As we head into a busy fall, a quick reminder from history: sailors once ate full rations and still succumbed to scurvy—not because they lacked calories, but because a critical nutrient never reached its target. That same pattern—a full plate with missing essentials—is echoing in modern life.
Today’s chronic disease landscape is broad. But in this piece we’re narrowing the lens to the gut–brain axis (GBA)—the supply line between your microbiome and your mind—and the specific ways it can shape mood, resilience, and brain aging.
Two things can be true at once:
-
Many of us don’t eat enough plants (and ultra-processed foods are common), so some people really are under-nourished in fiber and phytonutrients.
-
And yet, that alone doesn’t fully explain the rise in brain-related complaints or risk. Even when we do eat well, nutrients can still fail to arrive where they’re needed.
That’s the heart of our “Modern Scurvy” idea: a logistics problem inside the body. Food is the cargo, but the GBA is the supply line that decides what reaches the brain. When the line runs smoothly, microbial vitamins and postbiotic metabolites (like short-chain fatty acids) show up on time to support focus and calm. When it’s disrupted—by stress, dysbiosis, inflammation, antibiotics, or low-fiber routines—nutrients can be under-produced, over-consumed by microbes, chemically detoured, or even sequestered by disease processes before the brain ever sees them.
In the blog that follow, we’ll go beyond “eat more fruits and veggies” and examine where nutrients get lost even with a good diet:
-
B vitamins: why microbes can be producers or competitors, shifting your methylation and neurotransmitter pathways.
-
Redox balance: how certain microbes can spend your antioxidants before you can, nudging the gut (and then the brain) toward oxidative stress.
-
Lithium bioavailability: what it means when pathology can trap a protective micronutrient inside the brain.
Introduction
Think of your body as a logistics network. Food is the cargo, but the gut–brain axis (GBA) is the supply line that decides what actually reaches the brain. When the line runs smoothly, micronutrients and postbiotic metabolites arrive on time; when it’s disrupted, the brain experiences functional shortages—even if the diet looks great.
What the GBA does: It’s more than a “communication network.” Through neural, endocrine, immune, and metabolic channels, the gut and brain coordinate digestion, mood, cognition, and nutrient handling. As meals arrive, enteroendocrine cells and the microbiota sense their composition and trigger hormone and vagal signals that set appetite, motility, and inflammatory tone.
Why microbes are gatekeepers: Microbes convert dietary precursors into bioavailable micronutrients (notably B vitamins) and neuroactive compounds, and they shape absorption by maintaining barrier integrity and producing short-chain fatty acids that modulate transporters and immune tone (1,4,9). The colon expresses transporters for several vitamins, so bacterially produced vitamins can contribute to the host pool—especially when intake is marginal or demand is high (1).
When logistics fail: Stress, dysbiosis, and inflammation can derail this supply line: microbes may consume or inactivate vitamins, produce analogs that don’t help the host, or alter transporter expression and barrier function (1,4). The result is a functional deficiency—a shortfall in what reaches neural pathways—despite normal intake or even “normal” serum labs.
Key idea: The gut doesn’t just digest—it decides what your brain gets. (1,4,9)
Microbial B Vitamins: Producers, Competitors, and the Brain
Why B vitamins sit at the center. The B family (B₁, B₂, B₃, B₅, B₆, B₇, B₉, B₁₂) powers mitochondrial flux, myelin integrity, neurotransmitter synthesis, and one-carbon (methylation) chemistry. While most absorption occurs in the small intestine, colonic transporters allow host access to microbially synthesized vitamins (1). In eubiotic ecosystems, producer taxa (e.g., Bifidobacterium, Lactobacillus) help supply the pool; in dysbiosis, that vitamin economy can flip.
Competition changes the math—even with a good diet. An estimated 20–30% of gut taxa are auxotrophs for one or more B vitamins and must scavenge them (1). When consumer species bloom (e.g., SIBO, post-antibiotic shifts, low-fiber patterns), intraluminal demand can exceed supply, creating a host-level functional deficiency. Mechanisms include:
i) Microbial interception before host uptake (classic with B₁₂) (1)
ii) Production of unusable analogs or consumption of host-bound forms (1)
iii) Inflammation-driven transporter changes that blunt colonic salvage (1,4)
Signals from Parkinson’s disease (PD). Multi-cohort metagenomics show reduced microbial gene capacity for riboflavin (B₂) and biotin (B₇) in PD, alongside losses of butyrate producers (2). These vitamins feed redox enzymes and fatty-acid metabolism; their scarcity plausibly weakens epithelium, raises oxidative stress, and modulates α-synuclein biology—consistent with gut-origin PD models (2). Complementing this, Mendelian randomization links specific microbial signatures (e.g., Akkermansia, Lactococcus) to higher risk of B₁₂ (and other) deficiencies—supporting a causal role of microbiota in micronutrient status (3).
Neurochemical consequences. Folate/B₁₂ insufficiency elevates homocysteine (neurotoxic; linked to atrophy and vascular injury). B₆ enables GABA/serotonin synthesis; B₁ supports pyruvate dehydrogenase and neuronal glucose use. Over years, microbially mediated vitamin drag can plausibly accelerate cognitive decline, especially when stacked with inflammation and oxidative stress (1–3).
Key takeaways
-
Microbes can supply—or siphon—B vitamins, altering brain-relevant pathways. (1)
-
Dysbiosis shifts the “vitamin economy” toward consumption > production. (1–3)
-
PD data connect lost microbial B-vitamin capacity with disease biology, not just correlation. (2)
Redox Dysbiosis: When Microbes Hijack Antioxidants
Redox is the silent language of the GBA. Neurons are vulnerable to oxidative stress; the gut is a redox factory where diet, microbes, and host enzymes trade electrons. Microbes buffer or amplify oxidative tone via butyrate, flavin (B₂) chemistry, and antioxidant/polyphenol metabolism (4). Less antioxidant input—or more microbial “antioxidant theft”—shifts the lumen pro-oxidant, loosens tight junctions, and primes systemic inflammation that reaches the brain (4).
A striking example: ergothioneine cross-feeding. Humans don’t synthesize ergothioneine (EGT) but evolved a specific transporter to stockpile it. Recent work shows Clostridium symbiosum cleaves EGT to thiourocanic acid (TUA), which Bacteroides xylanisolvens uses as an electron acceptor to boost anaerobic growth—consuming host-available antioxidant capacity in the process (5). Individuals vary widely: some fecal communities barely touch EGT; others convert it rapidly—a person-specific antioxidant drain (5).
Why it matters upstream of the brain. Lower antioxidant availability weakens the barrier and permits LPS/inflammatory mediators to enter circulation, sensitizing microglia and raising CNS oxidative tone. Add reduced B₂/B₇ capacity (2) and you further erode redox enzymes and mitochondrial resilience—a stacked redox burden (2,4,5).
Practical inference (without overclaiming). We don’t yet have trials proving that preserving luminal EGT slows neurodegeneration. But the chain—microbial antioxidant use → mucosal redox stress → systemic inflammation → neuroinflammation—is biologically coherent and actionable via dietary fiber, polyphenols/mushrooms, and postbiotics that deliver metabolites without the variability of live strains (4,5,7).
Key takeaways
-
Redox balance is co-governed by microbes and vitamins; dysbiosis pushes pro-oxidant. (2,4)
-
EGT cross-feeding shows microbes can spend your antioxidants before you can. (5)
-
Barrier → inflammation → brain links convert gut redox signals into CNS stress. (2,4,5)
Lithium in Alzheimer’s: Nutrient Sequestration by Pathology
A different deficit: not intake—availability. At trace levels, lithium (Li) supports neural resilience (e.g., GSK-3β modulation, microglial tone). Human brain studies show Li is selectively reduced in MCI/AD cortex without consistent serum differences—implying intracerebral unavailability rather than dietary lack (6).
Amyloid as a molecular sponge. Mass-spec imaging and fractionation reveal Li co-localizes with amyloid plaques and is depleted from soluble cortical fractions that neurons use—pathology-driven sequestration creating a hidden deficiency despite “normal” blood (6).
Causality in vivo. When endogenous brain Li was reduced ~50% in AD-model mice, amyloid, tau phosphorylation, microglial activation, synapse loss, and memory decline all accelerated; lithium orotate (less amyloid binding) restored brain Li, curbed pathology, and protected cognition better than lithium carbonate in those models (6). This is not a license for casual lithium use; any dosing warrants clinical oversight.
Key takeaways
-
AD can trap lithium in plaques, lowering bioavailable Li in cortex. (6)
-
Experimental Li deficiency accelerates AD pathology—supporting causality. (6)
-
Formulation matters; amyloid-evading salts merit careful clinical study. (6)
Modern Scurvy: A Unifying Framework
From intake to impact—four failure modes:
-
Production failure (lost microbial vitamin capacity)
-
Competition (microbes consume/swap to analogs)
-
Conversion/consumption (microbes hijack antioxidants)
-
Sequestration (pathology binds/locks nutrients)
Any one can create functional deficiency; together, they compound.
Why this matters for neurodegeneration. When methylation underperforms (B₉/B₁₂), redox buffers thin (B₂/EGT), and kinases run hot (low Li → ↑GSK-3β), you lower the threshold for misfolding, synaptic loss, and network fragility—shaping the timeline of cognitive decline (1–6).
Clinical & Practical Implications (for Providers and Curious Readers)
Assess beyond serum. Normal B₁₂ with high homocysteine suggests functional deficiency; stool metagenomics can reveal producer erosion or consumer blooms (1–3). Consider SIBO in low B₁₂ with GI symptoms. For redox, pair diet history (polyphenols/mushrooms) with barrier/inflammation markers to infer luminal antioxidant pressure (2,4,5).
Intervene on ecosystem and endpoints.
-
Dietary pattern: fiber-diverse plants to fuel butyrate producers; add EGT-rich mushrooms and polyphenol sources; ensure adequate protein for mucosa (4,5).
-
Targeted nutrients: methylated B vitamins when homocysteine is high; riboflavin for redox/mitochondria; lithium only with clinician guidance in research-minded contexts (1–3,6).
-
Postbiotics: deliver SCFAs, vitamins, EPS without live-strain variability—useful when colonization or safety is a concern (7).
Match tool to task; avoid overclaiming. Start with measurable imbalances, prioritize low-risk, high-benefit changes, and monitor (homocysteine, CRP, cognition screens). Keep any lithium use under medical supervision (1–7).
References
-
Uebanso T, et al. Functional Roles of B-Vitamins in the Gut and Gut Microbiome. Mol Nutr Food Res. 2020;64:2000426.
-
Nishiwaki H, et al. Meta-analysis of shotgun sequencing of gut microbiota in Parkinson’s disease. NPJ Parkinson’s Dis. 2024;10:106.
-
Hou ZX, et al. Causal links between gut microbiota and vitamin deficiencies (Mendelian randomization). Curr Med Sci. 2024.
-
Fan L, et al. Gut microbiota bridges dietary nutrients and host immunity. Sci China Life Sci. 2023;66:2466–2514.
-
Zhou Z, et al. Metabolic cross-feeding of a dietary antioxidant enhances anaerobic energy metabolism by human gut bacteria. Cell Host Microbe. 2025;33:1321–1332.
-
Aron L, et al. Lithium deficiency and the onset of Alzheimer’s disease. Nature. 2025.
-
Scott E, De Paepe K, Van de Wiele T. Postbiotics and Their Health Modulatory Biomolecules. Biomolecules. 2022;12:1640.
-
Carabotti M, et al. The gut–brain axis: interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol. 2015;28:203–209.