Methylated B-Complex

B vitamins serve as coenzymes in energy metabolism, methylation cycle, neurotransmitter synthesis, and homocysteine clearance. RIBOFLAVIN / FAD CONTEXT (August 9, 2026): A peer-reviewed Immunity 2026 study (Wang et al.) identified flavin adenine dinucleotide — the riboflavin-derived cofactor produced by FAD synthase (FLAD1) — as an endogenous brake on the cytosolic nucleic-acid sensors cGAS and RIG-I, binding directly into their catalytic pockets. Loss of FLAD1 exacerbated sterile autoinflammation AND cellular senescence, placing riboflavin-derived FAD directly on the cGAS-STING inflammaging axis. This is mechanistically interesting given the B2 content of a B-complex, but it must not be over-read: the causal manipulation was intracellular FLAD1-dependent FAD availability in mice and cells, NOT oral riboflavin in humans, and the study provides no evidence that B2 supplementation alters inflammaging. The therapeutic window also cuts both ways — raising FAD would be expected to blunt antiviral type-I interferon at the same time as it damps sterile inflammation. Continue to dose B-complex for methylation and standard B-vitamin repletion indications, not as an anti-inflammaging strategy.