Question bank — Vitamins — fat-soluble (A, D, E, K) vs water-soluble (B-complex, C)

False. Vitamins have negligible caloric value; they act as coenzymes/regulators that help release energy from food (via carbohydrate and lipid metabolism) but are not themselves fuel.

Mostly true but not absolute. Excess washes out in urine so toxicity is rare, yet extreme mega-doses (e.g. B6) can still cause harm — "rare" is not "impossible."

False. Storage only delays deficiency; prolonged lack (or fat-malabsorption) still empties the store, giving e.g. rickets or night blindness — just more slowly than water-soluble ones.

False. C is ascorbic acid — a small polar sugar-acid (water-soluble); A is retinol — a long non-polar isoprenoid chain (fat-soluble). Opposite solubility families entirely.

False. "Cannot synthesise in adequate amounts" is the rule; vitamin D can be made in skin using sunlight, and gut bacteria make some vitamin K.

False. For water-soluble vitamins the practical danger is almost entirely deficiency; overdose is negligible. Solubility, not symmetry, sets which end is risky.

False. Most enzymes are proteins (though some RNA molecules — ribozymes — are also catalytic); vitamins are none of these — they are small organic micronutrients. Many B-vitamins become coenzymes that assist enzymes, but a vitamin is not an enzyme.

False. Hormones are synthesised internally by the body's glands; vitamins must be obtained from diet. Vitamin D blurs this line (skin-made, hormone-like) but the general distinction holds.

Error: scurvy is a vitamin C deficiency. Vitamin K deficiency causes prolonged clotting time / bleeding via low prothrombin — different mechanism, different vitamin.

Error: D is fat-soluble → stored → mega-doses accumulate → toxicity (hypercalcaemia). Only the water-soluble vitamins get flushed out.

Error: retinol is vitamin A (fat-soluble); ascorbic acid is vitamin C (water-soluble). Two different vitamins wrongly merged.

Error: count has nothing to do with solubility. The entire B-complex is water-soluble — they carry polar –OH, –NH₂, –COOH, phosphate groups and work in watery cytoplasm.

Error: the tissue location does not decide solubility; the molecule's structure does. Retinol's long hydrocarbon chain is non-polar, so A is fat-soluble.

Error: C is not stored (water-soluble), so surplus is excreted — you cannot bank it. Continuous daily intake, not a one-off surplus, is what protects you.

Error: gut bacteria synthesise vitamin K₂ (menaquinone); antibiotics kill them too, lowering K and prolonging bleeding time. A real drug–vitamin interaction.

Error: dietary K₁ (phylloquinone) comes from green plants, while K₂ (menaquinone) is made by gut bacteria. Both are fat-soluble and count as vitamin K, but they differ in source, which is why gut-flora loss hits K₂ specifically.

Because all three follow from one physical fact — "like dissolves like." Fat-soluble ⇒ dissolves into fat ⇒ stored ⇒ (not daily) + (can accumulate to toxic). Water-soluble ⇒ dissolves in blood ⇒ flushed out ⇒ (needed regularly) + (rarely toxic).

B-vitamins are studded with polar groups (–OH, –NH₂, –COOH, phosphate) that hydrogen-bond with water; A/D/E/K are built on long hydrocarbon or ring (isoprenoid/steroid) skeletons that are non-polar and repel water.

Vitamin C is not stored, and it is spent maintaining collagen, whose turnover means existing collagen slowly degrades over weeks. Once the small body pool of C (roughly 4–6 weeks' worth) is used up, new collagen cannot be cross-linked — so gums bleed after about a month or two at sea, not on short trips.

D is stored in fat and accumulates with continued high intake, reaching harmful levels; C is excreted in urine daily so it cannot build up.

The same flushing that makes them safe from overdose also means no reserve is kept, so a short spell of poor diet quickly causes deficiency.

Vitamins release no calories themselves; they enable the enzymes that unlock energy from carbohydrates and fats. Removing the fuel and keeping the vitamins would still leave you with no energy.

These vitamins dissolve in dietary fat and are absorbed along with it; if fat cannot be absorbed, the fat-soluble vitamins ride out with it and deficiency of all four can develop together.

B12 — dietary B12 binds intrinsic factor (a protein from the stomach), and this complex is taken up by specific receptor-mediated endocytosis in the ileum, then hoarded in the liver bound to transport proteins. Because uptake is receptor-controlled and losses are tiny, the liver store (a few milligrams) covers 3–5 years — so its deficiency appears years, not weeks, after intake stops.

Both fit: it is a dietary micronutrient (vitamin) yet the body can synthesise it in skin from sunlight and it acts on distant tissues like a hormone. It is the clearest boundary case between the two classes.

Bacterial K₂ synthesis alone is not reliably adequate (and is wiped out by antibiotics), so dietary K₁ from plants must still supply it — it meets the "cannot make enough internally" test.

Deficiency is still delayed, not instant — the liver/adipose store buffers the body for weeks to months before symptoms (e.g. night blindness) emerge.

Once tissues and enzymes are saturated, intake and urinary output balance — extra simply leaves in urine with little benefit and (usually) little harm.

Scurvy would become slow-onset and rare on short deprivation, mirroring fat-soluble deficiencies — showing that the storage property, not the specific vitamin, drives deficiency speed.