Vitamin E deficiency has been observed in individuals with severe malnutrition and conditions that result in poor absorption of fat from food (e.g., children with cystic fibrosis)
Severe vitamin E deficiency results mainly in neurological symptoms, including impaired balance and coordination (‘ataxia’), injury to the sensory nerves (‘peripheral neuropathy’), muscle weakness (‘myopathy’), and damage to the retina of the eye (‘pigmented retinopathy’).
The developing nervous system appears to be especially vulnerable to vitamin E deficiency: children who have severe vitamin E deficiency from birth and are not treated with vitamin E rapidly develop neurological symptoms.
In contrast, symptomatic vitamin E deficiency in healthy adult individuals who consume diets low in vitamin E has never been reported (3, 70).
Although overt vitamin E deficiency is rare, marginal intake and status is relatively common. A recent study systematically reviewed the published literature reporting vitamin E intake levels and serum concentrations to obtain a global overview of α-tocopherol status. Applying an RDA (recommended daily allowance) of 15 mg/day and EAR (estimated average requirement) of 12 mg/day to all populations with a minimum age of 14 years, 82 and 61 % were below the RDA and the EAR, respectively. Regarding serum concentrations, globally 13 % were below the functional deficiency threshold concentration of 12 µmol/L, mostly for newborns and children. Several prospective observational studies suggest that a serum α-tocopherol concentration of ≥30 µmol/L has beneficial effects on human health. Of the reported study populations and subpopulations, only 21 % reached this threshold globally. Thus, α-tocopherol status is inadequate in a substantial part of the studied populations (84).
Authored by Dr Peter Engel in 2010, reviewed and updated by Dr Szabolcs Peter on 18.06.2017
