Breakthrough: Researchers identify cause of heart failure in obese individuals
By dominguez // 2025-06-18
 
  • A study reveals that obesity triggers fat cells to release amyloid-beta 42 (AB42), an Alzheimer's-related protein, which travels to the heart and disrupts energy production.
  • AB42 accumulates in heart mitochondria, impairing energy generation and leading to heart dysfunction.
  • In experiments, mice injected with AB42 developed heart issues (e.g., reduced pumping efficiency), while obese mice showed high AB42 levels in heart cells.
  • An antibody that can block AB42 — designed to treat Alzheimer's — prevented heart damage in obese mice, suggesting existing drugs can be repurposed for heart disease.
  • AB42 may be a biomarker for obesity-related heart risk, highlighting overlap between metabolic and neurodegenerative diseases, with potential for cross-disciplinary therapies.
Obesity has been linked to a higher risk of heart disease, diabetes and even Alzheimer's. But how these conditions are connected has remained a mystery—until now. A groundbreaking study reveals that a protein best known for its role in Alzheimer's disease -- amyloid-beta 42 (AB42) -- may also be a hidden culprit behind heart damage in obese individuals.

Fat cells leak harmful Alzheimer's-related protein

Researchers found that fat tissue in obese mice releases unusually high levels of AB42 — a sticky protein that clumps together in the brains of Alzheimer's patients. Shockingly, this protein doesn’t just stay in the bloodstream; it travels to the heart, where it disrupts energy production in heart cells, leading to poor heart function. Researchers have long been aware that obesity strains the heart. The 2024 study, published in Nature Communications, reveals that AB42 acts like a metabolic saboteur — a chemical signal released by fat tissue that directly harms the heart. "We observed that amyloid beta accumulated in the mitochondria of the heart — the powerhouses of the cell that generate energy — and prevented energy generation in heart cells," Sean McGee, one of the study authors, told The Epoch Times. "Because the heart uses so much energy to pump blood, this is sufficient to cause heart disease." (Related: Your HEART could be decades older than you are.) In experiments, healthy mice injected with AB42 developed heart problems resembling those seen in obesity. These problems included slower heart relaxation, reduced pumping efficiency and abnormal fat buildup in heart tissue. Meanwhile, mice genetically prone to obesity showed high AB42 levels in their blood and heart mitochondria (the cell’s energy factories). Fortunately, McGee and his team also discovered a potential solution to this. They reported that blocking AB42 with an antibody originally developed for Alzheimer’s research prevented heart damage in obese mice. Even in already obese mice, the treatment stopped further decline in heart function.

Why this matters for humans

Heart failure linked to obesity — particularly the type that causes the heart to stiffen instead of weaken — is rising globally, with limited treatment options. The Nature Communications study suggests that:
  • AB42 could be a new biomarker for obesity-related heart risk
  • Alzheimer's drugs targeting AB42 might be repurposed to protect the heart
  • Mitochondrial dysfunction (impaired energy production) is a key player in heart disease progression
The study also hints at a fascinating overlap between Alzheimer's and metabolic diseases. In particular, AB42 isn't just a brain problem — it's a whole-body issue. While more research is needed, the study's findings open doors for cross-disciplinary treatments. Clinical trials testing AB42-blocking therapies in heart patients could be on the horizon. For now, the study underscores the importance of managing obesity — not just for weight-related health, but also to protect the heart from this stealthy protein. Find more stories like this at CensoredScience.com. Watch the following video to learn more about obesity, heart failure and the obesity paradox. This video is from the Daily Videos channel on Brighteon.com.

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