https://doi.org/10.1016/j.nut.2021.111525

https://pubmed.ncbi.nlm.nih.gov/34864433

Abstract

OBJECTIVES

This study evaluates the safety and feasibility of a normocaloric ketogenic diet (KD) in people with amyotrophic lateral sclerosis (ALS) for reducing hyperexcitability levels and modulating neuroinflammation.

METHODS

This is a prospective, open-label pilot study involving men and women diagnosed with ALS, ages 18 to 75 y. The primary outcome is the safety and reproducibility of the KD in people with ALS. We will monitor secondary clinical outcomes with the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale score, forced vital capacity, the Amyotrophic Lateral Sclerosis Assessment Questionnaire, blood parameters, and gut microbiota analyses. All participants will follow the KD for 8 wk. During the diet, the clinical status of all participants will be monitored every 15 d through neurologic and nutritional visits and biochemical markers. The research ethics committee approved the study.

RESULTS

Safety will be assessed by measuring the number and severity of adverse events, including death, and any changes in blood chemistry, vital signs, and clinical exam results. Tolerability will be assessed to complete the proposed 8 wk of treatment while maintaining adequate nutritional status without inducing malnutrition.

CONCLUSIONS

Adequate caloric intake is essential in ALS, because insufficient intake induces loss of body mass. We hope that the proposed study will provide a positive result in terms of the safety and feasibility of a KD in people ALS, with the purpose of developing a patient-centered diet program to limit disease progression and possibly improve survival.

------------------------------------------ Info ------------------------------------------

Open Access: False

Authors: F. De Marchi - A. Collo - A. Scognamiglio - M. Cavaletto - N. Bozzi Cionci - G. Biroli - D. Di Gioia - S. Riso - L. Mazzini -

Additional links: None found

Diets for Patients with Amyotrophic Lateral Sclerosis

Pay Attention to Nutritional Intervention

Yang, Li-Peng1,2; Fan, Dong-Sheng1,

Author InformationChinese Medical Journal: August 05, 2017 - Volume 130 - Issue 15 - p 1765-1767doi: 10.4103/0366-6999.211549

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INTRODUCTION

Amyotrophic lateral sclerosis (ALS) is characterized by the progressive degeneration of upper and lower motor neurons. Typical clinical features of ALS are limb paralysis, muscle atrophy, dysphagia, dysarthria, shortness of breath, and respiratory failure. Approximately 90% of ALS cases are classified as sporadic ALS, the remaining 10% are classified as familial.[12] Researchers have found that the survival of ALS patients is related to several factors, including clinical phenotype, age at onset, sex, early presence of respiratory failure, and treatment with riluzole. We recently found that there is a potential linear relationship in ALS between serum lactate and motor deterioration, and that slower lactate elimination rate might be associated with faster disease progression.[3] In addition, several studies have reported that nutritional status is closely related to the survival time of ALS patients, and there exists a U-shaped association between patients’ body mass index (BMI) and mortality.[14] The main cause of malnutrition (BMI ≤18.5 kg/m²) in ALS patients is an imbalance between intake and consumption, and some symptoms, such as dysphagia, can lead to insufficient energy intake. More importantly, recent studies have shown that ALS patients are in states of hypermetabolism.[56]

HYPERMETABOLISM IN AMYOTROPHIC LATERAL SCLEROSIS

It is difficult to explain the association between hypermetabolism and ALS, but it has been found in mutant Cu Zn-superoxide dismutase (SOD1) transgenic mice as well as in ALS patients. Resting energy expenditure (REE) is one reason for increased consumption for ALS.[6] Dupuis et al.[7] found that SOD1G86R and SOD1G93A mice have increased REE compared to control mice. Desport et al.[8] found that REE significantly increased by an average of 14% in 168 ALS patients compared to the calculated value, and 62.3% of ALS patients were considered hypermetabolic. Bouteloup et al.[5] confirmed that hypermetabolism existed in 48% of all AL

I have read many articles that states ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (stress/medication ) and the legalization of Marijuana could this lead down a bad path.

According to this study the C9orf72 gene is associated with ALS.

However, according to SNP "This repeat is not represented by a SNP, and, is not currently represented in SNPedia."

How can I check for it using https://promethease.com ?

I have read many articles that state ALS is from Excitotoxicity brought on by an excess of Glutamate in the brain. I find this interesting because there are food products that can increase Glutamate in the brain. Recently I read that an high dose of THC can also lead to Glutamate Excitotoxicity. I thought THC slowed down progresstion of ALS? Could it be possible that someone taking medication like anxiety pills and high dose of THC can actually give themselves ALS? The reason I am asking is because with the current state of mental health (anxiety medication) and the legalization of Marijuana (high does) could this lead down a bad path mixing the two?