Writing in the Journal of Neuroimmunology. the US-based team investigated the potential of different combinations of vitamin D therapy had benefit on the course of multiple sclerosis (MS) in a mouse model of the disease known as experimental autoimmune encephalomyelitis (EAE).
Led by Professor Colleen Hayes from the University of Wisconsin-Madison, the team assessed the outcomes of varying combinations of the active vitamin D hormone calcitriol and vitamin D3 from dietary supplements – finding that an initial single oral dose of calcitriol followed by daily supplementation with dietary vitamin D3 "was a runaway success."
“One calcitriol dose plus vitamin D3 supplementation sustainably reversed clinical EAE signs without inducing hypercalcemia," explained the research team - noting that the protocol 'rapidly and transiently' increased T regulatory (Treg) immune cells in the central nervous system of the mice and sustainably reduced CNS CD4+ T cells, and spinal cord and optic nerve pathology, "thereby promoting clinical recovery."
"All of the animals just got better and better, and the longer we watched them, the more neurological function they regained," explained Hayes.
In the current study, which was funded by the National Multiple Sclerosis Society, Hayes' team compared various vitamin D-based treatments to standard MS drugs. In each case, vitamin D-based therapy was found to be bettere than the drug alternative, the authors revealed – noting that the mice that received them showed fewer physical symptoms and cellular signs of disease.
In the first part of the study Hayes and his colleagues compared the effectiveness of a single dose of calcitriol to that of a comparable dose of a glucocorticoid, a drug that is currently given to MS patients who experience a bad neurological episode.
Calcitriol came out ahead, inducing a nine-day remission in 92% of mice on average, versus a six-day remission in 58% for mice that received glucocorticoid.
"So, at least in the animal model, calcitriol is more effective than what's being used in the clinic right now," says Hayes.
Next, the team tried a weekly dose of calcitriol – finding that such a strategy could reverse the disease and sustained remission indefinitely.
However, Hayes warned that calcitriol can carry some strong side effects and is a "biological sledgehammer" that can raise blood calcium levels in people.
Because of this, they tried a tried a third regimen: a single dose of calcitriol, followed by ongoing vitamin D supplements in the diet.
This "was a runaway success," she said. "One hundred percent of mice responded."
Hayes believes that the calcitriol may cause the autoimmune cells attacking the nerve cells' myelin coating to die, while the vitamin D prevents new autoimmune cells from taking their place.
While she said that she is excited about the prospect of her research helping MS patients someday, Hayes was quick to point out that the current findings are based on a mouse model of disease, not the real thing.
"So it's not certain we'll be able to translate [this discovery to humans]," she said. "But I think the chances are good because we have such a broad foundation of data showing protective effects of vitamin D in humans."
The next step is human clinical trials, a step that must be taken by a medical doctor, a neurologist, she said. If the treatment works in people, patients with early symptoms of MS may never need to receive an official diagnosis.
"It's my hope that one day doctors will be able to say, 'We're going to give you an oral calcitriol dose and ramp up the vitamin D in your diet, and then we're going to follow you closely over the next few months. You're just going to have this one neurological episode and that will be the end of it,'" said Hayes. "That's my dream."
Source:Journal of Neuroimmunology
Volume 263, Issues 1–2, Pages 64–74, doi: 10.1016/j.jneuroim.2013.07.016
"One calcitriol dose transiently increases Helios+FoxP3+ T cells and ameliorates autoimmune demyelinating disease"
Authors: Faye E. Nashold, Corwin D. Nelson, Lauren M. Brown, Colleen E. Hayes