#CONy16: Can Vitamin D Be Considered a Disease Modifier for Multiple Sclerosis?

Vitamin D is crucial for our general health and it is known that it modulates immune responses. While large studies have shown that supplemental vitamin D lowers the risk of multiple sclerosis (MS), not everyone is convinced.

In a debate at the 10th World Congress on Controversies in Neurology (CONy) March 17-20 in Lisbon, Portugal, researchers presented their views on vitamin D as a modifier of risk and disease progression in MS.

The debate, “Is vitamin D a substantial disease modifier in patients with MS?” was hosted by Jera Kruja, professor of neurology at the University of Medicine in Tirana in Albania.

Patients with multiple sclerosis show an accumulation of disability over time, and researchers have wondered if there is a biomarker that can explain the geographical, gender, and age distribution of the disease. Some argue that vitamin D might be such biomarker, but researcher Jacek Losy from the Poznan University of Medical Science in Poland is not convinced.

He agreed that there are studies showing that vitamin D lowers the risk of developing MS. Two population-based prospective studies, Nurses’ Health Study and Nurses’ Health Study II, that followed 187,563 women over at least 10 years, showed that vitamin D supplementation lowered the risk of developing multiple sclerosis by 40 percent. Women born to mothers who had a high vitamin D intake during pregnancy were also found to have a lower risk of developing the disease.

Losy also referred to studies showing the beneficial effects of vitamin D on disease progression, citing a prospective study of 145 relapsing-remitting MS patients who had a lower risk of relapse if they had high vitamin D levels, and a small study of 15 multiple sclerosis patients who received vitamin D3 supplements for 48 weeks, resulting in a lower rate of multiple sclerosis exacerbations at the end of the study.

He also mentioned a randomized controlled trial where vitamin D3 was given in addition to interferon beta 1b treatment, in which the patients who received supplements had less disease progression, measured by MRI, than patients receiving only interferon.

Based on these data, Losy said in the debate, “There is definitely an association with vitamin D and the risk of MS.”

Still, despite these findings, Losy argued that this does not constitute enough evidence that vitamin D can impact the course of multiple sclerosis, and he strongly disagreed with the idea of considering vitamin D a substantial disease modifier.

To defend his argument, he cited a clinical trial where 68 MS patients received 20,000 IU of vitamin D3 a week for 96 weeks. The study did not find evidence that the D3 supplements altered the relapse rate, expanded disability status scale (EDSS), MS Functional Composite measurements, or fatigue.

Losy concluded that vitamin D can be considered a supportive therapy in multiple sclerosis, especially given the “growing evidence supporting vitamin D deficiency as a risk factor for MS.”

But given the “inconsistent results on the effect of supplementation of vitamin D on the relapse rate in MS patients,” Losy maintained that researchers need to wait for results from currently ongoing clinical trials, or, more importantly, design large prospective trials to answer questions about a potential disease-modifying role of vitamin D.

Expressing an opposing opinion was Paul Friedemann, professor of neurology, NeuroCure Clinical Research Center in Germany. He believes that in addition to an important role in bone metabolism and calcium homeostasis, vitamin D can interfere in other processes. Due to its immunomodulatory capacity, vitamin D deficiency or disturbance in its metabolism might be a risk factor for the development of autoimmune diseases, including MS.

Friedemann said in the debate that the “immunomodulatory effects of vitamin D are relevant to MS,” supporting the idea that vitamin D supplementation might be a therapeutic option for the disease.

He emphasized that “strong epidemiological evidence points to vitamin D deficiency as an MS risk factor,” and that “animal models of MS suggest a role for vitamin D as a relevant disease-modifier.” Together, these data support an association between low vitamin D levels and the risk of developing MS, he said.

“Does vitamin D in regular diet influence MS risk?” Friedemann asked. “Yes,” he said, “studies show there is a significant risk reduction.”

“There may be a vulnerable phase where vitamin D deficiency causes more risk for MS,” primarily in infancy and adolescence, he said. According to Friedemann, vitamin D may be one of the long-searched-for environmental factors influencing MS development.

To support his arguments, he recalled that “clinical research has demonstrated a strong association of vitamin D levels with relapse rate and MRI activity,” and that the “relapse risk decreases when vitamin D levels are higher.”

“Do vitamin D levels predict disease course? Vitamin D levels are predictive of the further disease course,” Friedemann said, although he also indicated that more studies are needed.

Friedemann is also cautious about vitamin D supplementation as a way to prevent or modify the course of the disease. “The questions as to whether high-dose vitamin supplementation may beneficially influence MS disease course and prognosis remains to be answered,” he said.