Using vitamin E supplements for a long time may be associated with a risk reduction of the motor neurone disease amyotrophic lateral sclerosis (ALS), a pooled analysis from the USA of data from five prospective cohort studies suggests.
The large study analyzed longitudinal data from 1,055,546 people as the baseline population, among which 805 with ALS were identified during a follow-up period, ranging from 10 to 18 years across the five cohorts from the Nurses’ Health Study (1976–2004), the Health Professionals Follow-up Study (1986–2004), the Cancer Prevention Study II Nutrition Cohort (1992–2004), the Multiethnic Cohort Study (1993–2005), and the National Institutes of Health-AARP Diet and Health Study (1995–2005) (1). It investigated whether vitamin E intake was associated with ALS. The findings showed a suggestive inverse association between dietary vitamin E intake and ALS, that according to the authors “warrants further studies”.
ALS is the most common form of motor neurone disease (MND) that is characterized by progressive degeneration of the motor cells (neurones) in the brain and spinal cord. These cells control the muscle contractions, but without nerves to activate them, muscles gradually weaken and waste. ALS symptoms may include muscle weakness and paralysis, as well as impaired speaking, swallowing and breathing. For the most part, it does not affect intellect, memory or the senses. The disease progresses incurably and rapidly. Life expectancy is between two and five years from the onset of symptoms. The International Alliance of ALS/MND Associations reports that is more often found in 40–70 year old people, nearly 120,000 cases being diagnosed worldwide each year. 10% of all cases are inherited (genetic) and 90% of them sporadic without familial background.
The study was based on the suggestions of pprevious research, that a role for oxidative stress in the pathogenesis of ALS is supported by the presence of biomarkers of oxidative damage in sporadic ALS patients, and also by the occurrence of genetic ALS among carriers of mutations in the copper/zinc superoxide dismutase gene (SOD1), a critical component of cellular antioxidant defence. Vitamin E as an important cellular antioxidant has been shown to delay the onset of the clinical disease on animal model (transgenic mice). The authors point out that despite of ineffective vitamin E supplementation shown in randomized trials of patients with ALS, “it remains possible, that high vitamin E intake in apparently healthy persons could reduce disease risk or delay its onset”. Their results confirmed the inverse association between high dietary vitamin E intake and developing ALS, as reported from a recent case-control study from the Netherlands, but revealed no association of overall use of vitamin E supplements with ALS. However, they suggest “that long-term use of vitamin E supplements could be inversely associated with a risk of ALS”. Further studies to confirm a possible positive effect of vitamin E are necessary.