Vitamin A

BACKGROUND

Vitamin A is a fat-soluble vitamin which helps maintain normal reproduction, vision and immune function. It comes in a number of forms (as retinol, retinal, retinoic acid or retinyl ester). The term vitamin A is used in the context of dietary requirements to include provitamin A carotenoids that are dietary precursors of retinol. Of the many carotenoids in nature, several have provitamin A activity but food composition data are only readily available for α-carotene, β-carotene and β-cryptoxanthin. Preformed vitamin A is found only in animal-derived foods, whereas dietary carotenoids are found primarily in oils, fruits and vegetables.

Vitamin A intakes or requirements are generally expressed in terms of retinol equivalents (RE). One RE is defined as the biological activity associated with 1 µg of all-trans retinol. Although there is some ongoing discussion in the literature about the conversion rates for carotenes, 6 µg all-trans β-carotene and 12 µg of α-carotene, β-cryptoxanthin and other provitamin A carotenoids have been retained as the conversion figures as being equivalent to 1 RE. These traditional conversion rates align more with the sources of carotenes in the Australian and New Zealand diets. They are also in line with the most recent decision of the FAO, (FAO:WHO 2001) who concluded that the literature to date was insufficient to justify a change in conversion rates.

1 µg Retinol Equivalent = 1 µg of all-trans retinol
= 6 µg all-trans β-carotene
= 12 µg of α-carotene, β-cryptoxanthin and other provitamin A carotenoids
1 International Unit (IU) retinol = 0.3 µg Retinol Equivalents

Retinol is required for the integrity of epithelial cells throughout the body (Gudas et al 1994). Retinoic acid regulates the expression of various genes that encode structural proteins, enzymes, extracellular matrix proteins and retinol binding proteins and receptors. Retinoic acid plays an important role in embryonic development, particularly in the development of the spinal cord and vertebrae, limbs, heart, eye and ears (Morris-Kay & Sokolova 1996). It is also required to maintain differentiation of the cornea and conjunctiva, preventing xerophthalmia, as well as for photoreceptor rod and cone cells in the retina (Sommer & West 1996). The retinal form of vitamin A is also required by the eye to change light to neural signals for vision (Saari 1994). Retinol and its metabolites are necessary for maintenance of immune function (Katz et al 1987, Trechsel et al 1985, Zhao & Ross 1995).

An adequate supply of vitamin A also plays a role in preventing morbidity and mortality from infectious disease, particularly in children (Glasziou & Mackerras 1993). Infection and infestation can cause malabsorption of vitamin A (Mahalanabis et al 1979, Sivakumar & Reddy 1972, 1975). The matrix of foods eaten can affect the release of carotenoids from foods, however, processing of food (cutting up, cooking etc) greatly improves availability and thus absorption of carotenoids from foods (Micozzi et al 1992, Tang et al 2000, Torronen et al 1996). Some studies show improved absorption of carotenoids with increased fat intake (Jalal et al 1998, Reddy & Srikantia 1966, Roels et al 1963) but the data are not consistent (Borel et al 1997, Figuera et al 1969).

Positive interactions between iron or zinc status and vitamin A status have been reported in animal studies (Amine et al 1970, Rosales et al 1999) or within human population groups in developing countries (Bloem et al 1989) but the relevance to the Australia and New Zealand population is unclear. Deficiency can result in abnormal dark adaptation, followed by xerophthalmia but is uncommon in Australia and New Zealand. The New Zealand Children's Survey, 2002 (MOH 2003) did, however, state that a significant proportion of Pacific children and Maori males might be at risk of inadequate intakes. Chronically high levels of alcohol ingestion can negatively affect vitamin A status through an effect on the liver (Wang 1999).

Vitamin A status has been assessed using a variety of indicators including a dark adaptation test (Carney & Russell 1980), a pupillary response test (Stewart & Young 1989), plasma retinol concentration (Underwood 1984), total liver reserves by isotope dilution (Bausch & Rietz 1977, Furr et al 1989), relative dose response methods (Amedee-Manesme et al 1984, 1987, Loerch et al 1979, Mobarhan et al 1981) and/or immune function assessment (Butera & Krakowka 1986, Carman et al 1989, 1992, Cohen & Elin 1974, Friedman & Sklan 1989, Smith et al 1987). However, these methods have limitations in the context of setting EARs for the population. They are too specific (ie only related to visual outcomes), accurate only across a limited intake range or susceptible to confounding (FNB:IOM 2001).