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Riboflavin, or vitamin B-2, is an essential dietary component required
in small amounts for many functions, including regenerating the vital
antioxidant glutathione. Dietary riboflavin that is not being utilized
in riboflavin-dependent enzymes exists as free riboflavin. When we
consume riboflavin in excess of this requirement, there is a dramatic
increase in blood, tissue, and urine levels of free riboflavin.
Normally the body contains low levels of free riboflavin, but it's easy to
get abnormally high levels of riboflavin, simply because many of the supplements
available in today's marketplace contain an excess amount of riboflavin. This
is a particular concern because riboflavin has the ability to react with light,
resulting in adverse cellular effects. The combination of riboflavin and light
produces both toxic peroxides,1 and a unique riboflavin-tryptophan photo adduct
that is known to damage the liver and cells.2
This propensity for riboflavin to generate both damaging free radicals and
toxic photo adducts of amino acids has been especially troubling in the cases
of patients and infants who are fed intravenously. In these cases, riboflavin
catalyzed reactions formed from room light, irradiating the bags of liquid
nutrition, have often caused liver dysfunction.3
In fact, the naturally occurring riboflavin found in our skin and eyes has
been implicated to play a pivotal role in many of the damaging effects of UV
light exposure.4 This includes damage to our skin's connective tissue,5 the
induction of DNA lesions known to promote the development of skin cancer and
aging,6 and the impairment of mitochondria functioning resulting in cell death.7
High doses of riboflavin have also been shown to induce damage to retina cells
in the eyes of research animals.8
Surprisingly, while the combination of riboflavin and light has been studied
because of the adverse effects on cells grown in culture and exposed to light
- and riboflavin and light have been used as a model for inducing things as
diverse as liver dysfunction, cataracts and mutations - yet the nutrition industry
has failed to heed the warning that damage may be caused by high doses of riboflavin
supplements.
This is partly due to confusion because a diet deficient in riboflavin is a
risk factor for things like cataracts, while at the same time, the combination
of riboflavin and light is often used by scientists to cause cataracts in animal
research. As always, the dose makes the poison, and this means that if you
take nutritional supplements you should make sure you consume an adequate amount
of riboflavin daily, rather than an excess of riboflavin.
The human requirement for riboflavin is less than 2 milligrams a day, but many
common vitamin supplements contain 10s or 100s of milligrams. There is little
(if any) scientific justification for taking supplements of riboflavin greatly
in excess of the known dietary requirement. However, there is a lot of scientific
evidence and speculation that the combination of abnormally high blood, eye
and skin levels of riboflavin, combined with a lifetime of sun exposure, may
have serious negative consequences, and actually cause the damage we are trying
to prevent. The combination of sunlight and abnormally high tissue levels of
riboflavin from excess supplementation is a toxic combination that should be
avoided.
Adam Gisson and John Morgenthaler
For questions, correspondence, or to subscribe to Smart Publications
Health & Wellness
Update send email to riboflavin@smart-publications.com
References
1. Jernigan HM Jr., Role of hydrogen peroxide in riboflavin-sensitized
photodynamic damage to cultured rat lenses, Exp Eye Res 1985 Jul;41(1):121-9.
Kale H, Harikumar P, Kulkarni SB, Nair PM, Netrawali MS, Assessment
of the genotoxic potential of riboflavin and lumiflavin. B. Effect
of light, Mutat Res 1992 Nov;298(1):17-23.
2. Silva E, Salim-Hanna M, Edwards AM, Becker MI, De Ioannes AE, A
light-induced tryptophan-riboflavin binding: biological implications,
Adv Exp Med Biol 1991;289:33-48.
3. Chessex P, Lavoie JC, Rouleau T, Brochu P, St-Louis P, Levy E, Alvarez
F, Photooxidation of parenteral multivitamins induces hepatic steatosis
in a neonatal guinea pig model of intravenous nutrition, Pediatr Res
2002 Dec;52(6):958-63. Bhatia J, Moslen MT, Haque AK, McCleery R, Rassin
DK, Total parenteral nutrition-associated alterations in hepatobiliary
function and histology in rats: is light exposure a clue? Pediatr Res
1993 May;33(5):487-92.
4. Edwards AM, Silva E, Effect of visible light on selected enzymes,
vitamins and amino acids, J Photochem Photobiol B 2001 Oct;63(1-3):126-31.
5. Frati E, Khatib AM, Front P, Panasyuk A, Aprile F, Mitrovic DR,
Degradation of hyaluronic acid by photosensitized riboflavin in vitro.
Modulation of the effect by transition metals, radical quenchers, and
metal chelators, Free Radic Biol Med 1997;22(7):1139-44.
6. Riemschneider S, Podhaisky HP, Klapperstuck T, Wohlrab W, Relevance
of reactive oxygen species in the induction of 8-oxo-2'-deoxyguanosine
in HaCaT keratinocytes, Acta Derm Venereol 2002;82(5):325-8. Oikawa
S, Tada-Oikawa S, Kawanishi S, Site-specific DNA damage at the GGG
sequence by UVA involves acceleration of telomere shortening, Biochemistry
2001 Apr 17;40(15):4763-8.
7. Salet C, Moreno G, Photodynamic action increases leakage of the
mitochondrial electron transport chain, Int J Radiat Biol 1995 Apr;67(4):477-80.
Cho KS, Lee EH, Choi JS, Joo CK, Reactive oxygen species-induced apoptosis
and necrosis in bovine corneal endothelial cells, Invest Ophthalmol
Vis Sci 1999 Apr;40(5):911-9.
8. Eckhert CD, Hsu MH, Pang N, Photoreceptor damage following exposure
to excess riboflavin, Experientia 1993 Dec 15;49(12):1084-7
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