# Dietary Vitamin Intake and Blood Biomarkers in Relation to Muscle Activation in Amyotrophic Lateral Sclerosis: A Cross-Sectional Study

**Authors:** Jose Enrique de la Rubia Ortí, Guillermo Bargues-Navarro, Jesús Privado, Rubén Menarques-Ramírez, Claudia Emmanuela Sanchis-Sanchis, Sandra Sancho-Castillo, Camila Peres Rubio, Luis Pardo-Marin, María Benlloch, Julio Martín-Ruiz

PMC · DOI: 10.3390/nu17213345 · Nutrients · 2025-10-24

## TL;DR

This study explores how vitamin intake and blood biomarkers relate to muscle activation in ALS patients, finding some weak but notable associations.

## Contribution

The study identifies potential blood biomarkers and dietary vitamin associations with muscle function in ALS patients.

## Key findings

- Vitamin B9 intake showed a modest positive association with leg muscle activation.
- The B6/protein ratio had inconsistent associations across different muscle groups.
- Albumin emerged as the most consistent potential biomarker for muscle function.

## Abstract

Background/Objectives: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor function, which affects mobility and leads to secondary complications, including altered dietary intake due to dysphagia, fatigue, and hypermetabolism, particularly affecting vitamin consumption, which are essential micronutrients for neuromuscular performance. The specific relationship between vitamin intake and muscle activation is not well understood in patients with ALS; thus, it is relevant to identify blood biomarkers that reflect muscle status. Methods: A cross-sectional study was conducted with 61 patients with bulbar- or spinal-onset ALS. The dietary intake of B vitamins (B1, B2, B6, B12, folate, and niacin); vitamins C, A, D, and E; and the B6/protein ratio were assessed using a seven-day dietary record and a Food Frequency Questionnaire. Blood concentrations of butyrylcholinesterase (BuChE), albumin, haptoglobin, C-reactive protein (CRP), and paraoxonase 1 (PON1) were determined. Basal muscle activation was measured using surface electromyography of the biceps brachii, triceps brachii, rectus femoris, and tibialis anterior muscles. Two confirmatory predictive models were developed to evaluate the effects of muscle damage and vitamin intake on muscle strength. Results: Arm muscle activation was negatively predicted by the B6/protein ratio (β = −0.33). Leg activation was positively predicted by vitamin B9 (β = 0.39) and B6/protein (β = 0.17) and negatively predicted by vitamin A (β = −0.24). For biomarkers, albumin (β = 0.18) and PON1 (β = 0.28) positively predicted activation. For legs, albumin predicted activation (β = 0.31), whereas BuChE and haptoglobin predicted negative activation (β = −0.32 and β = −0.15, respectively). Conclusions: Weak associations were observed in patients with ALS: vitamin B9 intake showed a modest association with leg activation, the B6/protein ratio exhibited inconsistent associations across muscle groups, and vitamin A showed a negative association with leg activation. Albumin demonstrated the most consistent association as a potential biomarker of muscle function. These findings are exploratory and require validation in larger, longitudinal studies.

## Linked entities

- **Proteins:** LOC100189571 (uncharacterized LOC100189571)
- **Chemicals:** vitamin B1 (PubChem CID 1130), vitamin B2 (PubChem CID 493570), vitamin B6 (PubChem CID 1054), vitamin B12 (PubChem CID 73415824), folate (PubChem CID 135405876), niacin (PubChem CID 938), vitamin C (PubChem CID 54670067), vitamin A (PubChem CID 445354), vitamin E (PubChem CID 14985)
- **Diseases:** Amyotrophic lateral sclerosis (MONDO:0004976)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, BCHE (butyrylcholinesterase) [NCBI Gene 590] {aka BCHED, CHE1, CHE2, E1}, PON1 (paraoxonase 1) [NCBI Gene 5444] {aka ESA, MVCD5, PON}
- **Diseases:** neurodegenerative disease (MESH:D019636), fatigue (MESH:D005221), loss of motor function (MESH:D003291), muscle damage (MESH:D009133), ALS (MESH:D000690), hypermetabolism (MESH:C565498), dysphagia (MESH:D003680)
- **Chemicals:** vitamin A (MESH:D014801), folate (MESH:D005492), B1, B2, B6, B12 (-), niacin (MESH:D009525)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12608250/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12608250/full.md

## References

74 references — full list in the complete paper: https://tomesphere.com/paper/PMC12608250/full.md

---
Source: https://tomesphere.com/paper/PMC12608250