Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Nicotinamide Adenine Dinucleotide (NAD⁺) and its precursors (such as nicotinamide riboside and nicotinamide mononucleotide) have garnered interest for their potential to support nerve health due to their central role in cellular energy metabolism and mitochondrial function. Preclinical studies, mostly in animal models, suggest that boosting NAD⁺ levels can protect neurons from damage and reduce neuropathic pain by improving mitochondrial function, enhancing axonal regeneration, and reducing oxidative stress and inflammation. For example, studies in mice have shown that NAD⁺ supplementation or increasing NAD⁺ biosynthesis can delay or prevent axonal degeneration in models of traumatic or chemotherapy-induced peripheral neuropathy.

However, clinical evidence in humans remains limited. There are few published clinical trials evaluating NAD⁺ or its precursors specifically for peripheral neuropathy, and those that exist are generally small, preliminary, or focus on related conditions (such as diabetic neuropathy). As a result, while there is a plausible biological rationale and encouraging animal data, robust human evidence is lacking. Thus, NAD⁺ therapy for peripheral neuropathy is not yet standard care, and it should be considered experimental. Larger, well-controlled clinical trials are needed to establish efficacy and safety in this context.

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