Vitamin D supplementation can help overcome low levels of the vitamin often detected in people with amyotrophic lateral sclerosis (ALS). Still, such an alternative therapeutic approach has no meaningful clinical effect on progression of ALS-associated motor symptoms, a study suggests.
Increasing evidence suggests that an active form of vitamin D3 can protect nerve cells from damage triggered by several biological mechanisms, such as oxidative stress, inflammation, mitochondrial dysregulation, and cell death.
These different mechanisms are known to play roles in the underlying processes that support the development and progression of some human neurological disorders, including Alzheimer’s disease, Parkinson’s disease, and ALS.
Taken together, these findings have led researchers to evaluate the impact of vitamin D supplementation on the progression of these neurodegenerative disorders.
Preclinical studies of genetically engineered mice with ALS showed that vitamin D3 deficiency was linked to increased levels of markers of oxidative damage, cell death, and inflammation in the cerebrospinal fluid, which surrounds the brain and spinal cord.
Also, low vitamin D3 levels were found to be related to mice’s poor outcomes in motor functional tests. Importantly, when these ALS mice were treated with high-dose vitamin D3 supplements, researchers noted their motor function improved.
Supported by these positive results, researchers have explored the impact of vitamin D supplementation in patients with ALS.
One such study demonstrated that daily administration of 2,000 international units (IU) of vitamin D for nine months could significantly reduce motor function decline. However, other studies have failed to confirm the positive effects of vitamin D supplementation in ALS patients when administrating high doses.
Italian researchers conducted a pilot study to assess the impact of vitamin D supplementation in a population of ALS patients with low blood levels of active form of vitamin D3 (below 30 ng/mL).
The study enrolled 48 patients who were randomly assigned to take one of three different doses of vitamin D3: 50.000, 75.000, or 100.000 IU per month. Patients’ motor function was evaluated through the ALS Functional Rating Scale (ALSFRS-R) after six months of treatment.
Vitamin D supplementation with the two highest tested doses led to a significant improvement on blood levels of active form of vitamin D3. However, no meaningful changes on patients’ motor function outcomes were reported, regardless of the dose the patients took.
“On the basis of our findings, similarly to previous results (…), the oral supplementation of vitamin D revealed no effects on slowing ALS disease progression,” researchers wrote.
Despite these disappointing results, the team suggests that investigation of vitamin D status and its supplementation still should be recommended in ALS patients to avoid complications of its deficiency.
Future studies should focus on better understanding the bioavailable vitamin D3 in the body, researchers suggested.
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