EUROPE, Netherlands
Barbara M. van Amerongen, DDS, Ph.D.
Department of Molecular Cell Biology and Immunology,
VU University Medical Centre, Amsterdam, the Netherlands.
Department of Cariology Endodontology Pedodontology,
Academic Centre for Dentistry Amsterdam, Amsterdam, The Netherlands.
Born in the Netherlands on January 19, 1950. She went to dental school in Amsterdam, graduated in 1974 and did her PhD in 1985.
In 1998 she joined the Department of Molecular Cell Biology and Immunology and wrote a review about Multiple Sclerosis and vitamin D, with Professors Christine Dijkstra, Paul Lips and Chris Polman at the VU University Medical Center, which was published in 2004. They received a grant from Dutch MS Research for the role of vitamin D in MS (02-492). There we compared vitamin D levels between MS patients and controls in summer and in winter. The article was published in 2009.
References
VanAmerongen BM, Dijkstra CD, Lips P, Polman CH.
Multiple sclerosis and vitamin D: an update.
Eur J Clin Nutr. 2004 Aug;58(8):1095-109. Review.
Department of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands.
Abstract
MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), is a natural immunoregulator with anti-inflammatory action.
The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1 alpha-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH)(2)D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH)(2)D alters dendritic cell and T-cell function and regulates macrophages in EAE.
Interestingly, 1,25-(OH)(2)D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D(3) intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well.
Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.
Kragt J, van Amerongen B, Killestein J, Dijkstra C, Uitdehaag B, Polman Ch, Lips P.
Higher levels of 25-hydroxyvitamin D are associated with a lower incidence of multiple sclerosis only in women.
Mult Scler. 2009 Jan;15(1):9-15. Epub 2008 Aug 13.
Department of Neurology, VU University Medical Center, Amsterdam, the Netherlands.
Abstract
INTRODUCTION:
Multiple sclerosis (MS) is a chronic inflammatory disease with an as yet not fully understood etiological background. The geographical distribution of MS is striking with a prevalence that increases with latitude. For this reason, vitamin D deficiency is considered a possible pathogenic co-factor in MS. MATERIALS AND
METHODS:
To study the role of the vitamin D metabolism in MS, blood samples were taken twice (summer and winter) from 103 patients with MS and 110 healthy controls. Serum concentrations of 25-hydroxyvitamin D (25(OH) D) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) were measured, and detailed information on disease characteristics and environmental factors that might influence the vitamin D metabolite levels was collected.
RESULTS:
Mean serum 25(OH)D and 1,25(OH)(2)D concentrations were significantly higher in summer compared to winter in both patients and controls. Using logistic regression methods, we found that in women for every 10 nmol/L increase of serum 25(OH)D level the odds of MS was reduced by 19% (odds ratio 0.81; 95% confidence interval: 0.69-0.95), suggesting a "protective" effect of higher 25(OH)D serum levels. In addition, also restricted to women, a negative correlation was found between Expanded Disability Status Scale and 25(OH)D levels (r = -0.29, P = 0.020).
CONCLUSIONS:
Our data suggest that higher circulating levels of 25(OH)D are associated with a lower incidence of MS and MS-related disability in women. This may imply clues to the pathogenesis of the sex difference in risk and to the nature of the environmental factors involved in MS.