There is a link between hypothyroidism and poor MTHFR function. Basically, thyroxine (T4) is needed to convert riboflavin to riboflavin mononucleotide and then flavin adenine dinucleotide (FAD) the form best utilised by the body 2. In hypothyroidsim FAD levels are reduced to levels seen in riboflavin deficiency 2. This is because the thyroid regulates this conversion.
MTHFR is FAD dependent. FAD converts 5,10 mthf to 5 mthf which then converts homocysteine to methionine 1. MTHFR activity is lower in riboflavin deficient people (due to low levels of thyroxine) and homocysteine increases 1. High homocysteine and poor folate status is associated with Down Syndrome pregnancy 3.
Glutathione reductase is FAD dependent and is sensitive to riboflavin deficiency 1. So we see reduced glutathione and ability to detoxify in people with poor thyroid function.
MTHFR may be sensitive to riboflavin status particularly in people with the 677C-T variation of the MTHFR gene 1. In these people supplementation with higher doses of riboflavin could be necessary for the formation of 5-MTHF needed for homocysteine remethylation.
Therefore, using the reduced form of riboflavin as a supplement – FAD – may improve folate utilisation in people who don’t take thyroid medication. It would also reduce homocysteine and increase glutathione synthesis needed for detoxification and improve methylation function in general.
Riboflavin is made in the gut through the activity of bacteria, ensuring a healthy gut microbiome has positive effects on methylation and thyroid function also 4.
https://www.ncbi.nlm.nih.gov/books/NBK6145/
1. Riboflavin and Methylenetetrahydrofolate Reductase
https://www.ncbi.nlm.nih.gov/pubmed/3809170
2. Riboflavin metabolism in the hypothyroid human adult.
https://www.ncbi.nlm.nih.gov/pubmed/19524060
3. The complex relationship between folate/homocysteine metabolism and risk of Down syndrome.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919986/
4. Lactic acid bacteria as a cell factory for riboflavin production
