Vitamin B2, commonly called riboflavin, is one of eight water-soluble B vitamins. Like its close relative vitamin B1 (thiamine), riboflavin plays a crucial role in certain metabolic reactions, particularly the conversion of carbohydrates into sugar, which is "burned" to produce energy. Together, the eight B vitamins, often referred to as B complex vitamins, are also essential in the breakdown of fats and protein. In addition, B complex vitamins play an important role in maintaining muscle tone along the lining of the digestive tract and promoting the health of the nervous system, skin, hair, eyes, mouth, and liver.
Also called vitamin B2, it gives the body energy and helps normal growth of body tissues.
Riboflavin is important to energy metabolism (processing nutrients like protein, fat, carbohydrate and alcohol that have calories to a form of energy that the body can use - ATP), normal eyesight and healthy skin. Foods high in riboflavin are milk, yogurt, cheeses, meat, leafy green vegetables, whole and enriched grains. Riboflavin is an essential vitamin and is easily destroyed by light. Oral contraceptives may cause a riboflavin deficiency as well. Essential for healthy hair, skin and nails; helps treat acne.
Riboflavin is a water-soluble B-complex vitamin, also known as vitamin B2. In the body, riboflavin is primarily found as an integral component of the coenzymes, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN). Coenzymes derived from riboflavin are also called flavins. Enzymes that use a flavin coenzyme are called flavoproteins.
Living organisms derive most of their energy from oxidation-reduction (redox) reactions, which are processes involving the transfer of electrons. Flavin coenzymes participate in redox reactions in numerous metabolic pathways. Flavins are critical for the metabolism of carbohydrates, fats, and proteins. FAD is part of the electron transport (respiratory) chain, which is central to energy production. In conjunction with cytochrome P-450, flavins also participate in the metabolism of drugs and toxins.
Riboflavin deficiency alters iron metabolism. Although the mechanism is not clear, research in animals suggests that riboflavin deficiency may impair iron absorption, increase intestinal loss of iron, and/or impair iron utilization for the synthesis of hemoglobin. In humans, improving riboflavin nutritional status has been found to increase circulating hemoglobin levels. Correction of riboflavin deficiency in individuals who are both riboflavin deficient and iron deficient improves the response of iron-deficiency anemia to iron therapy.
Age-related cataracts are the leading cause of visual disability in the U.S. and other developed countries. Research has focused on the role of nutritional antioxidants because of evidence that oxidative damage of lens proteins from light may lead to the development of age-related cataracts. Two case-control studies found significantly decreased risk of age-related cataract (33% to 51%) in men and women in the highest quintile of dietary riboflavin intakes (1.6 to 2.2 mg/day) compared with those in the lowest quintile (0.08 mg/day). Individuals in the highest quintile of riboflavin nutritional status, as measured by red blood cell glutathione reductase activity, had approximately one half the occurrence of age-related cataract as those in the lowest quintile of riboflavin status, though the results were not statistically significant.
Recently, a cross-sectional study of 2,900 Australian men and women, 49 years of age and older, found that those in the highest quintile of intake for riboflavin were 50% less likely to have cataracts than those in the lowest quintile. A prospective study of more than 50,000 women did not observe a difference between rates of cataract extraction between women in the highest quintile of riboflavin intake (1.5 mg/day) and those in the lowest quintile (1.2 mg/day). However, the range between the highest and lowest quintiles was small, and median intake levels for both were above the current RDA for riboflavin. Although these observational studies provide support for the role of riboflavin in the prevention of cataracts, placebo-controlled intervention trials are needed to confirm the relationship.
Some evidence indicates that impaired mitochondrial oxygen metabolism in the brain may play a role in the pathology of migraine headaches. As the precursor of the two flavin coenzymes (FAD and FMN) required by the flavoproteins of the mitochondrial electron transport chain, supplemental riboflavin has been investigated as a treatment for migraine. A randomized placebo-controlled trial examined the effect of 400 mg of riboflavin/day for three months on migraine prevention in 54 men and women with a history of recurrent migraine headaches. Riboflavin was significantly better than placebo in reducing attack frequency and the number of headache days, though the beneficial effect was most pronounced during the third month of treatment. It should be noted, however, that only about 25 mg of riboflavin can be absorbed in a single oral dose. A more recent study by the same investigators found that treatment with either a medication called a beta-blocker or high-dose riboflavin resulted in clinical improvement, but each therapy appeared to act on a distinct pathological mechanism; beta-blockers on abnormal cortical information processing and riboflavin on decreased brain mitochondrial energy reserve. Though these findings are preliminary, they suggest that riboflavin supplementation might be a useful adjunct to pharmacologic therapy with beta-blockers in migraine prevention.
Levels of important nutrients are often quite low in people with anorexia or bulimia. At least 20% of people with anorexia admitted to a hospital for treatment are deficient in vitamins B2 and B6 (pyridoxine). Some research information suggests that as many as 33% of those with an eating disorder could be deficient in vitamins B2 and B6. Dietary changes alone, without additional supplements, can often bring vitamin B levels back to normal. However, extra B2 and B6 may be required (which will be determined by your doctor or nutritionist). Plus, B-complex vitamins may help alleviate stress and reduce symptoms of depression, frequently associated with eating disorders.
1. Siassi F, Ghadirian P. Riboflavin Deficiency and Esophageal Cancer: A Case Control-household Study in the Caspian Littoral of Iran. Cancer Detect Prev. 2005;29(5):464-9.
In a case-household-control-household study in two very high and low esophageal cancer (EC) risk regions of the Caspian Littoral of Iran, a total of 21 cases (12 subjects from the high risk and 9 subjects from the low-risk region) with a total of 91 household members (57 subjects from the high risk and 34 subjects from the low-risk region) were investigated. Cases were matched for sex and age (+/-5 years) with non-blood relative controls. METHODS: A standard 24-h dietary recall questionnaire was used to estimate riboflavin intake. The erythrocyte glutathione reductase activity coefficient (EGR-AC) was measured to assess riboflavin status. The Student t-test was used to test differences, and chi2 analysis was applied to test associations. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were also calculated.
Results indicated that in both regions, the mean daily intake of riboflavin for cases was less than that of the controls (0.66+/-0.43 mg/day versus 0.82+/-0.37 mg/day) whereas for their households, it was virtually the same. Both cases and control households showed riboflavin deficiency in two regions, with higher deficiency in the high risk area. Statistical analysis revealed significant differences between the two regions for EGR-AC (P<0.001). Odd ratios indicated that the risk of developing EC for persons living in riboflavin-deficient households was more than twice of non-deficient households.
This study suggests that riboflavin deficiency may play an important role in the etiology of esophageal cancer in the Caspian Littoral of Iran.
2. McCabe H. Riboflavin Deficiency in Cystic Fibrosis: Three Case Reports. J Hum Nutr Diet. 2001 Oct;14(5):365-70.
Three cases of clinical riboflavin deficiency are reported in children aged 2-10 years attending a regional Cystic Fibrosis clinic. Riboflavin deficiency presented as angular stomatitis in all three patients. Patients were confirmed to be riboflavin deficient by assaying the activity of erythrocyte glutathione reductase. Patients were not on routine supplements of water-soluble vitamins before presentation and were treated with riboflavin supplements as part of a water-soluble vitamin complex. At presentation, one patient had poor nutritional status, but two patients were adequately nourished, receiving overnight Gastrostomy feeds. Data on these two patients indicate an adequate dietary intake of riboflavin, suggesting a mechanism for increased requirements, inadequate absorption or utilization. Additional deficiencies of thiamin, pyridoxine and iron were also observed. This paper reports the occurrence of a vitamin deficiency not previously reported in the cystic fibrosis population.
3. Powers HJ. Riboflavin and Health. Am J Clin Nutr. 2003 Jun;77(6):1352- 60.
Riboflavin is unique among the water-soluble vitamins in that milk and dairy products make the greatest contribution to its intake in Western diets. Meat and fish are also good sources of riboflavin, and certain fruit and vegetables, especially dark-green vegetables, contain reasonably high concentrations. Biochemical signs of depletion arise within only a few days of dietary deprivation. Poor riboflavin status in Western countries seems to be of most concern for the elderly and adolescents, despite the diversity of riboflavin-rich foods available. However, discrepancies between dietary intake data and biochemical data suggest either that requirements are higher than hitherto thought or that biochemical thresholds for deficiency are inappropriate.
This article reviews current evidence that diets low in riboflavin present specific health risks. There is reasonably good evidence that poor riboflavin status interferes with iron handling and contributes to the etiology of anemia when iron intakes are low. Various mechanisms for this have been proposed, including effects on the gastrointestinal tract that might compromise the handling of other nutrients. Riboflavin deficiency has been implicated as a risk factor for cancer, although this has not been satisfactorily established in humans. Current interest is focused on the role that riboflavin plays in determining circulating concentrations of homocysteine, a risk factor for cardiovascular disease. Other mechanisms have been proposed for a protective role of riboflavin in ischemia reperfusion injury; this requires further study. Riboflavin deficiency may exert some of its effects by reducing the metabolism of other B vitamins, notably folate and vitamin B-6.
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