# Dietary Lithium, Silicon, and Boron: An Updated Critical Review of Their Roles in Metabolic Regulation, Neurobiology, Bone Health, and the Gut Microbiome

**Authors:** Eleni Melenikioti, Eleni Pavlidou, Antonios Dakanalis, Constantinos Giaginis, Sousana K. Papadopoulou

PMC · DOI: 10.3390/nu18030386 · Nutrients · 2026-01-24

## TL;DR

This review examines lithium, silicon, and boron as trace elements that may influence metabolism, brain function, bone health, and gut microbes, but more human studies are needed to confirm their benefits.

## Contribution

The paper provides a critical synthesis of the roles of lithium, silicon, and boron in overlapping biological pathways and identifies research gaps for future investigation.

## Key findings

- Lithium, silicon, and boron influence shared pathways like oxidative stress and inflammation.
- Human evidence for these elements is limited and mostly based on small trials or observational studies.
- Mechanistic synergies among the elements remain hypothetical and require further research.

## Abstract

Background/Objectives: Lithium (Li), silicon (Si), and boron (B) are proposed nutritional trace elements with potential roles in metabolic, neurobiological, endocrine, inflammatory, and bone-related processes. This review provides a critical synthesis of data on Li–Si–B, emphasizing (i) physiological and mechanistic pathways, (ii) human clinical relevance, (iii) shared biological domains, and (iv) safety considerations. Methods: A narrative review was conducted across PubMed, Scopus, and Web of Science from inception to January 2025. Predefined search strings targeted dietary, environmental, and supplemental exposures of lithium, silicon, or boron in relation to metabolism, endocrine function, neurobiology, inflammation, bone health, and the gut microbiome. Inclusion criteria required peer-reviewed studies in English. Data extraction followed a structured template, and evidence was stratified into human, animal, cellular, and ecological tiers. Methodological limitations were critically appraised. Results: Li, Si, and B influence overlapping molecular pathways including oxidative stress modulation, mitochondrial stability, inflammatory signaling, endocrine regulation, and epithelial/gut barrier function. Human evidence remains limited: Li is supported primarily by small trials; Si by bone-related observational studies and biomarker-oriented interventions; and B by metabolic, inflammatory, and cognitive studies of modest sample size. Convergence across elements appears in redox control, barrier function, and neuroimmune interactions, but mechanistic synergism remains hypothetical. Conclusions: Although Li–Si–B display compelling mechanistic potential, current human data are insufficient to justify dietary recommendations or supplementation. Considerable research gaps—including exposure assessment, dose–response characterization, toxicity thresholds, and controlled human trials—must be addressed before translation into public health policy.

## Linked entities

- **Chemicals:** lithium (PubChem CID 28486), silicon (PubChem CID 5461123), boron (PubChem CID 5462311)

## Full-text entities

- **Diseases:** inflammation (MESH:D007249), toxicity (MESH:D064420)
- **Chemicals:** Si (MESH:D012825), Li (MESH:D008094), Boron (MESH:D001895), Li-Si-B (-)
- **Species:** gut metagenome (species) [taxon 749906], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12899721/full.md

## References

78 references — full list in the complete paper: https://tomesphere.com/paper/PMC12899721/full.md

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Source: https://tomesphere.com/paper/PMC12899721