Author: ModernMedia

A Revolutionary Coral-inspired Material for Bone Repair

(Left) An image of a 3D-printed material implanted in vivo for 4 weeks. The photo was taken using a scanning electron microscope. Credit: Dr Zhidao Xia.
(Right) A photo of coral. Credit: Jesus Cobaleda.

Researchers at Swansea University have developed a revolutionary bone graft substitute inspired by coral which not only promotes faster healing but dissolves naturally in the body after the repair is complete.

This groundbreaking research, led by Dr Zhidao Xia from Swansea University Medical School in collaboration with colleagues from the Faculty of Science and Engineering and several external partners, has been patented and published in the leading journal Bioactive Materials.

Bone defects caused by conditions like fractures, tumours, and non-healing injuries are one of the leading causes of disability worldwide. Traditionally, doctors use either a patient’s own bone (autograft) or donor bone (allograft) to fill these gaps. However, these methods come with challenges, including a limited supply, the risk of infection and ethical concerns.

By using advanced 3D-printing technology, the team have developed a biomimetic material that mimics the porous structure and chemical composition of coral-converted bone graft substitute, blending perfectly with human bone and offering several incredible benefits:

  • Rapid Healing – It helps new bone grow within just 2–4 weeks.
  • Complete Integration – The material naturally degrades within 6–12 months after enhanced regeneration, leaving behind only healthy bone.
  • Cost-Effective – Unlike natural coral or donor bone, this material is easy to produce in large quantities.

In preclinical in vivo studies, the material showed remarkable results: it fully repaired bone defects within 3–6 months and even triggered the formation of a new layer of strong, healthy cortical bone in 4 weeks.

Most synthetic bone graft substitutes currently on the market can’t match the performance of natural bone. They either take too long to dissolve, don’t integrate well, or cause side effects like inflammation. This new material overcomes these problems by closely mimicking natural bone in both structure and biological behaviour.

Dr Xia explained: “Our invention bridges the gap between synthetic substitutes and donor bone. We’ve shown that it’s possible to create a material that is safe, effective, and scalable to meet global demand. This could end the reliance on donor bone and tackle the ethical and supply issues in bone grafting.”

Innovations like this not only promise to improve patient quality of life but also reduce healthcare costs and provide new opportunities for the biomedical industry.

The Swansea University team is now looking to partner with companies and healthcare organisations to bring this life-changing technology to patients around the world.

Source: Swansea University

The Heart has a ‘Brain’ of its Own

Human heart. Credit: Scientific Animations CC4.0

New research from Karolinska Institutet and Columbia University shows that the heart has a mini-brain – its own nervous system that controls the heartbeat. A better understanding of this system, which is much more diverse and complex than previously thought, could lead to new treatments for heart diseases. The study, conducted on zebrafish, is published in Nature Communications.

The heart has long been thought to be controlled solely by the autonomic nervous system, which transmits signals from the brain. The heart’s neural network, which is embedded in the superficial layers of the heart wall, has been considered a simple structure that relays the signals from the brain. However, recent research suggests that it has a more advanced function than that.

Controlling the heartbeat

Scientists have now discovered that the heart has its own complex nervous system that is crucial to controlling its rhythm.

“This ‘little brain’ has a key role in maintaining and controlling the heartbeat, similar to how the brain regulates rhythmic functions such as locomotion and breathing,” explains Konstantinos Ampatzis, principal researcher and docent at the Department of Neuroscience, Karolinska Institutet, Sweden, who led the study.

The researchers identified several types of neurons in the heart that have different functions, including a small group of neurons with pacemaker properties. The finding challenges the current view on how the heartbeat is controlled, which may have clinical implications.

Surprising complexity revealed

“We were surprised to see how complex the nervous system within the heart is,” says Konstantinos Ampatzis. “Understanding this system better could lead to new insights into heart diseases and help develop new treatments for diseases such as arrhythmias.” 

The study was conducted on zebrafish, an animal model that exhibits strong similarities to human heart rate and overall cardiac function. The researchers were able to map out the composition, organisation and function of neurons within the heart using a combination of methods such as single-cell RNA sequencing, anatomical studies and electrophysiological techniques.

New therapeutic targets

“We will now continue to investigate how the heart’s brain interacts with the actual brain to regulate heart functions under different conditions such as exercise, stress, or disease,” says Konstantinos Ampatzis. “We aim to identify new therapeutic targets by examining how disruptions in the heart’s neuronal network contribute to different heart disorders.”

Source: Karolinska Institutet

Home and Neighbourhood Environments Impact Sedentary Behaviour in Teens Globally

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The World Health Organization recommends no more than two to three hours per day of sedentary time for youth. However, adolescents worldwide are spending an average of 8 to 10 hours per day engaging in sedentary activities such as watching television, using electronic devices, playing video games and riding in motorised vehicles, according to a 15-country study published in the International Journal of Behavioral Nutrition and Physical Activity.

The most notable finding of the study, led by principal investigator James F. Sallis, PhD, distinguished professor at University of California San Diego, and colleagues from 14 countries, found that simply having a personal social media account was linked with higher total sedentary time in both males and females. Social media was also related to more self-reported screen time.

“Although there is great concern about negative effects of social media on youth mental health, this study documents a pathway for social media to harm physical health as well,” said Sallis, who is also a professorial fellow at the Australian Catholic University.

“These findings are concerning, as excessive sedentary behavior has been linked to a range of health problems, including obesity, diabetes and mental health issues.”

Researchers analysed accelerometer data from 3,982 adolescents aged 11 to 19 and survey measures of sedentary behaviour from 6,02 participants in the International Physical Activity and the Environment Network (IPEN) Adolescent Study, which covered 15 geographically and culturally diverse countries across six continents.

The number of electronic devices within a home, how many adolescents had their own social media accounts and neighbourhood walkability were significantly different across countries.

For example, adolescents from India had an average of 1.2 electronic devices in the bedroom and 0.5 personal electronic devices, while the average number of such devices in Denmark was 4.2 and 2.3, respectively. In India and Bangladesh, fewer than 30% of adolescents reported having their own social media account, compared to higher socio-economic status countries where it was over 90%.

Parents reporting on walkability identified Australia as having high access to parks, while Nigerian parents reported no access, and parents in Bangladesh and India reported poor access. Traffic was a concern among parents in Brazil, Malaysia, Bangladesh, India, and Israel, and concerns about crime were high in the first three countries.

Adolescents who reported less recreational screen time lived in walkable neighbourhoods and had better perceptions of safety from traffic and crime than others. Girls who lived in neighbourhoods designed to support physical activity were less likely to be sedentary.

Despite differences in culture, built environments and extent of sedentary time, patterns of association were generally similar across countries, said the study’s lead author Ranjit Mohan Anjana, MD, PhD, of Dr Mohan’s Diabetes Specialties Centre and Madras Diabetes Research Foundation in India.

“Together, parents, policymakers and technology companies can work together to reduce access to screens, limit social media engagement and promote more physical activity, thus helping adolescents develop healthier habits and reduce their risk of chronic diseases,” said Anjana.

The study’s findings have significant implications for public health policy and highlight the need for further research into the causes and consequences of sedentary behaviour among teenagers.

Source: University of California – San Diego

How Breast Cancer Cells Survive in Bone Marrow after Remission

Photo by National Cancer Institute on Unsplash

A new study has shed light on a previously poorly understood aspect of breast cancer recurrence: how cancer cells survive in bone marrow despite targeted therapies. The paper appears in the Journal of Clinical Investigation

Oestrogen receptor positive (OR+) breast cancer is the most common form of the disease, and cancer cells of this kind can live for years in bone marrow after remission. The persistence of these cells in marrow leads to the disease recurring about 40% of patients. This return can take the form of especially aggressive bone cancer with symptoms such as bone fractures and hypercalcaemia. 

The cells can also spread to other organs, causing recurrent disease that is currently incurable. 

To better understand how these cancer cells survive, and why they cause such aggressive returning disease, researchers investigated what happens to these dispersed cells in bone marrow. 

Their key finding was the mechanism by which a normal cell type, mesenchymal stem cells, in the bone marrow supports the cancer cells.

“We discovered that the breast cancer cells require direct contact with mesenchymal stem cells,” said Gary Luker, MD, senior author on the paper.  

“The cancer cells physically borrow molecules – proteins, messenger RNA – directly from the mesenchymal stem cells. Essentially the mesenchymal stem cells act as very generous neighbours in donating things that make the cancer cells more aggressive and drug resistant.”

In laboratory experiments, contact between cancer cells and mesenchymal stem cells induced changes in hundreds of proteins. Further analysis of which proteins allowed for survival of breast cancer cells led researchers to focus on GIV, also known as Girdin. The paper notes that GIV drives “invasiveness, chemoresistance, and acquisition of metastatic potential in multiple cancers.”

GIV makes these cancer cells specifically resistant to oestrogen-targeted therapies, such as the drug Tamoxifen. The researchers hope this understanding of the mechanism of cancer cell survival will one day lead to treatments that prevent OR+ breast cancers from returning.

Sleeper cells can awaken

“Sleeper cells can be reawakened and cause oestrogen receptor positive breast cancers to relapse years –in some cases as long as a decade – after patients were believed to be in remission,” said study author Pradipta Ghosh, M.D., a professor in the Departments of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine.

“Since these cancer cells ‘borrow’ essential proteins from stem cells in the bone marrow through cellular tunnels – much like smuggling – approaches for targeting the tunnels or proteins they smuggle could help prevent the relapse and metastasis of oestrogen receptor positive breast cancer.”

Source: University of Michigan

Deep Depletion of Blood Lipoprotein(a) Levels with New Drug

Image by Scientific Animations, CC4.0

In a new study, researchers found that a new drug under development, zerlasiran, depleted levels of lipoprotein(a) by more than 80% in participants with increased cardiovascular risk. The drug was well tolerated and the findings, published in JAMA Network, suggest that this could be the first viable treatment for elevated levels of lipoprotein(a).

Elevated levels of lipoprotein(a) (LPa) – a type of cholesterol – is a genetic risk factor for cardiovascular disease. Present in 20% of the population, it increases the risk of atherosclerotic cardiovascular disease (ASCVD) and aortic stenosis. Currently, there are no interventions which can bring down high LPa levels: it is unresponsive to diet, exercise, and other lifestyle changes and there is no available drug.

Zerlasiran, a small-interfering RNA that targets synthesis of LPa serum concentration, was developed to fill this gap. It is effectively a gene silencer that shuts down LPA, a gene which produces a protein found only in LPa. This in turn is expected to reduce cardiovascular risk.

A phase I clinical trial had shown that zerlasiran was safe and effective.

For the study, researchers enrolled 178 patients (average age 63.7 years, 46 female) with ASCVD and LPa concentrations greater than or equal to 125nmol/L. They were randomised to subcutaneously receive zerlasiran 300mg or 450mg, or a placebo, every 16 or every 24 weeks. The least-squares mean placebo-adjusted time-averaged percent change in LPa serum concentrations was −85.6%, −82.8%, and −81.3% for the 450mg every 24 weeks, 300mg every 16 weeks, and 300 mg every 24 weeks groups, respectively. The most common adverse events were injection site reactions, with mild pain occurring in 2.3% to 7.1% of participants in the first day following drug administration. There were 20 serious adverse events in 17 patients, none considered related to the study drug. For the group receiving a 300mcg dose every 16 weeks, it was found that even at the 60 week follow-up, 28 weeks after the last administration, that lipoprotein(a) serum concentrations were still 60% lower than baseline.

Pregnancy Enhances Natural Immunity to Block Severe Flu

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McGill University scientists have discovered that pregnancy may trigger a natural immunity to boost protection against severe flu infection. Contrary to the common belief that pregnancy increases vulnerability to infections, researchers found that it strengthened an immune defence in mice, blocking the Influenza A virus from spreading to the lungs, where it can cause severe infection.

Our results are surprising because of the current dogma, but it makes sense from an evolutionary perspective,” said co-lead author Dr Maziar Divangahi, Professor in McGill’s Faculty of Medicine and Health Sciences and Senior Scientist at the Research Institute of the McGill University Health Centre (The Institute).

“A mother needs to stay healthy to protect her developing baby, so the immune system adapts to provide stronger defenses. This fascinating response in the nasal cavity is the body’s way of adding an extra layer of protection, which turns on during pregnancy.”

Exploring benefits for pregnancy and beyond

The researchers used a mouse model to observe how a certain type of immune cell activates in the nasal cavity of mice during pregnancy, producing a powerful molecule that boosts the body’s antiviral defenses, especially in the nose and upper airways.

“Influenza A virus remains among the deadliest threats to humanity,” said first author Julia Chronopoulos, who carried out the research while completing her PhD at McGill. “This natural immunity in pregnancy could change the way we think about flu protection for expectant mothers.”

The Public Health Agency of Canada recommends pregnant women and pregnant individuals get the flu vaccine, as they are at high risk of severe illness and complications like preterm birth. The new insights offer promise for more targeted vaccines for influenza, which is among the top 10 leading causes of death in Canada.

“The broader population could also benefit, as our findings suggest the immune response we observed could be replicated beyond pregnancy,” said co-lead author Dr James Martin, Professor in McGill’s Faculty of Medicine and Health Sciences and Senior Scientist at the RI-MUHC. This could mean new nasal vaccines or treatments that increase protective molecules, known as Interleukin-17.

The team’s next focus is on finding ways to reduce lung damage during viral infections like the flu or COVID. Rather than targeting the virus, as previous research has done, they aim to prevent dysregulated immune systems from overreacting, an approach that could lower the risk of serious complications associated with flu infection.

Source: McGill University

T Cells Become Exhausted in Chronic Fatigue Syndrome Patients

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Debilitating chronic fatigue syndrome creates conditions T cells becomes exhausted, according to a new study published in Proceedings of the National Academy of Sciences. The findings point the way for important new lines of investigation. 

The study’s authors knew the immune system was dysregulated in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), so they began by asking, which parts shift with the condition? A systematic exploration revealed that key CD8+ T cells displayed one of the most pronounced signatures of dysregulation, with signs of constant stimulation that lead to an exhausted state, a condition that is well-studied in cancer.

ME/CFS affects an estimated 3 million people in the United States and some 65 million worldwide, leaving some patients ill for decades and unable to work. Symptoms include overwhelming fatigue that is not helped by rest, and can also include brain fog, body pains, headaches, difficulty sleeping and prolonged increases in symptoms after mild physical exertion or exercise. Causes are unknown and there is no treatment for the disease.

“This is an important finding for ME/CFS because now we can examine the T cells more carefully, and hopefully by looking in the exhausted cells we can start to get hints as to what they are responding to,” said Andrew Grimson, professor of molecular biology and genetics in the College of Arts and Sciences.

Grimson is co-corresponding author of the studyMaureen Hanson, Professor in the Department of Molecular Biology and Genetics, is the other corresponding author.

“Therapies have been developed to reverse T cell exhaustion as treatments for cancer,” Hanson said. “Our findings raise the question of whether such anti-exhaustion drugs might also be helpful in ME/CFS.”

Strong evidence for the phenomenon of T cell exhaustion in ME/CFS has also been reported in long COVID, Hanson added.

The study was led by co-first authors David Iu, a doctoral student in Grimson’s lab, and Jessica Maya, PhD ‘24, formerly in Hanson’s lab and currently a researcher at the Centers for Disease Control and Prevention. 

In a paper published earlier this year, Grimson and collaborators used a technology called single cell RNA sequencing to examine and identify all the circulating immune cells in ME/CFS patients. In the current paper, they used that data to examine which of the different types of T cells, including CD8+ T cells, were most altered in ME/CFS patients.

“That pointed us in the direction of CD8+ cells,” Grimson said. After purifying those cells, they used additional advanced technologies to precisely determine which genes were being expressed and pinpoint which genes were getting switched on or off. 

“When we looked at all of the differences [compared to normal functioning], they really pointed us towards an exhaustion-like state for the CD8+ T cells,” Grimson said. 

Meanwhile, in Hanson’s lab, Maya led a different approach of purifying patients’ T cells and then determining expression patterns of proteins on the surface of these cells. The team examined two series of different markers on the various proteins, one of which allowed them to subdivide all the different types of CD8+ T cells, while the other allowed them to detect proteins known to be involved in exhaustion.

“Immune cells from ME/CFS patients exhibited higher levels of proteins on their surface that are characteristic of cells that have become exhausted, which can be caused by long-term exposure to a virus protein or by continuous stimulation of the immune system, a state that is also found in cancer patients,” Hanson said. 

Future work will try to determine whether a virus is in fact involved, which is currently not known. “We need to understand what is pushing them to this exhausted state,” Grimson said.

The team also plans to take cells from patients and controls, purify those cells and treat patients with drugs that reverse exhaustion and see if the immune cells resume normal function. If CD8+ T cell exhaustion can be reversed, the next question is whether such reversal actually benefits a patient, as exhaustion can have protective qualities. 

Another future line of inquiry will include distinguishing T cell receptors in exhausted cells from patients, to try to find which molecules those T cell receptors are recognising, and if from those clues, they can work out whether specific pathogens are involved. 

Source: Cornell University

fMRI Brain Scan Predicts the Effectiveness of Spinal Cord Surgery

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A 10-minute brain scan can predict the effectiveness of a risky spinal surgery to alleviate intractable pain. The Kobe University result gives doctors a much-needed biomarker to discuss with patients considering spinal cord stimulation.

For patients with chronic pain that cannot be cured in any other way, a surgical procedure called “spinal cord stimulation” is seen as a method of last resort. The treatment works by implanting leads into the spine of patients and electrically stimulating the spinal cord. Because the spinal cord transmits sensations to the brain from all over the body, the position of the leads is adjusted so that the patients feel the stimulation at the site of the pain. The Kobe University anaesthesiologist Ueno Kyohei says: “A big issue is that the procedure is effective for some but not for other patients, and which is the case is usually evaluated in a short trial of a few days to two weeks prior to permanent implantation. Although this trial is short, it is still an invasive and risky procedure. Therefore, clinicians have long been interested in the possibility of predicting a patient’s responsiveness to the procedure through non-invasive means.”

Functional magnetic resonance imaging, or fMRI, has become a standard tool to visualize how the brain processes information. More precisely, it can show which parts of the brain are active in response to a stimulus, and which regions are thus functionally connected with each other. “In an earlier study, we reported that for the analgesic ketamine, pain relief correlates negatively with how strongly connected two regions of the default mode network are before the drug’s administration,” explains Ueno. The default mode network, which plays an important role in self-related thought, has previously been implicated in chronic pain. Another relevant factor is how the default mode network connects with the salience network, which is involved in regulating attention and the response to stimuli. Ueno says, “Therefore, we wanted to examine whether the correlation of the activities within and between these networks could be used to predict responsiveness to spinal cord stimulation.”

He and his team published their results in the British Journal of Anaesthesia. They found that the better patients responded to spinal cord stimulation therapy, the weaker a specific region of the default mode network was connected to one in the salience network. Ueno comments, “Not only does this offer an attractive biomarker for a prognosis for treatment effectiveness, it also strengthens the idea that an aberrant connection between these networks is responsible for the development of intractable chronic pain in the first place.”

Undergoing an fMRI scan is not the only option. Combining pain questionnaires with various clinical indices has been reported as another similarly reliable predictor for a patient’s responsiveness to spinal cord stimulation. However, the researchers write that “Although the cost of an MRI scan is controversial, the burden on both patients and providers will be reduced if the responsiveness to spinal cord stimulation can be predicted by one 10-minute resting state fMRI scan.”

In total, 29 patients with diverse forms of intractable chronic pain participated in this Kobe University study. On the one hand, this diversity is likely the reason why the overall responsiveness to the treatment was lower compared to similar studies in the past and also made it more difficult to accurately assess the relationship between brain function and the responsiveness. On the other hand, the researchers also say that, “From a clinical perspective, the ability to predict outcomes for patients with various conditions may provide significant utility.” Ueno adds: “We believe that more accurate evaluation will become possible with more cases and more research in the future. We are also currently conducting research on which brain regions are strongly affected by various patterns of spinal cord stimulation. At this point, we are just at the beginning of this research, but our main goal is to use functional brain imaging as a biomarker for spinal cord stimulation therapy to identify the optimal treatment for each patient in the future.”

Scientists Identify a Type of Brain Cell That is a Master Controller of Urination

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Researchers have identified a subset of brain cells in mice that act as the master regulators of urination.

The research, published as a Reviewed Preprint in eLife, is described by editors as an important study with convincing data showing that oestrogen receptor 1-expressing neurons (ESR1+) in the Barrington’s nucleus of the mouse brain coordinate both bladder contraction and relaxation of the external urethral sphincter.

Urination requires the coordinated function of two units of the lower urinary tract. The detrusor muscle of the bladder wall relaxes to allow the bladder to fill and empty, while the external sphincter opens when it’s appropriate to allow urine to flow out, but otherwise keeps tightly shut.

“Impairment of coordination between the bladder muscle and the sphincter leads to various urinary tract dysfunctions and can significantly degrade a person’s quality of life,” says first author Xing Li, Advanced Institute for Brain and Intelligence, School of Physical Science and Technology, Guangxi University, Nanning, China. “But although we know the individual nerve signalling pathways that control each of these urinary tract components, we don’t know which brain areas ensure they cooperate at the right time.”

To explore this, the authors used state-of-the-art live cell imaging to study the activity of brain cells in anaesthetised and awake mice during urination. They focused on a brain region called the pontine micturition centre (PMC), otherwise known as the Barrington’s nucleus, and compared the activity of different PMC nerve cell subtypes.

In their first experiments, they measured the activity of the cells as the bladder empties by measuring changes in levels of calcium. This revealed that the electrical firing rate of a subset of PMC cells expressing estrogen receptors (PMCESR1+ cells) was tightly linked to bladder emptying. When they combined this with monitoring bladder physiology, they found that it was not only the timing of PMCESR1+ cell activity that correlated with bladder emptying, but the strength of cell electrical activity, too.

Next, they tested what happened to urination if they blocked or triggered the PMCESR1+ cells. They found that when PMCESR1+ cell activity was blocked, the amount of urine the mice passed was significantly reduced and ongoing urination was suspended from the moment the cells were inactive. To understand the mechanism behind this, they measured the activity of the bladder muscle and sphincter. They discovered that both increase of bladder pressure and sphincter muscle bursting activity associated with bladder emptying both stopped when PMCESR1+ cell activity was blocked during an ongoing voiding even. Similarly, when PMCESR1+ cells were artificially activated using light, bladder emptying occurred 100% of the time. This suggests that PMCESR1+ cells work as a reliable master switch that either initiates or suspends bladder emptying.

To test whether PMCESR1+ cells can influence bladder emptying independently of controlling the sphincter, they disconnected either the nerve carrying messages from the brain to the sphincter, or the nerve carrying messages from the brain to the bladder. They found that PMCESR1+ cell control of the bladder was fully operational even when communication to the sphincter was blocked, and vice versa. This showed the cells could control the bladder and sphincter independently of one another, but the question remained: could they coordinate the action of the bladder muscle and sphincter together? That is, operate them in a controlled, perfectly timed manner, to trigger bladder emptying when appropriate?

To explore this, they simultaneously recorded bladder pressure and electromyography measurements of sphincter activity. The timing of bladder pressure changes immediately before sphincter bursting activity was consistent for both spontaneous bladder emptying and emptying caused by activating the PMCESR1+ cells, showing that these cells can coordinate the two steps in a precisely temporal sequence and controlled way.

“Our study shows that a subset of cells in the Barrington’s nucleus of the brain can initiate and suspend bladder emptying with 100% accuracy when needed, for example, to release only a small volume for landmarking by animals, or for a human to urinate into a small sample tube for a health check,” concludes senior author Xiaowei Chen, Third Military Medical University, and Chongqing Institute for Brain and Intelligence, China. “While other cells will no doubt be involved in perfect urination control, our pinpointing of PMCESR1+ cells’ crucial role in bladder–sphincter coordination will aid the development of targeted therapies for treating urination dysfunction caused by brain or spinal cord injury or peripheral nerve damage.”

Source: eLife

Five Years of Vitamin D Supplements Fails to Prevent Diabetes

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Using significantly higher doses of vitamin D than recommended for five years did not affect the incidence of type 2 diabetes in elderly men and women, according to a new study from the University of Eastern Finland which appears in Diabetologia.

In population studies, low levels of vitamin D in the body have been associated with a higher risk of type 2 diabetes, but such observational studies cannot directly prove a causative link. Experimental studies have shown that the use of significantly higher doses of vitamin D than recommended slightly reduces the risk of developing type 2 diabetes in individuals with impaired glucose metabolism, ie, those with prediabetes. In contrast, no effects have been observed in individuals without prediabetes. However, the studies with non-prediabetic subjects have used relatively small doses of vitamin D or have been short-term. Until now, there has been no research data on the effects of long-term use of high doses of vitamin D on the risk of type 2 diabetes in individuals without glucose metabolism disorders.

In the Finnish Vitamin D Trial (FIND) conducted at the University of Eastern Finland from 2012 to 2018, 2 495 men aged 60 and older and women aged 65 and older were randomised for five years into either a placebo group or groups receiving either 40 or 80 micrograms of vitamin D3 per day. In the statistical analyses of the now-published sub-study, 224 participants who were already using diabetes medications at the start of the study were excluded. Comprehensive information was collected from the participants on lifestyle, nutrition, diseases, and their risk factors. Data was also obtained from national health registers. About one-fifth were randomly selected for more detailed examinations, and blood samples were taken from them.

During the five years, 105 participants developed type 2 diabetes: 38 in the placebo group, 31 in the group receiving 40 micrograms of vitamin D3 per day, and 36 in the group receiving 80 micrograms of vitamin D3 per day. There was no statistically significant difference in the number of cases between the groups.

In the more closely studied group of 505 participants, the blood calcidiol level, which describes the body’s vitamin D status, was on average 75nmol/L at the start, and only 9% had a low level, ie, below 50nmol/L. After one year, the calcidiol level was on average 100nmol/L in the group that used 40 micrograms of vitamin D per day and 120nmol/L in the group that used 80 micrograms of vitamin D per day. There was no significant change in the placebo group. The effects of vitamin D on blood glucose and insulin levels, body mass index, and waist circumference were examined during the first two years of the study, but no differences were observed between the groups.

The findings of the FIND study reinforce the view that the use of higher doses of vitamin D than recommended does not significantly affect the risk of developing type 2 diabetes in individuals without prediabetes and who already have a good vitamin D status. So far, there is no research data on whether high doses of vitamin D can be beneficial in preventing type 2 diabetes in individuals without prediabetes but with vitamin D deficiency.

Source: University of Eastern Finland