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Diseases and Conditions

Midlife Weight Loss: The Key to a Longer, Healthier Life

Losing weight via lifestyle adjustments can deliver significant long-term health benefits, without the need for surgery or anti-obesity drugs. Alongside preventing diabetes, it can help ward off chronic conditions including arterial and pulmonary diseases as well as cancers.

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The study of a lifetime has shed new light on the benefits of midlife weight loss. Researchers from the University of Helsinki tracked an impressive 23,000 individuals from Finland and the UK over a period of 12 to 35 years, starting when participants were between 30 to 50 years old. The groundbreaking findings reveal that losing an average of 6.5% of body weight in early middle age and maintaining it throughout the follow-up period can lead to significant health benefits for overweight men and women.

Weight loss is not just a short-term fix; it’s about making lasting lifestyle changes. As noted by Professor Timo Strandberg, who led the study, “The benefits of lifestyle-based weight management are widely discussed, even though studies have found it surprisingly difficult to demonstrate health benefits beyond the prevention of diabetes.” This research fills that gap and provides hope for individuals seeking a longer, healthier life.

The findings also emphasize the importance of maintaining a healthy body mass index (BMI) throughout one’s life. The study suggests that aiming for a lifelong BMI under 25 is ideal for optimal health. As Professor Strandberg expresses, “I hope the findings will inspire people to see that lifestyle changes can lead to major health improvements and a longer life. This is particularly important today as more people are overweight than when our research data began 35 years ago.”

The study’s publication in JAMA Network Open serves as a reminder that with dedication and perseverance, individuals can achieve a healthier, happier life through simple yet effective lifestyle changes.

Alternative Medicine

Iron Overload: The Hidden Culprit Behind Early Alzheimer’s in Down Syndrome

USC researchers have uncovered a hidden driver behind the early and severe onset of Alzheimer’s in people with Down syndrome: iron overload in the brain. Their study revealed that individuals with both conditions had twice the iron levels and far more oxidative damage than others. The culprit appears to be ferroptosis, an iron-triggered cell death mechanism, which is especially damaging in sensitive brain regions.

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Scientists at the USC Leonard Davis School of Gerontology have made a groundbreaking discovery that sheds light on the unique challenges faced by people with Down syndrome who develop Alzheimer’s disease. Their research reveals a crucial link between high levels of iron in the brain and increased cell damage, providing a potential explanation for why Alzheimer’s symptoms often appear earlier and more severely in individuals with Down syndrome.

Down syndrome is caused by having an extra third copy (trisomy) of chromosome 21, which includes the gene for amyloid precursor protein (APP). People with Down syndrome tend to produce more APP, leading to an increased risk of developing Alzheimer’s disease. In fact, about half of all people with Down syndrome show signs of Alzheimer’s by the age of 60, which is approximately 20 years earlier than in the general population.

The researchers studied donated brain tissue from individuals with Alzheimer’s, those with both Down syndrome and Alzheimer’s (DSAD), and those without either diagnosis. They found that the brains of people with DSAD had twice as much iron and more signs of oxidative damage in cell membranes compared to the brains of individuals with Alzheimer’s alone or those with neither diagnosis.

This excess iron leads to ferroptosis, a type of cell death characterized by iron-dependent lipid peroxidation. In other words, iron builds up, drives the oxidation that damages cell membranes, and overwhelms the cell’s ability to protect itself.

The researchers also discovered that lipid rafts, tiny parts of the brain cell membrane crucial for cell signaling and protein processing, had more oxidative damage and fewer protective enzymes in DSAD brains compared to Alzheimer’s or healthy brains. These lipid rafts showed increased activity of the enzyme β-secretase, which interacts with APP to produce Aβ proteins, potentially promoting the growth of amyloid plaques.

The findings have significant implications for future treatments, especially for people with Down syndrome who are at high risk of Alzheimer’s. Early research in mice suggests that iron-chelating treatments may reduce indicators of Alzheimer’s pathology. Medications that remove iron from the brain or help strengthen antioxidant systems might offer new hope.

The study was supported by various organizations, including the National Institute on Aging and Cure Alzheimer’s Fund. These findings highlight the importance of understanding the biology of Down syndrome for Alzheimer’s research and could lead to new therapeutic approaches for this vulnerable population.

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Diseases and Conditions

The Cold Sore Virus’ Secret: Hijacking the Human Genome in 3D

Cold sore-causing HSV-1 doesn’t just hijack cells it reconfigures the entire architecture of our DNA to aid its invasion. Researchers discovered that it actively reshapes the 3D structure of the human genome within hours of infection, using host enzymes like topoisomerase I to gain access to crucial genetic machinery. Stunningly, blocking this single enzyme shuts the virus down completely.

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The herpes simplex virus-1 (HSV-1) is a cunning foe that has been infecting humans for centuries. While it’s well-known for causing cold sores, what’s less understood is how this virus hijacks our cells to reproduce itself. A recent study published in Nature Communications reveals the shocking truth: HSV-1 reshapes our genome in three-dimensional space, rearranging its structure to access host genes that help it multiply.

This “opportunistic interior designer” uses its precision to manipulate the human genome, choosing which bits to interact with and exploiting host resources. Researchers at the Center for Genomic Regulation (CRG) in Barcelona made this groundbreaking discovery using super-resolution microscopy and Hi-C techniques, which allowed them to visualize structures as small as 20 nanometers.

Within the first hour of infection, HSV-1 hijacks the human RNA-polymerase II enzyme to synthesize its own proteins. This is followed by the recruitment of topoisomerase I, an enzyme that snips DNA to release torsional stress, and cohesin, a structural protein. Three hours after infection, most polymerase and a sizeable fraction of the other two factors have abandoned human genes.

The consequences are devastating: transcription collapses across the host genome, causing chromatin to compact into a dense shell just 30% of its original volume. This was an unexpected finding, as the structure of chromatin is thought to dictate transcription. The relationship between activity and structure might be a two-way street.

This study has significant implications for public health, especially given the prevalence of HSV-1 worldwide. With nearly four billion people infected, treatments are available only to manage symptoms, while drug-resistant strains are on the rise. There is no cure.

The discovery of topoisomerase I as a potential target for therapy brings new hope. Inhibiting this enzyme stopped infection in cell culture before the virus could make a single new particle. This finding offers a potential new strategy to control HSV-1, which infects nearly four billion people worldwide.

The cold sore virus’ secret is out: it’s not just a harmless nuisance, but a cunning manipulator of our cells that’s been hijacking the human genome in 3D for centuries. The consequences are real, and the time to act is now.

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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.”

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