Riboflavin or vitamin B2 is a member of the group of vitamins referred to as vitamin B complex, which makes it a water-soluble vitamin. As a drug, healthcare providers often prescribe it in a combined formulation consisting of other B complex vitamins as a prophylactic supplement to prevent the development of deficiency.

Riboflavin deficiency is rare as it is ubiquitous in a variety of food choices. However, individuals following a diet scarce in milk and meat, which are one of the best sources of riboflavin, and also some specific groups of individuals as discussed below may be prone to its deficiency.[1]

Milk and dairy products have very high riboflavin content; dairy intake is the most significant contributor of the vitamin in Western diets, making riboflavin deficiency uncommon among water-soluble vitamins. However, in developed countries, there is an increased intake of semi-skimmed milk, depleting milk of its riboflavin content. Although relatively stable, it easily degrades by light exposure. Milk kept in a glass bottle may be susceptible to degradation through this route.

Grain products possess low natural amounts, but fortification practices ensure that certain breads and cereals have become sources of riboflavin. Therefore, according to an article by Morgan KJ et al., high riboflavin levels were found in those having cereals for breakfast.[2] Fatty fish are also excellent sources of riboflavin, and certain fruits and vegetables, especially dark green vegetables, contain reasonably high concentrations. Vegetarians with access to a variety of fruit and vegetables can avoid deficiency, although intake may be lower than omnivores, and elderly vegetarians are at a higher risk.[3]

Groups of Individuals at a Higher Risk for Low Riboflavin Intake

Pregnant/lactating women and infants

Pregnancy demands higher riboflavin intake as it crosses the placenta. If the maternal status is poor during gestation, the infant is likely to be born riboflavin deficient. Breast milk riboflavin content may reflect maternal intake and can be moderately increased by riboflavin concentration of the mother when maternal intake is low.

Schoolchildren

Riboflavin deficiency among children is present in many regions of the world where there are inadequate levels of milk and meat in their diet.[1] Riboflavin deficiency among children in the Western world seems to largely confine itself to adolescents, especially girls, because of increased metabolic demand.

The elderly

There is an increasing requirement of riboflavin with advancing age as a result of decreased efficiency of its absorption by the enterocytes.[4]

Athletes

Some studies report that vigorous exercise may deplete riboflavin due to its consumption in the metabolic pathways.[5]

Eating disorders

Young women practicing unorthodox eating habits accompanied by excessive exercise to lose weight have shown to have low levels of riboflavin.[5]

Prominent Features of Riboflavin Deficiency

Although clinical features of some vitamin deficiencies are similar and often coexist, the following are more common features of riboflavin deficiency are as follows[6]:

• Lips become red, dry, fissured, or ulcerated.
• Angular cheilitis is often a feature
• The tongue gets dry, atrophic, magenta red or sometimes blackish
• Seborrheic dermatitis may be present on the face
• Scrotum or vulva may get hyperpigmented resembling zinc deficiency
• Conjunctivitis can occur
• Sore throat
• Fatigue

Recommended Daily Allowance for Riboflavin[7]

• Adults (age 19 to 70 years): Women: 0.9 to 1.1 mg/dl and Men: 1.1 to 1.3 mg/d. (These values have their basis on clinical evidence of deficiency in intake less than 0.6 mg/d)
• Adolescents (Age 10 to 18 years): 0.9 to 1.3 mg/dl
• Children (Age 1 to 9 years): 0.5 to 0.6 mg/d
• Infants (Age: 0 to 12 mo): 0.3 to 0.4 mg/d

Apart from supplementation in deficiency, it is also prescribed in some clinical situations as follows: 

Migraine prophylaxis

Riboflavin may be effective for the prophylaxis of migraines (not FDA-approved) to minimize the frequency of attacks.[8]

Neonates undergoing phototherapy

Management of hyperbilirubinemia in the neonatal period is often with phototherapy. But it has been shown to degrade riboflavin and cause a deficiency in the newborns. A prophylactic daily oral dose of riboflavin prevents the development of the deficiency.[9]

Antiretroviral induced lactic acidosis

This rare syndrome results from a group of antiretroviral drugs used to treat HIV infection called nonnucleoside reverse transcriptase inhibitors (NNRTI). Discontinuation of the drug, along with treatment with riboflavin, causes its reversal.[10]

Corneal ectasia

This condition consists of gradual corneal narrowing caused by an alteration in the collagen matrix in the stroma, resulting in protrusion of the cornea in an irregular pattern. Therapy aims at correcting the refractory error until 1990; however, now a radical approach targeting the pathophysiology of the disease by cross-linking the corneal fibers is undertaken where the superficial epithelium gets removed, 0.1% riboflavin is applied for 30 minutes.[11] The cornea receives treatment with UVA for another 30 minutes.[12]

Riboflavin is involved in the metabolism of macronutrients as well as the production of some other B complex vitamins. It is known to participate in redox reactions in the metabolic pathways through cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), derived from riboflavin, by acting as electron carriers.[13] Inadequate intake of riboflavin would be expected to lead to a disturbance in the intermediate steps of metabolism, with specific functional implications.

It is also known for its role as an antioxidant due to its involvement in the regeneration of glutathione, a free radical scavenger.

Additionally, it is involved in growth and development, especially during fetal life, reproduction, and lactation.

A small amount of riboflavin is present in foods as free riboflavin, a majority as its derivative flavin adenine dinucleotide (FAD), and a smaller amount as flavin mononucleotide (FMN). A small amount, however, is also produced by the intestinal bacteria.[14]

For the absorption of dietary riboflavin, a prerequisite is the conversion of FAD and FMN to free riboflavin, catalyzed by enzymes called phosphatases in the enterocyte.[15] Absorption of the vitamin takes place predominantly in the proximal small intestine through a saturable, active, carrier-mediated transport process.

Riboflavin is relatively safe to administer as excess as enterocytes do not absorb the excess. Caution is necessary with the administration of large doses in pregnant women. It may cause urine discoloration (yellow-orange).

There are no absolute contraindications to riboflavin intake.