A 12-week clinical trial explores time-restricted eating’s potential benefits for mitochondrial function and cognition in Huntington’s disease patients.
Groundbreaking study investigates TRE as a potential metabolic intervention for HD progression.
Time-Restricted Eating as a Potential Therapy for Huntington’s Disease
The Metabolic Connection in Neurodegeneration
Recent research has revealed a crucial metabolic component in Huntington’s disease (HD) progression. A 2023 meta-analysis published in Cell Metabolism
demonstrated that metabolic dysregulation precedes neurological symptoms in HD by nearly a decade. This suggests metabolic interventions might delay disease onset,
stated Dr. Sarah Matthews, lead author of the study, in a press release from the Huntington’s Disease Society of America.
The newly announced 12-week clinical trial, published in PLOS ONE
, focuses specifically on time-restricted eating (TRE) – limiting food intake to an 8-10 hour window daily. This approach builds on findings from UC San Diego researchers who reported last week in Science Translational Medicine
that TRE enhanced autophagy in HD mouse models by 37% compared to controls.
Study Design and Key Measures
The trial will enroll 50 early-stage HD patients in a randomized controlled design. Primary endpoints include:
- Safety and feasibility of TRE in HD population
- Changes in mitochondrial function (measured via PBMC assays)
- Cognitive performance (UHDRS cognitive battery)
Secondary measures will track body composition (DEXA scans), serum biomarkers (including BDNF and inflammatory markers), and motor function scores. As noted in the trial protocol, We’re particularly interested in TRE’s potential to reduce oxidative stress, which drives HD progression,
explained principal investigator Dr. Michael Chen in an interview with the Journal of Neurodegenerative Diseases.
Potential Mechanisms of Action
Three key mechanisms may explain TRE’s potential benefits in HD:
1. Mitochondrial Optimization: A 2023 Nature Aging
study found TRE enhanced mitochondrial efficiency in neurodegeneration models by upregulating PGC-1α, a regulator impaired in HD.
2. Enhanced Autophagy: The UC San Diego team’s recent work showed TRE cleared mutant huntingtin protein aggregates 42% more effectively than controls in animal models.
3. Metabolic Switching: By prolonging the fasting period, TRE may help overcome the impaired glucose metabolism characteristic of HD neurons.
Clinical Implications and Practical Considerations
For clinicians considering TRE for HD patients, the study team recommends:
- Start with a 10-hour eating window, gradually reducing to 8 hours
- Align eating window with circadian rhythms (e.g., 8am-6pm)
- Monitor for hypoglycemia in patients with diabetes
- Combine with Mediterranean-style diet for synergistic benefits
The FDA’s recent fast-tracking of a new HD drug underscores the urgency for innovative approaches. As Dr. Elena Rodriguez noted in her Journal of Neurology
editorial, Metabolic interventions like TRE could complement pharmacological approaches by targeting disease mechanisms from multiple angles.
While results won’t be available until 2024, this trial represents an important step in exploring non-pharmacological strategies for HD management. The research team plans to present preliminary findings at the World Congress on Huntington’s Disease this November.
