The results of a new pilot clinical trial showcase the anti-inflammatory effects of a new drug product of interest. This is ChromaDex’s proprietary Niagen (patented nicotinamide riboside, ingredient in monocytes (a type of white blood cell) extracted from two groups: young, healthy subjects and patients diagnosed with systemic lupus erythematosus (SLE).
SLE is an autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs. It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.
The newly published data presents the 18th clinical trial demonstrating the health benefits of boosting NAD+ with Niagen.
Nicotinamide riboside is a part of the vitamin B3 family. It’s found in fruits, vegetables, meat, and milk. Nicotinamide riboside is changed in the body to a chemical called NAD+. The body needs NAD+ for many processes to work normally.
The study was a randomized, double-blinded, placebo-controlled pilot study featuring 35 healthy volunteers (of an average age of 24 and an average body mass index of 24 kilograms per square metre).
The volunteers had their diets supplemented with 1000mg of nicotinamide riboside or with a placebo for seven days. To assess the effects, the researchers extracted white blood cells from the young, healthy subjects as well as from middle-aged lupus patients.
The matched controls were then exposed to an inflammation inducer to assess nicotinamide riboside’s anti-inflammatory effects.
The results laid a foundation for further research into the implications of nicotinamide riboside supplementation for patients with autoimmune disorders like lupus.
According to lead researcher Michael N. Sack: “This study supplies a mechanistic foundation as to how NR blunts monocyte immunity and supports the need for future studies in patients with monocyte-driven inflammatory disease.”
The research findings have been published in the Journal of Clinical Investigation. The research is titled “Boosting NAD+ blunts toll-like receptor-4 induced type-I interferon in control and systemic lupus erythematosus monocytes.”