Vitamin A (VA) deficiency (VAD) and the
iodine deficiency disorders (IDD) affect > 30% of the global population and these deficiencies often coexist in vulnerable groups. VAD has multiple effects on the pituitary-thyroid axis; VA status modulates thyroid gland metabolism, peripheral metabolism of
thyroid hormone, and production of
thyrotropin (TSH) by the pituitary. Findings from Africa children indicate that VAD in severely-IDD-affected children increases TSH stimulation and thyroid size, and reduces risk for
hypothyroidism. In children with VAD, the higher TSH concentrations in the face of higher circulating total
thyroxine suggest central resistance to normal TSH suppression by
thyroid hormone. In IDD- and VAD-affected children receiving
iodized salt, concurrent VA supplementation improves
iodine efficacy. Recent VA and
iodine depletion studies in rats indicate moderate VAD alone has no measurable effect on the pituitary-thyroid axis; however, concurrent
iodine deficiency (ID) and VAD produce more severe
primary hypothyroidism than ID alone. Repletion studies in VA- and
iodine-deficient animals suggest: 1)
primary hypothyroidism in animals with concurrent moderate VAD and ID does not reduce the efficacy of high doses of oral
VA; 2) VAD does not reduce the efficacy of dietary
iodine to correct pituitary-thyroid axis dysfunction due to
iodine deficiency; and 3) given alone, without
iodine repletion, high-dose VA supplementation in combined VAD and ID may reduce thyroid hyperstimulation and reduce risk for
goiter.