Dietary sources of vitamin A
Vitamin A refers to retinol and its active metabolites, retinal and retinoic acid (5). Vitamin A is found in the diet as preformed retinol esterified to fatty acids. Preformed retinol is found in animal source foods such as liver, fish liver oils, dairy products, egg yolk, and breast milk. Provitamin A (PVA) carotenoids are found primarily in plant source foods such as dark green leafy vegetables (spinach, kale, etc.) and yellow or orange coloured fruits or vegetables (mango, papaya, carrot, pumpkin, orange-fleshed sweet potato), although PVA-carotenoids can also be found in animal source foods (liver, egg yolk) and in breast milk (1, 5).
Bioavailability
β-carotene, α-carotene and β-cryptoxanthin are the most common PVA carotenoids in human diets. PVA carotenoids can be bioconverted to retinol in human intestinal cells (5). Theoretically, β-carotene has twice the vitamin A activity of α-carotene and β-cryptoxanthin based on its chemical structure. When enzymatically cleaved in the central position, β-carotene can yield two molecules of retinol whereas α-carotene and β-cryptoxanthin can yield one molecule of retinol (5). Many diet and host-related factors can affect the bioavailability of PVA-carotenoids (6). Dietary fat and the use of food processing methods that disrupt the food matrix can enhance the bioavailability of PVA-carotenoids. The US Institute of Medicine (IOM) and the FAO/WHO have proposed vitamin A equivalence factors for dietary PVA-carotenoids. The US IOM factors are based on the retinol activity equivalent (RAE), where the 1 µg RAE is equivalent to 1 µg retinol, 12 µg β-carotene and 24 µg α-carotene or β-cryptoxanthin (7). The FAO/WHO factors are based on the retinol equivalent (RE), where 1 µg RE is equivalent to 1 µg retinol, 6 µg β-carotene and 12 µg α-carotene or β-cryptoxanthin (8). The values proposed by the US IOM and the FAO/WHO differ because of a difference in interpretation of data on absorption of dietary PVA-carotenoids (1).
Food fortification with vitamin A
Populations in low-income countries tend to rely mainly on PVA-carotenoids from plant source foods to meet their vitamin A needs because these foods tend to be more accessible and affordable than animal source foods (5). Food fortification is used as a strategy for increasing dietary vitamin A intake in many countries (9) (for more information, see the WHO publication (2006) Guidelines on Food Fortification with Micronutrients).
Staple foods such as cooking oil, sugar, wheat flour, and margarine, and processed foods such as infant cereals and snack foods have been fortified with vitamin A. Biofortification is used as a strategy for increasing intake of dietary PVA-carotenoids by breeding varieties of staple crops such as maize, orange-fleshed sweet potato, cassava and banana that contain higher amounts of PVA-carotenoids than traditional varieties (10) (for more information, see WHO eLENA – Biofortification of crops with vitamins and minerals; and this page from Harvest Plus).
Home-fortification is strategy for increasing dietary VA intake by providing households with sachets of micronutrient powders or micronutrient fortified lipid-based nutrient supplements that can be added to foods prepared in the home for young children (11)(see see WHO eLENA –Home fortification of foods with multiple micronutrient powders for health and nutrition in children under two years of age).
Supplementation is another strategy that is used to improve vitamin A status in young children in populations at risk of deficiency in low and middle-income countries. The WHO has developed a guideline for providing high-dose vitamin A supplements to children 6-59 months of age (12).
Are there populations at risk of excessive vitamin A intakes?
Excessive intake of preformed vitamin A from natural food sources is rare, although adverse health effects have been reported in individuals who consumed polar bear liver, which contains very high amounts of preformed vitamin A (13). High intake of PVA-carotenoids does not result in excessive body stores of vitamin A because intestinal bioconversion of PVA-carotenoids to vitamin A is downregulated when vitamin A status is adequate (5). There is concern that excessive vitamin A intake may occur in populations exposed to multiple vitamin A intervention programmes that provide preformed vitamin A, such as food fortification, high-dose supplementation, and home-fortification interventions (14). New biomarkers are needed to assess risk of excessive vitamin A intake and status. Vitamin A intervention programs should be monitored to assess the efficacy and safety of the interventions.