What is it?
Riboflavin is a type of B vitamin. It is water soluble, which means it is not stored in the body. You must replenish the vitamin in your body every day.
Riboflavin was originally recognized as a growth factor in 1879 and named vitamin B2 according to the British nomenclature system. It was first isolated from egg whites in 1934 and synthesized in 1935. Riboflavin fluoresces yellow-orange and gives the yellow-white hue to egg whites and milk.
What does it do?
Riboflavin and its active coenzymes function as hydrogen carriers in oxidation-reduction reactions.
Riboflavin has two active coenzyme forms;
- riboflavin 5’-phosphate (R5P; Flavin mononucleotide ) and
- Flavin adenine dinucleotide (FAD)
FAD is a cofactor in many reactions of intermediary metabolism, such as carbohydrate, fat, and amino acid synthesis; FAD and R5P are also necessary for the activation of other vitamins and enzyme systems. Folate (B9) and pyridoxine (B6) are vitamins that rely on riboflavin for activation. Flavocoenzymes, flavoproteins, and metalloproteins are examples of substrates that use FAD as a cofactor to drive reactions. Examples include amino acid oxidases, xanthine oxidases, beta oxidation of lipids, and dehydrogenase reactions in the citric acid cycle.
Riboflavin plays a role in erythropoiesis, epinephrine and norepinephrine catabolism, gluconeogenesis, activation of pyridoxine to active pyridoxal-5-phosphate, conversion of folate to 5-methyltetrahydrofolate (5-MTHF), and conversion of tryptophan to niacin and the synthesis of vitamin B12 is dependent on FAD.
Why supplement?
Riboflavin deficiency
A riboflavin deficiency is defined as ariboflavinosis. Clinical signs and symptoms of deficiency develop after inadequate dietary riboflavin for 3-8 months. Riboflavin deficiency, noted worldwide, is prevalent in underdeveloped countries. In the United States, riboflavin deficiency is common in pregnancy, infancy, alcoholism and the elderly. Rates of deficiency correlate with decreased dietary intake of meat and dairy products.
Riboflavin levels are decreased by interactions with tricyclic antidepressants, phenothiazines, oral contraceptives, and anti-malarial drugs. Probenecid decreases absorption of riboflavin in the gut.
Riboflavin deficiency could result in deficiencies of folate, vitamin B6, and vitamin B12.
Signs and symptoms of deficiency:
- Cataracts - Riboflavin deficiency is implicated in the formation of cataracts due to the concentration of reduced glutathione in the lens and its ability to protect the tissue from oxidative damage. Glutathione reductase, the enzyme responsible for the production of glutathione, is decreased in cataracts, and decreased enzymatic activity of glutathione reductase is associated with riboflavin deficiency.
- Hyperhomocysteinemia - There are two pathways that govern homocysteine metabolism; transsulfuration and remethylation. Transsulfuration is dependent on vitamin B6 and catabolizes homocysteine to cysteine, while remethylation of homocysteine to methionine is dependent on vitamin B12, folate, and riboflavin.
- Migraine
- Carpal tunnel syndrome
- Angular stomatitis
- Seborrhea
- Glossitis
- Neuropathy
- Anaemia
- Cheilosis
- Scrotal and vulvar dermatitis
- Seborrheic dermatitis
- Keratitis
- Ocular changes
- Severe deficiency states are associated with normochromic, normocytic anaemia and neuropathy.
How do I supplement?
Absorption is increased with food and delayed on an empty stomach.
Therapeutic daily dosages for riboflavin range widely, from 3-400 mg; while RDAs are 1.2-1.6 mg.
Dosages over 20 mg have been shown to exceed the carrier-mediated process. Most riboflavin in food is FAD, with a small proportion of free-form riboflavin and FMN comprising the remainder. FAD and FMN are usually found non-covalently bound to enzymes and must be converted back into Riboflavin before being absorbed.
Absorption studies demonstrate riboflavin bioavailability is not affected by different forms of dietary riboflavin.
