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Don't be a sad worm

The Longevity vs. Quality-of-Life Tradeoff

 

Aging research has shown that metabolic slowdown can extend lifespan. In C. elegans, the dauer state prolongs life significantly, but at the cost of reduced mobility, sensory function, and energy levels. ME/CFS presents a human parallel to this phenomenon, with patients exhibiting a hypometabolic state characterized by extreme fatigue, cognitive dysfunction, and immune abnormalities.

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This study investigates whether Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a condition characterized by a hypometabolic state, provides insights into lifespan extension without compromising function. Using biobank samples and citizen science data, we aim to determine whether ME/CFS slows or accelerates aging and what metabolic mechanisms govern this process.

Three
Pronged Approach

1. Biobank Analysis (Bioquest Study)

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2. Citizen Science  (Renegade Research)

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3. Combined Computational Analysis

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  • Compare metabolic, mitochondrial, and immune biomarkers in ME/CFS patients with illness onset before vs. after COVID-19.

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  • Utilize samples from three biobank sources (NIH and Open Medicine Foundation centers).

  • Collect real-world data from ME/CFS patients using self-reported symptoms, wearable devices (heart rate variability, energy expenditure), and at-home testing (blood-based immune/metabolomic profiling).

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  • Track symptom fluctuations and metabolic changes over time.

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  • Apply AI-driven data modeling to compare ME/CFS biomarker signatures to established aging and longevity markers.

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  • Identify whether ME/CFS represents an adaptive longevity mechanism or premature aging.

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