A 12-week clinical trial investigates time-restricted eating’s safety and efficacy in early-stage Huntington’s disease, focusing on mitochondrial function and cognitive outcomes.
Groundbreaking trial examines if time-restricted eating can slow Huntington’s progression through metabolic and circadian mechanisms.
Time-Restricted Eating Enters Huntington’s Disease Research
The first human clinical trial investigating time-restricted eating (TRE) in Huntington’s disease launched this month at the University of California, San Francisco. This 12-week study builds on compelling animal research showing TRE’s potential to modify disease progression.
As Dr. Sarah Tabrizi, director of University College London’s Huntington’s Disease Centre, noted in a May 2024 Lancet Neurology commentary: The translational leap from mouse models to human trials for metabolic interventions can’t come soon enough for Huntington’s patients.
Study Design and Scientific Rationale
The trial will enroll 50 participants with early-stage Huntington’s disease, randomizing them to either an 8-hour eating window (10am-6pm) or standard dietary patterns. Primary endpoints include safety measures and adherence rates, while secondary endpoints assess:
- Mitochondrial function via muscle biopsies
- Cognitive performance on the Unified Huntington’s Disease Rating Scale
- Autophagy markers in blood samples
This comes after a June 2024 Cell Metabolism study demonstrated TRE reduced mutant huntingtin aggregation by 30% in mouse models through enhanced mitophagy. Our animal data show TRE creates a metabolic environment hostile to protein aggregation,
said lead researcher Dr. Mark Mattson in the NIH press release announcing the new trial.
The Circadian Connection
Emerging research suggests TRE’s benefits may extend beyond caloric restriction. A April 2024 Brain study found Huntington’s patients with disrupted sleep cycles showed 40% faster motor symptom progression. TRE could help resynchronize peripheral clocks in organs that influence neurodegeneration,
explained circadian biologist Dr. Phyllis Zee in her recent Nature Reviews Neurology meta-analysis.
The trial incorporates actigraphy monitoring to track circadian rhythm changes, building on findings that huntingtin protein disrupts the SCN (suprachiasmatic nucleus), the brain’s master clock.
Future Implications
If successful, this trial could pave the way for larger phase 3 studies and combination therapies. The NIH’s recent $5 million funding initiative for metabolic approaches to neurodegeneration signals growing institutional support. As Dr. Claudia Testa, HD researcher at Virginia Commonwealth University, told Neurology Today: We’re entering an era where lifestyle interventions may become adjunct prescriptions for genetic disorders.
Researchers caution that while promising, TRE isn’t yet recommended outside clinical trials. The Huntington’s disease brain has unique energy demands,
notes trial principal investigator Dr. Adam Boxer. We need rigorous safety data before considering widespread adoption.
