I've been spending some time trying to absorb Dr. Ben Lynch's site, mthfr.net/ . One of many things I came across was this.
Proc Soc Exp Biol Med. 1987 Feb;184(2):151-3.
Riboflavin metabolism in the hypothyroid human adult.
Cimino JA, Jhangiani S, Schwartz E, Cooperman JM.
Abstract
It had been shown that thyroxine regulates the conversion of riboflavin to riboflavin mononucleotide and flavin adenine dinucleotide (FAD) in laboratory animals. In the hypothyroid rat, the flavin adenine dinucleotide level of the liver decreases to levels observed in riboflavin deficiency. We have shown that in six hypothyroid human adults, the activity of erythrocyte glutathione reductase, an accessible FAD-containing enzyme, is decreased to levels observed during riboflavin deficiency. Thyroxine therapy resulted in normal levels of this enzyme while the subjects were on a controlled dietary regimen. This demonstrates that thyroid hormone regulates the enzymatic conversion of riboflavin to its active coenzyme forms in the human adult.
ncbi.nlm.nih.gov/pubmed/?te...
The MTHFR gene defect also relates to thyroid problems.
Dr. Lynch:
Simple question: are you saying that MTHFR can cause thyroid disorders? How could so many people with thyroid disorders also have MTHFR and one not cause the other? Thanks.
Dr. Lynch Replied:
"Both ways – hypothyroidism can cause MTHFR downregulation – just like it would be having a snp for the MTHFR gene.
The MTHFR snp can cause thyroid issues due to lower biopterin recycling which causes decreased tyrosine levels and thus thyroid hormones."
It never gets any simpler. We are one complicated little bio-physics, bio-chemistry machine. PR