Time-restricted ketogenic diet in amyotrophic lateral sclerosis: a case study.

amyotrophic lateral sclerosis energy metabolism fasting ketogenic diet metabolic strategy mitochondria dysfunction motor neuron disease neurodegeneration

Journal

Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899

Informations de publication

Date de publication:
2023
Historique:
received: 29 10 2023
accepted: 27 12 2023
medline: 2 2 2024
pubmed: 2 2 2024
entrez: 2 2 2024
Statut: epublish

Résumé

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disorder. The most devastating variant is bulbar-onset ALS, which portends a median survival of 24 months from the onset of symptoms. Abundant evidence indicates that neuron metabolism and mitochondrial function are impaired in ALS. Metabolic strategies, particularly fasting and ketogenic diet protocols, alter neuron metabolism and mitochondria function in a manner that may mitigate the symptoms of this disorder. We report the case of a 64-year-old man with a 21-month history of progressive, deteriorating bulbar-onset ALS, with an associated pseudobulbar affect, who implemented a time-restricted ketogenic diet (TRKD) for 18 months. During this time, he improved in ALS-related function (7% improvement from baseline), forced expiratory volume (17% improvement), forced vital capacity (13% improvement), depression (normalized), stress levels (normalized), and quality of life (19% improvement), particularly fatigue (23% improvement). His swallowing impairment and neurocognitive status remained stable. Declines were measured in physical function, maximal inspiratory pressure, and maximal expiratory pressure. Weight loss was attenuated and no significant adverse effects occurred. This case study represents the first documented occurrence of a patient with ALS managed with either a fasting or ketogenic diet protocol, co-administered as a TRKD. We measured improved or stabilized ALS-related function, forced expiratory volume, forced vital capacity, swallowing, neurocognitive status, mood, and quality of life. Measurable declines were restricted to physical function, maximal inspiratory pressure, and maximal expiratory pressure. Now over 45 months since symptom onset, our patient remains functionally independent and dedicated to his TRKD.

Identifiants

pubmed: 38304328
doi: 10.3389/fneur.2023.1329541
pmc: PMC10830838
doi:

Types de publication

Case Reports

Langues

eng

Pagination

1329541

Informations de copyright

Copyright © 2024 Phillips, Johnston, Simpson, Chang, Mather and Dick.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Matthew C L Phillips (MCL)

Department of Neurology, Waikato Hospital, Hamilton, New Zealand.

Samuel E Johnston (SE)

Older Persons and Rehabilitation Service, Waikato Hospital, Hamilton, New Zealand.

Pat Simpson (P)

Department of Respiratory Medicine, Waikato Hospital, Hamilton, New Zealand.

David K Chang (DK)

Department of Speech Language Therapy, Waikato Hospital, Hamilton, New Zealand.

Danielle Mather (D)

Department of Speech Language Therapy, Waikato Hospital, Hamilton, New Zealand.

Rognvald J Dick (RJ)

Older Persons and Rehabilitation Service, Waikato Hospital, Hamilton, New Zealand.

Classifications MeSH