Neurodegeneration in equine grass sickness is not attributable to niacin deficiency.

Summary

Equine grass sickness remains a poorly understood condition characterised by neurodegeneration, prompting McGorum and colleagues to investigate whether niacin deficiency might be a contributory factor, given niacin's critical role in maintaining neural function and the potential for mycotoxigenic fungi on pasture to produce niacin antagonists. The team compared niacin status markers in affected horses, at-risk controls, and unaffected horses, measuring serum and tissue niacin concentrations alongside relevant biochemical indicators. Contrary to their hypothesis, horses with EGS showed normal niacin levels and metabolism comparable to healthy controls, effectively ruling out acute niacin deficiency as a primary mechanism in disease pathogenesis. Whilst this finding eliminates one proposed aetiological pathway, it underscores that EGS neurodegeneration likely involves different metabolic or toxicological mechanisms—information that should redirect research efforts and reassure practitioners that niacin supplementation is unlikely to represent a preventative or therapeutic strategy for this condition.

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Key Findings

• •The study tested the hypothesis that acute niacin (vitamin B3) deficiency contributes to neurodegeneration in equine grass sickness
• •Niacin deficiency was hypothesized to result from ingestion of niacin antagonists produced by pasture mycotoxigenic fungi
• •The research investigated whether neural homeostasis disruption through niacin deficiency plays a role in EGS pathogenesis

Conditions Studied

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