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Iodine and the Body

Iodine and the Breast  

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CLUR

Di-iodothyronine as part of the oestradiol and catechol oestrogen receptor--the role of iodine, thyroid hormones and melatonin in the aetiology of breast cancer.

Clur A.

Med Hypotheses. 1988 Dec;27(4):303-11. Review.

"Hypothyroidism and low iodine intake may be important aetiological factors in oestrogen dependent tumours of the breast, uterus and ovary. They are preventable risk factors. Iodine supplementation will hopefully lead to a decreased incidence of these cancers in future generations.

"The present author proposes that the tyrosyl residue in the hydrophobic oestrogen binding site of the oestrogen receptor is post translationally modified to monoiodotyrosine and hence 3,3' di-iodothyronine monoamine (T2) by peroxidase activity. He has previously proposed that various monoamine receptors are also T2 based. The densities of these receptors are increased in hypothyroidism and they exert control over release of prolactin and other hormones, including melatonin at multiple sites in the hypothalamic--pituitary axis. Melatonin is a metabolite of serotonin and hence melatonin receptors may be T2 or rT3 based as well. These factors could be significant in the aetiology of breast cancer as high prolactin and melatonin levels may be protective.

"Oestrogen receptor density may be increased in hypothyroidism as is certain monoamine receptor density. This would amplify the effect of high circulation oestrogen levels in hypothyroidism and may help explain why hypothyroidism and low iodine intake are risk factors for breast, uterine and ovarian cancer."

Hypothyroidism and hyperparathyroidism associated with lithium toxicity.

Clur AW

S Afr Med J. 1989 Aug 5;76(3):124.

Citation only

Reverse tri-iodothyronine as part of alpha 2 adrenergic receptors.

Clur A

Med Hypotheses. 1986 Nov;21(3):281-92.

Abstract only

"Thyroid hormones affect alpha and beta adrenergic receptor number profoundly. Presynaptic and post synaptic alpha 2 adrenergic receptor number is decreased in hypothyroidism. Behavioural studies show decreased presynaptic alpha 2 adrenergic function in hypothyroidism and increased function in hyperthyroidism. Reverse tri-iodothyronine (rT3) levels are also low in hypothyroidism and levels are high in hyperthyroidism induced by T4 administration. The present author has proposed that rT3 is incorporated into the alpha 2 adrenergic receptor where it provides the aromatic binding site. Tri-iodothyronine (T3) administration does not raise alpha 2 adrenergic receptor numbers above normal control values. This is consistent with the author's hypothesis as T3 cannot be converted to rT3. This paper describes how rT3 could provide the aromatic binding site for drugs that act on alpha 2 adrenergic receptors."

Iodothyronines and iodotyrosines as hypothetical receptors for catecholamines and opiates.

Clur A

Med Hypotheses. 1985 Feb;16(2):97-131.

Abstract only

"The signs and symptoms of hyperthyroidism are similar to those of phaeochromocytoma and adrenergic stimulation. These changes have been attributed to increased beta receptor numbers in hyperthyroidism, resulting in adrenergic supersensitivity. Beta blockers are used in treatment of hyperthyroidism and inoperable phaeochromocytomas. Beta receptor numbers increase in direct proportion to the dose of thyroid hormone given. Hypothyroidism decreases the number of alpha and beta receptors with greater reduction in beta receptor numbers. Beta responses predominate in hyperthyroidism and alpha responses in hypothyroidism. Hypothyroid patients show increased sensitivity to opiates while hyperthyroid patients are tolerant to opiates. In the present paper it is proposed that the various iodothyronine amino acids are incorporated into the various catecholamine and opiate receptors, providing the phenyl binding sites in the receptors. T3 and T4 are proposed as part of beta 1 chronotropic and inotropic receptors and those mediating vasodilation. T2 and rT3 are proposed as part of alpha 1 and alpha 2 receptors and dopamine and opiate receptors. T2 is probably incorporated into beta 2 receptors causing bronchodilation. The different structural features of the various amino acids would account in part for the selectivity of various drugs for various receptors."

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