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Last updated: March 4, 2021

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Vitamins are a group of chemically diverse organic compounds that an organism requires for normal metabolism. Apart from a few exceptions (e.g., vitamin D), the human body cannot synthesize vitamins on its own in sufficient amounts and must, therefore, ensure a steady supply through the diet. Vitamins are micronutrients that do not provide energy (like macronutrients) but instead have very specific biochemical roles. They can be coenzymes in various reactions (B vitamins, vitamins A and K) and/or antioxidants that protect the cell and its membrane from free radicals (vitamins C and E). They can also enable cell signaling (vitamin A) and gene transcription (vitamins A and E) or function as hormones (e.g., vitamin D). Vitamins are classified into fat-soluble vitamins, which the body can store, and water-soluble vitamins, which, with the exception of vitamins B9 (folate) and B12 (cobalamin), the body cannot store over significant periods of time and, therefore, require continuous intake. A balanced diet typically supplies the body with all vitamins it requires. Deficiencies occur mainly due to malnutrition, malabsorption disorders, or restrictive diets (e.g., vitamin B12 deficiency in a vegan diet).

Fat-soluble vs. water-soluble vitamins
Fat-soluble vitamins Water-soluble vitamins
  • Diet (except vitamin D which is predominantly synthesized in the body)
  • Intestinal flora: small amounts of vitamin K are synthesized by intestinal bacteria
  • Mainly diet
  • Intestinal flora: small amounts of vitamin B7, B9, and B12 are synthesized by intestinal bacteria
  • Absorption depends on intestinal and pancreatic function
  • Require lipids for absorption
  • Absorption in the intestine via specific luminal transporters
  • Not stored in the body, except vitamins B9 and B12, which are stored in the liver
    • B9 stores last for approx. 3–4 months.
    • B12 stores last for approx. 3–4 years
  • Oversupplementation → accumulation in adipose tissue → toxic excess
  • Toxicity occurs more often than with water-soluble vitamins
  • Accumulation and subsequent toxicity are very rare (kidneys detect and remove excess in urine).
  • No toxicity has been described for vitamins B1, B2, B5, B7, B9, and B12.

Accumulation and toxicity occur almost exclusively with fat-soluble vitamins.

Overview of fat-soluble vitamins


Active forms Sources Functions Deficiency Toxicity
Vitamin A (retinol)
Vitamin D (calciferol)
  • Cholecalciferol (provitamin D3): exposure to sunlight, fish, milk, plants
  • Ergocalciferol (provitamin D2): plants, fungi, yeast, fortified foods (e.g., milk, cereals, formula)
  • Calcium and phosphate homeostasis
  • ↑ Absorption of Ca2+ and PO43- in the intestine
  • ↑ Bone resorption at high levels
  • ↑ Bone mineralization at low levels
Vitamin E (tocopherol)
  • Meat, eggs, oils, leafy vegetables
  • Antioxidant
Vitamin K (K1: phytomenadione, phylloquinone, phytonadione; K2: menaquinone)
  • Green vegetables, e.g., broccoli, spinach
  • Synthesized by intestinal flora

Fat-soluble vitamins: The fat cat is in the attic (= “ADEK”).



Retinal is a major component of the retinal pigment rhodopsin in rods, which is necessary for vision, while retinoic acid and retinol are involved mainly in gene transcription and tissue maintenance.

Retinol (vitamin A) nurtures the retinA, acts as an Antioxidant, and can be used for Acne treatment.

Vitamin A deficiency [1]

Vitamin A toxicity

Isotretinoin is highly teratogenic. A negative pregnancy test and two forms of contraception are required before prescribing isoretinoin to women.

Therapeutic uses [3]

Vitamin A is contraindicated in pregnancy (teratogenic): A negative pregnancy test and two forms of contraception must be provided before isotretinoin can be prescribed to women.

Vitamin A should be given to measles patients with vitamin A deficiency to boost their immune system and reduce the risk of complications and mortality, especially in countries where vitamin A deficiency is endemic.


Vitamin D is the only vitamin that the human body can produce entirely on its own!


Vitamin D deficiency [6]

Vitamin D toxicity

Therapeutic uses



Vitamin E deficiency

Vitamin E toxicity

Therapeutic uses


  • Synonyms
  • Substance class: naphthoquinones
  • Chemical structure:
    • Vitamin K1
    • Vitamin K2
  • Inactive precursors (provitamins): none
  • Active form: vitamin K hydroquinone
    • Activation occurs via enzyme epoxide reductase.
    • Mutations in the VKORC1 (Vitamin K epOxide Reductase Complex subunit 1) gene impair the reduction of vitamin K epoxide, resulting in deficiencies in vitamin K-dependent clotting factors.
  • Sources
    • Leafy green vegetables (vitamin K1)
    • Eggs, dairy, and meat (vitamin K2)
    • Synthesized in small amounts by intestinal bacteria
  • Transport: via lipoproteins; no specific protein
  • Storage: liver
  • Excretion: bile and urine


Koagulation requires Vitamin K.

Vitamin K deficiency [10]

Warfarin inhibits the vitamin K-dependent synthesis of clotting factors and proteins.

Vitamin K toxicity

Therapeutic uses

Overview water-soluble vitamins
Name Active forms Sources Functions Deficiency Toxicity
Vitamin B1 (thiamine)
  • Whole grain cereals (e.g., whole wheat, brown rice), yeast, pork, legumes
  • No toxicity has been described
Vitamin B2 (riboflavin)
  • Meat, fish, eggs, milk, green vegetables, yeast
Vitamin B3 (niacin, nicotinic acid)
  • Meat (liver), cereals, seeds, legumes
Vitamin B5 (pantothenic acid)
  • No toxicity has been described
Vitamin B6 (pyridoxine)
  • Meat, nuts, whole grains, vegetables

Vitamin B7 (biotin)

  • Eggs, meat, fish, seeds, nuts
  • Cofactor for carboxylases, transcarboxylases, and decarboxylases
  • No toxicity has been described
Vitamin B9 (folate)
  • Green leafy vegetables, dried legumes

Vitamin B12 (cobalamin)

  • Cobamamide
  • Methylcobalamin
  • Meat and dairy products
Vitamin C (ascorbic acid)
  • Fruits: citrus fruits, strawberries, tomatoes
  • Vegetables: potatoes, cabbage, spinach


  • Synonyms: thiamine
  • Inactive precursor (provitamin): none
  • Active form: thiamine pyrophosphate (TPP); activation via intracellular phosphorylation of thiamine
  • Sources: whole-grain cereals (e.g., whole wheat, brown rice), yeast, pork, legumes [12]
  • Resorption: via thiamine transporter-2 (ThTR2)
  • Transport in blood: mainly via blood cells; only ∼10% is free or bound to albumin


Enzymes thiamine is a cofactor for: Thiamine PATs your Back! (Pyruvate dehydrogenase, Alpha-ketoglutaric acid dehydrogenase, Transketolase, Branched-chain ketoacid dehydrogenase).

Vitamin B1 deficiency [13]

In malnourished or alcohol-dependent patients, always administer thiamine before giving dextrose to decrease the risk of precipitating or exacerbating Wernicke encephalopathy.

Vitamin B1 deficiency causes Ber1Ber1.


  • Synonyms: riboflavin
  • Substance class: flavins
  • Inactive precursor (provitamin): none
  • Active forms: flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD)
  • Sources: meat, fish, eggs, milk, green vegetables, yeast[12]
  • Resorption: flavoproteins are cleaved into riboflavin in the intestine
  • Transport in blood: via albumin and immunoglobulins

Active forms of riboFlavin are FMN and FAD.


Vitamin B2 deficiency [14][15]

The 2 C's of Vitamin B2 deficiency: Corneal vascularization and Cheilitis!


Active forms of Niacin are NAD+ and NADP+.


Vitamin B3 deficiency [12]

3 typical features of severe vitamin B3 Deficiency: Dermatitis, Diarrhea, and Dementia.

Vitamin B3 toxicity

Therapeutic use



Vitamin B5 deficiency [12]

Deficiency is rare.

Vitamin B5 is pentothenic acid, as in “penta,” the Greek word for “five.”


  • Synonyms: pyridoxine
  • Substance class: pyridoxine
  • Inactive precursor (provitamin): none
  • Active form: pyridoxal phosphate (PLP)
  • Sources: nuts, whole grains, vegetables, yeast, meat (esp. liver and poultry) [12]
  • Resorption: cleavage by phosphorylases and subsequent resorption by the intestine
  • Transport in blood: partially free, partially bound to albumin


Vitamin B6 deficiency [17]

Vitamin B6 toxicity

Although rare, excess pyridoxine can lead to irreversible sensory neuropathy.

Therapeutic use


  • Synonyms: biotin
  • Inactive precursor (provitamin): none
  • Active form: biotin
  • Sources
    • Plants (e.g., soy products, nuts), animal products (e.g., liver, egg yolk, dairy products)
    • Small amounts are synthesized by intestinal flora
  • Resorption: pancreatic enzyme biotinidase cleaves protein-bound biotin into free biotin active intestinal resorption
  • Transport in blood: mainly free


Biotin is a coenzyme in all carboxylase enzyme complexes that are not vitamin K-dependent.

Vitamin B7 deficiency (biotin deficiency)

Biotin binds to avidin, which is found in raw egg whites: Biotin loves avidin!


  • Synonyms: folic acid, folate
  • Substance class: pteridines
  • Inactive precursor (provitamin): none
  • Active form: tetrahydrofolic acid (THF)
  • Sources
    • Leafy green vegetables, fortified foods (e.g., bread, flour, and cereal)
    • Small amounts are synthesized in intestinal flora
  • Resorption: jejunum via specific transporters
  • Transport in blood: via folate-binding transport proteins
  • Storage: small reserve in the liver (enough for approx. 3–4 months)

Foliage (leafy green vegetables) contains Folate.


Vitamin B9 deficiency [18]

Unlike vitamin B12 deficiency, folate deficiency is not associated with neurologic symptoms.

Therapeutic uses


Vitamin B12 is the only water-soluble vitamin that is stored in the body in significant amounts!


Vitamin B12 deficiency

Therapeutic uses

  • Prenatal supplementation for vegetarians (2 μg per day)


  • Synonyms: ascorbic acid, ascorbate
  • Substance class: lactones
  • Inactive precursor (provitamin): none
  • Active form: ascorbate
  • Sources: fruits and vegetables
  • Resorption
    • Passive resorption via oral mucosa
    • Active resorption in the intestine (especially jejunum)
  • Transport in blood: mainly free, only very small amounts as dehydroascorbate
  • Storage: no specialized vitamin C stores; high concentrations in organs that require vitamin C as a cofactor (e.g., adrenal gland)


Think of vitamin C as “absorbic acid” since it promotes the intestinal absorption of iron.

Vitamin C deficiency [12]

Vitamin C deficiency results in sCurvy due to impaired Collagen synthesis.

Vitamin C toxicity

Therapeutic use

  • Supportive treatment for methemoglobinemia: Vitamin C reduces Fe3+ to Fe2+
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