Zoology · Biomolecules

Vitamins — Classification & Deficiency Diseases

Vitamins are accessory organic micronutrients required by the body in very small amounts; they do not yield energy but act as biocatalysts, several of them feeding into the coenzymes that drive enzyme catalysis. NEET treats vitamins as a high-yield matching topic — fat-soluble versus water-soluble, the specific deficiency disease, the principal food source — and weaves them back into the Biomolecules chapter through the niacin–NAD coenzyme link. This page goes deep on all thirteen recognised vitamins, their target symptoms and their dietary sources.

NCERT grounding

The NCERT Class XI Biology chapter on Biomolecules does not list the deficiency diseases as a separate section, but it anchors the whole subtopic through one important coenzyme statement under enzyme cofactors: "The essential chemical components of many coenzymes are vitamins, e.g., coenzyme nicotinamide adenine dinucleotide (NAD) and NADP contain the vitamin niacin." This single sentence is why NEET examiners can pull vitamins into a Biomolecules question. The fuller classification, daily requirements and deficiency diseases come from the NIOS Senior Secondary Biology supplement (Chapter 28, "Nutrition and Health"), which the syllabus uses as the standard reference for the water-soluble and fat-soluble groups.

"Vitamins are complex chemical substances required by the body in very small amounts. They do not yield energy but act as biocatalysts in the body."

NIOS Senior Secondary Biology · §28.2.4

What vitamins are and how they are classified

A vitamin is an organic compound that the body requires in trace amounts for normal growth, normal metabolism and resistance to disease, but which the body in general cannot synthesise for itself. Vitamins are therefore essential nutrients that must be supplied through the diet. They are micronutrients in the strict sense — nutrients required in small amounts — and along with the minerals they make up the protective or regulatory part of food. They do not act as fuel; they do not yield energy on oxidation. Instead, several of them act as biocatalysts, either by directly forming the catalytic portion of a coenzyme or by maintaining the structure of an enzyme or a tissue.

The standard NEET classification is built on a single physical property — solubility. Vitamins that dissolve in fats are grouped together; vitamins that dissolve in water form a second group. The grouping is not just bookkeeping. It dictates how the vitamin is absorbed (fat-soluble vitamins ride along with dietary fats and require bile salts for absorption), how it is transported, whether it is stored in the body, and what happens if it is taken in excess.

Fat-soluble versus water-soluble vitamins

Fat-soluble — A, D, E, K

A · D · E · K

Four members

  • Absorbed with dietary fats; require bile salts.
  • Stored in the liver and adipose tissue.
  • Daily intake from food not required every single day.
  • Excess intake (A and D) can be toxic — hypervitaminosis.
  • Vitamin D can be synthesised by the body itself in the skin on exposure to sunlight.
VS

Water-soluble — B-complex and C

B-complex · C

B1, B2, B3, B5, B6, B7, B9, B12 and C

  • Absorbed directly in the aqueous medium of the gut.
  • Not stored in significant amounts; excess is excreted in urine.
  • Must be supplied regularly through the diet.
  • Excess intake usually does not cause harm.
  • Several act as coenzymes — niacin in NAD/NADP, riboflavin in FAD-type carriers, pantothenic acid in coenzyme A.

One often-tested point is that the human body cannot synthesise most vitamins; they must be supplied through food. The standard NIOS exception is vitamin D, which the body can produce on its own with the help of sunlight acting on the skin. This makes vitamin D a kind of intermediate between a vitamin and a hormone, but for the purposes of NEET it is still tabulated as a fat-soluble vitamin.

Fat-soluble vitamins: A, D, E, K

The four fat-soluble vitamins are absorbed together with the dietary lipids in the small intestine. Bile salts emulsify the fats and the vitamins ride along inside the lipid droplets. Once across the intestinal wall, they enter the lymphatic system and ultimately reach the liver, which is the principal storage site for vitamins A and D (and, to a lesser extent, E and K). This storage capacity is what makes the daily requirement of these vitamins less rigid than for the water-soluble group, but it is also why an unchecked daily overdose can accumulate to toxic levels.

Vitamin A (retinol) and night blindness

Vitamin A is essential for the maintenance of vision and for the synthesis of the visual pigment in the retina. It is also needed to keep epithelia healthy by directing their proper keratinisation. The best food sources are milk, cheese, butter, eggs, cod liver oil, carrots, mangoes, papaya, yellow pumpkin, spinach and sweet potato. The orange and yellow vegetables are rich in the carotene pigment, which the body converts to retinol; the NIOS cell-structure chapter notes that vitamin A is present in the carotene pigment of carrot.

The first clinical sign of vitamin A deficiency is night blindness — the inability to see in dim light, because the visual pigment cannot be regenerated quickly enough between flashes of light. With continued deficiency the conjunctiva and cornea dry out, a condition called xerophthalmia, the epithelia keratinise abnormally and the skin becomes dry. NEET tabulates "night blindness, xerophthalmia, retarded keratinisation of epithelia and dry skin" as the symptoms of vitamin A deficiency.

Vitamin D (calciferol) and rickets/osteomalacia

Vitamin D keeps the teeth and bones healthy by promoting the intestinal absorption of calcium and phosphorus. The body can synthesise it in the skin on exposure to sunlight, but it is also obtained from milk, cheese, egg yolk, cod liver oil, fish and butter. Deficiency of vitamin D in growing children prevents the bones from calcifying properly and produces rickets, recognised by bow legs, pigeon chest and softening of the bones. The NIOS figure of a child with rickets shows a large head, a bulging forehead, curved limb bones, a protruding abdomen, leg deformities and enlarged ankle epiphyses. In adults the same deficiency, acting on bones whose growth is already complete, produces osteomalacia, marked by painful bones and spontaneous fractures.

Vitamin E (tocopherol) and reproductive failure

Vitamin E acts as an antioxidant and is sometimes called the ageing vitamin in older texts because of its protective role against oxidative damage. It is obtained from grains, vegetable oils, green leafy vegetables, nuts and liver. NEET-standard deficiency symptoms are reproductive failure in both males and females — sterility in males, and miscarriage or death of embryos during pregnancy in females.

Vitamin K (phylloquinone) and faulty blood clotting

Vitamin K is required for the clotting of blood; without it the clotting cascade cannot produce a stable clot. It is obtained from green leafy vegetables, soyabean and tomatoes. Deficiency results in faulty blood clotting and haemorrhage — delayed blood clotting is the NIOS-listed symptom. This is the reason newborns are sometimes given a vitamin K supplement at birth, as their gut flora has not yet established and intestinal synthesis has not begun.

Fat-soluble fingerprint. A → vision and skin; D → calcium handling and bone mineralisation; E → reproduction and antioxidant; K → blood clotting. Memorise the disease that maps to the deficiency, and the food source list.

A

Vitamin A — Retinol

Function: Maintenance of vision; synthesis of visual pigment; healthy epithelia.

Deficiency: Night blindness, xerophthalmia.

Sources: Carrot, milk, butter, eggs, cod liver oil, mango, papaya, pumpkin.

D

Vitamin D — Calciferol

Function: Absorption of calcium and phosphorus; healthy bones and teeth.

Deficiency: Rickets in children; osteomalacia in adults.

Sources: Sunlight on skin, cod liver oil, egg yolk, milk, fish, butter.

E

Vitamin E — Tocopherol

Function: Antioxidant; supports reproduction; "ageing vitamin".

Deficiency: Sterility in males; miscarriage in females.

Sources: Grains, vegetable oils, green leafy vegetables, nuts, liver.

K

Vitamin K — Phylloquinone

Function: Clotting of blood.

Deficiency: Faulty blood clotting; haemorrhage.

Sources: Green leafy vegetables, soyabean, tomatoes.

Figure 1 Skeletal signs of rickets in vitamin D deficiency Bulging forehead Pigeon chest Protruding abdomen Curved limb bones (bow legs) Enlarged ankle epiphyses VITAMIN D DEFICIENCY

Figure 1. Classical skeletal signs of rickets — vitamin D deficiency in a growing child: bow legs, pigeon chest, enlarged ankle epiphyses, protruding abdomen and bulging forehead. The same deficiency in adults, where bone growth is already complete, manifests instead as osteomalacia with painful bones and spontaneous fractures.

Water-soluble vitamins: B-complex and C

The water-soluble vitamins comprise the B-complex group and vitamin C. They dissolve in the watery medium of the gut and are absorbed without the help of bile salts. Because they are not stored in significant amounts, the body needs them regularly through food. Any excess is excreted through the urine, which is why excessive intake of water-soluble vitamins generally does not cause harm.

Vitamin B1 (thiamine) and beriberi

Vitamin B1 supports carbohydrate metabolism, sharpens appetite and is required for the proper functioning of the heart, nerves and muscles. The best food sources are yeast, liver, milk, cheese, leafy vegetables, meat and whole-grain cereals. Deficiency of B1 causes beriberi, whose NEET-listed symptoms are pain in hands and feet, swelling of the body, paralysis of limbs and oedema.

Vitamin B2 (riboflavin) and cheilosis

Vitamin B2 is required for carbohydrate and protein metabolism and keeps the skin healthy. It is obtained from milk, liver meat, eggs, peas, yeast, whole grains and green leafy vegetables. Its deficiency produces riboflavinosis, with cracking of the skin at the corners of the mouth (the classical sign of cheilosis), lesions of the eyes, photophobia, retarded growth and mental disorder.

Vitamin B3 (niacin) and pellagra

Vitamin B3 — niacin — acts as a coenzyme for the metabolism of proteins, fats and carbohydrates and keeps the skin healthy. It is obtained from fish, eggs, meat, legumes, whole grains, leafy vegetables, peanuts, beans, tomato and potato. Niacin is the vitamin embedded in NAD and NADP, the two main electron-carrier coenzymes referenced by the NCERT Biomolecules chapter. Its deficiency produces pellagra, classically remembered as the "three D's" — dermatitis (bad skin), diarrhoea (loose motions) and dementia (mental disorder).

Vitamin B5, B6 and B7 — pantothenic acid, pyridoxine, biotin

Although the NIOS table tabulates only B1, B2, B3, B12 and C explicitly, the broader B-complex group of NEET importance includes pantothenic acid (B5), pyridoxine (B6) and biotin (B7). Pantothenic acid deficiency produces the "burning-feet syndrome" with painful sensations in the soles. Pyridoxine deficiency leads to anaemia, peripheral neuropathy and dermatitis. Biotin deficiency, rare in normal diets, causes dermatitis and hair loss. Pantothenic acid is the vitamin component of coenzyme A, which carries acyl groups in fatty-acid and citric-acid-cycle metabolism.

Vitamin B9 (folate/folic acid) and megaloblastic anaemia

Folic acid is essential for nucleic acid synthesis and for the maturation of red blood cells. Its deficiency produces megaloblastic anaemia, in which the bone marrow releases large, immature red cells because DNA synthesis cannot keep pace with cytoplasmic growth. Folic acid is especially important during pregnancy for the development of the embryo's neural tube.

Vitamin B12 (cyanocobalamin) and pernicious anaemia

Vitamin B12 is required for blood formation, nervous tissue metabolism and nucleic acid synthesis. It is obtained from liver, fish, cheese, milk, eggs and meat — the strict NIOS list is exclusively animal-source foods, which is why a poorly planned vegan diet can produce B12 deficiency. Its deficiency produces pernicious anaemia, whose symptoms are paleness of skin, breathlessness and retarded growth. NIOS Chapter 13 also lists the storage of vitamin B12 (along with vitamins A and D) as one of the liver's functions.

The NIOS iron-deficiency text adds a clinically important point that NEET sometimes recycles: iron-deficiency anaemia is treated with foods rich in iron and in vitamin B12, because B12 is required for blood formation in the bone marrow. The two anaemias — iron-deficiency and pernicious — are different in origin but related in treatment.

Vitamin C (ascorbic acid) and scurvy

Vitamin C builds resistance to infections, keeps teeth, gums and joints healthy, heals cuts and wounds, and maintains connective tissue. It is obtained from amla, cabbage, tomatoes, lemon, orange, mangoes, chillies, guava, pineapple and sprouted grams. Its deficiency produces scurvy, with bleeding gums, pain in joints and general weakness. NIOS Chapter 4 makes the same point in compact form: "Water soluble e.g. vitamin B and ascorbic acid and fat soluble vitamins; deficiency of vitamin B causes beriberi and that of vitamin C causes scurvy."

The reason the Biomolecules chapter touches vitamins at all is because several of them are the active chemical core of coenzymes. The NCERT text is explicit on this point: cofactors are non-protein constituents bound to the enzyme to make it catalytically active, and three kinds of cofactors are recognised — prosthetic groups, coenzymes and metal ions. Coenzymes are organic compounds whose association with the apoenzyme is only transient, occurring during the course of catalysis, and which serve as cofactors in many enzyme-catalysed reactions. Their essential chemical components are vitamins.

Vitamin → Coenzyme → Active enzyme

Three coenzymes that NEET routinely pulls back into Biomolecules
  1. B3

    Niacin

    Niacin is the vitamin core of NAD and NADP, the dehydrogenase coenzymes that shuttle hydride ions in respiration and biosynthesis.

    NAD / NADP
  2. B2

    Riboflavin

    Riboflavin is the vitamin core of flavin coenzymes such as FAD, used by the dehydrogenases of the electron transport chain.

    FAD-type carriers
  3. B5

    Pantothenic acid

    Pantothenic acid is part of coenzyme A (CoA), which carries acetyl and acyl groups into the citric-acid cycle and fatty-acid metabolism.

    Coenzyme A
  4. Result

    Holoenzyme

    Apoenzyme (protein) plus its bound coenzyme (carrying the vitamin) is the catalytically active holoenzyme. Remove the coenzyme — catalytic activity is lost.

    Catalysis

This is also why the absence of a vitamin can have such wide-ranging metabolic consequences: a missing vitamin disables every enzyme that needs the corresponding coenzyme. A diet poor in niacin disables every NAD-dependent dehydrogenase; a diet poor in pantothenic acid disables every CoA-mediated acyl transfer. The clinical picture (pellagra, burning-feet syndrome) is the integrated signature of those many small failures.

Figure 2 Vitamin → coenzyme → active enzyme Apoenzyme (protein, inactive) + Coenzyme NAD / NADP niacin (B3) Holoenzyme (catalytically active) ACTIVE Apoenzyme + Coenzyme → Holoenzyme. The coenzyme carries the vitamin (e.g., niacin in NAD).

Figure 2. The vitamin–coenzyme–enzyme link. The protein apoenzyme by itself is inactive. It becomes the catalytically active holoenzyme only when it binds the coenzyme that carries the vitamin — here, niacin (vitamin B3) embedded inside NAD/NADP.

Hypervitaminosis — too much of a vitamin

"Hypervitaminosis" is the disease caused by the presence of vitamins in excessive quantities in the body. Excessive intake of water-soluble vitamins, that is the B-complex group and vitamin C, may not cause any harm because they are excreted out through the urine. Intake of the fat-soluble vitamins A and D, however, can be toxic to the body and lead to specific disease states. This asymmetry between water-soluble and fat-soluble vitamins comes from storage: fat-soluble vitamins build up in the liver, water-soluble vitamins flush out in the urine.

Both deficiency and excess of nutrients are harmful to the body. This is the standard NEET take-home from the nutrition module, and it explains why the daily requirements tabulated in the NIOS chapter are bracketed — too little produces a deficiency disease, too much (for the fat-soluble group) produces hypervitaminosis.

Worked examples

Worked example 1

Which of the following is a fat-soluble vitamin: vitamin B1, vitamin C, vitamin D, vitamin B12?

Vitamin D. The fat-soluble group consists of vitamins A, D, E and K; the rest are water-soluble. NEET routinely places one fat-soluble vitamin among water-soluble distractors, and "vitamin D" is the standard correct answer because it is also the only vitamin the body can synthesise on its own.

Worked example 2

Match the vitamin with its deficiency disease: (a) Vitamin A, (b) Vitamin B1, (c) Vitamin B3, (d) Vitamin C.

(a) Vitamin A → Night blindness (and xerophthalmia on prolonged deficiency). (b) Vitamin B1 → Beriberi (pain in hands and feet, swelling of body, paralysis of limbs, oedema). (c) Vitamin B3 → Pellagra (the three D's — dermatitis, diarrhoea, dementia). (d) Vitamin C → Scurvy (bleeding gums, pain in joints, general weakness). Each disease is tied to one specific vitamin, and the match is the standard NEET question format.

Worked example 3

Which vitamin's deficiency causes faulty blood clotting and haemorrhage?

Vitamin K. It is the fat-soluble vitamin required for the clotting of blood; its deficiency produces faulty blood clotting and haemorrhage. The principal sources are green leafy vegetables, soyabean and tomatoes.

Worked example 4

Coenzyme nicotinamide adenine dinucleotide (NAD) contains which vitamin as its essential chemical component?

Niacin (vitamin B3). The NCERT Biomolecules chapter states explicitly: "The essential chemical components of many coenzymes are vitamins, e.g., coenzyme nicotinamide adenine dinucleotide (NAD) and NADP contain the vitamin niacin." This is the question that drags vitamins back into Biomolecules from a Nutrition table.

Common confusion & NEET traps

NEET PYQ Snapshot — Vitamins & Deficiency Diseases

Concept drills built on the NCERT coenzyme statement and the NIOS vitamin table that NEET examiners draw from.

Concept

The essential chemical component of the coenzyme nicotinamide adenine dinucleotide (NAD) is the vitamin

  1. Thiamine (B1)
  2. Riboflavin (B2)
  3. Niacin (B3)
  4. Ascorbic acid (C)
Answer: (3)

Why: NCERT Biomolecules states: "The essential chemical components of many coenzymes are vitamins, e.g., coenzyme nicotinamide adenine dinucleotide (NAD) and NADP contain the vitamin niacin." This is the line that links vitamins to the Biomolecules chapter and the line examiners build matching questions around.

Concept

Match the vitamin with its deficiency disease.
(a) Vitamin A — (i) Beriberi
(b) Vitamin B1 — (ii) Night blindness
(c) Vitamin C — (iii) Rickets
(d) Vitamin D — (iv) Scurvy

  1. (a)-(ii), (b)-(i), (c)-(iv), (d)-(iii)
  2. (a)-(i), (b)-(ii), (c)-(iii), (d)-(iv)
  3. (a)-(iii), (b)-(iv), (c)-(i), (d)-(ii)
  4. (a)-(iv), (b)-(iii), (c)-(ii), (d)-(i)
Answer: (1)

Why: Vitamin A deficiency → night blindness; vitamin B1 deficiency → beriberi; vitamin C deficiency → scurvy; vitamin D deficiency → rickets. The NIOS Chapter 28 table fixes these pairings, and they form the most frequently tested matching set in this topic.

Concept

Which of the following vitamins can be synthesised in the human body?

  1. Vitamin A
  2. Vitamin B12
  3. Vitamin C
  4. Vitamin D
Answer: (4)

Why: "Since vitamins cannot be made in our body except for vitamin D, they need to be supplied through food that contain them" (NIOS §28.2.4). Vitamin D is synthesised in the skin on exposure to sunlight; the other three must be supplied through the diet.

Concept

Deficiency of which vitamin in growing children causes rickets, recognised by bow legs, pigeon chest and softening of bones?

  1. Vitamin A
  2. Vitamin C
  3. Vitamin D
  4. Vitamin K
Answer: (3)

Why: Vitamin D deficiency in growing children leads to failure of bones to calcify — bow legs, pigeon chest and softening of bones — the clinical picture of rickets. In adults the same deficiency causes osteomalacia (painful bones, spontaneous fractures).

FAQs — Vitamins & Deficiency Diseases

Quick clarifications on the points NEET examiners trap students on.

Why are vitamins classified as fat-soluble and water-soluble?

Vitamins are grouped into two classes on the basis of solubility. The fat-soluble vitamins are A, D, E and K; they dissolve in lipids and can be stored in the liver and adipose tissue. The water-soluble vitamins are the B-complex group and vitamin C; they dissolve in water and excess amounts are excreted through the urine, so they are not stored in significant quantities and must be supplied regularly through the diet.

Which vitamin can the human body synthesise on its own?

Of all the vitamins, only vitamin D can be produced by the human body itself. Skin synthesises vitamin D on exposure to sunlight, with the help of sunlight acting on a precursor in the skin. All the remaining vitamins cannot be made in our body and must be supplied through food that contains them.

How are vitamins related to coenzymes?

Coenzymes are organic compounds whose association with the apoenzyme is only transient and which serve as cofactors in many enzyme-catalysed reactions. The essential chemical components of many coenzymes are vitamins. For example, the coenzymes nicotinamide adenine dinucleotide (NAD) and NADP contain the vitamin niacin. So a vitamin can be thought of as a precursor of a coenzyme without which the corresponding enzyme cannot catalyse its reaction.

What is the difference between beriberi, pellagra and scurvy?

All three are water-soluble vitamin deficiency diseases, but they involve different vitamins. Beriberi is caused by deficiency of vitamin B1 (thiamine) and shows up as pain in hands and feet, swelling of the body, paralysis of limbs and oedema. Pellagra is caused by deficiency of vitamin B3 (niacin) and is recognised by dermatitis, diarrhoea and dementia. Scurvy is caused by deficiency of vitamin C (ascorbic acid) and presents with bleeding gums, pain in joints and general weakness.

Why does deficiency of vitamin A cause night blindness?

Vitamin A (retinol) is essential for the synthesis of the visual pigment in the eye and for the maintenance of vision. When the diet lacks vitamin A over a long period, the pigment cannot be regenerated in sufficient quantity, and the person cannot see in dim light. This early symptom is called night blindness. Prolonged deficiency causes drying of the conjunctiva and cornea, a condition called xerophthalmia, along with retarded keratinisation of epithelia and dry skin.

What is hypervitaminosis and which vitamins commonly cause it?

Hypervitaminosis is the disease caused by the presence of vitamins in excessive quantities in the body. Excess intake of water-soluble vitamins, that is the B-complex group and vitamin C, usually does not cause harm because they are excreted through urine. Intake of the fat-soluble vitamins A and D in excess can be toxic. Excess vitamin A accumulates in the liver and produces loss of hair, drowsiness, painful swelling of long bones, loss of appetite, nausea and vomiting. Excess vitamin D raises calcium absorption from the intestine and causes deposition of calcium in soft tissues such as the kidney, along with drowsiness, nausea and loss of weight.