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Table of Contents | |
VITAMIN B-2, RIBOFLAVIN
Thyroidal function: Facilitates copper metabolism and
therefore slows the thyroid. Supplementation of riboflavin without copper may
deplete copper and promote hyperthyroidism. A deficiency of riboflavin may be a
causative factor in Thyroid Eye Disease (TED).
Vitamin B-2 is the yellow colored B vitamin and is the one
responsible for making your urine yellow. If your urine is not yellow you may
not be getting enough B-2.
Deficiency symptoms: Itchy eyes and eyelids.
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Acta Psychiatr Scand 1992 May;85(5):360-3 |
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Low thyroxine levels in female psychiatric inpatients
with riboflavin deficiency: implications for folate-dependent methylation.
Bell IR, Morrow FD, Read M, Berkes S, Perrone G
Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont.
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 (B2)-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 B2 deficiency (i.e., insufficient FAD activity) on a functional red
blood cell enzyme assay, but only one B2-deficient individual showed
deficiency in another B-complex vitamin (folate). All patients with B2
deficiency were women, who were also significantly younger than the rest of
the sample. The B2-deficient women had significantly lower thyroxine levels,
even when controlling for sex and covarying for age. B2-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 B2 (FAD) activity may serve as a
sensitive marker of thyroxine status in certain female psychiatric
inpatients and that B2 deficiency may play an etiological role in defects of
the methylation pathways in a subset of mentally ill individuals.
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