Riboflavin is one of the eight B-group vitamins that are responsible for converting glucose into energy. It’s also involved in fat and protein metabolism. All of the B vitamins are water soluble, which means the body doesn’t store them, but instead constantly excretes them in urine. Riboflavin is that magical B vitamin that turns your urine a fluro yellow color.
Vitamin B2 is intricately involved in the Citric Acid Cycle, where it helps to convert succinate into fumurate, which inevitably goes on to produce ATP (which is basically the body’s energy source). It’s also needed to convert tryptophan into niacin, to activate vitamin B6 and folate, and it plays a major role in the function of glutathione reductase, which is responsible for regenerating the body’s most important antioxidant, glutathione. B2 is also essential for immune function, tissue repair, healthy growth of skin, nails, and hair, and is involved in red blood cell production.
The recommended dietary intake for riboflavin is 1.3mg/day for men and 1.1mg/day for women.
The best sources of riboflavin include brewer’s yeast, almonds, organ meats, whole grains, wheat germ, wild rice, mushrooms, soybeans, milk, yogurt, eggs, broccoli, Brussels sprouts, and spinach. Flours and cereals are often fortified with riboflavin.
In Western countries poor riboflavin status is mainly seen in children and the elderly, although I personally see it in other groups. Vitamin B2 is converted to flavin adenine dinucleotide (FAD), which requires thyroxine (T4), produced by the thyroid gland. For those with impaired thyroid function, B2 deficiency can quite often be a factor.
The main deficiency signs involve the eyes, due the function of glutathione perioxidase in this area. Poor B2 status means impaired antioxidant function in the lens of the eye, which exposes it to an increased amount of oxidative damage. Also, photoreceptors in the eye are riboflavin-dependant, which can cause issues with dark adaption.
Deficiency signs can include sensitivity to light, constant blood shot eyes, night blindness and cataracts in older people. Other deficiency symptoms may include an inflamed tongue, cracked lips or split corners of the mouth, cold sores, swollen tongue or throat, hair loss, dermatitis and fatigue.
Other deeper pathologies include poor iron handling and anaemia, increased risk of cervical dysplasia, migraines, elevated homocysteine, and hypertension in those with the C667T MTHFR phenotype.
B2 is the co factor for the MTHFR enzyme, which is needed to convert 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate (active folate).
It’s also needed as a cofactor for methionine synthase reductase (MTRR). MTRR is an enzyme that is catalyzed by methionine synthase (MTR), but MTR is reduced by the continual oxidation of cobalamin (B12). Vitamin B12 is needed to regenerate MTRR, so it can pass a methyl group to methionine. Methionine then goes on to form S-adenosylmethionine (SAMe).
Those people with heterozygous or homozygous MTHFR mutations should make sure they’re including adequate B2 containing foods in their diet.
Australian Government. Department of Health and Ageing, National Health and Medical Research Council, Ministry of Health. Nutrient reference values for Australia and New Zealand – Executive summary. Canberra: Commonwealth of Australia, 2006.
Braun L, Cohen M, 2010. Herbs & Natural Supplements – an evidence-based guide, 3rd edn. Churchill Livingston, Elsevier, NSW
Breen C, Crowe A, Roelfsema HJ, Saluja IS, Guenter D, 2003. High-dose riboflavin for prophylaxis of migraine. Can Fam Physician. Vol.49, pp.1291-93.
Genecards, 2014. “5-Methyltetrahydrofolate-Homocysteine Methyltransferase”. Viewed 21st July 2014 from www.genecards.org/cgi-bin/carddisp.pl?gene=MTRR
Powers H, 2003. Riboflavin (vitamin B-2) and health. Amer. Jour. Clin. Nut. Vol.77, pp.1352-60.
Head KA, 2001. Natural Therapies for Ocular Disorders, part two: cataracts and glaucoma. Altern Med Rev, Vol.6, no.2, pp.141-6
Hustad S, Ueland M, Schneede J, Vollset S, Ulvik A et al, 2004. Phenotypic expression of the methylenetetrahydrofolate reductase 677C-T polymorphism and flavin cofactor availability in thyroid dysfunction. Am J Clin Nutr. Vol.80, pp.1050-7.
Liu T, Soong SJ, Wilson NP, 1993. A case cortrol study of nutritional factors and cervical dysplagia. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. Vol.2, pp.525-30.
Moat SJ, Ashfield-Watt PA, Powers HJ, 2003. Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype. Clin Chem. Vol.4, no.2, pp.295-302.
Miyamoto Y, Sancar A, 1998. Vitamin B2-based blue-light photorecptors on the retinohypothalamic tract as the photoactive pigments for setting the circadian clock in mammals. National Academy of Science. Vol.95, pp.6097-102.
Schoenen J, Jacuy J, Lenaerts M, 1998. Effectiveness of high-dose riboflavin in migraine prophylaxis – a random controled trial. American Academy of Neurology. Vol.50, pp.467-70.
University of Maryland Medical Center, 2013. “Vitamin B2 (riboflavin)”. Viewed 21st July 2014 from http://umm.edu/health/medical/altmed/supplement/vitamin-b2-riboflavin#ixzz38574G3IU
Wahlqvist M, 2002. Australian and New Zealand Food and Nutrition, 2nd edn. Allen & Unwin, NSW.
Wilson CP McNulty H, Ward M, Strain JJ, Trouton TG, Hoeft BA, Weber P, et al, 2013. Blood pressure in treated hypertensive individuals with the MTHFR 677TT genotype is responsive to intervention with riboflavin: findings of a targeted randomized trial. Hypertension. Vol.61, no.6, pp.1302-8.