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Diabetes

A Breakthrough in Fitness Tracking: New Algorithm Accurately Measures Calories Burned by People with Obesity

Fitness trackers often fail people with obesity by underestimating their energy burn, leading to discouraging results and misguided health data. A scientist’s frustrating experience in an exercise class with his mother-in-law where her effort wasn t reflected on the fitness leaderboard sparked a breakthrough. His team at Northwestern developed a new open-source smartwatch algorithm that accurately captures energy expenditure for individuals with obesity, rivaling gold-standard lab equipment and paving the way for more inclusive, empowering health tracking.

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The article’s content has been rewritten to improve clarity, structure, and style while maintaining the core ideas.

For many, fitness trackers have become indispensable tools for monitoring how many calories they’ve burned in a day. However, these devices often inaccurately measure activity, particularly for those living with obesity. This is because current algorithms were built for people without obesity, and hip-worn trackers misread energy burn due to gait changes and device tilt. Wrist-worn models promise better comfort, adherence, and accuracy across body types, but no one has rigorously tested or calibrated them for this group.

A team of scientists at Northwestern University has developed a new algorithm that enables smartwatches to more accurately monitor the calories burned by people with obesity during various physical activities. The technology bridges a critical gap in fitness technology, making it easier for more people with obesity to track their daily activities and energy use.

The algorithm was tested against 11 state-of-the-art algorithms designed by researchers using research-grade devices and wearable cameras to catch every moment when wrist sensors missed the mark on calorie burn. The findings were published in Nature Scientific Reports.

The exercise class that motivated the research
Alshurafa was motivated to create the algorithm after attending an exercise class with his mother-in-law who has obesity. She worked harder than anyone else, yet when they glanced at the leaderboard, her numbers barely registered. This moment hit him: fitness shouldn’t feel like a trap for the people who need it most.

Algorithm rivals gold-standard methods
By using data from commercial fitness trackers, the new model rivals gold-standard methods of measuring energy burn and can estimate how much energy someone with obesity is using every minute, achieving over 95% accuracy in real-world situations. This advancement makes it easier for more people with obesity to track their daily activities and energy use.

How the study measured energy burn
In one group, 27 study participants wore a fitness tracker and metabolic cart – a mask that measures the volume of oxygen the wearer inhales and the volume of carbon dioxide the wearer exhales to calculate their energy burn (in kilocalories/kCals) and resting metabolic rate. The study participants went through a set of physical activities to measure their energy burn during each task. The scientists then looked at the fitness tracker results to see how they compared to the metabolic cart results.

In another group, 25 study participants wore a fitness tracker and body camera while just living their lives. The body camera allowed the scientists to visually confirm when the algorithm over- or under-estimated kCals.

At times, Alshurafa said he would challenge study participants to do as many pushups as they could in five minutes.
Many couldn’t drop to the floor, but each one crushed wall-pushups, their arms shaking with effort. We celebrate ‘standard’ workouts as the ultimate test, but those standards leave out so many people. These experiences showed me we must rethink how gyms, trackers, and exercise programs measure success – so no one’s hard work goes unseen.

The study is titled, “Developing and comparing a new BMI inclusive energy burn algorithm on wrist-worn wearables.”

Cancer

A Breakthrough in Inflammation Control: Scientists Discover ‘Off Switch’ Enzyme to Combat Heart Disease and Diabetes

Researchers at UT Arlington have discovered a key enzyme, IDO1, that when blocked, helps immune cells regain their ability to properly process cholesterol—something that breaks down during inflammation. This breakthrough could offer a powerful new way to fight heart disease, diabetes, cancer, and more. By “turning off” this enzyme, the team restored cholesterol absorption in macrophages, potentially stopping disease at the source. Even more promising, they found a second enzyme, NOS, that makes things worse—raising hopes that targeting both could pave the way for transformative treatments for millions suffering from inflammation-driven conditions.

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The discovery of an “off switch” enzyme that can help prevent heart disease and diabetes is a significant breakthrough in the medical field. Scientists at The University of Texas at Arlington have identified an enzyme called IDO1, which plays a crucial role in inflammation regulation. By blocking this enzyme, researchers believe they can control inflammation and restore proper cholesterol processing.

Inflammation is a natural response to stress, injury, or infection, but when it becomes abnormal, it can lead to chronic diseases such as heart disease, cancer, diabetes, and dementia. The team found that IDO1 becomes activated during inflammation, producing a substance called kynurenine that interferes with how macrophages process cholesterol.

When IDO1 is blocked, however, macrophages regain their ability to absorb cholesterol, suggesting a new way to prevent heart disease by keeping cholesterol levels in check. The researchers also discovered that another enzyme linked to inflammation, nitric oxide synthase (NOS), worsens the effects of IDO1.

The findings are crucial because they suggest that understanding how to prevent inflammation-related diseases could lead to new treatments for conditions like heart disease, diabetes, cancer, and others. The research team plans to further investigate the interaction between IDO1 and cholesterol regulation, with the goal of finding a safe way to block this enzyme and develop effective drugs to combat chronic diseases.

The discovery is supported by grants from the National Institutes of Health (NIH) and the National Science Foundation (NSF), indicating the importance of this research in advancing our understanding of inflammation-related diseases. With further study, it’s possible that we may see a new era in disease prevention and treatment, giving hope to millions of people affected by these conditions.

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Diabetes

The Ancient Longevity Switch: How Morning Coffee Could Be Slowing Down Your Ageing Process

Caffeine appears to do more than perk you up—it activates AMPK, a key cellular fuel sensor that helps cells cope with stress and energy shortages. This could explain why coffee is linked to better health and longer life.

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The scientific community has made another groundbreaking discovery that reveals how our beloved morning coffee might be doing more than just waking us up. A recent study conducted by researchers at Queen Mary University of London’s Cenfre for Molecular Cell Biology sheds light on the potential anti-ageing properties of caffeine, the world’s most popular neuroactive compound.

The research, published in the journal Microbial Cell, delves into the intricate mechanisms within our cells and how they respond to stress and nutrient availability. The scientists used a single-celled organism called fission yeast as a model to understand how caffeine affects ageing at a cellular level.

One of the key findings was that caffeine doesn’t act directly on the growth regulator called TOR (Target of Rapamycin), which is responsible for controlling energy and stress responses in living things for over 500 million years. Instead, it works by activating another crucial system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics, and Fundamental Cell Biology at Queen Mary University of London, the study’s senior author. “And our results show that caffeine helps flip that switch.”

The implications of this discovery are significant, as AMPK is also the target of metformin, a common diabetes drug being studied for its potential to extend human lifespan together with rapamycin. The researchers demonstrated using their yeast model that caffeine’s effect on AMPK influences how cells grow, repair their DNA, and respond to stress – all of which are tied to ageing and disease.

These findings open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines. So, the next time you reach for your coffee, remember that it might be doing more than just boosting your focus – it could also be giving your cells a helping hand in slowing down your ageing process.

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Alzheimer's

Groundbreaking Study Suggests Link Between Semaglutide and Lower Dementia Risk in Type 2 Diabetes Patients

A blockbuster diabetes and weight-loss drug might be doing more than controlling blood sugar—it could also be protecting the brain. Researchers at Case Western Reserve University found that people with type 2 diabetes who took semaglutide (the active ingredient in Ozempic and Wegovy) had a significantly lower risk of developing dementia. The benefit was especially strong in women and older adults.

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A recent study by researchers at the Case Western Reserve School of Medicine has made an astonishing discovery that may revolutionize the way we approach dementia prevention. The research team found that semaglutide, a popular medication used to treat diabetes and aid in weight loss, could significantly lower the risk of dementia in people with type 2 diabetes (T2D).

Dementia is a devastating condition that affects millions worldwide, causing memory loss and cognitive decline. It occurs when brain cells are damaged, disrupting their connections and ultimately leading to this debilitating state. Encouragingly, studies indicate that approximately 45% of dementia cases could be prevented by addressing modifiable risk factors.

The study, published in the Journal of Alzheimer’s Disease, analyzed three years’ worth of electronic records from nearly 1.7 million T2D patients nationally. The researchers used a statistical approach that mimicked a randomized clinical trial to determine the effectiveness of semaglutide in preventing dementia.

Their findings suggest that patients prescribed semaglutide had a significantly lower risk of developing Alzheimer’s disease-related dementia compared to those taking other anti-diabetic medications, including GLP-1R-targeting medications. These results were even more pronounced in women and older adults.

Semaglutide, a glucagon-like peptide receptor (GLP-1R) molecule that decreases hunger and regulates blood sugar levels in T2D patients, has shown remarkable benefits beyond its primary use as a diabetes treatment. It also reduces the risk of cardiovascular diseases, further solidifying its potential in preventing dementia.

The study’s lead researcher, biomedical informatics professor Rong Xu, stated, “There is no cure or effective treatment for dementia, so this new study provides real-world evidence for its potential impact on preventing or slowing dementia development among at-high risk populations.”

While the findings are promising, it’s essential to note that further research through randomized clinical trials will be necessary to confirm the causal relationship between semaglutide and dementia prevention. Nevertheless, this groundbreaking study offers a glimmer of hope in the quest to combat dementia and improve the lives of millions worldwide.

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