Riboflavin (Vitamin B2): Interactions

Interactions of riboflavin (vitamin B2) with other micronutrients (vital substances):

Vitamin B complex

Because flavoproteins interfere with the metabolism of some other vitamins such as vitamin B6, niacin, and folic acid, a marked riboflavin deficiency affects diverse enzyme systems. The conversion of naturally occurring vitamin B6 to its co-enzyme form – pyridoxal 5′-phosphate (PLP) – requires an FMN-dependent enzyme – pyridoxine 5′-phosphate oxidase (PPO). Scientific studies in the elderly demonstrate significant interactions between the nutritional status of vitamin B6 and riboflavin. Synthesis of the niacin-containing co-enzymes, NAD and NADP, from the amino acid tryptophan requires an FAD-dependent enzyme. Marked riboflavin deficiency may reduce the conversion of tryptophan to NAD and NADP, increasing the risk of niacin deficiency. Methylene tetra-hydro-folate reductase (MTHFR) is an FAD-dependent enzyme that plays an important role in obtaining a specific folate co-enzyme. This is required to form methionine from homocysteine. As with other B vitamins, increased riboflavin intake is associated with decreased homocysteine plasma levels. It is considered proven that increased riboflavin plasma serum levels with concomitant decreased homocysteine concentrations are mainly seen in individuals who were homozygous for the C677T polymorphism of the MTHFR gene and whose folate intake was low. Such results illustrate the complicated interactions between genetic and dietary factors.

Iron

Riboflavin deficiency clearly has a negative effect on iron metabolism. Although the mechanism has not yet been elucidated, it has been demonstrated in animals that riboflavin deficiency impairs iron absorption, increases intestinal loss of iron, and/or impedes iron binding for hemoglobin synthesis. In humans, it has been found that improved riboflavin status also improved hemoglobin levels. In individuals with both riboflavin and iron deficiency, correction of riboflavin deficiency improved the success of iron therapy for iron deficiency anemia.