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Vitamins may be fat soluble (vitamins A, D, E, and K) or water soluble (B vitamins and vitamin C). The B vitamins include biotin, folate, niacin, pantothenic acid, riboflavin (B2), thiamin (B1), B6 (eg, pyridoxine), and B12 (cobalamins). For dietary requirements, sources, functions, effects of deficiencies and toxicities, blood levels, and usual therapeutic dosages for vitamins, see Table 1: Vitamin Deficiency, Dependency, and Toxicity: Recommended Daily Intakes for Vitamins and Table 2: Vitamin Deficiency, Dependency, and Toxicity: Sources, Functions, and Effects of Vitamins .
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Table 1
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| Recommended Daily Intakes for Vitamins |
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Age (yr)
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Folate (μg)
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Niacin (mg NE*)
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Riboflavin (mg)
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Thiamin (mg)
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Vitamin A (μg)
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Vitamin B6 (mg)
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Vitamin B12 (μg)
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Vitamin C (mg)
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Vitamin D (IU)†
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Vitamin E (mg)
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Vitamin K (μg)
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Infants
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0–6 mo
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65
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2
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0.3
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0.2
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400
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0.1
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0.4
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40
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400
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4
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2.0
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7–12 mo
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80
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4
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0.4
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0.3
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500
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0.3
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0.5
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50
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400
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5
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2.5
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Children
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1–3
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150
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6
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0.5
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0.5
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300
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0.5
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0.9
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15
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600
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6
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30
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4–8
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200
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8
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0.6
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0.6
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400
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0.6
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1.2
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25
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600
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7
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55
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Males
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9–13
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300
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12
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0.9
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0.9
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600
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1.0
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1.8
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45
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600
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11
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60
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14–18
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400
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16
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1.3
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1.2
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900
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1.3
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2.4
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75
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600
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15
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75
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19–70
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400
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16
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1.3
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1.2
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900
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1.3
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2.4
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90
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600
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15
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120
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> 70
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400
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16
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1.3
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1.2
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900
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1.7
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2.4
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90
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800 ‡
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15
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120
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Females
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9–13
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300
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12
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0.9
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0.9
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600
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1.0
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1.8
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45
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600
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11
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60
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14–18
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400
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14
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1.0
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1.0
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700
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1.2
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2.4
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65
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600
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15
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75
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19–70
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400
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14
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1.1
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1.1
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700
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1.3
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2.4
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75
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600
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15
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90
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≥ 70
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400
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14
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1.1
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1.1
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700
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1.5
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2.4
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75
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800 ‡
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15
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90
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Pregnant women
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19–50 yr
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600
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18
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1.4
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1.4
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770
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1.9
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2.6
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85
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600
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15
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90
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Breastfeeding women
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19–50 yr
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500
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17
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1.6
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1.4
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1300
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2.0
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2.8
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120
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600
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19
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90
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Upper limit (UL)§
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1000
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35
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ND
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ND
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3000
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100
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ND
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2000
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4000
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1000
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ND
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Note: Recommended dietary allowances (RDAs) are shown in regular type. RDAs are set to meet the needs of 97 to 98% of healthy people.
Adequate intakes (AIs) are shown in bold type. When data to calculate the RDA for a nutrient are insufficient, AIs are based on observed or experimentally determined estimates of nutrient intake by healthy people.
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*1 niacin equivalent (NE) equals 1 mg niacin or 60 mg dietary tryptophan.
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†200 IU of vitamin D equals 5 μg cholecalciferol.
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‡800 IU of vitamin D is recommended for people ≥ 70 yr.
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§UL is the largest amount of a nutrient that most adults can ingest daily without risk of adverse effects. The more the UL is exceeded, the greater the risk of adverse effects.
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ND = not determinable because of lack of data (sources of intake should be limited to foods); RAE = retinol activity equivalents (1 µg RAE of preformed vitamin A= 3.33 IU).
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Adapted from Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Washington, DC: National Academy Press.
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Table 2
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| Sources, Functions, and Effects of Vitamins |
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Nutrient
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Principal Sources
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Functions
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Effects of Deficiency and Toxicity
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Folate (folic acid)
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Fresh green leafy vegetables, fruits, organ meats (eg, liver), enriched cereals and breads
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Maturation of RBCs
Synthesis of purines, pyrimidines, and methionine
Development of fetal nervous system
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Deficiency:
Megaloblastic anemia, neural tube birth defects, mental confusion
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Niacin (nicotinic acid, nicotinamide)
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Liver, red meat, fish, poultry, legumes, whole-grain or enriched cereals and breads
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Oxidation-reduction reactions
Carbohydrate and cell metabolism
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Deficiency:
Pellagra (dermatitis, glossitis, GI and CNS dysfunction)
Toxicity:
Flushing
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Riboflavin (vitamin B2)
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Milk, cheese, liver, meat, eggs, enriched cereal products
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Many aspects of carbohydrate and protein metabolism
Integrity of mucous membranes
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Deficiency:
Cheilosis, angular stomatitis, corneal vascularization
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Thiamin (vitamin B1)
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Whole grains, meat (especially pork and liver), enriched cereal products, nuts, legumes, potatoes
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Carbohydrate, fat, amino acid, glucose, and alcohol metabolism
Central and peripheral nerve cell function
Myocardial function
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Deficiency:
Beriberi (peripheral neuropathy, heart failure), Wernicke-Korsakoff syndrome
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Vitamin A (retinol)
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As preformed vitamin: fish liver oils, liver, egg yolks, butter, vitamin A–fortified dairy products
As provitamin carotenoids: dark green and yellow vegetables, carrots, yellow and orange fruits
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Formation of rhodopsin (a photoreceptor pigment in the retina)
Integrity of epithelia
Lysosome stability
Glycoprotein synthesis
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Deficiency:
Night blindness, perifollicular hyperkeratosis, xerophthalmia, keratomalacia, increased morbidity and mortality in young children
Toxicity:
Headache, peeling of skin, hepatosplenomegaly, bone thickening, intracranial hypertension, papilledema
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Vitamin B6 group (pyridoxine, pyridoxal, pyridoxamine)
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Organ meats (eg, liver) whole-grain cereals, fish, legumes
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Many aspects of nitrogen metabolism (eg, transaminations, porphyrin and heme synthesis, tryptophan conversion to niacin)
Nucleic acid biosynthesis
Fatty acid, lipid, and amino acid metabolism
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Deficiency:
Seizures, anemia, neuropathies, seborrheic dermatitis
Toxicity:
Peripheral neuropathy
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Vitamin B12 (cobalamins)
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Meats (especially beef, pork, and organ meats [eg, liver]), poultry, eggs, fortified cereals, milk and milk products
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Maturation of RBCs, neural function, DNA synthesis, myelin synthesis and repair
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Deficiency:
Megaloblastic anemia, neurologic deficits (confusion, paresthesias, ataxia)
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Vitamin C (ascorbic acid)
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Citrus fruits, tomatoes, potatoes, broccoli, strawberries, sweet peppers
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Collagen formation
Bone and blood vessel health
Carnitine, hormone, and amino acid formation
Wound healing
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Deficiency:
Scurvy (hemorrhages, loose teeth, gingivitis, bone defects)
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Vitamin D (cholecalciferol, ergocalciferol)
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Direct ultraviolet B irradiation of the skin (main source), fortified dairy products (main dietary source), fish liver oils, fatty fish, liver
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Ca and phosphate absorption
Mineralization and repair of bone
Tubular reabsorption of Ca
Insulin and thyroid function, improvement of immune function, reduction of autoimmune disease
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Deficiency:
Rickets (sometimes with tetany), osteomalacia
Toxicity:
Hypercalcemia, anorexia, renal failure, metastatic calcifications
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Vitamin E group (α-tocopherol, other tocopherols)
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Vegetable oils, nuts, legumes
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Intracellular antioxidant
Scavenger of free radicals in biologic membranes
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Deficiency:
RBC hemolysis, neurologic deficits
Toxicity:
Tendency to bleed
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Vitamin K group (phylloquinone, menaquinones)
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Green leafy vegetables (especially collards, spinach, and salad greens), soy beans, vegetable oils
Bacteria in the GI tract after neonatal period
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Formation of prothrombin, other coagulation factors, and bone proteins
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Deficiency:
Bleeding due to deficiency of prothrombin and other factors, osteopenia
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Table 3
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| Potential Vitamin-Drug Interactions |
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Nutrient
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Drug
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Biotin
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Antibiotics, anticonvulsants
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Folate
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Alcohol, 5-fluorouracil, metformin, methotrexate, oral contraceptives, anticonvulsants (eg, phenobarbital, phenytoin, primidone), sulfasalazine, triamterene, trimethoprim
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Niacin
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Alcohol, isoniazid
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Riboflavin
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Alcohol, barbiturates, phenothiazines, thiazide diuretics, tricyclic antidepressants
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Thiamin
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Alcohol; oral contraceptives; thiamin antagonists in coffee, tea, raw fish, and red cabbage
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Vitamin A
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Cholestyramine, mineral oil
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Vitamin B6
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Alcohol, anticonvulsants, corticosteroids, cycloserine, hydralazine, isoniazid, levodopa, oral contraceptives, penicillamine
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Vitamin B12
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Antacids, metformin, nitrous oxide (repeated exposure)
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Vitamin C
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Corticosteroids
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Vitamin D
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Antipsychotics, corticosteroids, mineral oil, anticonvulsants (eg, phenobarbitol, phenytoin, primidone), rifampin
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Vitamin E
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Mineral oil, warfarin
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Vitamin K
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Antibiotics, anticonvulsants, mineral oil, rifampin, warfarin
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Dietary requirements for vitamins (and other nutrients) are expressed as daily recommended intake (DRI). There are 3 types of DRI:
In developed countries, vitamin deficiencies result mainly from poverty, food faddism, drugs (see Nutrition: General Considerations: Nutrient-Drug Interactions and Table 3: Vitamin Deficiency, Dependency, and Toxicity: Potential Vitamin-Drug Interactions), alcoholism, or prolonged and inadequately supplemented parenteral feeding. Mild vitamin deficiency is common among frail and institutionalized elderly people who have protein-energy undernutrition. In developing countries, deficiencies can result from lack of access to nutrients. Deficiencies of water-soluble vitamins (except vitamin B12) may develop after weeks to months of undernutrition. Deficiencies of fat-soluble vitamins and of vitamin B12 take > 1 yr to develop because the body stores them in relatively large amounts. Intakes of vitamins sufficient to prevent classic vitamin deficiencies (such as scurvy or beriberi) may not be adequate for optimum health. This area remains one of controversy and active research.
Vitamin dependency results from a genetic defect involving metabolism of a vitamin. In some cases, vitamin doses as high as 1000 times the DRI improve function of the altered metabolic pathway.
Vitamin toxicity (hypervitaminosis) usually results from taking megadoses of vitamin A, D, C, B6, or niacin.
Because many people eat irregularly, foods alone may provide suboptimal amounts of some vitamins. In these cases, the risk of certain cancers or other disorders may be increased. However, routine daily multivitamin supplements have not been proved to reduce cancer.
Last full review/revision December 2012 by Larry E. Johnson, MD, PhD
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