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Low thyroxine levels in female psychiatric inpatients with riboflavin deficiency: implications for folate‐dependent methylation
Author(s) -
Bell I. R.,
Morrow F.D.,
Read M.,
Berkes S.,
Perrone G.
Publication year - 1992
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1992.tb10319.x
Subject(s) - flavin adenine dinucleotide , riboflavin , etiology , depression (economics) , b vitamins , medicine , schizophrenia (object oriented programming) , endocrinology , tricyclic , methylation , psychiatry , physiology , cofactor , enzyme , biology , biochemistry , pharmacology , gene , macroeconomics , economics
Intermediates in the folate‐dependent methylation pathways may play a role in the etiology and treatment of such mental disorders as major depression. These pathways include a step dependent on a riboflavin (B 2 )‐derived coenzyme, flavin adenine dinucleotide (FAD), which is reportedly sensitive to thyroid status and to phenothiazine and tricyclic drug exposure. In a sample of 52 male and female acute psychiatric inpatients, 17% ( n = 9) showed B 2 deficiency (i.e., insufficient FAD activity) on a functional red blood cell enzyme assay, but only one B 2 ‐deficient individual showed deficiency in another B‐complex vitamin (folate). All patients with B 2 deficiency were women, who were also significantly younger than the rest of the sample. The B 2 ‐deficient women had significantly lower thyroxine levels, even when controlling for sex and covarying for age. B 2 ‐deficient patients exhibited a nonsignificant trend toward more unipolar depression (44% vs 14%), but not toward bipolar or schizophrenic disorders. As in a previous study, drug exposure did not show a relationship to riboflavin deficiency in this sample. The findings suggest that B 2 (FAD) activity may serve as a sensitive marker of thyroxine status in certain female psychiatric inpatients and that B 2 deficiency may play an etiological role in defects of the methylation pathways in a subset of mentally ill individuals.