Vitamin B2 (Riboflavin)

Posted on 17 Feb 2011 16:46

By Ken Adams, M.D. and Scott E. Conard, M.D.

Sources and Physiologic Functions

Sources: Liver is an excellent source of riboflavin. Milk, cheese, egg whites, legumes, peanuts, fish, meats, broccoli, spinach, and fortified grains are good sources. The UV component of sunlight destroys Riboflavin. Hence, milk should be protected in opaque cartons from bright light during storage. Proteins, dextrins, and starch decrease the need for this vitamin.

Populations at risk

Alcoholics and poorer populations of the United States may be deficient in Riboflavin, among other nutrients. Deficiency is widespread in under-developed countries. As it is mainly absorbed in the ileum, total/subtotal gastrectomised patients develop a deficiency. Chronic infection, malignancy, pregnancy, lactation, and consumption of broad-spectrum antibiotics and chloramphenicol are other risk factors. A dietary interview conducted in 403 elderly people showed that the majority had sufficient amounts of riboflavin from the diet, but the margin towards deficiency was small. Hence, elderly people should be considered a vulnerable group with respect to the intakes of vitamins and minerals.

An adolescent population ranging in age from 13 to 19 years and of a low socioeconomic status in New York City, was surveyed for riboflavin deficiency. Deficiency was determined from estimation of erythrocyte glutathione reductase activity, an accurate reflector of riboflavin nutritional status. The overall prevalence of deficiency among those not on vitamin supplements was 26.6%. The prevalence did not depend on sex or age. There was a correlation between milk consumption and riboflavin nutritional status. The prevalence was highest among those consuming less than 1 cup/week and least among those taking 3 or more cups a day. The latter group was comparable in this respect to those receiving daily vitamin supplements. Adolescents are at a high risk for nutritional deficiencies because of their notoriously poor dietary habits, and the estimation of riboflavin deficiency may be an indicator of overall nutritional status.

Signs and Symptoms of Deficiency

Lesions of the mouth like Cheilitis, angular stomatitis, and glossitis occur. Cheilitic lesions are painful and may result in bleeding. Purplish discoloration of the tongue - magenta tongue, is seen. Skin lesions include seborrheic dermatitis and rash on the scrotum and vulva. Ocular burning, dim vision, and photophobia are other symptoms.


Riboflavin is essentially non-toxic. After absorption from the gut, it binds loosely to serum albumin and rarely accumulates in the cell. When absorbed in excess, it is promptly excreted in the urine.


The two biologically active forms of Riboflavin are Flavin mononucleotide (FMN) and Flavin adenine dinucleotide (FAD) and are called Flavins. Flavins are used as a cofactor in the energy producing Kreb's cycle at the pyruvate dehydrogenase step. FMN and FAD are each capable of accepting two hydrogen atoms forming FMNH2 and FADH2. Bound to flavoenzymes, they catalyze the oxidation or reduction of a substrate. Flavins are lost from the body as intact Riboflavin, rather than breakdown products. Vitamin status may be assessed by measuring the level of urinary Riboflavin or glutathione reductase assay.

Recommendations: RDA in mg

  • Infants birth to 6 mos - 0.4mg
  • Infants 6 mos to 1 yr - 0.5mg
  • Children 1 yr to 3 yr - 0.8mg
  • Children 4 yr to 6 yr - 1.1mg
  • Children 7 yr to 10 yr - 1.2mg
  • Adolescent males 11yr to 14 yr - 1.5mg
  • Adolescent females 11 yr to 14 yr - 1.3mg
  • Adolescent males 15 yr to 18 yr - 1.8mg
  • Adolescent females 15 yr to 18 yr - 1.3mg
  • Adult males 19 yr to 50 yr - 1.7mg
  • Adult females 19 yr to 50 yr - 1.3mg
  • Adult males 51 yr plus - 1.4mg
  • Adult females 51 yr plus - 1.2mg
  • Pregnant Women - 1.6mg
  • Lactating Mothers (1st 6 months) - 1.8mg
  • Lactating Mothers (2nd 6 months) - 1.7mg

Riboflavin - B2 Food Sources

Food Serving Size/Amount # of mg/serving
Liver (beef braised) 3.5 oz 4.10 mg
Liver (veal braised) 3.5 oz 1.94 mg
Cheddar Cheese 3.5 oz. 38 mg
Monterrey Cheese 1.0 oz. 23 mg
Peanuts (roasted) 1.0 oz. 04 mg
Broccoli (boiled) 1/2 cup. 09 mg
Broccoli (raw) 1/2 cup 41.00 mg
Spinach (boiled) 1/2 cup. 21 mg
Spinach (raw) 1/2 cup. 05 mg
Milk 2% 8 fl oz. 40 mg
Pinto beans (boiled) 1 cup. 16 mg



Riboflavin enhances erythropoiesis and may have a beneficial effect in improving hematologic status in certain conditions like sickle cell disease. The effect of riboflavin supplementation (5mg twice daily for 8 weeks) on reduced blood glutathione (GSH) and iron status was assessed in 18 patients with sickle cell disease (SCD-HbSS). Twelve SCD patients and 13 normal (Hb-AA) subjects served as the control. The total iron binding capacity (TIBC) and serum ferritin (SF) were significantly higher (p < 0.01), but GSH level, hemoglobin and transferring saturation (TS) were significantly lower (p < 0.001) in SCD patients than in normal subjects. The administration of riboflavin elicited a significant increase (p < 0.01) in serum iron and TS, but a non significant increase in SF and circulating Hb. The GSH level varied little in riboflavin supplemented but decreased significantly in unsupplemented SCD. The disparity in GSH concentration might reflect availability of FAD for regeneration of GSH from glutathione. Likewise, the hematological improvement in the supplemented group supports the assertion that riboflavin enhances erythropoiesis. For an effective management of SCD in Africa, a closer attention should be directed to the riboflavin status in hemolytic disorders. In another study, riboflavin deficiency caused a significantly lower glutathione reductase activity and higher methhemoglobin concentrations.


In migraine prophylaxis, a significant breakthrough came from riboflavin 400 mg, which has an outstanding efficacy side-effect profile. A deficit of mitochondrial energy metabolism may play a role in migraine pathogenesis. Riboflavin (400 mg) was compared to placebo in 55 patients with migraine in a randomized trial of 3 months duration. Riboflavin was found to be superior to placebo in reducing attack frequency and headache days. Regarding the latter, the proportion of patients who improved by at least 50%, i.e. "responders," was 15% for placebo and 59% for riboflavin (p = 0.002) and the number-needed-to-treat for effectiveness was 2.3. Three minor adverse events occurred; two in the riboflavin group (diarrhea and polyuria), and one in the placebo group (abdominal cramps). None was serious. Because of its high efficacy, excellent tolerability, and low cost, riboflavin is an interesting option for migraine prophylaxis and a candidate for a comparative trial with an established prophylactic drug.

Aphthous ulcers

In an evaluation of the thiamine, riboflavin, and pyridoxine (vitamin B1, B2 and B6) status of 60 patients with recurrent mouth ulcers, 17 patients (28.2%) were found to be deficient in one or more of these vitamins. Replacement therapy of these vitamins was given to a study group of deficient patients and a non-deficient group for one month. At the end of therapy and after a follow-up period of 3 months, only those patients who had a B complex deficiency had a significant sustained clinical improvement in their mouth ulcers. Vitamin B1, B2, and B6 deficiencies should, therefore, be considered as another possible precipitating factor in recurrent aphthous ulceration.


Riboflavin is essentially non-toxic. Deficits in Riboflavin are rare but do occur in malnourished individuals and alcoholics as well as people who have received gastric bypass surgery. Deficiencies mostly manifest as skin and tongue lesions include seborrheic dermatitis and rashes on the scrotum and vulva. Ocular burning, dim vision, and photophobia are other symptoms.

People with sickle cell anemia, migraines, and aphthous ulcers have noted improvement in their conditions with supplementation.


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