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Vitamin D Deficiency and Possible Role in Multiple Sclerosis
Michael F Holick, 1 Stuart Cook, 2 Gustavo Suarez 3 and Mark Rametta 4
1. Boston University School of Medicine, Boston, US; 2. Department of Neurology, New Jersey Medical School, Rutgers,New Jersey, US;
3. Global Medical Affairs, Neurology, Bayer HealthCare Pharmaceuticals, Inc. Whippany, New Jersey, US; 4. US Medical Affairs, Neurology,
Bayer HealthCare Pharmaceuticals, Inc., Whippany, New Jersey, US
Abstract Vitamin D is not only an essential nutrient for bone homeostasis but has also been implicated in many other disorders including
cardiovascular disease (CVD) and autoimmune diseases. Here we review the problem of vitamin D deficiency and guidelines to help
achieve adequate levels in both the general population and in multiple sclerosis (MS) patients and its role in MS and impact on treatment.
Although there is a lack of consensus on vitamin D deficiency and insufficiency, they have been defined as a serum level of 25(OH)D
<50 nmol/L or 52.5–72.5 nmol/L, respectively. Deficiency is common in all age groups. Vitamin D is probably involved in the prevention
of a number of disease states and 25(OH)D is thought to regulate at least 2,000 genes. Vitamin D toxicity is very rare, with none seen
at doses up to 20,000 IU/day. However, the majority of primary care clinicians are not aware of the recommended dose for vitamin D
supplementation and optimum serum level in terms of patients with MS. Several organisations have concluded that vitamin D screening
cannot be recommended in the general population. Guidelines have been published on treatment and prevention of vitamin D deficiency,
particularly for at-risk groups and during pregnancy. There is much evidence for the protective effects of vitamin D in MS. A higher level of
sun exposure and intake of vitamin D as well as of serum 25 (OH)D, are associated with a lower risk of MS. It also has a beneficial effect on
the clinical course of MS, such as lowering the risk of relapses. Growing evidence indicates that the effects of interferon-beta are additively
enhanced by 25(OH)D in MS and this may be due to its modulating vitamin D metabolism.
Keywords Vitamin D, 25-hydroxyvitamin D, deficiency, supplementation, multiple sclerosis, cardiovascular disease
Disclosure: Michael F Holick serves as a consultant for Bayer HealthCare Pharmaceuticals, Inc. Stuart Cook has received prior grant support from Bayer HealthCare
Pharmaceuticals, Inc. and Biogen and has received prior honoraria from Bayer, Biogen and EMD Serono. Gustavo Suarez is an employee of Bayer HealthCare Pharmaceuticals.
Mark Rametta is an employee of Bayer HealthCare Pharmaceuticals.
Acknowledgement: Medical writing support, including preparation of the drafts under the guidance of the authors, was provided by Ray Ashton, Richmond Medical
Communications. and funded by Bayer HealthCare Pharmaceuticals, Inc. All named authors meet the criteria of the International Committee of Medical Journal Editors for
authorship for this manuscript, take responsibility for the integrity of the work as a whole and have given final approval for the version to be published.
Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, adaptation,
and reproduction provided the original author(s) and source are given appropriate credit.
Received: 20 October 2015 Accepted: 30 November 2015 Citation: European Neurological Review, 2015;10(2):131–8
Correspondence: Michael F Holick, Boston University School of Medicine, 85 E. Newton St Fuller Building, Boston, US. E: [email protected]
Support: The publication of this article was supported by Bayer HealthCare Pharmaceuticals, Inc. The views and opinions expressed in the article are those of the authors
and not necessarily those of Bayer HealthCare Pharmaceuticals, Inc.
Vitamin D is an essential nutrient for bone homeostasis that has also
been implicated in numerous other disorders, such as cardiovascular
disease (CVD) and autoimmune diseases. Originally vitamin D
in MS and its impact on MS treatment. In addition, the extent and
consequences of vitamin D deficiency and guidelines to help the
general population and those with MS achieve sufficient levels will
deficiency was associated only with rickets and it was considered
that the fortification of food resolved this disorder. However, it is now
realised that rickets represents just one manifestation of vitamin D
deficiency. 1,2 The recommended Dietary Reference Intakes are solely
based on the skeletal effects of vitamin D, with the recommended
dietary allowance (RDA) ranging from 400 to 800 IU/day depending
on age as recommended by the Institute of Medicine to maintain
blood levels of 25-hydroxyvitamin D (25[OH]D) of at least 50 nmol/L
(20 ng/mL). However to achieve non-skeletal benefits of vitamin D, a
multitude of studies have suggested that maintenance of a level of
25[OH]D >30 ng/mL may be required. The majority of primary care
clinicians are not aware of the recommended dose for vitamin D
supplementation and the optimum level in terms of patients with
multiple sclerosis (MS). This article reviews the role of vitamin D
TOU CH MED ICA L MEDIA
Vitamin D Deficiency and its Consequences
There is considerable debate on the blood level of 25[OH]D that
constitutes deficiency in both the general population and with respect
to certain disorders, such as MS. Conflicting recommendations have
been published by different organisations. Experts disagree on the
optimal 25(OH)D concentration and thus many definitions of deficiency
and insufficiency have been proposed. In the general population, a
serum level of at least 50 nmol/L 25(OH)D is generally considered to be
required for maximum bone health and thus vitamin D deficiency has
been defined as a 25(OH)D <50 nmol/L. 3,4 The Endocrine Society also
recognised that vitamin D had non-skeletal health benefits, and defined
vitamin D insufficiency as a 25(OH)D level of 51–74 nmol/L.