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B2 - Riboflavin

Updated: Feb 8

I believe you will benefit from this article if you are interested in oxidative stress, glutathione, neurotransmitters, histamine, activation of Vitamin B6, nitric oxide, migraines, hypertension, Chrone’s Disease, neuro degenerative disorders (AD, PD, MS, etc) , mitochondrial energy production (Complex I), homocysteine, recovery from ME/CFS, recovery from brain injury, MCS, SIBO – especially hydrogen sulfide (H2S) SIBO, or glutamate toxicity / NMDA receptor activation.

The Technicals - Riboflavin

B2 is a key component of enzymes involved in antioxidant function, energy production, detoxification, methionine metabolism and vitamin activation. Riboflavin helps to metabolize food into energy; and is converted into its active forms (FAD) and FMN. FMN is a precursor to FAD and is involved in a myriad of metabolic reactions. RFK encodes for riboflavin kinase which catalyzes the critical phosphorylation of riboflavin (vitamin B2) to flavin mononucleotide (FMN), an essential step in the utilization of the vitamin.

FAD and FMN are cofactors in many reactions for flavoproteins, and are used to create cellular energy production and respiration. Riboflavin is a cofactor for glutathione reductase (GSR), which recycles glutathione back to its reduced state from its oxidized state, and is also a cofactor for NOS enzyme function (nitric oxide synthase: NOS1, NOS2, NOS3).

FAD is a cofactor in the electron transport chain, to produce energy in the mitochondria, especially Complex I. FAD is a cofactor in both creating energy from carbohydrates and through fatty-acid oxidation. FAD is also a cofactor for some CYP450 enzymes.

Riboflavin (as FAD or FMN) is is needed to create niacin from tryptophan, and in the synthesis of vitamin B6 and iron. FAD is required as a cofactor for methylenetetrahydrofolate reductase (MTHFR). Xanthine oxidase, where FAD is a cofactor, oxidizes hypoxanthine and xanthine to uric acid, which 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. [2]. Riboflavin also supports conversion of choline to TMG. Riboflavin also supports the release of methyl groups from Glycine, synthesized by GCAT, SMHT1, and SHMT2. Riboflavin also supports the release of carbon from Glycine as an extra source of methyl groups.


SLC52A3 is a transporter of riboflavin across the intestinal barrier into the blood stream. SLC52A2 known as RFVT2 and has an important role in riboflavin absorption. Riboflavin supplementation may be beneficial in individuals with significant SLC52A2 mutations. Riboflavin is absorbed in the upper part of the small intestines, so people with SIBO/ oxalate / gut issues may have problems with riboflavin deficiency. Riboflavin-specific transporters move it across cell membranes and into the mitochondria. Mutations in this transporter (SLC52A2 gene) cause Brown-Vialetto-Van Laere syndrome, which is a rare neurological order that may be helped by riboflavin supplementation in some cases.

Riboflavin Deficiency

Riboflavin may be depleted by excessive or chronic alcohol consumption, high fat diets, and exercise. Burning fat requires more riboflavin, take note those on a Keto based diet! [4]

Frank deficiency of riboflavin is rare, however, marginal deficiency is common. Deficiency of riboflavin is associated with fatigue/weakness. Signs of deficiency include depression, dizziness, sore or burning lips, mouth, tongue, photophobia, burning, itching, or teary eyes, and loss of visual acute in early stages. As the deficiency progresses, symptoms can include: dermatitis, glossitis, cheilosis, angular stomatitis, and corneal vascularization. Deficiencies often overlaps with b3, b6 or iron deficiencies. [4]

Riboflavin Intake / Foods / Supplementation

Who is at risk? People more likely to suffer from riboflavin deficiency include the elderly, women on birth control, vegans, and alcoholics, and people with malabsorption issues (SIBO, high oxalates, gut dysbiosis, etc).

Food sources high in riboflavin include: organ meats, dairy foods, eggs, leafy greens (spinach), broccoli, liver, enriched grains, nutritional yeast, almonds, eggs, beef, chicken, asparagus, mushrooms, and salmon. [3]

The RDA for riboflavin is 1.7 mg/day. Common levels of therapeutic intake of riboflavin are 25-50 mg/day. No UL for riboflavin has been set.[4]

Research in animals reveals that riboflavin deficiency impairs iron absorption, increases intestinal loss of iron, and/or impairs iron utilization for the synthesis of hemoglobin. In humans, low intake of riboflavin is correlated with an increased risk of anemia. Riboflavin supplementation increases circulating hemoglobin levels. Supplementation in individuals improves the response to iron therapy. Riboflavin deprivation resulted in higher levels of cardiac biomarkers, histopathological abnormalities, and reduced mitochondrial membrane potential which shows the role of riboflavin in the prevention of cardiovascular pathogenesis [3].

Treatment of Deficiency - Riboflavin

Treatment of manifestations: High-dose oral supplementation of riboflavin (vitamin B ) between 10 mg and 50 mg/kg/day improves symptoms and signs on clinical examination, improves objective testing (vital capacity, brain stem evoked potentials, nerve conduction studies), and normalizes acylcarnitine levels. When riboflavin supplementation is given earlier in the disease course, the response can be very good; if given later in the disease course, the response is less, likely reflecting the effect of existing neuronal damage. Because oral riboflavin supplementation is effective (and possibly lifesaving), it should begin as soon as a riboflavin transporter deficiency is suspected and continued lifelong unless molecular genetic testing fails to identify biallelic pathogenic variants in either SLC52A2 or SLC52A3. Supportive care includes respiratory support; physiotherapy to avoid contractures; occupational therapy to support activities of daily living; orthotics for limb and trunk bracing; speech and language therapy to avoid choking and respiratory problems; wheelchair as needed; low vision aids as needed; routine management of scoliosis to avoid long-term respiratory problems; and routine management of depression. [11]

Riboflavin – Reduces Frequency of Migraine headaches

Some evidence indicates that impaired mitochondrial oxygen metabolism in the brain may play a role in the pathology of migraine headaches. Since 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 controlled trial examined the effect of very high dose riboflavin (400 mg/day) for three months on migraine prevention in 54 men and women with a history of recurrent migraine headaches. Riboflavin compared to placebo reduced attack frequency and the number of headache days, though the beneficial effect was most pronounced during the third month of treatment. 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. A single-blinded, randomized, parallel group trial in 85 patients with migraine headaches (ages 15-55 years), high-dose riboflavin supplementation (400 mg/day) for 12 weeks decreased migraine frequency, duration, and severity compared to baseline. Thus, although the available trials have been small and short term, most studies to date suggest that high-dose riboflavin supplementation might be a useful adjunct therapy in adults with migraine headaches.[2]

A recent trial found a benefit of intervention with higher dose riboflavin: children with migraine treated with 400 mg/day of riboflavin for 12 weeks (n=30) had reductions in migraine frequency and duration, but not intensity, compared to placebo (n=30), yet no benefit was seen in children taking 200 mg/day for 12 weeks in this study. Additionally, a randomized controlled trial in 98 adolescents, ages 12 to 19 years, found that 400 mg/day of riboflavin for three months decreased both headache frequency and duration and improved migraine-related disability compared to placebo. Retrospective studies of children and adolescents suffering from migraine have also suggested some benefit associated with supplemental riboflavin. [2]

Patients received 400 mg riboflavin capsules per day. Headache frequency, duration, intensity and the use of abortive drugs were recorded at baseline and 3 and 6 months after treatment. Headache frequency was significantly reduced from 4 days/month at baseline to 2 days/month after 3 and 6 months (P < 0.05). We could demonstrate a significant reduction of headache frequency following riboflavin treatment. In addition, the number of abortive anti-migraine tablets was reduced. In line with previous studies our findings show that riboflavin is a safe and well-tolerated alternative in migraine prophylaxis.[7]

Riboflavin in Treatment of High Blood Pressure / HyperTension

Thus, studies to date indicate that riboflavin supplementation may have benefits in lowering blood pressure and reducing hypertension in individuals (and sub-populations) affected by the common MTHFR C677T polymorphism. [9]

Riboflavin In Treatment Of Neuro-Degeneration and Mitochondrial Dysfunction

Riboflavin regulates the structure and function of flavoenzymes through its cofactors FMN and FAD and, thus, protects the cells from oxidative stress and apoptosis. Hence, it is not surprising that any disturbance in riboflavin metabolism and absorption of this vitamin may have consequences on cellular FAD and FMN levels, resulting in mitochondrial dysfunction by reduced energy levels, leading to riboflavin associated disorders, like cataracts, neurodegenerative and cardiovascular diseases, etc. Furthermore, mutations in either nuclear or mitochondrial DNA encoding for flavoenzymes and flavin transporters significantly contribute to the development of various neurological disorders. Moreover, recent studies have evidenced that riboflavin supplementation remarkably improved the clinical symptoms, as well as the biochemical abnormalities, in patients with neuronopathies, like Brown-Vialetto-Van-Laere syndrome (BVVLS) and Fazio-Londe disease. This review presents an updated outlook on the cellular and molecular mechanisms of neurodegenerative disorders in which riboflavin deficiency leads to dysfunction in mitochondrial energy metabolism, and also highlights the significance of riboflavin supplementation in aforementioned disease conditions. [5]

Treatment of Chrone’s Disease and Anti Enterobacteriaceae

Three weeks of riboflavin supplementation resulted in a reduction in systemic oxidative stress, mixed anti-inflammatory effects, and a reduction in clinical symptoms [HBI]. FISH analysis showed decreased Enterobacteriaceae in patients with CD with low FC levels, though this was not observed in MGS analysis. Our data demonstrate that riboflavin supplementation has a number of anti-inflammatory and anti-oxidant effects in CD. [6]

MTHFR C677 TT – Riboflavin reduces homocysteine

Meta-analyses predict that a 25% lowering of plasma homocysteine would reduce the risk of coronary heart disease by 11% to 16% and stroke by 19% to 24%. Individuals homozygous for the methylenetetrahydrofolate reductase (MTHFR) 677C→T polymorphism have reduced MTHFR enzyme activity resulting from the inappropriate loss of the riboflavin cofactor, but it is unknown whether their typically high homocysteine levels are responsive to improved riboflavin status. From a register of 680 healthy adults 18 to 65 years of age of known MTHFR 677C→T genotype, we identified 35 with the homozygous (TT) genotype and age-matched individuals with heterozygous (CT, n=26) or wild-type (CC, n=28) genotypes to participate in an intervention in which participants were randomized by genotype group to receive 1.6 mg/d riboflavin or placebo for a 12-week period. Supplementation increased riboflavin status to the same extent in all genotype groups (8% to 12% response in erythrocyte glutathione reductase activation coefficient; P<0.01 in each case). However, homocysteine responded only in the TT group, with levels decreasing by as much as 22% overall (from 16.1±1.5 to 12.5±0.8 μmol/L; P=0.003; n=32) and markedly so (by 40%) in those with lower riboflavin status at baseline (from 22.0±2.9 and 13.2±1.0 μmol/L; P=0.010; n=16). No homocysteine response was observed in the CC or CT groups despite being preselected for suboptimal riboflavin status. Although previously overlooked, homocysteine is highly responsive to riboflavin, specifically in individuals with the MTHFR 677 TT genotype. Our findings might explain why this common polymorphism carries an increased risk of coronary heart disease in Europe but not in North America, where riboflavin fortification has existed for >50 years. [9]

Neuro-Inflammation Protection - Riboflavin

The neurotoxic triad is characterized by excitotoxicity, oxidative stress, and neuroinflammation, with each aspect of the triad being able to perpetuate the others inside of the nervous system. It has been suggested in the literature that to adequately address oxidative stress as a contributor to neurodegeneration, that we must also simultaneously address excitotoxicity (Li et al., 2013), but dietary micronutrients may offer an even better solution by reducing all three aspects of the neurotoxic triad, including neuroinflammation. Vitamin C, vitamin E, vitamin D, and riboflavin are key dietary antioxidants which simultaneously protect against excitotoxicity, oxidative stress, and neuroinflammation. Similarly, glutathione also appears to directly affect all three aspects of the neurotoxic triad. Future dietary research should examine how increased intake of these micronutrients, along with other nutrients like vitamins B6 and B12, and magnesium, may be protective against excitotoxicity, oxidative stress, and neuroinflammation. [5,12]

Riboflavin in Protection Against Oxidative Stress, Parkinson’s and Neuro-Degeneration

Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson’s disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future. [5,13]

Riboflavin is a potential neuroprotective agent. In fact, riboflavin has demonstrated its ability to tackle significant pathogenesisrelated mechanisms in neurological disorders, exemplified by the ones attributed to the pathogenesis of PD and migraine. Indeed, riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which are involved in the pathogenesis of a wide range of neurological disorders. In addition, riboflavin is required for pyridoxine activation. Riboflavin and PLP, the active form of pyridoxine, play essential roles in homocysteine metabolism, and tryptophankynurenine pathway. Indeed, any accumulation of homocysteine or kynurenines due to vitamin insufficiency can lead to significant neurological consequences. [13]

Neuro-Protection From Excess Glutamate – Riboflavin

We examined the effect of riboflavin, vitamin B2, on the release of endogenous glutamate from nerve terminals purified from rat cerebral cortex. The release of glutamate evoked by 4-aminopyridine was inhibited by riboflavin. Further experiments indicated that riboflavin-mediated inhibition of glutamate release (i) results from a reduction of vesicular exocytosis, not from an inhibition of nonvesicular release; (ii) is associated with a decrease in presynaptic N-type and P/Q-type voltage-dependent Ca channel activity. These findings are the first to suggest that, in rat cerebrocortical nerve terminals, riboflavin suppresses voltage-dependent Ca channel activity and in so doing inhibits evoked glutamate release. This finding may explain the neuroprotective effects of vitamin B2 against neurotoxicity.[14]

In conclusion, riboflavin and vitamin E had a protective effect on the GTN-induced brain injury by inhibiting free radical production, regulation of calcium-dependent processes, and supporting the antioxidant redox system. [15]

Riboflavin Clears Excess Glutamate - Coincidental with Hydrogen Sulfide SIBO

Hydrogen sulfide SIBO - produces much too much H2S in the gut from the combination of sulfur in the diet and sulfur producing bacteria like Dulsulfivibrio bacteria. Hydrogen Sulfide SIBO tends to be the most recalcitrant of the 3 SIBO types. It also has the most cognitive issues coincidentally. It is by no coincidence that NMDA receptors are activated directly by H2S, and also indirectly from H2S through the TRP receptors[16]. With a compromised gut barrier (intestinal tight juncture compromise), H2s makes its way into the blood stream, and to the brain - causing neuro inflammation and excitatory issues related to NMDA receptors. These features are common in both ME/CFS and MCS (Multiple Chemical Sensitivity) according to Martin Pall [17, 18]. It is also not a coincidence that NMDA receptors and over-active / neuro sensitization with the NMDA receptors based on Martin Pall's work [17, 19]. So, why do i put this here ? B2 clears excess glutamate from the NMDA receptors, and thus calms down the excitatory activity of the NMDA receptors - which calms down some of the neuro inflammation. [19] A breakdown of the blood brain barrier also occurs under these conditions for a variety of cascading factors [19].

Riboflavin in Treatment of Corneal disorders

Corneal ectasia is an eye condition characterized by irregularities of the cornea that affect vision. Corneal cross-linking – a fairly new procedure used by professionals to limit the progression of corneal damage –involves the use of topical riboflavin in conjunction with ultraviolet-A irradiation. Riboflavin functions as a photosensitizer in the reaction. Cross-linking modifies the properties of the cornea and strengthens its architecture.[2]

Riboflavin In Treatment of Multiple sclerosis

Multiple sclerosis (MS) is an autoimmune disease of unknown etiology that is characterized by the progressive destruction of myelin and nerve fibers in the central nervous system, causing neurological symptoms in affected individuals. Riboflavin appears to have a role in the formation of myelin, and oxidative stress has been implicated in the pathogenesis of MS; thus, riboflavin may be helpful in treatment of the disease. A strong inverse association between dietary riboflavin intake and risk for MS was initially observed in a case-control study. In a mouse model of MS (i.e., experimental autoimmune encephalomyelitis), riboflavin supplementation improved clinical measures of the disease. However, a randomized, double-blind, placebo-controlled pilot study in 29 patients with MS found that supplementation with 10 mg/day of riboflavin for six months had no effect on MS-related disability, assessed by the Expanded Disability Status Scale. Large-scale randomized, placebo-controlled trials are needed to determine whether riboflavin supplementation has a beneficial effect in the treatment of MS.[2]

Riboflavin in Treatment of CoQ Enzyme Mutations In Mitochondria (Complex I)

MADD is caused by autosomal recessive mutations in genes that impair the activity of enzymes involved in the transfer of electrons from acyl-coenzyme A (acyl-CoA) to coenzyme Q10/ubiquinone inside the mitochondria. ETFA, ETFB, and ETFDH code for the two subunits of the electron transfer flavoprotein (ETF-A and -B) and for ETF dehydrogenase/ubiquinone oxidoreductase (ETFDH/ETFQO), respectively. Deficiencies in these enzymes (ETF or ETFDH) lead to a decrease in oxidized FAD, which becomes unavailable for FAD-dependent dehydrogenation reactions, including the first step in β-oxidation – a major fatty acid catabolic process that takes place in the mitochondria. A defect in fatty acid β-oxidation causes lipid accumulation in skeletal muscles, leading to lipid storage myopathy characterized by muscle pain and weakness and exercise intolerance.

Together with a low-fat, high-carbohydrate diet, riboflavin supplementation has led to significant clinical improvements in patients with ETFDH mutations. The specific type of the mutation in ETF/ETFDH contributes to age of onset, severity, and responsiveness to riboflavin treatment. Additionally, the report of a 20-year-old man with riboflavin-responsive MADD failed to find mutations in ETF and ETFDH genes, suggesting that other sites of mutation should not be excluded. Finally, secondary deficiencies in the respiratory chain are observed in MADD and appear to respond favorably to riboflavin supplementation. [2]

Acyl-CoA dehydrogenase 9 deficiency (ACAD9) – Mito Complex I

Acyl-CoA dehydrogenase family member 9 (ACAD9) is an FAD-dependent enzyme with important roles in both the electron transport chain and β-oxidation of fatty acids in the mitochondria. Recessive mutations in the ACAD9 gene coding for ACAD9 have been found in patients with mitochondrial complex I deficiency, a respiratory chain disorder. Complex I carries electrons from NADH to coenzyme Q10 in the electron transport chain. Defective oxidative phosphorylation (ATP synthesis by the respiratory chain) due to complex I deficiency has been linked to a broad variety of clinical manifestations, from neonatal death to late-onset neurodegenerative diseases. The clinical symptoms of complex I deficiency due to ACAD9 mutations typically include muscle weakness, exercise intolerance, lactic acidosis, and hypertrophic cardiomyopathy. However, symptoms can be of varying severity, likely due to the remaining functional activity of ACAD9. For example, affected patients have been reported to exhibit a spectrum of cardiac deficits, including isolated, mild ventricular hypertrophy to severe hypertrophic cardiomyopathy.[2]

Riboflavin supplementation (100-300 mg/day) has been shown to increase complex I activity in patients with childhood-onset clinical forms of ACAD9 deficiency. Improvements in muscle strength and exercise tolerance have also been associated with riboflavin supplementation. A review of cases of ACAD9 deficiency presenting in infancy (i.e., cases with severe symptoms) found riboflavin treatment to be associated with improved survival: 7 of 22 patients treated with riboflavin succumbed to the illness compared to 16 out of 17 untreated patients. [2]

Multiple acyl-CoA dehydrogenase deficiency (MADD)

MADD, also known as type II glutaric aciduria (or acidemia), is a fatty acid metabolism disorder characterized by the accumulation of short-, medium-, and long-chain acyl-carnitines in various tissues. MADD is classified into three separate types based on age of onset and clinical symptoms: type I MADD is evident in the neonatal period and is characterized by the presence of congenital anomalies; type II MADD is present in the neonatal period but lacks congenital defects; and type III is characterized by late onset, from infancy through adulthood, and even as late as the seventh decade of life. Clinical symptoms of type I and II MADD present shortly after birth and include hypoglycemia, hyperammonemia, metabolic acidosis, hepatomegaly, and respiratory distress; these forms of MADD are often fatal in infancy, even if treated. Type III MADD usually presents later in life and includes milder symptoms, varying from periodic vomiting, rhabdomyolysis, muscle pain and weakness, and exercise intolerance. Peripheral neuropathy has also recently been reported as a symptom of adult-onset MADD.[2]

Riboflavin-responsive trimethylaminuria

Primary trimethylaminuria is caused by defective oxidation of trimethylamine by a liver flavoprotein called flavin containing mono-oxygenase 3 (FMO3). Individuals with FMO3 deficiency have increased levels of trimethylamine in urine, sweat, and breath. This socially distressing condition is known as "fish odor syndrome" due to the fishy odor and volatile nature of trimethylamine. FMO3 gene mutations are usually associated with mild or intermittent trimethylaminuria; the condition is sometimes limited to peri-menstrual periods in female subjects or to the consumption of trimethylamine-rich food. The clinical management of the condition includes dietary restriction of trimethylamine and its precursors, such as foods rich in choline and seafood, as well as cruciferous vegetables that contain both trimethylamine precursors and FMO3 antagonists. The use of riboflavin supplements was reported in a 17-year-old female patient affected by pyridoxine non-responsive homocystinuria. The disease was initially treated with betaine (a choline derivative), which caused body odor secondary to FMO3 deficiency. Riboflavin supplementation (200 mg/day) reduced trimethylamine excretion and the betaine treatment-related body odor. Similar effects were seen with riboflavin supplementation in two pediatric patients. The data suggest that riboflavin might help maximize residual FMO3 enzyme activity in patients with primary trimethylaminuria. Moreover, a recent case report in a 35-year-old male with HIV described supplemental riboflavin as an effective treatment for secondary trimethylaminuria caused by antiretroviral therapy.[2]


[1] Riboflavin Responsive Mitochondrial Dysfunction in Neurodegenerative Diseases. Tamilarasan Udhayabanu,1 Andreea Manole. J Clin Med. 2017 May; 6(5): 52. Published online 2017 May 5. doi: 10.3390/jcm6050052. PMCID: PMC5447943. PMID: 28475111

[2] Linus Pauling Institute, MicroNutrient Information Center

[3] Adaptive regulation of riboflavin transport in heart: effect of dietary riboflavin deficiency in cardiovascular pathogenesis. Tamilarasan Udhayabanu 1, Sellamuthu Karthi. Mol Cell Biochem. 2018 Mar;440(1-2):147-156. doi: 10.1007/s11010-017-3163-1. Epub 2017 Aug 23. 1, Ayyavu Mahesh 2, Perumal Varalakshmi 3, Andreea Manole 4, Henry Houlden 4, Balasubramaniem Ashokkumar . PMID: 28836047. DOI: 10.1007/s11010-017-3163-1

[4] Riboflavin Deficiency. Navid Mahabadi 1, Aakriti Bhusal 2, Stephen W. Banks. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan. 2022 Jul 18. PMID: 29262062. Bookshelf ID: NBK470460. J Clin Med. PMC5447943

[5] Riboflavin Responsive Mitochondrial Dysfunction in Neurodegenerative Diseases. Tamilarasan Udhayabanu,1 Andreea Manole. J Clin Med. 2017 May; 6(5): 52. Published online 2017 May . doi: 10.3390/jcm6050052. PMCID: PMC5447943. PMID: 28475111. J Clin Med. PMC5447943

[6] Riboflavin Supplementation in Patients with Crohn's Disease [the RISE-UP study]. Clinical Trial. J Crohns Colitis. 2020 Jun 19;14(5):595-607. doi: 10.1093/ecco-jcc/jjz208. Julius Z H von Martels 1, Arno R Bourgonje. Et al. PMID: 31873717. PMCID: PMC7303596. DOI: 10.1093/ecco-jcc/jjz208

[7] High-dose riboflavin treatment is efficacious in migraine prophylaxis: an open study in a tertiary care centre. C Boehnke 1, U Reuter, U Flach, S Schuh-Hofer, K M Einhäupl, G Arnold. PMID: 15257686. DOI: 10.1111/j.1468-1331.2004.00813.x Clinical Trial. Eur J Neurol. . 2004 Jul;11(7):475-7. doi: 10.1111/j.1468-1331.2004.00813.x.

[8] Prophylaxis of migraine headaches with riboflavin: A systematic review. D F Thompson 1, H S Saluja. PMID: 28485121. DOI: 10.1111/jcpt.12548. Review J Clin Pharm Ther. 2017 Aug;42(4):394-403. doi: 10.1111/jcpt.12548. Epub 2017 May 8.

[9] Riboflavin Lowers Homocysteine in Individuals Homozygous for the MTHFR 677C→T Polymorphism. Helene McNulty, Le Roy C. Dowey, J.J. Strain, Adrian Dunne, Mary Ward, Anne M. Molloy, Liadhan B. McAnena, Joan P. Hughes, Mary Hannon-Fletcher and John M. Scott. Originally published27 Dec 2005 2006;113:74–80

[10] Review Neurotoxicology. . 2004 Jan;25(1-2):63-72. doi: 10.1016/S0161-813X(03)00114-1. The FAD binding sites of human monoamine oxidases A and B. Dale E Edmondson 1, Claudia Binda, Andrea Mattevi. PMID: 14697881 DOI: 10.1016/S0161-813X(03)00114-1

[11] Riboflavin Transporter Deficiency. Elisa Cali, MD, Natalia Dominik, BSc, MSc, Andreea Manole, BSc, PhD, and Henry Houlden, MD, PhD. NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. Initial Posting: June 11, 2015; Last Update: April 8, 2021. Adam MP, Everman DB, Mirzaa GM, et al., editors. Seattle (WA): University of Washington, Seattle; 1993-2023.

[12] Micronutrients May Be a Unique Weapon Against the Neurotoxic Triad of Excitotoxicity, Oxidative Stress and Neuroinflammation: A Perspective Kathleen F. Holton*. Nutritional Neuroscience Lab, Department of Health Studies, Center for Neuroscience and Behavior, American University, Washington, DC, United States. This article was submitted to Neuroenergetics, Nutrition and Brain Health, a section of the journal Frontiers in Neuroscience Received: 16 June 2021. Accepted: 31 August 2021. Published: 22 September 2021

[13] Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine Eyad T. Marashly* and Saeed A. Bohlega Department of Neurosciences, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia. This article was submitted to: Neurodegeneration, a section of the journal Frontiers in Neurology Received: 26 April 2017. Accepted: 26 June 2017. Published: 20 July 2017

[14] Vitamin B2 inhibits glutamate release from rat cerebrocortical nerve terminals Su-Jane Wang , Wen-Mein Wu, Feili-Lo Yang, Guoo-Shyng Wang Hsu, Chia-Yu Huang . 2008 Aug 27;19(13):1335-8. doi: 10.1097/WNR.0b013e32830b8afa. PMID: 18695519 DOI: 10.1097/WNR.0b013e32830b8afa [15] Riboflavin and vitamin E increase brain calcium and antioxidants, and microsomal calcium-ATP-ase values in rat headache models induced by glyceryl trinitrate.cBütün A1, Nazıroğlu M, Demirci S, Çelik Ö, Uğuz AC Author information The Journal of Membrane Biology, 26 Nov 2014, 248(2):205-213. DOI: 10.1007/s00232-014-9758-5 PMID: 25425044

[17] NMDA sensitization and stimulation by peroxynitrite, nitric oxide, and organic solvents as the mechanism of chemical sensitivity in multiple chemical sensitivity. Martin L Pall. FASEB J. 2002 Sep;16(11):1407-17. doi: 10.1096/fj.01-0861hyp. PMID: 12205032 DOI: 10.1096/fj.01-0861hyp

[18] Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism. Martin L Pall. Environ Health Perspect. 2003 Sep; 111(12): 1461–1464. doi: 10.1289/ehp.5935. PMCID: PMC1241647. PMID: 12948884

[19] Multiple Chemical Sensitivity: Toxicological Questions and Mechanisms. Martin L. Pall. General and Applied Toxicology, Online  2009 John Wiley & Sons, Ltd. This article is  2009 John Wiley & Sons, Ltd. DOI: 10.1002/9780470744307.gat091. General, Applied and Systems Toxicology in 2011 John Wiley & Sons, Ltd.

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