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B2 Riboflavin and me

Discussion in 'General Treatment' started by justy, Mar 19, 2012.

  1. justy

    justy Donate Advocate Demonstrate

    Hi, i saw this link posted on another thread about B2 and was so struck by how much it related to my own experiences over the years that i needed to give it a seperate thread.

    Below i have taken exracts from this paper that relate to my health and may have implications for others with M.E. I dont currently take a B vitamin (its complicated) but am now going to add B2 to the mix.

    Extracts taken from : Riboflavin (vitamin B-2) and health1,2
    Hilary J Powers
    1 From The Centre for Human Nutrition, The University of Sheffield, Sheffield, United Kingdom

    **As shown on my mitochondrial profile test Acumen labs

    **My translocator protein studies show an accumulation of fatty acids deposited on my mitochondrial membranes, most notably oleic and linoleic acids

    ** have had problems with iron transportation and storage for years.

    **Adrenal problems exacerbated by steroid use for lung condition.

    ** Anemia again, plus I have neurological problems and vision problems. I have subclinical hypothyroidsim, but due to adrenal issues cant tolerate supplementing with thyroxine.


    I have had surgery for cervical dysplasia, 3 years ago.

    **Cant directly relate to my experience, but I know its to do with the methylation cycle and so must be important for us.

    **I have had a problem with night blindness since I first became ill. Driving at night ios almost completely impossible it was one of my symptoms that stayed when I was in remmission.

    67. Prentice AM, Bates CJ. A biochemical evaluation of the erythrocyte glutathione reductase (EC test for riboflavin status. 1. Rate and specificity of response in acute deficiency. Br J Nutr 1981;45:3752.[Medline]
    68. Prentice AM, Bates CJ. A biochemical evaluation of the erythrocyte glutathione reductase (EC test for riboflavin status. 2. Dose-response relationships in chronic marginal deficiency. Br J Nutr 1981;45:5365.[Medline]
    71. Hoppel CL, DiMarco JP, Tandler B. Riboflavin and rat hepatic structure and function. Mitochondrial oxidative metabolism in deficiency states. J Biol Chem 1979;254:416470.[Free Full Text]
    72. Olpin SE, Bates CJ. Lipid metabolism in riboflavin deficient rats II. Mitochondrial fatty acid oxidation and microsomal desaturation pathway. Br J Nutr 1982;47:58996.[Medline]
    73. Goodman SI. Organic aciduria in the riboflavin deficient rat. Am J Clin Nutr 1981;34:24347.[Free Full Text]
    74. Hoppel CL, Tandler B. Riboflavin deficiency. In: Tanaka K, Coates PM, eds. Fatty acid oxidation: chemical, biochemical and molecular aspects. New York: Alan R Liss, 1988:23348.
    75. Veitch K, Draye JP, Van Hoof F, Sherratt HS. Effects of riboflavin deficiency and clofibrate treatment on the five acyl CoA dehydrogenases in rat liver mitochondria. Biochem J 1988;254:47781.[Medline]
    80. Foy H, Kondi A. A case of true red cell aplastic anaemia successfully treated with riboflavin. J Pathol Bacteriol 1953;65:55964.[Medline]
    81. Foy H, Kondi A. Anaemias of the tropics: East Africa, with special reference to proteins and liver damage. Trans R Soc Trop Med Hyg 1958;52:4670.[Medline]
    82. Foy H, Kondi A, Mbaya V. Effects of riboflavin deficiency on bone marrow function and protein metabolism in baboons. Br J Nutr 1964;18:30717.[Medline]
    83. Foy H, Kondi A. A comparison between erythroid aplasia in marasmus and kwashiorkor and the experimentally induced erythroid aplasia in baboons by riboflavin deficiency. Vitam Horm 1968;26:65379.[Medline]
    91. Decker K, Dotis B, Glatzle D, Hinselmann M. Riboflavin status and anaemia in pregnant women. Nutr Metab 1977;21(suppl):179.[Medline]
    92. Buzina R, Jusic M, Milanovic N, Sapurnar J, Brubacher G. The effects of riboflavin administration on iron metabolism parameters in a school-going population. Int J Vitam Nutr Res 1979;49:13643.[Medline]
    93. Powers HJ, Bates CJ, Prentice AM, Lamb WH, Jepson M, Bowman H. The relative effectiveness of iron and iron with riboflavin in correcting a microcytic anaemia in men and children in rural Gambia. Hum Nutr Clin Nutr 1983;37C:41325.
    94. Powers HJ, Wright AJA, Fairweather-Tait SJ. The effect of riboflavin deficiency in rats on the absorption and distribution of iron. Br J Nutr 1988;59:3817.[Medline]
    95. Powers HJ, Weaver LT, Austin S, Wright AJA, Fairweather-Tait SJ. Riboflavin deficiency in the rat: effects on iron utilization and loss. Br J Nutr 1991;65:48796.[Medline]
    106. Leshner RT. Riboflavin deficiencya reversible neurodegenerative disease. Ann Neurol 1981;10:2945.
    107. Bell IR, Morrow FD, Read M, Berkes S, Perrone G. Low thyroxine levels in female psychiatric patients with riboflavin deficiency: implications for folate-dependent methylation. Acta Psychiatr Scand 1992;85:3603.[Medline]
    118. Lui T, Soong SJ, Wilson NP, et al. A case control study of nutritional factors and cervical dysplasia. Cancer Epidemiol Biomarkers Prev 1993;2:52530.[Abstract/Free Full Text]
    122. Stampfer MJ, Malinow MR, Willett W, et al. A prospective study of plasma homocysteine and risk of myocardial infarction in US physicians. JAMA 1992;268:87781.[Abstract/Free Full Text]
    123. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA 1995;274:104957.[Abstract/Free Full Text]
    124. Homocysteine-Lowering Trialists Collaboration. Lowering blood homocysteine with folic acid supplements: meta-analysis of randomised trials. BMJ 1998;316:8948.[Abstract/Free Full Text]
    125. Selhub J, Miller JW. The pathogenesis of homocysteinemia: interruption of the coordinate regulation by S-adenosylmethionine of the remethylation and transsulfuration of homocysteine. Am J Clin Nutr 1992;55:1318.[Abstract/Free Full Text]
    126. Morrison HI, Schaubel D, Desmeules M, Wigle DT. Serum folate and the risk of fatal coronary heart disease. JAMA 1996;275:18936.[Abstract/Free Full Text]
    127. Kang SS, Wong P, Susmano A, Sora J, Norusis M, Ruggie N. Thermolabile methylene tetrahydrofolate reductase: an inherited risk factor for coronary artery disease. Am J Hum Genet 1991;48:53645.[Medline]
    128. Lakshmi R, Lakshmi AV, Bamji MS. Mechanisms of impaired skin collagen maturity in riboflavin or pyridoxine deficiency. J Biosci 1990;15:28995.
    129. Hustad S, Ueland PM, Vollset SE, Zhang Y, Bjorke-Monsen AL, Schneede J. Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clin Chem 2000;46:106571.[Abstract/Free Full Text]
    130. Jacques PF, Bostom AG, Wilson PW, Rich S, Rosenberg IH, Selhub J. Determinants of plasma homocysteine concentration in the Framingham Offspring cohort. Am J Clin Nutr 2001;73:61321.[Abstract/Free Full Text]
    131. Moat SJ, Ashfield-Watt PAL, Powers HJ, Newcombe RG, McDowell IFW. The effect of riboflavin status on the homocysteine-lowering effect of folate in relation to MTHFR genotype. Clin Chem 2003;49:295302.[Abstract/Free Full Text]
    135. Venkataswamy G. Ocular manifestations of vitamin B complex deficiency. Br J Ophthalmol 1967;51:74954.[Free Full Text]
    136. Miyamota Y, Sancar A. Vitamin B2 based blue photoreceptors in the retinohypothalamic tract as the photoactive pigments for setting the circadian clock in mammals. Proc Natl Acad Sci U S A 1998;95:6097102.[Abstract/Free Full Text]
    137. Batey DW, Daneshgar KK, Eckhert CD. Flavin levels in the rat retina. Exp Eye Res 1992;54:6059.[Medline]
  2. Rand56

    Rand56 Senior Member

    Myrtle Beach, SC
  3. Sparrow

    Sparrow Senior Member

    Fascinating. I had to up my riboflavin lots because despite frequent doses, I was still getting test results back that suggested a shortage. I wonder if this explains part of why. Thanks for sharing.
    keenly likes this.
  4. Dog Person

    Dog Person

    Hi Justy,

    Excellent research! I posted some more information on "B2 I Love You" thread you might want to read as well.
  5. justy

    justy Donate Advocate Demonstrate

    Thanks dogperson, will check that out later. I havent started taking B2 yet, but will order some today. B12 has been so beneficail for me, i'm hoping the B2 can do the same.
  6. justy

    justy Donate Advocate Demonstrate

    Thanks for this link. B2 seems to be so important for so many processes, but also for methylation. I wonder if it should be added as a seperate b vitamin on the SMP. It seems some may not be able to utilise it properly and may need higher doses to keep their levels up.
  7. baccarat

    baccarat Senior Member

    Overview from the Linus Pauling database

    yes interesting threads. thanks for highlighting this!

    good point! see interactions with other nutrients further down.


    Riboflavin is a water-soluble B 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) (1). Coenzymes derived from riboflavin are termed flavocoenzymes, and enzymes that use a flavocoenzyme are called flavoproteins (2).


    Oxidation-reduction (redox) reactions

    Living organisms derive most of their energy from oxidation-reduction (redox) reactions, which are processes that involve the transfer of electrons. Flavocoenzymes participate in redox reactions in numerous metabolic pathways (3). Flavocoenzymes 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, flavocoenzymes also participate in the metabolism of drugs and toxins (4).

    Antioxidant functions

    Glutathione reductase is a FAD-dependent enzyme that participates in the redox cycle of glutathione. The glutathione redox cycle plays a major role in protecting organisms from reactive oxygen species, such as hydroperoxides. Glutathione reductase requires FAD to regenerate two molecules of reduced glutathione from oxidized glutathione. Riboflavin deficiency has been associated with increased oxidative stress (4). Measurement of glutathione reductase activity in red blood cells is commonly used to assess riboflavin nutritional status (5).

    Glutathione peroxidase, a selenium-containing enzyme, requires two molecules of reduced glutathione to break down hydroperoxides (see diagram).

    Xanthine oxidase, another FAD-dependent enzyme, catalyzes the oxidation of hypoxanthine and xanthine to uric acid. Uric acid is one of the most effective water-soluble antioxidants in the blood. Riboflavin deficiency can result in decreased xanthine oxidase activity, reducing blood uric acid levels (6).

    Nutrient Interactions

    B-complex vitamins

    Because flavoproteins are involved in the metabolism of several other vitamins (vitamin B6, niacin, and folic acid), severe riboflavin deficiency may affect many enzyme systems. Conversion of most naturally available vitamin B6 to its coenzyme form, pyridoxal 5'-phosphate (PLP), requires the FMN-dependent enzyme, pyridoxine 5'-phosphate oxidase (PPO) (7). At least two studies in the elderly have documented significant interactions between indicators of vitamin B6 and riboflavin nutritional status (8, 9). The synthesis of the niacin-containing coenzymes, NAD and NADP, from the amino acid, tryptophan, requires the FAD-dependent enzyme, kynurenine mono-oxygenase. Severe riboflavin deficiency can decrease the conversion of tryptophan to NAD and NADP, increasing the risk of niacin deficiency (3). Methylene tetrahydrofolate reductase (MTHFR) is a FAD-dependent enzyme that plays an important role in maintaining the specific folate coenzyme required to form methionine from homocysteine (see diagram). Along with other B vitamins, increased riboflavin intake has been associated with decreased plasma homocysteine levels (10). Recently, increased plasma riboflavin levels were associated with decreased plasma homocysteine levels, mainly in individuals homozygous for the C677T polymorphism of the MTHFR gene and in individuals with low folate intake (11). Such results illustrate that chronic disease risk may be influenced by complex interactions between genetic and dietary factors.


    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 and iron deficient improves the response of iron-deficiency anemia to iron therapy (12).


    Ariboflavinosis is the medical name for clinical riboflavin deficiency. Riboflavin deficiency is rarely found in isolation; it occurs frequently in combination with deficiencies of other water-soluble vitamins. Symptoms of riboflavin deficiency include sore throat, redness and swelling of the lining of the mouth and throat, cracks or sores on the outsides of the lips (cheliosis) and at the corners of the mouth (angular stomatitis), inflammation and redness of the tongue (magenta tongue), and a moist, scaly skin inflammation (seborrheic dermatitis). Other symptoms may involve the formation of blood vessels in the clear covering of the eye (vascularization of the cornea) and decreased red blood cell count in which the existing red blood cells contain normal levels of hemoglobin and are of normal size (normochromic normocytic anemia) (1, 3). Severe riboflavin deficiency may result in decreased conversion of vitamin B6 to its coenzyme form (PLP) and decreased conversion of tryptophan to niacin (see Nutrient Interactions).

    Preeclampsia is defined as the presence of elevated blood pressure, protein in the urine, and edema (significant swelling) during pregnancy. About 5% of women with preeclampsia may progress to eclampsia, a significant cause of maternal death. Eclampsia is characterized by seizures, in addition to high blood pressure and increased risk of hemorrhage (severe bleeding) (13). A study in 154 pregnant women at increased risk of preeclampsia found that those who were riboflavin deficient were 4.7 times more likely to develop preeclampsia than those who had adequate riboflavin nutritional status. The cause of preeclampsia-eclampsia is not known. Decreased intracellular levels of flavocoenzymes could cause mitochondrial dysfunction, increase oxidative stress, and interfere with nitric oxide release and thus blood vessel dilationall of these changes have been associated with preeclampsia (14). However, a small randomized, placebo-controlled, double-blind trial in 450 pregnant women at high risk for preeclampsia found that supplementation with 15 mg of riboflavin daily did not prevent the condition (15).

    Risk factors for riboflavin deficiency

    Alcoholics are at increased risk for riboflavin deficiency due to decreased intake, decreased absorption, and impaired utilization of riboflavin. Additionally, anorexic individuals rarely consume adequate riboflavin, and lactose intolerant individuals may not consume milk or other dairy products which are good sources of riboflavin. The conversion of riboflavin into FAD and FMN is impaired in hypothyroidism and adrenal insufficiency (3, 4). Further, people who are very active physically (athletes, laborers) may have a slightly increased riboflavin requirement. However, riboflavin supplementation has not generally been found to increase exercise tolerance or performance (16).

    The Recommended Dietary Allowance (RDA)

    The RDA for riboflavin, revised in 1998, was based on the prevention of deficiency. Clinical signs of deficiency in humans appear at intakes of less than 0.5-0.6 milligrams (mg)/day, and urinary excretion of riboflavin is seen at intake levels of approximately 1 mg/day (1).

    Recommended Dietary Allowance (RDA) for Riboflavin
    Life Stage Age Males (mg/day) Females (mg/day)
    Infants 0-6 months 0.3 (AI) 0.3 (AI)
    Infants 7-12 months 0.4 (AI) 0.4 (AI)
    Children 1-3 years 0.5 0.5
    Children 4-8 years 0.6 0.6
    Children 9-13 years 0.9 0.9
    Adolescents 14-18 years 1.3 1.0
    Adults 19 years and older 1.3 1.1
    Pregnancy all ages - 1.4
    Breast-feeding all ages - 1.6

    Disease Prevention


    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 light-induced oxidative damage of lens proteins may lead to the development of age-related cataracts. A case-control study found significantly decreased risk of age-related cataract (33% to 51%) in men and women in the highest quintile of dietary riboflavin intake (median of 1.6 to 2.2 mg/day) compared to those in the lowest quintile (median of 0.08 mg/day in both men and women) (17). Another case-control study reported that 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 (18). 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 riboflavin intake were 50% less likely to have cataracts than those in the lowest quintile (19). 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 (median of 1.5 mg/day) and women in the lowest quintile (median of 1.2 mg/day) (20). However, the range between the highest and lowest quintiles was small, and median intake levels for both quintiles were above the current RDA for riboflavin. A recent study in 408 women found that higher dietary intakes of riboflavin were inversely associated with five-year change in lens opacification (21). 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.

    Disease Treatment

    Migraine headaches

    Some evidence indicates that impaired mitochondrial oxygen metabolism in the brain may play a role in the pathology of migraine headaches. Because riboflavin is the precursor of the two flavocoenzymes (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 (22). 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. 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 (23). A small study in 23 patients reported a reduction in median migraine attack frequency after supplementation with 400 mg of riboflavin daily for three months (24). Additionally, a 3-month randomized, double-blind, placebo-controlled study that administered a combination of riboflavin (400 mg/day), magnesium, and feverfew to migraine sufferers reported no therapeutic benefit beyond that associated with taking a placebo containing 25 mg/day of riboflavin (25). Compared to baseline measurements in this trial, both the placebo and treatment groups experienced some benefits with respect to the mean number of migraines, migraine days, or migraine index (25). Although these findings are preliminary, data from most studies to date suggest that riboflavin supplementation might be a useful adjunct to pharmacologic therapy in migraine prevention.


    Food sources

    Most plant and animal derived foods contain at least small quantities of riboflavin. In the U.S., wheat flour and bread have been enriched with riboflavin (as well as thiamin, niacin, and iron) since 1943. Data from large dietary surveys indicate that the average intake of riboflavin for men is about 2 mg/day and for women is about 1.5 mg/day; both intakes are well above the RDA. Intake levels were similar for a population of elderly men and women (1). Riboflavin is easily destroyed by exposure to light. For instance, up to 50% of the riboflavin in milk contained in a clear glass bottle can be destroyed after two hours of exposure to bright sunlight (6). Some foods with substantial amounts of riboflavin are listed in the table below along with their riboflavin content in milligrams (mg). For more information on the nutrient content of foods, search the USDA food composition database.

    Food Serving Riboflavin (mg)
    Fortified cereal 1 cup 0.59 to 2.27
    Milk (nonfat) 1 cup (8 ounces) 0.34
    Cheddar cheese 1 ounce 0.11
    Egg (cooked) 1 large 0.27
    Almonds 1 ounce 0.23
    Salmon (cooked) 3 ounces* 0.12
    Halibut (broiled) 3 ounces 0.08
    Chicken, light meat (roasted) 3 ounces 0.08
    Chicken, dark meat (roasted) 3 ounces 0.16
    Beef (cooked) 3 ounces 0.16
    Broccoli (boiled) 1/2 cup chopped 0.10
    Asparagus (boiled) 6 spears 0.13
    Spinach (boiled) 1/2 cup 0.21
    Bread, whole wheat 1 slice 0.06
    Bread, white (enriched) 1 slice 0.08
    *A 3-ounce serving of meat is about the size of a deck of cards.


    The most common forms of riboflavin available in supplements are riboflavin and riboflavin 5'-monophosphate. Riboflavin is most commonly found in multivitamin and vitamin B-complex preparations (26).



    No toxic or adverse effects of high riboflavin intake in humans are known. Studies in cell culture indicate that excess riboflavin may increase the risk of DNA strand breaks in the presence of chromium (VI), a known carcinogen (27). This may be of concern to workers exposed to chrome, but no data in humans are available. High-dose riboflavin therapy has been found to intensify urine color to a bright yellow (flavinuria), but this is a harmless side effect. The Food and Nutrition Board did not establish a tolerable upper level of intake (UL) when the RDA was revised in 1998 (1).

    Drug interactions

    Several early reports indicated that women taking high-dose oral contraceptives (OC) had diminished riboflavin nutritional status. However, when investigators controlled for dietary riboflavin intake, no differences between OC users and non-users were found (1). Phenothiazine derivatives like the anti-psychotic medication chlorpromazine and tricyclic antidepressants inhibit the incorporation of riboflavin into FAD and FMN, as do the anti-malarial medication, quinacrine, and the cancer chemotherapy agent, adriamycin (4). Long-term use of the anti-convulsant, phenobarbitol may increase destruction of riboflavin, by liver enzymes, increasing the risk of deficiency (3).

    Linus Pauling Institute Recommendation

    The RDA for riboflavin (1.3 mg/day for men and 1.1 mg/day for women), which should prevent deficiency in most individuals, is easily met by eating a varied diet. Consuming a varied diet should supply 1.5 mg to 2 mg of riboflavin a day. Following the Linus Pauling Institute recommendation to take a multivitamin/multimineral supplement containing 100% of the Daily Values (DV) will ensure an intake of at least 1.7 mg of riboflavin/day.

    Older adults (50 years of age and older)

    Some experts in nutrition and aging feel that the RDA (1.3 mg/day for men and 1.1 mg/day for women) leaves little margin for error in people over 50 years of age (28, 29). A recent study of independently living people between 65 and 90 years of age found that almost 25% consumed less than the recommended riboflavin intake, and 10% had biochemical evidence of deficiency (30). Additionally, epidemiological studies of cataract prevalence indicate that riboflavin intakes of 1.6 to 2.2 mg/day may reduce the risk of developing age-related cataracts. Individuals whose diets may not supply adequate riboflavin, especially those over 50, should consider taking a multivitamin/multimineral supplement, which generally provides at least 1.7 mg of riboflavin/day.


    Written in September 2002 by:
    Jane Higdon, Ph.D.
    Linus Pauling Institute
    Oregon State University

    Updated in June 2007 by:
    Victoria J. Drake, Ph.D.
    Linus Pauling Institute
    Oregon State University

    Reviewed in June 2007 by:
    Donald B. McCormick, Ph.D.
    F. E. Callaway Professor, Emeritus
    Department of Biochemistry
    Emory University School of Medicine

    Copyright 2000-2012 Linus Pauling Institute
  8. merylg

    merylg Senior Member

    Sydney, NSW, Australia
    Hi justy,

    I also show quite a few signs of B2 (Riboflavin) deficiency, and have just started a revised kind of protocol that re-assesses everything I have been taking.

    One symptom, severe itching, flaking, at times blistering, bleeding dermatitis covering 1/2 palm and one finger of my right hand, plus one finger of my left hand, has started to heal almost completely after only a couple of days!

    Last night I slept better, breathed better & all my skeletal muscles were relaxed when I woke, instead of being tight. My eyes were not as dry as interesting point is that it has been the lipid layer that has been missing from my tear film...partially improved after a month or so of taking Fish Oil...further improved on B2 12.5 mg 3 x a day.

    I was still lacking in energy through the day, but I have been so debilitated that I expect it may take some time to work through any healing process full of metabolic complexities involving the liver.

    Other things that tie in, include my fatty liver, damaged liver, oesophagitis, gastritis, bowel polyps, family history of bowel cancer, stomach cancer, liver cancer...etc etc...
  9. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

    Mackay, Aust
    Hi Meryl. Is this right - 12.5mg -10 times RDA? I've only just picked up on the B2 thread. Can't find dosage anywhere.

    PS. I just realised I have ordered 100mg B2 from iHerb.
  10. merylg

    merylg Senior Member

    Sydney, NSW, Australia
    Hi RustyJ,
    I am just starting out with B2 Riboflavin, but I am working with Dog Person & will be adding other things as I go.
    It's interesting as in the past I took 400mg/day as prescribed by my Neuro for migraine prevention. It was the only treatment that worked, of a list of about 9 or so treatments I tried. Of course, it was last on the list!
    The study from which this treatment derives showed no ill effects from this dose.

    So 12.5 mg 3 x day is not a high dose & it's got nothing to do with RDA. It's more about each individual tolerating & managing the effects from the treatment.
  11. Rand56

    Rand56 Senior Member

    Myrtle Beach, SC
    hi merylg

    How did you take that 400mg per day? Did you titrate up and only had a response at that dosage....or did you take numerous smaller dosages frequently throughout the day? According to Dog Person, at most a person absorbs at any one time is 25mg's.
  12. merylg

    merylg Senior Member

    Sydney, NSW, Australia
    3 x before treatment photos of dermatitis on hands and 1 x after B2 (Riboflavin) treatment
    (which involved ceasing any B multi, any folate, any methylfolate (Metafolin), any folinic acid)

    photo(38).JPG photo(39).JPG photo(40).JPG
    anne_likes_red likes this.
  13. Rand56

    Rand56 Senior Member

    Myrtle Beach, SC
    That is very interesting that you had to cease taking methylfolate. I wonder if additional methylfolate depletes B-2 stores further. I have a question concerning this to Dog Person on the other Riboflavin thread asking her this because currently I am taking 15mg's per day of methylfolate for my depression. Hope she can weigh in on this.
  14. merylg

    merylg Senior Member

    Sydney, NSW, Australia
    I'm not sure Rand56. I stopped Methyl B12 and Methylfolate (Metafolin) more for personal reasons that they make me feel ill...cannot tolerate them.
  15. aquariusgirl

    aquariusgirl Senior Member

    about the linus pauling post: many of us are gluten & dairy free so that could reduce dietary sources of B2,. add to that malabsorption, hypothyrodism, adrenal fatigue ....and you could severely compromise your intake and usage of B2 I would guess.
  16. justy

    justy Donate Advocate Demonstrate

    I've just ordered my B2 from natures own in the uk who make food state vitamins and minerals. The lowest dose i could find was 20mg - so yes waaaayyy over the RDA. Most companies seem to sell a 100mg, but i figured i would just pee it all out.
    I also saw the research that suggests 400mg a day for migraine - it doesnt have any known toxicity.

    Meryl - really interesting to hear about (and see) your small improvements with B2 after such a short time. I also have the anemia and low b12 so am hoping it will help in my absorption of the iron and b12 im taking.

    I can't believe - after all the links ive read the past few days about b2 that i havent considered it before. I'ts also not particularly flagged up on the mito profile test from Acumen, which is surprising given its importance in ox phos and energy transport and metabolism.
    Fingers crossed, Justy.
  17. Dog Person

    Dog Person

    Hello Everyone,

    Please know that I am working on this as quickly as I can. One reason I wanted Brenda to remove her specific supplement protocol (which she kindly did) is because it was designed for her; I saw her chart. B2 can interact with many medications (which I will list) so I do not want everyone to suddenly take what she takes and possibly have issues. I know the National Research Council states that no tolerable upper limit has been set due to its lack of side effects. However this recommendation was made based on a healthy individual taking high doses of riboflavin, not a nutritional imbalanced person with high levels of lead and possibly iron. This is why its important that you understand what I believe the imbalance is, what has caused the imbalance and how it affects your energy system.

    Possible Interactions with: Vitamin B2 (Riboflavin)
    If you are currently being treated with any of the following medications, you should not use vitamin B2 supplements without first talking to your health care provider.
    Anticholinergic Drugs -- Used to treat a variety of conditions, including gastrointestinal spasms, asthma, depression, and motion sickness, these drugs may inhibit the body's ability to absorb riboflavin.
    Tetracycline -- Riboflavin interferes with the absorption and effectiveness of tetracycline, an antibiotic. (All vitamin B complex supplements act in this way.) You should take riboflavin at a different time during the day from when you take tetracycline.
    Tricyclic Antidepressants -- Tricyclic antidepressants may reduce levels of riboflavin in the body. In addition to raising levels of the vitamin in the body, taking riboflavin may also improve the effects of these antidepressants. They include:
    Imipramine (Tofranil)
    Desimpramine (Norpramin)
    Amitriptyline (Elavil)
    Nortriptyline (Pamelor)
    Antipsychotic Medications -- Antipsychotic medications called phenothiazines (such as chlorpromazine or Thorazine) may lower riboflavin levels.
    Doxorubicin -- Riboflavin may deactivate doxorubicin, a medication used for the treatment of certain cancers. In addition, doxorubicin may deplete levels of riboflavin in the body. Your doctor will let you know whether you need to take a riboflavin supplement or not.
    Methotrexate -- Methotrexate, a medication used to treat cancer and autoimmune diseases such as rheumatoid arthritis, can inhibit the body from using riboflavin.
    Phenytoin -- Phenytoin (Dilantin), a medication used to control epileptic seizures, may affect riboflavin levels in the body.
    Probenecid -- This medication used for gout may decrease the absorption of riboflavin from the digestive tract and increase the excretion in the urine.
    Thiazide Diuretics -- Diuretics (water pills) that belong to a class known as thiazides, such as hydrochlorothiazide, may cause you to excrete more riboflavin in your urine.
    Drug Interactions:
    Antimalarial MedicationsAntipsychotic MedicationsBirth Control MedicationsDoxorubicinPhenytoin-containing MedicationsSelegilineTetracyclineTricyclic Antidepressants

    This may not be a complete list, thus you should check with your healthcare provider and/or pharmacist regarding any medications you currently are taking to see if there are any known side effect with riboflavin supplementation.
  18. taniaaust1

    taniaaust1 Senior Member

    Sth Australia
    Thanks to justy and those who have posted on this thread. Its helped me to see that I probably do definately need to be trialing B2 as dogperson had suggested to me. I suddenly feel like a piece of the puzzle has actually just dropped into place.

    So many of those things mentioned on justy's mitochondrial profile test Acumen labs... are issues I have. I have an issue with my lipids (and hence get very high cholestrol not related to eatting cholestrol containing foods), I have issue with my adrenals (low cortisol), I have an issue with my iron (I dont store it) etc

    I also have MTHFR polymorphism C677T so there is a need to keep my homocysteine levels down as mine tend to go on high side.. so thanks for your post bacarrat on how B2 relates to it.. I wonder why my specialist who has me on various things for the MTHFR issue has missed putting me on B2 for it.
    Im glad I didnt run out and buy some B2 right away cause I was currently trialing one of the drugs not to be taken with it and at times currently also taking others in that list too. (I stopped my Amitriptyline trial a couple of days ago..another failure, it didnt help sleep at all).
  19. Dog Person

    Dog Person

    You may be thinking of the MTHFR enzyme, which converts 5,10 methylene tetrahydrofolate to 5-methyltetrahydrofolate. This enzyme does require FAD as a cofactor, which is one of the two coenzyme forms of riboflavin.

    Rich posted this to one of my posts. So you can see that MTHFR relates to riboflavin now.
  20. merylg

    merylg Senior Member

    Sydney, NSW, Australia
    I can't remember, but I quickly found that after awhile, even lower doses of B2 (Riboflavin) were effective for me in preventing my migraines. Here is one of the original studies:

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