Not just "salt": the gradient that runs your nerves, heart and nutrient absorption.
Mechanisms, studies and evidence grades for each claim above.
Roughly 2–3 g/day, increasing with sweat loss.
↑ back to summaryRegulates water retention, blood volume, and cellular hydration.1 Works with potassium and chloride to maintain osmotic gradients and membrane potential, keeping electrolytes in balance.3
↑ back to summaryElectrical signaling in cardiac tissue depends on sodium gradients;3 also maintains blood volume and circulation.1
↑ back to summarySodium influx generates action potentials (nerve signaling).2 Sodium-dependent transporters (SVCT2) also deliver vitamin C to neurons.4 Imbalance (hyponatremia) can cause neurological dysfunction.5
↑ back to summaryRequired for muscle contraction and prevention of dysfunction from electrolyte imbalance.3
↑ back to summarySodium-dependent transport improves nutrient absorption and vitamin uptake, including SVCT1-mediated dietary vitamin C absorption in intestinal tissue.46 Also enables absorption of glucose and amino acids via sodium-coupled cotransporters. (the two citations originally linked for glucose/amino-acid cotransport point to Notion pages that no longer resolve — flagged rather than silently dropped)
↑ back to summarySodium balance influences hormonal regulation (RAAS, stress response) and circulatory stability;7 dysregulation in either direction (too low or too high) is a physiological stressor.7
↑ back to summaryIndirectly supports antioxidant systems by enabling vitamin C transport into cells.4 See Vitamin C and Glycine / Collagen for where that connects to collagen synthesis.
↑ back to summaryHyponatremia: confusion, headache, seizures.
↑ back to summarySodium is not just "salt" — it's a central regulator of fluid balance, cellular energy systems, and nutrient delivery, especially for compounds like vitamin C that feed directly into collagen synthesis and antioxidant defense.8
↑ back to summaryTODO — the source page also cited two references for glucose and amino-acid sodium-cotransport that point to broken/deleted Notion pages (no longer resolvable). Worth re-sourcing those two claims directly against primary literature (SGLT1 for glucose, PMID 30231979 above is adjacent but not the original cite; amino acid cotransport has no substitute yet).