First, I would like to thank Laura for recognizing my innate righteousness.

Second, there seems to be some major linkages beginning to come to light involving, not only thyroid problems but also vitamin D3 and electrolytes and neurological disorders and our misbehaving immune systems. And it is all so stress responsive. In short, all the things we have been blathering about for the last couple of years is lying there in a great big pile if we can just untangle it.

Here is an abstract of interest (full text is available)-


1. Endocrinology. 2009 Feb;150(2):1051-60. Epub 2008 Oct 16.

Vitamin D deficiency modulates Graves' hyperthyroidism induced in BALB/c mice by
thyrotropin receptor immunization.

Misharin A, Hewison M, Chen CR, Lagishetty V, Aliesky HA, Mizutori Y, Rapoport B,
McLachlan SM.

Autoimmune Disease Unit, Cedars-Sinai Research Institute and University of
California Los Angeles, UCLA School of Medicine, Los Angeles, CA 90095, USA.

TSH receptor (TSHR) antibodies and hyperthyroidism are induced by immunizing mice
with adenovirus encoding the TSHR or its A-subunit. Depleting regulatory T cells
(Treg) exacerbates thyrotoxicosis in susceptible BALB/c mice and induces
hyperthyroidism in normally resistant C57BL/6 mice. Vitamin D plays an important
role in immunity; high dietary vitamin D intake suppresses (and low intake
enhances) adaptive immune responses. Vitamin D-induced immunosuppression may
enhance Treg. Therefore, we hypothesized that decreased vitamin D intake would
mimic Treg depletion and enhance hyperthyroidism induced by A-subunit adenovirus
immunization. BALB/c mice had a reduced ability vs. C57BL/6 mice to generate the
active metabolite of vitamin D (1,25-dihydroxyvitamin D3). Vitamin D deficiency
induced subtle immune changes in BALB/c (not C57BL/6) mice. Compared with mice
fed regular chow, vitamin D-deprived BALB/c mice had fewer splenic B cells and
decreased interferon-gamma responses to mitogen and lacked memory T-cell
responses to A-subunit protein. However, vitamin D deficiency did not alter TSHR
antibody responses measured by ELISA, TSH binding inhibition, or cAMP generation
from TSHR-expressing cells. Unexpectedly, compared with vitamin D-sufficient
mice, vitamin D-deficient BALB/c mice had lower preimmunization T(4) levels and
developed persistent hyperthyroidism. This difference was unrelated to the
immunological changes between vitamin D-deficient or -sufficient animals.
Previously, we found that different chromosomes or loci confer susceptibility to
TSHR antibody induction vs. thyroid function. Our present studies provide
evidence that an environmental factor, vitamin D, has only minor effects on
induced immunity to the TSHR but directly affects thyroid function in mice.

PMCID: PMC2646531
PMID: 18927213 [PubMed - indexed for MEDLINE]