Vitamin B3 Boosts Muscle Health in Mitochondrial Myopathy, Study Suggests
Niacin, vitamin B3, can help to normalize muscle metabolism in people with mitochondrial myopathy, a study based on a small pilot trial in patients suggests.
Titled, “Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy,” the study was published in the journal Cell Metabolism.
Nicotinamide adenine dinucleotide (NAD+) is a molecule that is critical for cell metabolism due to its function as an electron carrier. Niacin is a vitamin used by cells to produce NAD+.
Previous research in a mouse model of mitochondrial myopathy suggested that vitamin B3 supplements could promote the formation of new mitochondria in skeletal muscle and fat tissue, as well as delay disease progression.
A team led by researchers at the University of Helsinki reports the results of a clinical trial (NCT03973203) testing niacin supplements in up to 15 patients with mitochondrial myopathy. People without this disease, who were matched in terms of sex and age to the patient group, were also analyzed (control group).
Trial participants were given the vitamin B3 supplements starting at 250 mg a day, with the dose increased by 250 mg/day every month up to a maximum of 750 mg to 1,000 mg daily. Patients were given supplements for a total of 10 months, and controls for four months.
At baseline (study start), results showed that patients with mitochondrial myopathy had lower-than-normal levels of NAD+ in their blood and muscle tissue.
Following the use of niacin supplements, NAD+ levels in patients blood rose by as much as eight-fold, and the levels of NAD+ in muscle rose to levels indistinguishable from those observed in controls.
Muscle strength and the formation of new mitochondria (mitochondrial biogenesis) increased in all participants after niacin supplementation.
Overall, the metabolic profile of patients with mitochondrial myopathy shifted to be more similar to that of healthy controls after niacin’s use.
“Our results are a proof-of-principle that NAD+ deficiency exists in humans and that NAD+ boosters can delay progression of mitochondrial muscle disease,” Anu Suomalainen-Wartiovaara, a professor at the University of Helsinki and study co-author, said in a press release. “The study is a significant leap in the development of targeted therapy options for energy metabolic diseases.”
The researchers, however, noted that niacin supplements are best taken by individuals who have demonstrably low NAD+ levels, as seen, for example, in blood tests.
“Our evidence indicates that blood analysis is useful in identifying NAD+ deficiency and points niacin to be an efficient NAD+ booster for treating mitochondrial myopathy,” the researchers wrote.