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Cholesterol

Rewiring Cellular Energy Processing for Drastic Weight Loss: A Breakthrough Mechanism

Mice genetically engineered to lack the amino acid cysteine, and fed a cysteine-free diet, lost 30 percent of their body weight in a week.

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Researchers at NYU Grossman School of Medicine have made a groundbreaking discovery that sheds light on how cells process energy from food. A study published online in Nature reveals a novel mechanism that enables drastic weight loss by manipulating cellular energy processing. The findings, which detail the effects of cysteine depletion on mammalian metabolism, have far-reaching implications for our understanding of how to induce weight loss.

In the study, mice genetically engineered to lack cysteine, an essential amino acid found in most foods, were fed a diet devoid of cysteine. Within one week, these animals experienced significant weight loss, dropping 30% of their body weight on average. This drastic reduction was achieved by disrupting normal metabolic pathways used by cells to convert food into energy.

The researchers identified coenzyme A (CoA), a small molecule involved in over 100 intermediate metabolic reactions and serving as a partner for nearly 4% of all enzymes in the body, as the key factor contributing to this weight loss. By depleting CoA levels through cysteine restriction, cells were forced to rapidly burn stored fat reserves, leading to the observed weight reduction.

What is remarkable about this study is that it was previously impossible to directly examine CoA’s function due to the fact that mice with defective CoA synthesis typically do not survive beyond three weeks of age. The researchers have now been able to detail how CoA shapes metabolism in adult mice, providing new insights into cellular energy processing.

While achieving a truly cysteine-free diet would be challenging for most people, this study highlights the potential benefits of reducing cysteine intake through dietary modifications. For example, fruits, vegetables, and legumes contain lower levels of cysteine compared to red meat.

The authors caution that eliminating cysteine or inhibiting its production could have unintended consequences on organ function, particularly in vulnerable individuals who may be more susceptible to everyday toxins, including medications. However, this research opens up new avenues for understanding how cellular energy processing can be manipulated to induce weight loss without completely removing cysteine from the diet.

Future studies will focus on hijacking parts of this process to safely and effectively induce weight loss in humans while minimizing potential risks associated with cysteine depletion. This breakthrough mechanism has far-reaching implications for our understanding of how to tackle obesity, a major public health concern worldwide.

Cholesterol

The Hidden Cancer Epidemic: How Obesity is Driving Rising Deaths Nationwide

Obesity-related cancer deaths in the U.S. have tripled in just two decades, with women, older adults, and minority groups most affected. New research presented at ENDO 2025 highlights how obesity—linked to 13 different cancers—is now a major contributor to cancer mortality, especially in underserved and rural populations. Despite the growing awareness of obesity’s broader health impacts, this surge in cancer fatalities reveals an urgent need for targeted public health interventions and equitable access to care.

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The article highlights a disturbing trend in the United States – cancer deaths linked to obesity have tripled over the past two decades. A study presented at the Endocrine Society’s annual meeting in San Francisco examined more than 33,000 deaths from obesity-associated cancers and revealed sharp increases in cancer deaths, particularly among women, older adults, Native Americans, and Black Americans.

“Obesity is a significant risk factor for multiple cancers, contributing to significant mortality,” said lead researcher Faizan Ahmed. “This research underscores the need for targeted public health strategies such as early screening and improved access to care, especially in high-risk rural and underserved areas.”

The study used mortality data from the Centers for Disease Control and Prevention (CDC) to analyze U.S. deaths from obesity-associated cancers between 1999 and 2020. The results showed age-adjusted mortality rates increased from 3.73 to 13.52 per million over two decades, with steep increases among certain groups.

Obesity is a complex disease resulting from multiple genetic, physiological, hormonal, environmental, and developmental factors. It raises the risk of developing serious chronic conditions such as high blood pressure, high cholesterol, prediabetes, type 2 diabetes, heart disease, and chronic and end-stage kidney disease.

In addition to certain types of cancer, obesity is associated with a higher risk of developing 13 types of cancer, according to the CDC. These cancers make up 40% of all cancers diagnosed in the United States each year.

The regions with the highest rates of obesity-related cancer deaths were identified as follows:

* The Midwest had the highest rate.
* Vermont, Minnesota, and Oklahoma had the highest state-level rates.
* Utah, Alabama, and Virginia had the lowest state-level rates.

This research emphasizes the need for targeted public health strategies to combat the growing epidemic of obesity-related cancer deaths. Early screening and improved access to care are crucial in reducing mortality rates among high-risk groups.

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Cholesterol

The Dark Side of Healthy Fats: How Oleic Acid May Be Fueling Obesity

A popular fat found in olive oil may not be as innocent as it seems. Scientists discovered that oleic acid, a major component of many high-fat foods, uniquely spurs the growth of new fat cells by manipulating specific proteins in the body. Unlike other fats, it boosts the number of “fat cell soldiers,” setting the stage for obesity and possibly chronic diseases. This unexpected twist reveals that the type of fat we eat, not just how much, may play a crucial role in our health.

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The article discusses how consuming high levels of oleic acid, a type of monounsaturated fat commonly found in olive oil, may be contributing to obesity. Research published in the journal Cell Reports suggests that oleic acid can cause the body to produce more fat cells by boosting a signaling protein called AKT2 and reducing the activity of a regulating protein called LXR.

Lead researcher Michael Rudolph, Ph.D., notes that while it’s difficult to isolate specific fatty acids in human diets due to the complexity of food combinations, there is evidence that oleic acid levels are increasing in the food supply. This is particularly concerning for individuals with limited access to dietary variety and those who rely heavily on fast food.

The study involved feeding mice specialized diets enriched with different types of fatty acids, including those found in coconut oil, peanut oil, milk, lard, and soybean oil. Oleic acid was the only type that caused an increase in precursor cells that give rise to fat cells, ultimately leading to a higher capacity for storing excess nutrients.

Rudolph emphasizes the importance of moderation and variety when it comes to consuming fats. He suggests that relatively balanced levels of oleic acid may be beneficial, but higher and prolonged levels could be detrimental, particularly for individuals at risk for heart disease.

The take-home message is clear: while some types of healthy fats are essential for our well-being, overconsumption or imbalance can have negative consequences. By being mindful of the fatty acids in our diets and consuming a variety of sources, we can minimize the risks associated with obesity and related health issues.

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Anemia

Hidden Risk: Three Genetic Variants That Raise Clot Risk by 180%

Genetic research in Sweden has unveiled three new gene variants that dramatically increase the risk of venous blood clots, sometimes by up to 180%. These discoveries build on existing knowledge of Factor V Leiden and suggest that genetics plays a bigger role than previously thought, especially for clots in the legs that can lead to life-threatening pulmonary embolisms.

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The risk of blood clots is a serious concern worldwide, with venous thrombosis being one of the most common causes of death globally. A recent study from Lund University in Sweden has shed light on three genetic variants that significantly increase the risk of blood clots in the leg by up to 180%.

While arterial and venous blood clots have different causes and consequences, understanding the risk factors is crucial for prevention and treatment. In Sweden, over 10,000 people suffer from venous thromboembolism each year, with age being a strong risk factor.

“Venous thrombosis is a common disease that has always been somewhat overshadowed by arterial blood clots,” says Bengt Zöller, a specialist in general medicine at Skåne University Hospital and professor of general medicine at Lund University. “However, it’s essential to acknowledge its significance and take steps to prevent it.”
The risk factors for venous thrombosis include age, being overweight or tall, and lack of physical activity. Smoking is considered only a weak to moderate risk factor, while high blood pressure and high levels of blood lipids are associated with arterial clots, not venous ones.

Research suggests that commercial fishermen have a lower risk due to their diet rich in omega-3 fatty acids. Additionally, ultra-processed foods have been linked to an increased risk of blood clots, whereas plant-based diets may reduce this risk.
“Prophylaxis in the form of blood thinners may be particularly important if other risk factors are also present,” advises Zöller.

The three genetic variants identified by Bengt Zöller and his fellow researchers are ABO, F8, and VWF. These variants increase the risk of venous blood clots by 10-30% each, with an individual having five of these gene variants having a 180% higher risk.
“These genetic variants are present in all populations, making it essential to investigate how the number of risk genes affects the duration of treatment with anticoagulants after a blood clot,” concludes Zöller.

To prevent blood clots, one can take steps such as maintaining physical activity, monitoring blood pressure and lipid levels, quitting smoking, and eating a balanced diet rich in omega-3 fatty acids. Tailoring treatment based on risk assessment will become increasingly important in the future.
“Tailoring treatment based on risk assessment will become increasingly important,” concludes Bengt Zöller.

In summary, understanding the three genetic variants that increase the risk of blood clots by up to 180% is crucial for prevention and treatment. By acknowledging these risk factors, individuals can take steps to reduce their likelihood of developing venous thrombosis.
“Blood clot prevention is a vital aspect of healthcare, and awareness about the risks is essential,” emphasizes Zöller.

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