Vitamin C modulates gene expression to control inflammation

Vitamin C supplementation is controversial because, as with most any other micronutrient, taking it is only going to help when it is needed due to deficiency or increased demand (a fact often overlooked in flawed studies). A fascinating study just published in the journal Genes and Nutrition reveals that vitamin C supplementation in a non-deficient, normal physiologic state has no significant effect. But in the presence of an inflammatory trigger vitamin C modulates gene expression to control inflammation. The authors state:

"In order to study the effects of vitamin C supplementation on gene expression and compare its action between physiological and inflammatory conditions, a pilot study was set up utilizing microarray and qPCR technologies."

They supplemented healthy volunteers with 1 gram of vitamin C per day for five consecutive days and examined peripheral blood mononuclear cells (PBMNC) before and just after the last supplementation for RNA expression. They also treated the PBMNC with lipopolysaccharide (LPS, a stimulator of inflammation), and again quantified gene expression. Their observations are revealing:

"Only a very moderate effect on the baseline gene expression modulation was associated with vitamin C supplementation. However, in spite of the limited number of subjects analyzed, vitamin C supplementation resulted in a markedly different modulation of gene expression upon the inflammatory stimulus, specifically at the level of the MyD88-dependent pathway and of the anti-inflammatory cytokine IL-10 synthesis."

The authors articulate the significance of their findings:

"This study suggests that vitamin C supplementation in healthy subjects, not selected according to a specific genetic profile, consuming an adequate amount of vitamin C, and having a satisfactory vitamin C plasma concentration at the baseline, does not result in a significant modification of gene expression profile. Under this satisfactory micronutrient status, supplementation of vitamin C is “buffered” within a homeostatic physiological equilibrium. Differently, following a second “hit” constituted of an inflammatory stimulus such as LPS, able to trigger a critical burst to the normal physiological state, the higher availability of ascorbic acid emerges, and results in a significant modulation of cell response."

Bottom line: vitamin C supplementation may do nothing in a replete individual free of inflammation, but in the presence of an inflammatory response to an immune trigger it can modulate gene expression in a favorable way to help regulate inflammation. This is an action model to consider for other micronutrients in case management.