Vitamins

A sailor on a six-week voyage with no fresh fruit develops bleeding gums and joints that ache at every step. A child raised indoors, rarely in the sun, grows up with soft, bowed legs. Two very different bodies, two very different failures — yet both trace back to the same kind of gap: a vitamin missing from the diet. Vitamins are organic compounds the body needs in tiny amounts to run its everyday chemistry, but usually cannot make for itself, so they must arrive with food. What decides how a shortage plays out — how fast the symptoms appear, how the body stores (or fails to store) the vitamin, how dangerous an overdose can be — is a single physical property: whether the vitamin dissolves in fat or in water. This article builds the classification of vitamins around that one idea, then works through the functions and deficiency diseases the syllabus expects you to name on sight.

The core insight

A vitamin's solubility in fat versus water decides whether it is stored in the body (fat-soluble A, D, E, K — slow deficiency, risk of toxic build-up) or not stored and needing frequent replenishment (water-soluble B-group and C — fast deficiency, excess simply excreted).

The core idea

Vitamins are catalysts of metabolism, not fuel or building blocks. Unlike carbohydrates, fats, and proteins, vitamins supply no significant energy and are not incorporated into body structure in bulk. Instead, most function as coenzymes or coenzyme precursors — small helper molecules that enzymes need to carry out reactions such as energy release, blood clotting, or collagen synthesis. Because the body needs only milligram or microgram quantities, a diet that looks adequate in calories can still be badly deficient in a single vitamin.

The one property that organises the whole topic is solubility. Vitamins A, D, E, and K dissolve in fats and oils; they travel through the body along with dietary lipids and can be stored in fatty tissue and the liver. The B-group vitamins and vitamin C dissolve in water; they move freely in blood and body fluids but are not retained in any depot, so what is not used is filtered out by the kidneys and lost in urine.

That single fact predicts almost everything examinable about a vitamin. Because fat-soluble vitamins are stored, a person who stops eating them does not fall ill immediately — the body draws on its reserve — but for the same reason, taking too much over time lets the vitamin accumulate to toxic levels, a condition called hypervitaminosis (well documented for vitamins A and D). Because water-soluble vitamins have no reserve, a shortage in the diet shows up as a deficiency disease within weeks, but there is very little risk of toxic accumulation from an oral excess, since the surplus is excreted rather than stored.

Fat-soluble vitamins (A, D, E, K). Vitamin A (retinol) is required for the visual pigment rhodopsin and for healthy epithelial tissue; deficiency causes night blindness and, if prolonged, damage to the cornea. Vitamin D (calciferol) promotes intestinal absorption of calcium and phosphorus for mineralising bone and teeth, and is also made in the skin on sunlight exposure; deficiency causes rickets in children and osteomalacia in adults. Vitamin E (tocopherol) is an antioxidant that protects cell membranes; deficiency is linked to fragile red blood cells. Vitamin K is needed to synthesise blood-clotting factors; deficiency impairs clotting.

Water-soluble vitamins (B-group and C). Vitamin B₁ (thiamine) supports carbohydrate metabolism and nerve function; deficiency causes beriberi. Vitamin B₂ (riboflavin) is a coenzyme precursor for cellular energy metabolism; deficiency causes cheilosis (cracked lips and mouth corners). Vitamin B₃ (niacin) is likewise a metabolic coenzyme precursor; deficiency causes pellagra. Vitamin B₆ (pyridoxine) supports amino acid metabolism; deficiency causes anaemia and nerve disorders. Vitamin B₁₂ (cobalamin) is needed for red blood cell formation; deficiency causes pernicious anaemia. Vitamin C (ascorbic acid) is required for collagen synthesis and wound healing — humans cannot make it at all, so diet is the only source; deficiency causes scurvy.

Figure
Two columns of vitamins sorted by solubility, fat soluble stored in the body on the left and water soluble not stored and excreted on the right
Solubility decides storage and deficiency speed Fat soluble: A, D, E, K dissolve with dietary fat stored in fatty tissue and liver deficiency develops slowly excess can build up to toxic levels A: night blindness D: rickets, osteomalacia K: poor blood clotting Water soluble: B group, C dissolve in blood and body fluids not stored in the body deficiency develops within weeks excess simply excreted in urine B1: beriberi, B2: cheilosis, B3: pellagra B12: pernicious anaemia C: scurvy

Why it works

This topic has no formula to derive — the syllabus asks you to reason from the fat-soluble versus water-soluble split, so that reasoning is spelled out here instead of a derivation. Start from the physical fact: fat mixes with fat, water mixes with water. Vitamins A, D, E, and K share chemical structures rich in hydrocarbon chains or rings, so they dissolve preferentially in lipids; they are absorbed in the small intestine packaged with dietary fat, and any surplus partitions into the body's own fat stores rather than staying dissolved in blood plasma. That storage depot is the whole story for fat-soluble vitamins: it acts as a buffer, so a few weeks of poor diet barely dents the reserve, and deficiency symptoms take a long time — often months — to appear. The same depot, run in reverse, is why overdosing on A or D is a real clinical risk: the vitamin keeps accumulating in fat and liver tissue rather than being flushed out, so an excess dose today adds to yesterday's rather than being cleared. The B-group vitamins and vitamin C, by contrast, are small polar molecules that mix readily with water and poorly with fat. They are absorbed directly into the bloodstream, distributed through watery body fluids, and — because there is no fatty depot for them to hide in — any amount beyond what the tissues can use immediately is filtered by the kidneys and lost in urine within hours. With no reserve to draw on, cutting off the dietary supply of a water-soluble vitamin causes symptoms to appear within days to a few weeks, which is exactly the timeline seen in classic deficiency diseases like scurvy and beriberi. This is also why doctors advise regular, even daily, replenishment of vitamin C and the B vitamins, while emphasising caution around large supplemental doses of vitamin A or D.

Worked example

Question. A sailor on a long voyage with no access to fresh fruits or vegetables develops bleeding gums, joint pain, and slow wound healing after several weeks. A second patient, a child kept mostly indoors and rarely exposed to sunlight, develops soft, bowed leg bones and delayed tooth development. For each case, identify the vitamin deficiency, classify the vitamin by solubility, and explain the difference in how quickly each set of symptoms appeared.

Step 1. Match symptoms to disease for the sailor. Bleeding gums, joint pain, and poor wound healing are the classic presentation of scurvy, caused by deficiency of vitamin C (ascorbic acid), which is required for collagen synthesis.

Step 2. Match symptoms to disease for the child. Soft, bowed leg bones and delayed tooth development are classic signs of rickets, caused by deficiency of vitamin D (calciferol), needed for intestinal absorption of calcium and phosphorus for bone and tooth mineralisation.

Step 3. Classify each vitamin by solubility. Vitamin C is water-soluble (with the B-group vitamins); vitamin D is fat-soluble (with A, E, K).

Step 4. Explain the timing difference. Vitamin C is not stored in the body, so once fresh-produce intake stopped, the sailor's supply depleted within weeks and scurvy appeared quickly — the classic reason sailors on long voyages developed it historically. Vitamin D is fat-soluble and can be stored in the liver and fatty tissue (and is normally topped up by skin synthesis on sunlight exposure), so its deficiency in the child developed only gradually, over a much longer period of inadequate sun exposure and diet.

Answer: the sailor has scurvy from water-soluble vitamin C deficiency (fast onset, no storage); the child has rickets from fat-soluble vitamin D deficiency (slow onset, drawn down from body stores before symptoms show).

Common traps

  • Being asked for the chemical structure or IUPAC name of a vitamin — the syllabus excludes this; only the name, solubility class, function, and deficiency disease are examinable.
  • Mixing up fat-soluble versus water-soluble — the fat-soluble set is small and fixed (A, D, E, K); everything else commonly tested (the B-group and C) is water-soluble.
  • Assigning the wrong deficiency disease, such as confusing beriberi with pellagra, or rickets with osteomalacia — rickets is the childhood form and osteomalacia the adult form of vitamin D deficiency.
  • Assuming all vitamins are safe in unlimited amounts — fat-soluble vitamins can accumulate to toxic levels (hypervitaminosis) since they are stored in the body, a risk that barely applies to water-soluble vitamins.

Ask the tutor: want a quick quiz matching each named vitamin to its deficiency disease, or a memory trick for which vitamins are fat-soluble?

If vitamin C is destroyed by cooking, why isn't scurvy common today?

Modern diets normally include fresh fruits and vegetables — citrus, tomatoes, leafy greens — eaten raw or lightly cooked often enough to supply the small daily amount of vitamin C the body needs, since it cannot be stored. Scurvy became historically famous among sailors precisely because long voyages removed access to any fresh produce for months at a time, cutting off the only source of a vitamin the body cannot make or save. Where fresh produce is scarce or diets are very restricted, scurvy can still occur today.

Why does vitamin D deficiency cause different diseases in children and adults?

Vitamin D governs how the body absorbs calcium and phosphorus and lays them down as bone mineral. In children, bones are still actively growing and lengthening, so a shortage of mineral produces soft, poorly formed, easily bowed bone — rickets. In adults, the skeleton is already formed but bone is continuously remodelled and re-mineralised throughout life; a shortage there weakens and softens existing bone without the growth-related deformities — osteomalacia. Same vitamin, same underlying mineralisation failure, different result depending on whether the skeleton is still growing.

Can taking extra vitamin C ever be harmful, the way excess vitamin A is?

Not in the same way. Because vitamin C is water-soluble, the kidneys excrete what the body does not immediately use, so there is no fatty-tissue depot where it can build up to toxic levels the way vitamin A or D can. Very large doses may cause minor digestive upset, but this is a different and far less serious effect than the true toxicity (hypervitaminosis) seen with excess fat-soluble vitamins, which genuinely accumulate in the body over time.

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