Abdominal Obesity and Vitamin D Deficiency Together More Than Double the Risk of Death After 50
Key Takeaways:
- In people aged 50 and over, having both abdominal obesity and vitamin D deficiency was linked to a 123% higher risk of death.
- Alone, abdominal obesity raised that risk by 47% and vitamin D deficiency by up to 91% – together, the two amplify one another.
- Abdominal fat sequesters circulating vitamin D, and the resulting deficiency worsens the chronic inflammation driven by excess fat.
A six-year study of ageing in England
New research has put a figure on something clinicians have long suspected: that two common and often overlooked problems in later life are considerably more dangerous when they occur together than either is alone.
The study, in the journal Diabetes, Obesity and Metabolism, followed 5,520 people aged 50 and older over a six-year period. It found that people with both abdominal obesity and vitamin D deficiency had a 123% higher risk of death than people without these conditions.
The work was coordinated by Tiago Silva Alexandre, a professor in the Department of Gerontology at the Federal University of São Carlos (UFSCar) in Brazil, and carried out in collaboration with University College London (UCL) in the United Kingdom. Participants were drawn from the English Longitudinal Study of Ageing (ELSA), one of the world’s largest studies on ageing.
The central message is not that either condition is newly dangerous, but that their combination multiplies risk.
“Abdominal obesity is a well-known risk factor because it’s associated with inflammation and metabolic problems. Vitamin D, on the other hand, is a hormone that acts on various organs, and its deficiency impairs several bodily functions. When these two conditions occur together, one amplifies the effects of the other, further increasing the risk of death,” explains Alexandre. “For that reason, monitoring vitamin D levels and treating excess abdominal fat are essential measures to prevent premature death, especially after age 50,” he adds.
How the two conditions were defined
The researchers used established thresholds for both measures, which makes the findings straightforward to translate into everyday practice.
Vitamin D deficiency was defined as a level below 30 nmol/L. Abdominal obesity was defined by waist circumference – greater than 102 centimetres (40 inches) for men and greater than 88 centimetres (35 inches) for women.
Both are measures that can be captured in a routine consultation, one through a standard blood test and the other with a tape measure, without recourse to specialist equipment or imaging.
Each condition carries risk on its own
When the two conditions were examined separately, the data produced a result that may surprise some practitioners: vitamin D deficiency alone posed a greater risk than abdominal obesity alone.
Abdominal obesity on its own was associated with a 47% increase in the risk of death. Vitamin D deficiency on its own raised that risk by up to 91%. When both were present, the risk of death more than doubled.
That pattern is what makes the combination clinically significant. The elevated risk seen in people with both conditions is greater than would be expected from simply adding the two individual risks together, which points towards a biological interaction rather than two independent problems sitting side by side in the same person.
Why the two conditions amplify one another
According to Alexandre, abdominal obesity and vitamin D deficiency feed into each other, creating what he describes as a vicious cycle.
The first mechanism is storage. Abdominal fat “sequesters” circulating vitamin D and holds it within adipocytes, or fat cells, preventing the vitamin from reaching the bloodstream in useful quantities.
“This means that although the body may have the vitamin stored in fat, it isn’t freely available in the blood to perform vital functions in other organs and systems,” he says.
In other words, a blood test may show deficiency even where the body’s total stores are not depleted, because the vitamin is effectively locked away where it cannot be used.
The second mechanism concerns metabolism. People with obesity have lower expression of the enzymes needed to metabolise vitamin D, which further reduces the amount available to the body.
The consequences then loop back on themselves. “Abdominal obesity reduces circulating vitamin D, and that deficiency impairs the immune system, exacerbating the chronic inflammation caused by excess fat and drastically increasing the risk of mortality,” Alexandre explains to Agência FAPESP.
Ageing, inflammation and a loss of regulation
The picture is complicated further by the biology of ageing itself. Later life is naturally marked by a process known as inflammaging – a state of low-grade chronic inflammation that develops with age.
Vitamin D ordinarily acts as a brake on that process. Where levels fall and abdominal fat is present, that brake is weakened at precisely the point where it is most needed.
“Under normal conditions, vitamin D acts as a regulator of the immune system, preventing inflammation from getting out of control. When vitamin D levels are low and there’s excess abdominal fat, an unfavorable systemic environment develops that accelerates cardiovascular and metabolic diseases, as well as muscle loss,” he stresses.
Part of a wider cascade
This study is the most recent in a series by the same group investigating the role of vitamin D in ageing, and its findings sit alongside earlier work linking deficiency to functional decline.
“In previous studies, we identified a cascade effect. Vitamin D deficiency leads to a loss of strength, which results in reduced walking speed, causing a loss of independence and greater dependence in daily activities,” Alexandre explains.
A further study by the group found that vitamin D deficiency increases the risk of cognitive decline.
Taken together, these strands describe a hormone with a reach that extends well beyond bone health.
“Vitamin D is a hormone with various functions. It plays a role in regulating blood pressure, heart rate, the central nervous system, the immune system and the endocrine system. Therefore, when its levels are low, several essential bodily functions are compromised,” he says.
What this means for practice
For healthcare professionals working with people over 50, the practical implication is a case for looking at these two markers together rather than in isolation. A raised waist circumference and a low vitamin D level each warrant attention on their own terms, but the study suggests that the presence of one should prompt closer interest in the other.
It also reinforces the value of waist circumference as an assessment measure in its own right, given that it is central adiposity – rather than body weight alone – that drives the inflammatory and metabolic processes described here.
Building that broader assessment skill set, and the confidence to act on it as part of whole-person care, is the focus of professional training such as the College of Contemporary Health’s Obesity Essentials, a CPD-accredited online short course covering the assessment and management of overweight and obesity.
As Alexandre puts it, monitoring vitamin D levels and treating excess abdominal fat are essential measures to prevent premature death after the age of 50 – two simple assessments that, on this evidence, carry considerable weight together.
CCH insight
This is an interesting study. At CCH we have held a longstanding interest in the wide- ranging functions of vitamin D, especially its role in immune function. These results suggest that vitamin D status should be checked routinely in patients with abdominal obesity, and any deficiency should be treated immediately. This would be a simple and inexpensive protocol and could significantly reduce premature death in this group.
Findings like these are a reminder that excess abdominal fat rarely acts alone – its metabolic and inflammatory effects reach into hormone regulation, immune function and, ultimately, life expectancy. CCH’s Obesity Essentials CPD short course (10 CPD hours, fully online, CPD-accredited) helps healthcare professionals assess and manage patients living with overweight and obesity using a rounded, evidence-based approach that looks beyond a single number on the scale to the wider systemic picture.
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Belly Weight Predicts Heart Health Better Than BMI, Study Indicates
Key Takeaways:
- Fat stored around the waist is a stronger predictor of heart disease than body mass index alone.
- People with preclinical obesity face a raised cardiovascular risk despite appearing healthy.
- Researchers estimate early intervention could prevent 45% of new cardiovascular disease cases.
Why waist size matters more than the scales
People living with overweight or obesity can carry a higher risk of heart disease even when they appear to be perfectly healthy, according to new research presented at the International Congress on Obesity in Mexico City (15–17 July). Combining waist-based measurements with body mass index (BMI) to detect this hidden risk and act early could, over the years ahead, prevent hundreds of thousands of people from dying from heart attacks, strokes and other cardiac problems, researchers from the University of Glasgow, Glasgow, UK, said.
“We know that excess weight, particularly around the waist, increases the risk of heart disease,” said lead researcher Estefania Fuentes Avalos. “In 2021, an estimated 1.9 million cardiovascular disease deaths – almost one in 10 heart-related deaths worldwide – were attributed to high body mass index.
“The link between central, or abdominal, obesity and heart disease is especially strong because fat stored around the waist, known as visceral fat, is metabolically active and releases inflammatory substances into the bloodstream. Over time, this chronic inflammatory state can damage blood vessels and accelerate the buildup of arterial plaque, significantly increasing the risk of heart attacks.”
The limits of BMI
BMI, a measure of weight compared with height, is routinely used to assess a person’s weight status, defining whether they have a normal weight, overweight or obesity. However, it does not take into account where fat is stored in the body.
To address this and other shortcomings of BMI, The Lancet Diabetes & Endocrinology Commission recently proposed a different way of assessing obesity status. The Lancet Commission framework uses BMI together with central adiposity markers – waist measurements – to determine whether a person has excess body fat. People with excess body fat are then categorised as having either preclinical obesity or clinical obesity, depending on whether they also have long-term obesity-related conditions such as high blood pressure, joint pain and sleep apnoea.
The new study set out to establish whether this method is better at identifying people at high risk of cardiovascular disease than BMI alone.
“Detecting cardiovascular risk at an early stage is essential, particularly at the preclinical stage of obesity, as it provides a window of opportunity to implement timely, targeted interventions before obesity-related complications such as high blood pressure arise,” Fuentes Avalos said.
“This underpins our focus on risk stratification in this group, with the aim of detecting high-risk individuals who may otherwise be overlooked.”
What the study looked at
Fuentes Avalos examined data on 382,769 adults of white ethnicity in the UK Biobank study (age range 40–69 years, average age 56 years, 53% women).
Under The Lancet Commission framework, 285,190 (74%) of the participants had excess body fat, based on BMI and central adiposity markers. Within this group, 102,237 (26.7%) were classified as having preclinical obesity – excess body fat without long-term obesity-related conditions – and 182,953 (47.8%) as having clinical obesity, meaning excess body fat alongside long-term obesity-related conditions. The remainder had neither excess body fat nor long-term obesity-related conditions; they were classified as not having obesity and served as the reference group.
None of the participants had cardiovascular disease at the start of the study. Hospital and death records provided information about diagnoses of, and deaths from, heart attacks, strokes and other forms of cardiovascular disease over the following 12 years. During this time, there were 41,742 new cases of, and 8,832 deaths from, cardiovascular disease. Studies of this scale underline how much practical assessment skill clinicians need when supporting patients with excess weight – a competency CCH’s Obesity Essentials short course is designed to build.
Clinical obesity carried the sharpest risk
Analysis of the data showed that people with clinical obesity were far more likely to develop, or die from, cardiovascular disease than those without obesity.
Women with clinical obesity developed cardiovascular disease at a rate 2.5-fold higher than women without obesity, and died from it at an almost threefold (2.8-fold) higher rate. Men with clinical obesity developed cardiovascular disease at an almost twofold higher rate (1.9-fold) and had a 2.6-fold higher rate of cardiovascular death than men without obesity.
The hidden risk in preclinical obesity
People with preclinical obesity were also at greater risk, despite having no obesity-related conditions and appearing to be in good health.
Women with preclinical obesity developed cardiovascular disease at a 38% higher rate and died from it at a 46% higher rate than women without obesity. For men, preclinical obesity was associated with an 18% higher rate of developing cardiovascular disease and a 52% higher rate of cardiovascular death.
All of the results were adjusted for socioeconomic status and lifestyle factors, including smoking and alcohol consumption.
More waist markers, more risk
Further analysis showed that the more high-risk central adiposity markers a person had, the more likely they were to develop heart disease. For example, a woman with one high-risk marker – waist circumference, waist-to-hip ratio or waist-to-height ratio – was 17% more likely to develop cardiovascular disease than a woman with no high-risk waist measurements. Having all three high-risk measurements increased the risk by 64%. The study also found that waist measurements were more accurate at predicting cardiovascular disease than BMI.
A window of opportunity
The researchers concluded that people with preclinical obesity are at higher risk of developing, and dying from, cardiovascular disease despite appearing to be healthy.
“Preclinical obesity is a critical window of opportunity to improve heart health. Routinely measuring waist circumference, waist-to-hip ratio and waist-to-height ratio along with BMI would identify high-risk individuals who might be overlooked by assessing BMI alone,” Fuentes Avalos said.
“They could then be offered intensive diet and exercise programs to improve their cardiac and overall health.
“We have calculated that early intervention could prevent 45% of new cases of cardiovascular disease and 41% of cardiovascular disease deaths in similar populations.
“Given that cardiovascular disease remains a leading cause of ill health and death globally, routinely taking waist measurements along with BMI could prevent hundreds of thousands of deaths over a decade alone.”
CCH insight
This is very important work on two levels. Firstly, it not only re-enforces the importance of waist circumference measures as superior indicators of disease risk compared to the traditional BMI measure, but also suggests that calculating three waist circumference markers gives a more accurate indication of CV risk than just one. And secondly, it feeds into the current debate around the terms ‘clinical’ and ‘pre-clinical’ obesity coined by The Lancet Diabetes & Endocrinology Commission. The results indicate that, while people with clinical obesity have a far higher risk of cardiovascular disease or death, those with pre-clinical obesity are still at risk and still therefore warrant intervention. Depending on your perspective, you could argue this supports the Commission’s findings or contradicts them!
Findings like these are only useful in practice if clinicians feel confident assessing excess weight and having sensitive, evidence-based conversations with patients about it. CCH’s Obesity Essentials – an online CPD short course offering 10 CPD hours – equips healthcare professionals with the practical skills to assess and manage patients living with overweight and obesity, from measurement through to compassionate communication.
Explore Obesity Essentials and strengthen your day-to-day weight-management practice.
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Four Weeks of Tomato-Soy Juice Lowered Inflammation in Adults with Obesity
Key Takeaways:
- In a four-week study, a tomato-soy juice rich in lycopene and soy isoflavones significantly reduced three blood markers of systemic inflammation in healthy adults with obesity, while a control tomato juice lacking those compounds did not.
- The researchers chose a low-carotenoid tomato juice as the comparison drink, rather than water, so they could isolate the effects of the lycopene and isoflavones rather than the effects of tomato juice in general.
- Building on these results and supporting animal data, the team has secured federal funding for a pilot clinical trial examining whether the same juice can ease inflammation in people living with pancreatitis.
A food-based approach to inflammation
Drinking a tomato-soy juice packed with plant compounds previously shown in animal studies to support health lowered pro-inflammatory proteins in healthy adults with obesity after four weeks, according to a new study. The researchers say the findings point to the juice’s potential as a functional food that could help rein in the persistent, unchecked inflammation that underpins a wide range of chronic conditions.
The juice was formulated to deliver high levels of two plant-based compounds, lycopene and soy isoflavones, both of which earlier research suggests have antioxidant and anti-inflammatory properties. Measured against a control tomato juice that lacked these compounds, the tomato-soy juice produced a significant drop in the blood levels of three proteins that serve as markers of systemic inflammation.
“The idea is, can we use food-based interventions to modulate inflammation?” said lead author Jessica Cooperstone, associate professor of horticulture and crop science at The Ohio State University. “And can we test this in a rigorous way so that we can really see this is affecting inflammation, versus just saying something is anti-inflammatory?”
The study was published recently in the journal Molecular Nutrition & Food Research.
What is in the juice
Lycopene is a carotenoid, the class of pigments responsible for the colours of tomatoes and various other vegetables. Soy isoflavones are flavonoids that mimic the action of the hormone oestrogen. Both are phytochemicals, naturally occurring compounds that help plants thrive.
Years ago, drawing on studies that linked diets rich in either tomato products or soy with a reduced risk of prostate cancer, Ohio State researchers developed the tomato-soy juice. It was made using tomatoes bred to contain a high concentration of lycopene – varieties also developed and grown at Ohio State – and then enriched with a soy isoflavone extract.
Subsequent research at the university connected a higher intake of the tomato-soy juice with reduced prostate-specific antigen levels in some men with prostate cancer. Studies conducted elsewhere have likewise suggested that tomatoes and soy, whether eaten separately or together, can influence inflammatory and metabolic pathways tied to obesity and other chronic illnesses.
“There’s been enough compelling evidence that compounds from tomatoes and soy might be modulating inflammation that we decided to test this in people,” Cooperstone said.
How the study was carried out
For the new study, 12 healthy adults with obesity drank two 6-ounce cans of the tomato-soy juice every day for four weeks. Following a washout period, the same participants then consumed the low-carotenoid control tomato juice for a further four weeks.
The choice of comparison drink was deliberate. Rather than pitting the juice against plain water, the team selected a tomato juice stripped of the key compounds so that any difference could be attributed to those compounds specifically.
“The hypothesis is that it’s the lycopene from the tomatoes and the isoflavones from the soy that’s inducing the effect, so we didn’t want to have a control that’s just water,” Cooperstone said.
What the blood tests showed
Before and after each four-week period, the researchers collected blood samples and tested them for cytokines, the pro-inflammatory proteins produced by the immune system. Only the tomato-soy juice produced significant reductions, and it did so in three cytokines: interleukin (IL)-5, IL-12p70 and granulocyte-macrophage colony-stimulating factor (GM-CSF). The juice was also associated with a downward trend in tumour necrosis factor alpha (TNF-a), although that particular change did not reach statistical significance.
Clues from the urine analysis
The team also examined participants’ urine before and after each trial period, looking for changes in metabolites. Metabolites are the molecular products of the biochemical reactions that break down nutrients to generate energy and carry out other essential functions in the body.
The analysis revealed that both the tomato-soy juice and the control tomato juice prompted some of the same shifts in metabolite profiles, indicating that certain tomato-driven effects occurred even in the absence of lycopene. Among the changes specifically induced by the tomato-soy juice, shifts in soy isoflavone metabolites stood out. The researchers note that, while more investigation is warranted, these changes offer further evidence that the food-based intervention is acting on human biology.
“This is probably a function of the fact that there’s more to our intervention agents than just these two compounds,” Cooperstone said. “Ultimately, we want to have a better understanding of how the foods that we eat are relating to our health. And when we really want to be sure, we need to test them in clinical trials. And that’s what we’re doing here.”
Next steps: a pancreatitis trial
On the strength of these results and additional data, Cooperstone and her colleagues have received funding from the National Institute of Diabetes and Digestive and Kidney Diseases for a pilot clinical trial. That trial will test whether consuming the same tomato-soy juice reduces inflammation in people living with pancreatitis.
The team has also gathered evidence from an animal model suggesting that the tomato-soy juice can lessen both inflammation and the severity of chronic pancreatitis. Those findings support the central prediction behind the new clinical trial, namely that the intervention could improve outcomes for people with the condition.
“Care for patients with pancreatitis is palliative, focused on controlling pain and GI symptoms. Our hypothesis is that the tomato-soy juice may serve as an intervention to decrease inflammation and hopefully increase patients’ quality of life,” Cooperstone said.
Funding and contributors
The work was supported by the U.S. Department of Agriculture, the National Institutes of Health, the Lisa and Dan Wampler Endowed Fellowship for Foods and Health Research, and the Foods for Health Initiative at Ohio State.
Co-authors include first author Maria Sholola, along with Jenna Miller, Emma Bilbrey, David Francis and Thomas Mace, all of Ohio State, and Janet Navotny of the USDA. Mace is the lead principal investigator on the pancreatitis trial. Cooperstone, Philip Hart and Kristen Roberts of Ohio State are also principal investigators on that trial.
Source: Eureka Alert!
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Scientists Discover Key Protein Triggering Inflammation Linked to Obesity and Type 2 Diabetes
Key Takeaways:
- Researchers have identified FAM20C as a protein that triggers inflammation and insulin resistance in fat cells, a process linked to type 2 diabetes.
- Blocking or removing the FAM20C gene in mice improved insulin sensitivity and reduced inflammation, even without weight loss.
- High levels of FAM20C in human fat tissue are associated with insulin resistance, suggesting a potential new therapeutic target.
Early trigger identified in obesity-related inflammation
Investigators at Weill Cornell Medicine have uncovered an early step in the chain of events that links obesity to inflammation and insulin resistance – key contributors to the development of type 2 diabetes.
Their findings, published on 28 October in the Journal of Clinical Investigation, identify a protein known as FAM20C as a critical “switch” that initiates inflammation within fat cells. The study, conducted in mice, shows that when this protein is removed or blocked, metabolic health improves markedly, even without weight loss.
“By inhibiting or getting rid of FAM20C in fat cells, the mice became healthier even at the same body weight,” said senior author Dr James Lo, the Rohr Family Clinical Scholar and an Associate Professor of Medicine in the Division of Cardiology at Weill Cornell Medicine. “Their fat becomes metabolically healthier, reducing harmful inflammation in fat cells that can lead to chronic diseases like type 2 diabetes, fatty liver disease and heart disease.”
FAM20C: A molecular switch for inflammation
The research team, led by first author Dr Ankit Gilani, a Research Associate in Medicine at Weill Cornell Medicine, discovered FAM20C while screening genes that were switched on in the fat cells of mice with obesity and inflammation. FAM20C belongs to a class of enzymes known as kinases, which work by adding phosphate groups to other proteins – a process that can alter their activity and influence gene expression.
When the researchers increased the production of FAM20C in fat cells, the cells began releasing inflammatory molecules and became resistant to insulin. In contrast, blocking or deleting the gene in mice with obesity had the opposite effect – it reduced inflammation, improved insulin sensitivity, and decreased the accumulation of visceral fat (fat surrounding internal organs), even when total body weight remained unchanged.
“During obesity, when this gene is switched on in the adipose tissue, it causes inflammation,” Dr Gilani explained. “It drives the expression of other inflammatory genes, and then it causes insulin resistance, which can lead to type 2 diabetes.”
Evidence from human fat tissue
To determine whether the same mechanism operates in humans, the researchers analysed visceral fat tissue samples from individuals living with obesity. They found that higher levels of FAM20C were associated with insulin resistance – a key driver of type 2 diabetes – while people with lower FAM20C levels tended to exhibit better metabolic health despite having overweight or obesity.
These findings suggest that the FAM20C pathway could play a pivotal role in determining whether fat tissue becomes inflamed and metabolically harmful or remains relatively benign.
Next Steps: Targeting FAM20C and its downstream pathways
The research team now plans to investigate how FAM20C influences other tissues involved in metabolism and metabolic disease. They are particularly interested in a protein called CNPY4, which is activated by FAM20C and appears to be central to the inflammatory process.
“CNPY4 is going to be a major focus of future research to see how strongly it affects insulin resistance, and whether it could be a target for therapies to treat or prevent insulin resistance,” said Dr Lo, who is also a member of the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine, and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center.
Ultimately, the team hopes to develop small-molecule drugs that can block FAM20C or CNPY4 activity. Such therapies could reduce inflammation, lower visceral fat levels, improve insulin sensitivity, and help prevent or treat type 2 diabetes. Dr Lo noted that these treatments might one day be used alongside weight loss medications, or to support people who continue to experience metabolic inflammation and cardiovascular risk even after losing weight.
Funding and support
This research was supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH), through grants R01DK121140 and R01DK121844.
CCH insights
For a long time now we have known that inflammation in visceral adipose tissue is a major factor in insulin resistance, but it is still unknown why some people with obesity experience this adipose tissue inflammation and subsequent metabolic dysfunction, while other people with obesity do not. This research suggests that the FAM20C protein may contribute to this switch from healthy adipose tissue to inflamed, dysfunctional adipose tissue, and could offer an exciting new therapeutic pathway for type 2 diabetes and other cardiometabolic conditions.
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Strawberries May Support Glucose Control and Reduce Inflammation in Prediabetes, Study Finds
Key Takeaways:
- Daily intake of freeze-dried strawberries for 12 weeks improved fasting glucose and reduced inflammation in adults with prediabetes.
- Antioxidant biomarkers including superoxide dismutase, glutathione, and β-carotene significantly increased during strawberry supplementation.
- Findings suggest strawberries could serve as a practical, food-based intervention to prevent progression to type 2 diabetes.
Strawberries and prediabetes: A promising link
A new randomised controlled trial published in Antioxidants has found that consuming freeze-dried strawberries (FDS) daily may help reduce fasting blood glucose and vascular inflammation in adults with prediabetes. The research also showed marked improvements in antioxidant status, highlighting the potential of strawberries as a simple dietary intervention for metabolic health.
The authors concluded that “strawberries may represent a practical dietary intervention that improves fasting glucose and strengthens antioxidant defence in adults with prediabetes.”
Understanding prediabetes and oxidative stress
Prediabetes represents a critical stage between normal glucose metabolism and type 2 diabetes mellitus (T2DM). It is characterised by mildly elevated blood glucose levels, which contribute to oxidative stress and low-grade inflammation.
High glucose levels increase reactive oxygen species (ROS), impairing insulin function and damaging pancreatic β-cells. Proinflammatory cytokines such as tumour necrosis factor-alpha (TNF-α) further aggravate insulin resistance by interfering with glucose uptake and triggering inflammatory pathways. Over time, these effects contribute to vascular dysfunction and atherosclerosis through increased endothelial adhesion molecules and reduced antioxidant enzyme activity.
Dietary antioxidants – including vitamins, polyphenols, and carotenoids – can neutralise oxidative stress. However, studies using supplements have produced inconsistent results due to differences in absorption and bioavailability. Evidence from clinical trials and meta-analyses indicates that plant-based antioxidants can improve total antioxidant capacity and glycaemic outcomes in people with prediabetes or T2DM.
Berries, particularly strawberries, are rich in polyphenols such as anthocyanins and ellagic acid, which are known to enhance antioxidant enzyme activity and improve insulin sensitivity. Previous studies using FDS have already shown benefits for inflammation and oxidative stress in metabolic disorders, providing a foundation for this new research.
Study design and methodology
Researchers at the University of Nevada, Las Vegas, conducted a 28-week randomised controlled crossover trial involving 25 adults who met the American Diabetes Association’s diagnostic criteria for prediabetes.
Each participant completed two 12-week phases: one with daily FDS intake and another control period without strawberries, separated by a four-week washout. Participants were randomly assigned to begin with either the FDS or control phase.
During the intervention, participants consumed 32 grams of FDS powder per day – equivalent to roughly 2.5 servings of fresh strawberries – containing dietary fibre, polyphenols, flavonols, and anthocyanins. They were instructed to maintain their usual diet and physical activity throughout the trial.
Compliance was carefully monitored using dietary logs, returned powder packets, and plasma ellagic acid levels. Blood samples were collected at baseline, 12, 16, and 28 weeks to measure fasting glucose, antioxidant enzyme activity, total antioxidant capacity, and vascular adhesion molecules using standardised assays. Carotenoid levels were analysed via high-performance liquid chromatography (HPLC).
A mixed-model analysis of variance (ANOVA) was used to evaluate treatment effects while accounting for treatment period, randomisation order, age, sex, fasting glucose, and baseline values. Power analysis confirmed the study was adequately powered to detect meaningful changes in metabolic and antioxidant markers.
Improvements in antioxidant and metabolic markers
Results showed high adherence rates, with more than 85% compliance confirmed by elevated plasma ellagic acid during the FDS phase.
Compared with the control period, strawberry supplementation produced significant improvements in several antioxidant biomarkers, including superoxide dismutase, glutathione (GSH), total antioxidant capacity (AC), and β-carotene. No significant changes were observed in catalase, glutathione reductase, glutathione peroxidase, or α-carotene.
Fasting blood glucose levels also decreased significantly during the FDS period, indicating better glycaemic control. Moreover, markers of vascular inflammation – particularly intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) – were notably reduced. Levels of P-selectin and E-selectin remained unchanged.
Correlation analyses revealed modest inverse relationships between ICAM and GSH, AC, and β-carotene, and between VCAM and AC, suggesting that stronger antioxidant status was associated with reduced vascular inflammation.
Only minor side effects were reported, such as mild gastrointestinal discomfort and headaches.
Implications and limitations
The findings suggest that incorporating strawberries into the diet could help strengthen antioxidant defences, lower inflammation, and improve fasting glucose regulation in people with prediabetes. These benefits may be linked to polyphenols enhancing glutathione synthesis and superoxide dismutase activity, alongside carotenoids and anthocyanins reducing oxidative stress and endothelial dysfunction.
The study’s strengths include its randomised crossover design, objective biomarker measurements, and the use of a realistic dietary dose of strawberries. However, the relatively small and predominantly female sample, the absence of a placebo control drink, lack of participant blinding, and single-site recruitment limit the generalisability of results.
The study was funded by the California Strawberry Commission.
A food-based approach to diabetes prevention
In summary, consuming a daily portion of freeze-dried strawberries for 12 weeks led to measurable improvements in antioxidant capacity, fasting glucose, and vascular inflammation among adults with prediabetes.
While further research in larger, more diverse populations is needed, these results point to strawberries as a simple, accessible dietary strategy that could help prevent the progression from prediabetes to type 2 diabetes in everyday clinical and public health settings.
CCH insights
It is great to have research that shows health benefits from eating strawberries, because nearly everyone loves strawberries and there aren’t many foods that are extremely popular and good for us. However, the amount of freeze-dried strawberries consumed in this study would set you back about £20 per week – not a huge amount, but during a cost-of-living crisis might not be feasible for many people. This study was, unsurprisingly, funded by the California Strawberry Commission, and it begs the question whether eating other berries or certain other foods might not have a similar effect – but credit to the strawberry industry for making the effort to do the research.
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