Synopsis

Source of validity: Scientific
Rating (out of 5): 4

Vitamin B2, also known as riboflavin, is supported by scientific evidence for its role in mitochondrial function. Riboflavin acts as a precursor for the cofactors flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), both of which are essential for the activity of several mitochondrial enzymes involved in the electron transport chain and energy (ATP) production. Deficiency of riboflavin impairs mitochondrial oxidative phosphorylation, leading to reduced cellular energy output and increased oxidative stress. Clinical studies have demonstrated that riboflavin supplementation can improve mitochondrial function in certain disorders, such as multiple acyl-CoA dehydrogenase deficiency (MADD) and some mitochondrial myopathies. Additionally, riboflavin has been studied as a supportive treatment in migraine, which is hypothesized to involve mitochondrial dysfunction. These findings are documented in peer-reviewed literature, including reviews and clinical trials, affirming riboflavin’s biochemical and physiological necessity for mitochondrial health. However, while there is strong mechanistic and clinical support for riboflavin’s involvement in mitochondrial processes, the evidence for benefit in people without a deficiency or specific mitochondrial disorder is less robust. Overall, the use of Vitamin B2 to support mitochondrial function is justified by scientific understanding of its metabolic role and clinical evidence from deficiency and certain mitochondrial disorders.

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