TL;DR
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In the 410-participant NOPARK phase III trial, nicotinamide riboside did not improve the primary clinical measure in people with early Parkinson’s disease over 52 weeks. Scores worsened modestly more in the supplement group than in the placebo group, despite a clear rise in blood NAD levels.
A phase III trial of 410 people with early Parkinson’s disease found that the over-the-counter supplement nicotinamide riboside did not improve clinical outcomes over 52 weeks, with the treatment group’s scores worsening modestly more than those of the placebo group. The NOPARK findings, reported in JAMA, do not support using the NAD-boosting supplement to slow Parkinson’s progression.
The primary outcome was change in total scores on the Movement Disorder Society Unified Parkinson Disease Rating Scale (MDS-UPDRS), which includes a motor examination and assessments of daily living. At week 52, scores had worsened by an average of 2.45 points in the nicotinamide riboside group; the placebo group’s scores trended toward improvement. The adjusted mean difference was 2.72 points (95% confidence interval 0.47 to 4.98; P=0.02).
Researchers also reported greater worsening in nonmotor symptom burden among participants taking the supplement. There was no significant difference between groups in changes to cognitive scores, and brain imaging showed no evidence that treatment slowed or accelerated changes in the dopamine system. The EQ-5D-5L quality-of-life index was lower in the supplement group.
The trial tested 500 milligrams twice daily for one year. Participants were enrolled at 11 centers in Norway, had been diagnosed within the previous two years, and were receiving stable dopaminergic treatment. Adherence was high, with median adherence to nicotinamide riboside reported at 99.6%. Treatment raised blood NAD levels substantially, but that biological change did not correspond to clinical improvement.
What the Results Mean for Supplement Users
Nicotinamide riboside is sold without a prescription as a vitamin B3 form and NAD precursor, and is often marketed in the longevity supplement category. The trial tests a proposed disease benefit, not every possible use of the supplement: its findings specifically do not support nicotinamide riboside as a way to slow early Parkinson’s disease.
The results show that an increase in a biological marker does not necessarily correspond to improvement in a clinical outcome. Although treatment increased NAD metabolism and blood NAD, participants did not show a clinical benefit on the main measure. The investigators said the modest difference was below commonly cited thresholds for a minimum clinically important difference, while noting consistent findings across clinical outcomes and analyses.
The trial does not establish that the supplement caused Parkinson’s to worsen, nor does it settle its safety or value for other groups or purposes. People considering supplements alongside Parkinson’s medication should discuss that decision with a qualified health professional.
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Why Researchers Tested NAD Supplementation
Nicotinamide riboside is a precursor to NAD+, a molecule involved in cellular energy metabolism, DNA repair and inflammation regulation. Animal research and smaller human studies had suggested that raising NAD levels might help in Parkinson’s disease, providing the biological rationale for the larger NOPARK trial.
The randomized study assigned 206 participants to nicotinamide riboside and 204 to placebo. The cohort had a mean age of 66, and 66% were men. Participants had relatively early disease and stable dopaminergic treatment; people with dementia, atypical parkinsonism, other neurodegenerative disorders or recent high-dose vitamin B3 use were excluded. The study is described as the largest trial to date of an NAD-boosting treatment in a neurologic disorder.
“Nicotinamide riboside clearly increased NAD metabolism, but this did not translate into clinical improvement.”
— Charalampos Tzoulis, trial investigator, in a statement
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Why the Scores Worsened More
The trial found an association between treatment assignment and modestly worse scores relative to placebo, but it did not establish why the difference occurred or prove that nicotinamide riboside directly worsened the disease. The researchers proposed that sustained NAD augmentation could have unfavorable biological effects in Parkinson’s disease, or that the supplement might interact with dopaminergic medication; both remain possibilities, not demonstrated explanations.
Interpretation is also limited by the absence of a washout phase, which could have helped distinguish lasting disease progression from effects related to treatment or medication. The investigators said dopamine transporter imaging has limited sensitivity for detecting subtle changes over one year. The placebo group’s lack of apparent disease progression may partly reflect dopaminergic therapy. The study also does not answer whether nicotinamide riboside has effects in other populations or for other outcomes.
Serious adverse events occurred in 8.3% of the supplement group and 14.1% of the placebo group. Hypertension was the most common adverse event in both groups, and most events were judged unrelated or unlikely to be related to treatment. One participant in the nicotinamide riboside group had cardiac arrest and died; the supplied report does not establish that the supplement caused the death.
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Further Trials Will Test Other Uses
Nicotinamide riboside remains under study, but NOPARK’s authors said its results do not support using it to slow Parkinson’s disease. A separate research direction is planned by Niagen Bioscience, which recently announced plans for a large randomized, placebo-controlled trial with Mass General Brigham to study healthy-aging outcomes and related biomarkers.
That planned study addresses different outcomes and does not resolve the Parkinson’s findings. The source report did not provide a start date, full protocol or results for the proposed trial. Any further Parkinson’s research would need to clarify the reasons for the NOPARK score differences and assess outcomes over an appropriate period.
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Key Questions
Did nicotinamide riboside slow Parkinson’s disease in the trial?
No. The 52-week NOPARK trial found no clinical benefit on its primary measure in people with early Parkinson’s disease.
Were outcomes worse for participants taking the supplement?
Average MDS-UPDRS scores worsened by 2.45 points in the supplement group, while placebo scores trended toward improvement. The adjusted difference between groups was 2.72 points. This finding does not by itself prove the supplement caused disease worsening.
Did nicotinamide riboside raise NAD levels?
Yes. The trial reported a substantial increase in blood NAD measures among participants taking the supplement, but the increase did not translate into clinical improvement.
Was the supplement linked to the death in the trial?
One participant in the nicotinamide riboside group had cardiac arrest and died. The available report does not establish that the supplement caused the death; most adverse events were considered unrelated or unlikely to be related to treatment.
Does the study settle whether nicotinamide riboside is useful for other purposes?
No. NOPARK tested whether the supplement could help people with early Parkinson’s disease. It does not answer whether it affects other populations or health outcomes.
Source: rss
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