retained lean muscle,” said lead author and exercise physiologist Dr Grace Rose of the University of the Sunshine Coast.
The study examined how the intensity of different exercises could influence body composition in healthy older adults.
“While moderate training reduced fat mass, it also caused a small decline in lean muscle,” she said. “Both high and moderate intensities improved the composition of weight carried around the middle. Further analysis is needed of the low intensity results.” Dr Rose said the findings were particularly useful because body composition was implicated in the progression of many chronic diseases as people aged.
More than 120 healthy older adults from the Greater Brisbane region participated in the study, completing three exercise sessions a week in the gym for six months.
Their average age was 72 years old and average body mass index was 26kg/m2, categorised as normal for people aged over 65.
UniSC Associate Professor of Physiology and co-author Mia Schaumberg welcomed the the paper published in the journal Maturitas, with collaborators including UniSC’s Healthy Ageing Research Cluster and The University of Queensland.
“High intensity training in this study involved repeated short bursts, or intervals, of very hard exercise – where breathing is heavy and conversation is difficult – alternated with easier recovery periods. More than 120 healthy older adults from the Greater Brisbane region participated in the study, completing three exercise sessions a week in the gym for six months.
Their average age was 72 years old and average body mass index was 26kg/m2, categorised as normal for people aged over 65.
UniSC Associate Professor of Physiology and co-author Mia Schaumberg welcomed the timing of the paper published in the journal Maturitas, with collaborators including UniSC’s Healthy Ageing Research Cluster and The University of Queensland.
“High intensity training in this study involved repeated short bursts, or intervals, of very hard exercise – where breathing is heavy and conversation is difficult – alternated with easier recovery periods,” she said.
“HIIT likely works better because it puts more stress on the muscles, giving the body a stronger signal to keep muscle tissue rather than lose it.”
52% of postmenopausal women experience female-pattern hair loss, according to peer-reviewed research published in Menopause, the journal of the North American Menopause Society. Hot flushes – one of the symptoms that owns many public conversations about menopause – affect a larger proportion of women, but the disparity is not in the data. It is in how medicine responds to them. At more than one in two women, female-pattern hair loss is routinely absent from clinical consultations, rarely investigated at first presentation, and almost universally met with the same advice: give it time.
Why timing matters
During and after menopause, declining oestrogen levels and shifts in androgen balance cause susceptible hair follicles to gradually shrink. Each hair grows finer and shorter, with a briefer growth period per cycle. Left long enough without intervention, some follicles reach a point of no return, and the damage becomes irreversible.
“When we say irreversible, we mean that the follicle has become so damaged or inactive that it can no longer reliably regenerate a healthy terminal hair on its own,” says Dr Kashmal Kalan, Medical Director at Alvi Armani South Africa. “Medical therapies may help stabilise surrounding hair at that stage, but they may not recover what has already been lost,” says Dr Kalan.
For many women, that window closes not because they made an informed decision, but because nobody told them they had options. The advice they received – that gradual thinning is normal, that stress is a likely factor, that it may settle with time – sounded measured.
The cost of being dismissed
When the condition is classified as cosmetic, clinical urgency disappears. The patient is reassured rather than assessed, even though menopausal thinning is frequently a visible signal of systemic change. Hormonal shifts, nutritional deficiencies, thyroid dysfunction, and inflammatory or metabolic factors are all documented contributors, and none of them are cosmetic.
The consequences reach well beyond the scalp. Research published in the British Journal of Dermatology found that over 60% of women with hair loss actively avoided social interactions because of it. A separate study in the Journal of Cosmetic Dermatology found that affected women reported significantly higher social anxiety, lower self-esteem, and reduced life satisfaction compared to men experiencing the same condition. What begins on the scalp moves into how a woman presents professionally, how she engages socially, and how she sees herself.
A clinical framework built for men, applied to women
The protocols widely used to assess and treat this condition were largely developed around male patients. Defined hairline recession, concentrated donor areas, and linear progression are all considered male presentations. As a result, women have largely been assessed within a framework built for someone else.
“Applying male-based protocols to women can absolutely compromise outcomes. Female hair restoration requires an understanding of female-specific patterns of loss, progression risk, and the long-term hormonal picture. Preservation of softness, natural density gradients, and age-appropriate framing are considerations with no real equivalent in the male framework. In experienced hands, those distinctions are built into every stage of assessment and planning – not treated as secondary.”
What rigorous care looks like
At Alvi Armani, the first step is not a treatment recommendation – it is a diagnosis. A comprehensive workup, including blood investigations, is conducted before any intervention is discussed, because in menopausal women the drivers are rarely singular and what is visible on the scalp is seldom the whole picture.
“Not every patient is an immediate candidate for surgical restoration and recognising this is itself part of responsible practice. Medical stabilisation, non-surgical therapies, and hormonal management in collaboration with relevant specialists all form part of the treatment landscape – guided by individual diagnosis, not assumption,” Dr Kalan concludes.
“If any of this sounds familiar – the gradual changes, the concerns dismissed, the years of quietly adapting – it is worth knowing that the window is not necessarily closed. But it is also not standing still. Hair loss during menopause is extremely common – but common does not mean insignificant, and it does not mean inevitable.”
A 3-month-old African turquoise killifish, left, and a 5-month-old killifish, right, show aging much like that in humans.
Researchers have identified a gene that directly links early-life growth and reproductive success with accelerated ageing and increased cancer risk later in life, offering new insight into a longstanding theory in evolutionary biology.
Now, an international team of researchers provides experimental evidence for the theory of antagonistic pleiotropy, the idea that certain genes can provide advantages early in life while contributing to disease and decline in old age.
What’s fascinating – and slightly terrifying – is that the cancer we see in these fish isn’t a random accident. It’s the direct shadow of their youthful vitality
Prof Itamar Harel
While widely accepted in theory, scientists have struggled to identify specific genes responsible for such trade-offs in vertebrates. Using the African turquoise killifish, a short-lived species recently pioneered by Harel and colleagues for genetic ageing research, the team focused on the gene vgll3, which has been previously linked to the timing of human puberty and maturation in other species, particularly Atlantic salmon.
By modifying this gene using CRISPR technology, the researchers observed clear effects. Fish with altered vgll3 grew faster and reached sexual maturity earlier, traits that could offer a reproductive advantage in natural environments.
However, these benefits came with significant long-term costs. The same fish showed reduced lifespans and a higher incidence of age-related tumours, including melanoma-like cancers.
“We have effectively caught evolution in the act of making a trade-off. For years, we’ve asked why our bodies can’t just maintain themselves indefinitely. This gene gives us a direct answer: nature doesn’t prioritise longevity; it prioritises continuity. We are built to sprint, not to marathon,” said Prof Itamar Harel at Hebrew University.
Further analysis showed that the gene influences key biological processes, including cell division, stem cell activity, and DNA repair. Increased cellular activity may help explain both the rapid development observed in younger fish and the accumulation of damage that leads to disease in older individuals.
The researchers also developed a new immunodeficient killifish model, enabling them to transplant and study tumour cells in ways not previously possible in this system.
“What’s fascinating – and slightly terrifying – is that the cancer we see in these fish isn’t a random accident. It’s the direct shadow of their youthful vitality. The same machinery that drives a cell to build a young body is hijacking the system to build a tumour in the old one. If we can understand this mechanism, we might finally learn how to decouple healthy growth from the disease of ageing,” Dr Harel added.
Because vgll3 is conserved in humans, the findings may have broader implications for understanding human development, ageing, and age-related diseases. While previous association studies have linked the gene to puberty timing and hormone levels, functional data were missing until now.
The discovery could contribute to future efforts in cancer prevention and research aimed at extending healthy lifespan. Researchers say the next step will be to explore whether it is possible to separate the gene’s beneficial early-life effects from its harmful consequences later in life.
Calcium, vitamin D, or combined supplements offer little to no clinically meaningful benefit on fracture and fall prevention in most older people, finds an in-depth review of the latest evidence published by The BMJ.
Almost a third of people aged 65 and older fall each year, often resulting in fractures, which are linked to pain, reduced quality of life, and the need for residential care. Preventing falls and fractures is therefore a global public health priority.
Several previous evidence reviews have found no reduction in fractures with either calcium or vitamin D supplements and results are inconsistent for combined use. The benefit of vitamin D on falls also remains unclear.
Yet despite this, many clinicians, guidelines, and regulatory agencies recommend vitamin D supplements (with or without calcium) for bone health, and prescriptions have increased substantially in recent years.
To address this uncertainty, researchers in Canada reviewed the results of 69 randomised controlled trials involving 153,902 adults that assessed the effect of calcium or vitamin D supplements – or a combination of both – on reducing the number of fractures and falls compared with placebo or no treatment.
The trials were of varying quality, but the researchers were able to assess their risk of bias and certainty of evidence using established tools.
After agreeing on clinically meaningful thresholds, the researchers found little to no effect for experiencing any fracture from use of calcium supplements (moderate certainty evidence from 11 trials; 9,067 participants), vitamin D supplements (high certainty evidence from 36 trials; 92 045 participants), or combined supplementation (high certainty evidence from 15 trials; 51 126 participants).
Calcium, vitamin D, or combined supplementation also appeared to have little to no effect on specific fractures, such as hip fractures, or falls, based largely on moderate to high certainty of evidence.
The researchers acknowledge that some analyses included a small number of trials and participants, so these findings should be interpreted with caution, and results may not apply to individuals with specific bone disorders or to those receiving drug treatment for osteoporosis.
However, the findings were consistent after further analyses to account for differences such as participant age, sex, history of fractures and falls, and average dietary calcium intake, supporting the strength of their conclusions.
As such, they say these findings “do not support routine supplementation with calcium or vitamin D, or combined supplementation to prevent fractures and falls” and they suggest clinicians, guideline panels, and regulatory agencies “should re-evaluate their general recommendations for calcium and vitamin D supplementation in light of current evidence.”
Evidence from rigorous and well-powered trials is needed to inform recommendations for supplementation in higher-risk groups, say researchers in a linked editorial.
In the meantime, they suggest that focus and funding should be redirected towards interventions that have been shown to offer meaningful prevention of falls and falls related injuries, such as balance and resistance exercise, and interventions that combine elements like exercise, hazard assessment or education, tailored to individual risk.
