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Vitamin B2 (Riboflavin)

Nutrient Name: Vitamin B2, riboflavin.
Synonyms: 7,8-dimethyl-10-(11-D-ribityl)isoalloxazine, 7,8-dimethyl-10-(D-ribo-2,3,4,5-tetrahydroxypentyl)isoalloxazine, flavin, flavine, hepatoflavin, lactoflavin, lyochrome, ovoflavin, riboflavine, uroflavin, vitamin B2, vitamin G.
Trade Names Include: Aqua-Flave, Beflavin, Beflavina, Béflavine, Beflavit, Berivine, Dolo-Neurotrat, Flavaxin, Ribobis, Ribobutin, Ribipea.
Related Substance: Riboflavin-5-phosphate: Alloxazine mononucleotide, coflavinase, cytoflav, flavine mononucleotide, FMN, riboflavin phosphate.

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Anticonvulsant medications
/ /
Anticonvulsant medications, especially those that induce cytochrome P450, may alter riboflavin metabolism and interfere with activity of riboflavin-related coenzymes and deplete riboflavin. Riboflavin is essential to the function of folate, MTHFR, and pyridoxine. Coadministration can mitigate adverse effects. Further research needed.Riboflavin (and folate) coadministration may be beneficial, but interaction can vary depending on medication. Requires clinical management.
Antimalarial drugs
/ / /
Strong evidence indicates that low riboflavin status is protective against malaria and advantageous in reducing the severity of malarial symptoms. Several antimalarial medications appear to act as riboflavin antagonists. Riboflavin intake is generally contraindicated in both prevention and treatment. However, limited research indicates that high doses of riboflavin may exert activity against Plasmodium falciparum . Further research needed.Avoid concomitant riboflavin intake, as well as vitamin E, iron, and folate, except as indicated by extraordinary circumstances and then only under medical supervision.
Antiretroviral agents
Nucleoside (analog) reverse-transcriptase inhibitors (NRTIs)
/ /
Drug-induced mitochondrial toxicity associated with riboflavin deficiency contributes to lactic acidosis in patients treated with NRTIs. Riboflavin coadministration can prevent or reverse these and other adverse effects. Further research warranted to confirm consistent but limited evidence.Coadministration, preferably with thiamine, can be beneficial. Supervise closely and monitor regularly.
Boric acid, borate, and boron
Boron, in various forms, tends to complex with riboflavin and thereby reduce absorption and increase urinary excretion. Effects are rapid, and continued use may cause riboflavin deficiency. Separation of intake can reduce gut absorption interference. Conversely, riboflavin may be used to treat acute boric acid poisoning.Separate intake of boron/boric acid and riboflavin unless binding is intentional.
Phenothiazine antipsychotics
/ /
Chlorpromazine and other phenothiazines can inhibit hepatic flavokinase and conversion of riboflavin to FMN and FAD. Binding and increased excretion may also occur; thus, simultaneous intake might impair activity of both agents. Interrelationships reported linking unipolar depression, low thyroxine status, deficiency of riboflavin, and folate. Riboflavin (or FAD) may protect against chlorpromazine-induced arrhythmia and mitochondrial dysfunction.Consider coadministration of riboflavin (and folic acid), especially in unipolar depression. Separate intake. Evaluate and monitor riboflavin, FAD, and thyroxine status.
/ / / / /
Doxorubicin can inhibit the conversion to FMN and FAD but coadministration of riboflavin may not adequately counteract resulting toxic effects. Binding and increased excretion may also occur; thus, simultaneous intake might impair activity of both agents. Sunlight exposure in the presence of riboflavin may deactivate doxorubicin. Further research needed.Coadministration, especially with coenzyme Q10, can be beneficial but may not be adequate. Separate intake. Sunlight avoidance may be prudent with coadministration. Supervise closely and monitor regularly.
Oral contraceptives (OCs)
/ /
Mixed OCs may reduce levels of riboflavin (as well as B6, folate, and B12). Evidence mixed as to clinical significance of effects, but risk appears higher with high-dose hormones, high metabolic demands, poor nutritional status, and during initial months. Nutritional support may prevent or reverse adverse effects on riboflavin and related nutrients. Continued research necessary for conclusive determination of effects and susceptibility and effective clinical response.Coadministration of a B-complex formulation can be beneficial. No adverse effects probable.
Probenecid can adversely affect riboflavin through several mechanisms, including impaired absorption in gastrointestinal tract, inhibited renal tubular secretion, and decreased urinary excretion. Evidence limited but generally accepted as plausible. Probable that riboflavin administration can prevent or reverse adverse drug-induced effects.Coadminister riboflavin, especially with nutritionally compromised patients and with long-term therapy. Monitor for signs of deficiency.
Propantheline appears to elevate riboflavin levels by decreasing salivary flow and decreasing rate of gastric emptying and gastrointestinal motility. Minimal evidence, but low probability of significant risk due to minimal toxicity of riboflavin. Substantive research necessary for conclusive determination of effects and appropriate clinical response.No response necessary. Patients need not avoid riboflavin in multivitamin.
Tetracycline antibiotics Other antibiotics
Simultaneous intake of riboflavin and other B vitamins with tetracycline-class antibiotics can reduce absorption and bioavailability of both/all agents. Antibacterial effect on intestinal flora and gut ecology can produce secondary adverse effects on B-vitamin status and inflammatory processes.Separate intake if concurrent administration indicated or necessary. Probiotic flora beneficial after antibiotic therapy.
Thyroid hormones

Hypothyroidism and riboflavin deficiency share many characteristics. Triiodothyronine (T3) enhances biosynthesis of FMN through the expression of riboflavin kinase. Thyroid status appears to influence activity of riboflavin (and folate) and response to tricyclic antidepressants and phenothiazines.Coadministration may be beneficial, except with malaria susceptibility or treatment.
Tricyclic antidepressants (TCAs)
/ /
TCAs can adversely affect riboflavin activity (and increase requirements) by impairing absorption and inhibiting synthesis of FMN and FAD. Coadministration may prevent or reverse depletion as well as augment clinical response to TCAs through an additive or synergistic effect. Continued research warranted. Coadministration potentially beneficial in migraine.Coadministration of riboflavin can be protective and may enhance clinical response, especially with deficiency. Consider B1, B6, B12, and folic acid. Check thyroxine status. Supervise closely and monitor regularly.
MTHFR, 5,10-Methylenetetrahydrofolate reductase; FMN , flavin mononucleotide; FAD , flavin adenine dinucleotide.
nutrient description

Chemistry and Forms

  • Riboflavin names:   7,8-dimethyl-10-(11-D-ribityl)isoalloxazine, 7,8-dimethyl-10-(D-ribo-2,3,4,5-tetrahydroxypentyl)isoalloxazine, and 7,8-dimethyl-10-ribitylisoalloxazine.

  • Formula:   C17H20N4O6.

  • Molecular weight:   376.4 daltons.

Riboflavin is stable to heat, oxidation, and acid; it is destroyed by alkali and light, especially fluorescent light. Riboflavin is partially soluble in water.

Riboflavin is a water-soluble member of the B-vitamin family. The originally termed “yellow enzyme,” which became known as “flavin mononucleotide” or “riboflavin phosphate,” was initially synthesized in 1935. The name “riboflavine” was initially chosen because it contained the pentose side chain ribitol, and flavius is Latin for “yellow,” in recognition of the deep color of the crystals formed from the pure vitamin and the deep-yellow color it imparts to urine. The final “e” was later dropped on learning that it really was not an amine. In 1952 the Commission on Biochemical Nomenclature formally adopted the name riboflavin . At this time, riboflavin is the Approved Name for use on pharmaceutical labels in Britain.

Physiology and Function

Riboflavin plays a critical role as a component of several key metabolic substances involved in oxidation of glucose, fatty acids, and certain amino acids; reactions with several intermediaries of the Krebs cycle; activation of pyridoxine phosphate (B6) to form pyridoxal phosphate, its biologically active form; conversion of folate to its coenzymes; conversion of tryptophan to niacin; and support of antioxidant activity through flavin adenine dinucleotide (FAD) and reduced glutathione. Riboflavin exerts minimal direct or intrinsic metabolic activity, and only a small portion of the total flavin pool in the human body remains as riboflavin, primarily stored in the liver. Most is converted into coenzyme derivatives flavin mononucleotide (FMN) and its product, the more predominant FAD, before these flavins form complexes with numerous flavoprotein dehydrogenases and oxidases. Notably, flavokinase, the enzyme required for the production of FAD and FMN, is regulated by thyroxin so that thyroid hormones increase the synthesis of flavin cofactors.

As flavocoenzymes, FMN and FAD participate in oxidation-reduction reactions in metabolic pathways and in energy production through the respiratory chain. The isoalloxazine ring system of riboflavin serves as the functional moiety in both FAD and FMN by acting as a two-electron acceptor in enzymatic biochemical reductions. This property enables FMN and FAD to act as cofactors for flavoproteins, the enzymes involved in oxidation-reduction reactions of organic substrates and in intermediary metabolism. FAD and FMN serve as intermediate hydrogen carriers in the mitochondrial electron transport chain, accepting hydrogen ions and transferring electrons to the cytochrome system as part of the metabolism of carbohydrates to produce adenosine triphosphate (ATP). Riboflavin aids in beta oxidation in lipid metabolism and is involved, as a coenzyme component of the dehydrogenases, in the first step in glucose metabolism.

Xanthine oxidase, nicotinamide-adenine dinucleotide phosphate (NADP)–cytochrome c reductase, andD- andL-amino acid oxidase are among the key riboflavin-dependent flavoenzymes. Succinic dehydrogenase, monoamine oxidase (MAO), and other flavoenzymes have FAD covalently bound to them. As a component of these flavin coenzymes, riboflavin serves as a cofactor in numerous respiratory enzymes, including glutaryl coenzyme A dehydrogenase, erythrocyte glutathione reductase, sarcosine dehydrogenase, NADH dehydrogenase, electron-transferring flavoprotein, and ETF dehydrogenase. Flavocoenzymes are also involved in the biosynthesis of niacin-containing coenzymes from tryptophan (via FAD-dependent kynurenine hydroxylase), the FMN-dependent conversion of the 5′-phosphates of vitamin B6to pyridoxal 5′-phosphate, the FAD-dependent dehydrogenation of 5,10-methylenetetrahydrofolate to the 5′-methyl product, and the vitamin B12–dependent formation of methionine and sulfur amino metabolism.

Riboflavin participates in other self-regulatory and protective processes, particularly by facilitating destruction of reactive oxygen species and prevention of cellular oxidative injury in a range of tissues. Glutathione reductase is a FAD-containing enzyme that generates reduced glutathione, which acts as a cofactor in the formation of glutathione peroxidases, major selenium-containing antioxidant enzymes central to the regulation of lipid peroxidation. The availability of riboflavin is also essential to maintaining the mitochondrial pool of reduced glutathione necessary to the activities of the flavoenzymes reduced nicotinamide-adenine dinucleotide phosphate (NADPH)–cytochrome P450 (CYP450) reductase and NADPH–cytochrome b reductase. Riboflavin may also play a role in maintaining the integrity of erythrocytes and nerve tissue. Flavin reductase , also known as methemoglobin reductase, is an NADPH-dependent enzyme that appears to provide protection against oxidative forms of hemeproteins, such as those involved in reperfusion injury. In this process, riboflavin acts as an antioxidant through its conversion to dihydroriboflavin, with methemoglobin reduced while riboflavin is oxidized. The dihydroriboflavin not only maintains the hemeproteins in their lower oxidation states, but also rapidly reduces higher oxidation states of hemeproteins and prevents peroxidative damage to the heme and protein groups. Moreover, because the 5,10-methylenetetrahydrofolate reductase gene product (MTHFR) is a riboflavin/FAD-dependent enzyme, riboflavin status modifies the metabolic effect of the MTHFR 677C→T polymorphism, a critical factor in regulation of plasma concentrations of total homocysteine (tHcy), coronary artery disease, and colon cancer risk. For individuals who carry the 677C→T polymorphism, improving both riboflavin and folate nutriture is protective.

Riboflavin is also required for gluconeogenesis, erythropoiesis, thyroid enzyme regulation, and the production of corticosteroids. Riboflavin is also important in deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) metabolism and can be found in high concentration in the retina.

In normal physiological settings, riboflavin is readily absorbed in the upper gastrointestinal tract, principally in the duodenum, through a saturable active transport system. The presence of food can increase absorption fourfold when riboflavin is ingested with meals rather than taken separately. The gastric environment is important because acid is responsible for releasing B2from noncovalent bonding in foods so that it may be absorbed. Hepatitis, cirrhosis, or biliary obstruction can also significantly impair its absorption. Riboflavin absorption is increased in hypothyroidism and decreased in hyperthyroidism. Riboflavin and a number of other water-soluble vitamins can be synthesized by the microflora that should normally populate the large intestine. Circulating riboflavin can complex with a variety of proteins, including plasma albumin. Conversion of riboflavin to its coenzymes forms (e.g., FAD) predominantly takes place in the liver, heart, and kidneys, but also to some degree in most tissues. In the body tissue, riboflavin is predominantly present as the coenzyme FAD. Riboflavin is stored in the liver to a limited extent, but hepatic reserves will only reduce to 50% of maximum storage when availability is low. Riboflavin is excreted primarily in the urine, predominantly as metabolites, with a typical half-life elimination of 66 to 84 minutes. Excess riboflavin, approximately 9%, is excreted unchanged, imparting the well-known yellow color to urine. Riboflavin crosses the placenta readily and is also excreted in breast milk.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Treatment of ariboflavinosis (riboflavin deficiency) is the primary application of riboflavin recognized in conventional medical practice. An emerging body of evidence supporting the efficacy of riboflavin for the prevention of migraine and ocular cataract is becoming more widely recognized but is still generally viewed as mixed. Nevertheless, clinical experience and a close review of the literature reveal a solid basis for further research through well-designed and high-powered clinical trials aimed at developing guidelines for therapeutic application. The use of riboflavin in conjunction with antiviral regimens, especially nucleoside analog reverse-transcriptase inhibitors (NNRTIs), is well established, particularly for treatment and prevention of lactic acidosis.

Riboflavin is most often administered in conjunction with other nutrients, especially B vitamins, because its physiological functions and activities as well as its depletion patterns tend to cluster, and their coadministration produces a synergistic effect.

Historical/Ethnomedicine Precedent

Vitamin B2(riboflavin) has not been used historically as an isolated nutrient.

Possible Uses

Anemia, anorexia, aphthous ulcers, ariboflavinosis (riboflavin deficiency), bulimia, burn recovery, burning feet syndrome, carpal tunnel syndrome, cataracts, depression, esophageal cancer (risk reduction and treatment), ethylmalonic encephalopathy, fatigue, glaucoma, human immunodeficiency virus (HIV) support, hyperhomocysteinemia, involuntary eye movement, ischemia-reperfusion injury, malaria, methemoglobinemia (congenital), migraine headache (prophylaxis), mitochondrial encephalomyopathy (MEM), multiple acyl-coenzyme A dehydrogenase deficiency, neonatal jaundice (with phototherapy), Parkinson's disease, posttransplant headache, preeclampsia, red blood cell aplasia, sickle cell anemia, sports performance enhancement, thyroid disorders.

Deficiency Symptoms

Cheilosis, glossitis, and angular stomatitis (cracking at lip corners) are classic deficiency symptoms, but both hyporiboflavinosis and ariboflavinosis can also manifest as lethargy, depression, generalized weakness, hyperemia, edema of the pharyngeal and oral mucous membranes, dermatitis (particularly seborrheic dermatitis affecting the scrotum or labia majora and nasolabial folds), photosensitivity, burning and itching of the eyes, corneal vascularization, and normochromic normocytic anemia, leukopenia, and thrombocytopenia, sometimes associated with pure erythrocyte cytoplasia of the bone marrow. These clinical signs of deficiency in humans may appear at intakes less than 0.5 to 0.6 mg per day. Isolated riboflavin deficiency is rare and usually occurs in conjunction with broader nutritional deficiency patterns, particularly involving other B vitamins and contexts associated with increased vulnerability. Symptoms of niacin and vitamin B6deficiency may also appear because riboflavin is necessary to their metabolic activity.

The U.S. recommended dietary (daily) allowance (RDA) for riboflavin (vitamin B2), as revised in 1998, was established based on dosage level necessary to prevent the pathophysiological changes associated with riboflavin deficiency, not to maintain normal enzyme function, promote optimal health, or treat specific conditions.

The most common cause of insufficient riboflavin status is unbalanced, nutritionally deficient diets, particularly affecting infants and children, elderly persons, low-income populations, and those in areas characterized by deprivation. Individuals in particular groups tend to be especially at risk for riboflavin deficiency, including chronic heavy alcohol use, people with chronic illnesses (especially chronic liver disease), patients with severe burns or sickle cell anemia, patients receiving total parenteral nutrition (TPN) with inadequate riboflavin, and gastric bypass bariatric surgery patients, if they neglect to take high-potency B-complex supplements. Impaired absorption and reduced assimilation of riboflavin can result from abnormal digestion caused by various conditions, including gastrointestinal (GI) infections or parasites, infectious enteritis, GI and biliary obstructions, chronic diarrhea, decreased GI passage time, celiac disease, tropical sprue, malignancy, and resection of the small intestine, as in management of patients with Crohn's enteritis. Infants receiving phototherapy for neonatal jaundice are also at risk for riboflavin deficiency. Inadequate thyroid hormone and cataract formation can also be associated with impaired riboflavin status. Inborn errors of metabolism affecting the formation of a flavoprotein, such as acyl-coenzyme A dehydrogenases, can cause deficiency in relatively rare cases. Children may be at increased risk of deficiency during phases of rapid growth. Riboflavin deficiency is relatively common in children with cardiac disease, especially congestive heart failure. Low milk consumption and lactose intolerance can also contribute to decreased riboflavin intake. Vegetarians tend to have depressed riboflavin levels, and vegans are considered at increased risk of riboflavin deficiency, although nutritional yeast is an excellent source for vegans. Individuals engaged in strenuous athletic activities tend to have increased riboflavin requirements and may be more susceptible to deficiency. Women using oral contraceptives tend to lower levels of riboflavin and other B vitamins. In many women, riboflavin levels tend to be lower during periods of exercise and calorie-restrictive dieting.

Dietary Sources

Even though all plant and animal cells contain riboflavin and it is widely distributed in foodstuffs, few foods provide abundant sources of this essential nutrient. The richest dietary sources of riboflavin are calf liver and other organ meats, torula (nutritional) yeast, brewer's yeast, and mushrooms. Milk products (especially yogurt), spinach, asparagus, broccoli and other leafy green vegetables, egg whites, fish roe, almonds and other nuts, legumes, sunflower seeds, whole grains (especially wild rice), wheat germ, and fortified grains can also contain significant amounts of vitamin B2. Regular daily intake of riboflavin is important because, as with other B vitamins, vitamin B2is not stored in appreciable amounts. Healthy subjects restricted to a riboflavin-free diet may demonstrate symptoms of riboflavin deficiency within 7 days. 1 The requirement for riboflavin appears to be related more to nitrogen balance than to caloric intake.

The availability and stability of riboflavin vary with different food sources. Riboflavin from animal sources is better absorbed and thus exhibits higher bioavailability than from vegetable sources. Vegetarians, and vegans in particular, therefore are more susceptible to inadequate riboflavin intake. The milling and processing of grains usually result in substantial loss of riboflavin because the vitamin is concentrated in the germ and bran. Furthermore, being water soluble, the riboflavin in grains and vegetables is often leached away during cooking, unless those fluids are reused as soups and sauces. The riboflavin in milk is relatively abundant and generally stable, although it was often degraded by light exposure when distributed in clear-glass bottles.

Nutrient Preparations Available

Riboflavin and riboflavin 5′-monophosphate are the most common forms of riboflavin available in supplements. Riboflavin is rarely administered as a monotherapy or dispensed as an individual nutrient; it is almost always part of a multinutrient formulation, particularly as a component of a B-vitamin complex. In general, such coadministration is superior because vitamin B2is most effective in combination with vitamins B1, B3, and B6.

Dosage Forms Available

  • Oral:   Capsule, soft elastic capsule, tablet, enteric-coated tablet, extended-release tablet.

  • Injection:   Injectable riboflavin sodium phosphate is available by prescription. Riboflavin is moderately unstable in glucose–amino acid solutions but is stabilized with addition of a lipid, typically a 3:1 mixture, in TPN admixtures.

Dosage Range


  • Dietary:   5 to 30 mg per day. However, a survey conducted by the U.S. Department of Agriculture estimated that daily riboflavin intake less than the RDA occurs in about a third of Americans. In the United Kingdom the average adult daily diet for men provides 2.24 mg and 1.98 mg for women.

  • Supplemental/Maintenance:   The ideal level of riboflavin intake has not been established, but the 25 to 50 mg typically contained in nutritional supplements is generally considered more than adequate for most individuals.

In the United States the Food and Nutrition Board of the Institute of Medicine of the National Academy of Sciences recommends the following dietary reference intakes (DRIs) for riboflavin:

  • Men (>18 years): 1.3 mg
  • Women (>18 years): 1.1 mg
  • Pregnant women (any age): 1.4 mg
  • Lactating women (any age): 1.6 mg

Pharmacological/Therapeutic: 10 to 100 mg/day, although 400 mg/day is often administered for migraine prophylaxis.

Toxic: None established. The evidence on adverse effects has been deemed insufficient to set a tolerable upper intake level (UL) for riboflavin.

Pediatric (<18 Years)

  • Dietary: 2.5 to 10 mg/day.
  • Infants, birth to 6 months: 0.3 mg/day (AI, adequate intake)
  • Infants, 7 to 12 months: 0.4 mg/day (AI)
  • Children, 1 to 3 years: 0.5 mg/day (RDA)
  • Children, 4 to 8 years: 0.6 mg/day (RDA)
  • Children, 9 to 13 years: 0.9 mg/day (RDA)
  • Adolescents, 14 to 18 years: 1.0 mg/day for females; 1.3 mg/day for males (RDA)

  • Supplemental/Maintenance:   0.4 to 1.8 mg/day.

  • Pharmacological/Therapeutic:   Riboflavin is generally not administered in pharmacological doses to infants or children. Riboflavin at levels five times that in formulas for term infants is often provided in augmented preterm infant formulas (PIFs) administered enterally to very-low-birth-weight (VLBW) infants; 5 mg three times daily has been used during phototherapy for neonatal jaundice.

Toxic: Not established.

Laboratory Values

  • Erythrocyte riboflavin: This test is generally not considered to provide a sensitive index. Levels below 15 µg/dL of red blood cells indicate deficiency.
  • Red blood cell FAD and FMN: Because these forms constitute more than 90% of riboflavin, these levels (obtained after modest hydrolysis from FAD) have been used as indicators of the cellular concentration of riboflavin in its form as coenzyme.
  • Urinary riboflavin: Urinary excretion of riboflavin reflects an excess of current intake beyond tissue requirements. A normal adult excretes 120 µg or more in 24 hours. Excretion of less than 100 µg daily indicates deficiency.
  • Erythrocyte glutathione reductase (EGR) activity coefficients: Stimulation of FAD-dependent EGR in vitro, which relies on an associated oxidation of NADPH, can be readily monitored spectrophotometrically and expressed as an activity coefficient (AC) indicating the ratio of activities in the presence and absence of added FAD. Assessment of this riboflavin-dependent enzyme provides a reliable indicator of functional riboflavin status but has known limitations, particularly in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
  • An activity coefficient less than 1.2 is defined as “acceptable,” 1.2 to 1.4 as indicating low riboflavin status, and greater than 1.4 indicating deficiency.
  • Capillary electrophoresis with laser-induced fluorescence detection: This test may provide an effective tool for accurate assessment of riboflavin status by allowing detection of all riboflavin vitamers below physiological concentrations.

Urinary riboflavin levels are often measured to assess compliance with medication regimens, particularly with patients being treated for alcohol dependence, mental disorders, and other conditions.

High intake levels of riboflavin are known to interfere with the accuracy of many laboratory tests, including urinalysis based on spectrometry, drugs of abuse assays, and fluorometric determinations of catecholamines and urobilinogen.

safety profile


Riboflavin (vitamin B2) is generally considered to be nontoxic at typical supplemental and dietary dosage levels. Its limited intestinal absorption and water solubility make riboflavin toxicity highly improbable.

Nutrient Adverse Effects

General Adverse Effects

Beyond flavinuria, the yellow discoloration of urine, with high doses and extremely rare instances of allergic reactions, riboflavin toxicity in humans is unknown. Although indications of serious adverse effects are lacking, very high doses have reportedly caused itching, numbness, and burning or prickling sensations. Only two minor, nonspecific adverse events (diarrhea and polyuria) were reported during the 4-month course of a clinical trial involving 400 mg per day for migraine prophylaxis. 2 A potential risk from the photosensitizing properties of riboflavin has been raised, but no substantial evidence is available to confirm such a concern as clinically significant.


None has been found on testing or has otherwise been proposed or suspected.

Pregnancy and Nursing

Riboflavin is excreted in breast milk but is generally considered safe during pregnancy and lactation at usual dosage levels.


None has been reported.

Infants and Children

No pediatric adverse effects from vitamin B2have been established.


No contradictions have been established for riboflavin.

Precautions and Warnings

No warnings or precautions have been established for vitamin B2, other than known allergy to constituents of the formulation.

interactions review

Strategic Considerations

The administration of riboflavin as a monotherapy is atypical in conventional practice and nutritionally oriented therapeutics; its use in migraine prophylaxis represents its most well-known monotherapeutic application. Supplementation is usually unnecessary for individuals with a balanced diet and healthy lifestyle, although requirements can be increased with stresses such as poor nutritional intake (of riboflavin and other B vitamins), chronic illness, malabsorption disorders, alcohol consumption, hemodialysis, chemotherapy, or even vigorous athletic activity. The diagnosis of riboflavin deficiency is usually based on the symptoms and evidence of general undernutrition. Angular stomatitis is the most readily observable sign of emerging deficiency but frequently goes unrecognized at early stages. Diagnostic tests to confirm riboflavin deficiency are not readily available or particularly sensitive to functional depletion. In cases of frank riboflavin deficiency, high doses are typically administered orally until symptoms resolve. Impairment and deficiencies involving B vitamins are highly interdependent, and these nutrients are usually most effective when administered concomitantly. Riboflavin is generally considered to be nontoxic at typical supplemental and dietary dosage levels, with flavinuria (yellow-colored urine) being the primary side effect.

Although evidence from focused clinical trials is limited, adverse effects from coadministration appears to be improbable with most medications, given basic intake timing precautions. The major exception is individuals at high risk for malaria or being treated with antimalarial medications. Coadministration of riboflavin is particularly indicated with the several pharmaceuticals that impair riboflavin absorption and the many that inhibit conversion of riboflavin to its active coenzymes, FAD and FMN. The concomitant use of riboflavin and thiamine with the nucleoside analog reverse-transcriptase inhibitors used in HIV pharmacotherapy can prevent or reverse the uncommon but usually irreversible lactic acidosis caused by drug-induced mitochondrial toxicity and riboflavin deficiency. Coadministration with tricyclic antidepressants appears not only to counter drug-induced adverse effects but also to enhance therapeutic response, especially in depressed patients with low folate levels, defective methylation functions, and low thyroxine levels. Less dramatically, riboflavin's lack of toxicity suggests that it can be broadly prescribed to prevent or reverse drug-induced depletion effects, even in the absence of deficiency signs, as with oral contraceptives and CYP450-inducing antiseizure medications. Riboflavin appears to be safe even in the case of the anticholinergic agent propantheline, which can elevate riboflavin levels. Concomitant administration of other B vitamins is often indicated for full effectiveness of vitamin B2.

Tetracycline-class antibiotics, chlorpromazine and d phenothiazine antipsychotics, and boric acid are prominent among the drugs with notable pharmacokinetic interactions with riboflavin, typically involving binding that impairs absorption of both substances. Chlorpromazine and boric acid and its derivatives promote renal excretion of riboflavin. Preliminary evidence suggests that riboflavin could theoretically impair the therapeutic activity of doxorubicin, selegiline, and some sulfa drugs in individuals exposed to sunlight or other bright light.

The role of riboflavin in cardiovascular function is emerging as an area of significant scientific research, providing new data on interactions involving related medications. Research involving patients with migraine demonstrated a decreased mitochondrial phosphorylation potential between migraine attacks and suggests that decreased brain mitochondrial energy reserve between attacks is related to the activity of flavoenzymes, particularly FMN and FAD, in the electron transport chain and the production of cellular energy. The pivotal role of riboflavin in FAD, which is the cofactor for the MTHFR enzyme, as well as the role of MTHFR in the regulation of homocysteine, may bring riboflavin into equal prominence with folic acid, vitamins B6and B12, and possibly thiamine as a key agent in remethylation processes and modulation of risks associated with hyperhomocysteinemia. The antioxidant activity of vitamin B2and its clinical implications have yet to be fully elucidated but are derived from its role as a component of FAD and the role of this cofactor in the production of the antioxidant peptide reduced glutathione, as well as from its conversion to dihydroriboflavin. By affecting the mitochondrial pool of reduced glutathione, riboflavin deficiency in turn affects the activities of the flavoenzymes NADPH-CYP450 reductase, NADPH–cytochrome b reductase, and NADPH-dependent methemoglobin reductase (i.e., flavin reductase).

Oxidative forms of hemeproteins have been implicated in reperfusion injury, and elevated riboflavin levels have been reported to provide protection against such altered hemeproteins and reperfusion injury. 3-6Continued research into these activities and functions will provide new insight into the importance of riboflavin nutriture, suggest expanded therapeutic uses for riboflavin administration, and present new challenges for understanding both beneficial and harmful interactions with conventional medications.

nutrient-drug interactions
Anticonvulsant Medications and Related Barbiturates
Antimalarial Drugs
Antiretroviral Agents, Nucleoside (Analog) Reverse-Transcriptase Inhibitors (NRTIs or NNRTIs)
Boric Acid, Borate, and Boron
Chlorpromazine and Related Phenothiazine Antipsychotics
Doxorubicin and Related Anthracycline Chemotherapy
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Propantheline Bromide (Pro-Banthine)
Tetracyclines and Other Antibiotics
Thyroid Hormones
Tricyclic Antidepressants (TCAs)
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Acetylsalicylic Acid
Beta-1-Adrenoreceptor Antagonists (Beta-Adrenergic Blocking Agents)
Bile Acid Sequestrants
Imidazole Antibiotics
Thiazide Diuretics
Trimethoprim and Trimethoprim-Sulfamethoxazole
nutrient-nutrient interactions
Folate (Folic Acid)
Psyllium, Fiber, and Related Laxatives
Vitamin B 3 (Niacin)
Vitamin B 6 (Pyridoxine)
Vitamin B 12
Vitamin E
Citations and Reference Literature
  • 1.Tillotson JA, Baker EM. An enzymatic measurement of the riboflavin status in man. Am J Clin Nutr 1972;25:425-431.View Abstract
  • 2.Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis: a randomized controlled trial. Neurology 1998;50:466-470.View Abstract
  • 3.Xu F, Hultquist DE. Coupling of dihydroriboflavin oxidation to the formation of the higher valence states of hemeproteins. Biochem Biophys Res Commun 1991;181:197-203.View Abstract
  • 4.Hultquist DE, Xu F, Quandt KS et al. Evidence that NADPH-dependent methemoglobin reductase and administered riboflavin protect tissues from oxidative injury. Am J Hematol 1993;42:13-18.View Abstract
  • 5.Christensen HN. Riboflavin can protect tissue from oxidative injury. Nutr Rev 1993;51:149-150.View Abstract
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