NHS Evidence – Complementary and alternative medicine – Guest editorial: Vitamin D to prevent MS?

NHS Evidence – complementary and alternative medicine

formerly a Specialist Library of the National Library for Health

Guest editorial: Vitamin D to prevent MS?

Could supplementation of something as safe as vitamin D prevent MS? A series of studies offer the suggestion that this may be the case and following significant media coverage clinicians running MS clinics know that this is becoming a familiar theme. What is the background?

The striking variation in MS prevalence with latitude – increasing further from the equator  – has exercised epidemiologists for the majority of the 20th century. The first suggestion that this might relate to sunlight was made in 1960 and gained ground with the understanding of the relationship between sunlight exposure and vitamin D production. Limited vitamin D in the western diet (oily fish, sealion and polar bear are good sources…) means that production in the skin is the major source. A significant proportion of populations in temperate regions are deficient, particularly in winter months.

The discovery that vitamin D influences immune function – exerting anti-inflammatory influence on immune function (Smolders et al, 2008) – offered biological plausibility.

Circumstantial support comes from the observation of seasonal variation in birth rate, more patients with MS are born in May than November (Willer CJ, 2005), suggesting a seasonal environmental factor influencing disease risk in utero. Additional studies have shown children and adults with MS to be relatively deficient in vitamin D (Ascherio A, 2007) and that supplementation may reduce disease risk (Munger KL, 2004).

Further data comes from two recent publications. Ramagopalan and colleagues looked for evidence to link genetic predisposition to MS, driven by the association with HLA, to vitamin D (Ramagopalan SV, 2009). They screened the MHC class II region for genetic sequences coding for vitamin D response elements (VDRE) and found one such region, in the promoter region of HLA-DRB1. Sequencing of this region revealed absolute conservation in the MS associated haplotype (HLA-DRB1*15) with variation only in non-MS associated haplotypes. Further studies confirmed the VDRE to be functional and that vitamin D was able to increase expression of HLA-DRB1 on lymphoid cells. The study provides the first biological link between the strongest epidemiological and genetic features of the disease.

Correale and colleagues reported that patients with relapsing remitting MS (N=92), in relapse and remission, had lower vitamin D levels than controls (60) and patients with primary progressive MS (40) and that levels were lowest in relapse (Correale J, 2009). They also studied the effect of vitamin D on CD4+ T cells and showed that vitamin D has the potential to down-regulate auto-immune activity in vitro, suggesting that supplementation may have a role not only in reducing disease risk but also activity.

So how to advise patients? The case for vitamin D supplementation undoubtedly gets stronger, though is far from proven. For who, when and by how much are far from clear.

Supplementation is straightforward and safe – though current RDA (200-400IU/day) are insufficient to reliably maintain adequate levels. No significant problems have been associated with supplementation of 1000IU in children and 4000IU in adults.

Parents with MS, whose children have a 2-4% risk of the disease, will be motivated to consider interventions that may reduce this risk. Should we advise supplementation in pregnancy? Possibly – the seasonal variation in birth rate argues for such an intervention – and again supplementation appears safe. It is difficult to see how large scale, long term, intervention studies can be undertaken to generate the proof that some may require.

For patients with MS the evidence is weakest; here replication of the study from Correale would be welcome. A simple intervention which influences disease risk and outcome would be very welcome – polar bear anyone?

References

Ascherio A, Munger KL. (2007) Environmental risk factors for multiple sclerosis. Part II: Noninfectious factorsAnn Neurol. 61(6):504-13.

Correale J, Ysrraelit MC, Gaitán MI. (2009) Immunomodulatory effects of Vitamin D in multiple sclerosis. Brain 132 (Pt 5):1146-60.

Munger KL, Zhang SM, O’Reilly E, Hernán MA, Olek MJ, Willett WC, Ascherio A. (2004) Vitamin D intake and incidence of multiple sclerosis. Neurology 62(1):60-5.

Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton SM, Dyment DA, Deluca GC, Herrera BM, Chao MJ, Sadovnick AD, Ebers GC, Knight JC. (2009) Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D. PLoS Genet. 5(2):e1000369. Epub 2009 Feb 6.

Smolders J, Damoiseaux J, Menheere P, Hupperts R. (2008) Vitamin D as an immune modulator in multiple sclerosis, a review. J Neuroimmunol. 194(1-2):7-17.

Willer CJ, Dyment DA, Sadovnick AD, Rothwell PM, Murray TJ, Ebers GC; Canadian Collaborative Study Group. (2005) Timing of birth and risk of multiple sclerosis: population based study. BMJ. Jan 15;330(7483):120.

  • Publication Date: 12 Jun 2009
  • Publication Type: Editorial or Opinion Piece
  • Creator: NHS Evidence – neurological conditions Project Team
  • Contributor: Mike Boggild
  • Next Review Date: 12 Jun 2010
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