Iodine Articles 4

© 2012

Triiodothyronine and thyroxine in the serum and thyroid glands of iodine-deficient rats

            (Abrams and Larsen 1973) Download

Triiodothyronine (T(3)) and thyroxine (T(4)) were measured by immunoassay in the serum and thyroid hydrolysates of control (group A), mildly iodine-deficient (group B), and severely iodine-deficient rats (group C). These results were correlated with changes in thyroidal weight, (131)I uptake and (127)I content as well as with the distribution of (131)I in Pronase digests of the thyroid. There was a progressive increase in thyroid weight and (131)I uptake at 24 h with decrease in iodine intake. The (127)I content of the thyroids of the group B animals was 44% and that of the group C animals 2% of that in group A. The mean labeled monoiodotyrosine/diiodotyrosine (MIT/DIT) and T(3)/T(4) ratios in group A were 0.42+/-0.07 (SD) and 0.12+/-0.01, 0.59+/-0.06 and 0.11+/-0.03 in group B, and 2.0+/-0.3 and 1.8+/-0.9 in the group thyroid digests.Mean serum T(4) concentration in the control rats was 4.2+/-0.6 (SD) mug T(4)/100 ml, 4.5+/-0.3 mug/100 ml in group B animals, and undectectable (<0.5 mu(4)/100 ml) in group C animals. There was no effect of iodine deficiency on serum T(3) concentrations, which were 44+/-9 (Mean+/-SD) ng/100 ml in A animals, 48+/-6 ng/100 ml n B animals, and 43+/-6 ng/100 ml in the C group. Thyroidal digest T(3) and T(4) concentrations were 39 and 400 ng/mg in group A animals and were reduced to 5 and 1% of this, respectively, in group C. The molar ratio of T(3)/T(4) in the thyroid digests of the groups A and B animals was identical to the ratio of labeled T(3)/T(4) and was slightly less (1.0+/-0.9) than the labeled T(3)/T(4) ratio in the group C animals. The mean ratio of labeled T(4) to labeled T(3) in the serum of the severely iodine-deficient animals 24 h after isotope injection was 11+/-1 (SEM). With previously published values, it was possible to correlate the ratio of labeled T(4)/T(3) in the thyroid digest with the labeled T(4)/T(3) ratio in the serum of each iodine-deficient animal. This analysis suggested that the labeled thyroid hormones in the severely iodine-deficient rat were secreted in the ratio in which they are present in the gland. Kinetic analysis of total iodothyronine turnover indicated that two-thirds of the T(3) utilized per day by the iodine-sufficient rat arises from T(4). If the T(4)-T(3) conversion ratio remains the same in iodine deficiency, then the analysis suggests that about 90% of the T(3) arises directly from the thyroid. Therefore, it would appear that absolute T(3) secretion by the thyroid increases severalfold during iodine deficiency. The fact that serum T(3) remains constant and T(4) decreases to extremely low levels, combined with previous observations that iodine-deficient animals appear to be euthyroid, is compatible with the hypothesis that T(4) in the normal rat serves primarily as a precursor of T(3).

Potassium iodide in bronchial asthma

            (Bernecker 1969) Download

An evaluation of potassium iodide as a therapeutic agent in the treatment of experimental hypercholesteremia and atherosclerosis

            (Byers, Friedman et al. 1956) Download

Blood Iodine Studies : VII. The Relation of the Basal Metabolic Rate to the Blood Iodine in Thyroid Disease

            (Curtis and Fertman 1945) Download

Iodine deficiency disease

            (Edward 1948) Download

The Effect of Iodine and Thyroid Feeding on the Thyroid Gland

            (Frazier and Mosser 1929) Download

The Use of Potassium Iodide in Hyperthyroidism

            (Frazier 1932) Download

The Effect of Potassium Iodide, Thyroid Extract and Anterior Pituitary Extract Upon Regeneration and Early Compensatory Hypertrophy of the Thyroid Gland

            (Gray 1929) Download

The Effect of Combined Potassium Iodide and Thyroid Substance Upon the Thyroid Gland

            (Gray and Rabinovitch 1929) Download


Hypothesis: dietary iodine intake in the etiology of cardiovascular disease

            (Hoption Cann 2006) Download

This paper reviews evidence suggesting that iodine deficiency can have deleterious effects on the cardiovascular system, and correspondingly, that a higher iodine intake may benefit cardiovascular function. In recent years, public health bodies have aggressively promoted sodium restriction as a means of reducing hypertension and the risk of cardiovascular disease. These inducements have led to a general decline in iodine intake in many developed countries. For example, a United States national health survey conducted in the early 1970s observed that 1 in 40 individuals had urinary iodine levels suggestive of moderate or greater iodine deficiency; twenty years later, moderate to severe iodine deficiency was observed in 1 in 9 participants. Regional iodine intake has been shown to be associated with the prevalence of hypothyroidism and hyperthyroidism, where autoimmune hypothyroidism is the more common of the two in regions with moderate to high iodine intake. Both of these thyroid abnormalities have been shown to negatively affect cardiovascular function. Selenium, an important antioxidant in the thyroid and involved in the metabolism of iodine-containing thyroid hormones, may play an interactive role in the development of these thyroid irregularities, and in turn, cardiovascular disease. Iodine and iodine-rich foods have long been used as a treatment for hypertension and cardiovascular disease; yet, modern randomized studies examining the effects of iodine on cardiovascular disease have not been carried out. The time has come for investigations of sodium, hypertension, and cardiovascular disease to also consider the adverse effects that may result from mild or greater iodine deficiency.

Triiodothyronine, thyroxine, and iodine in purified thyroglobulin from patients with Graves' disease

            (Izumi and Larsen 1977) Download

Previous studies have suggested that there is an overproduction of triiodothyronine (T(3)) relative to thyroxine (T(4)) in patients with thyrotoxicosis associated with Graves' disease. To evaluate whether or not an increased ratio of T(3) to T(4) in thyroidal secretion could be contributing to this relative T(3) hyperproduction, T(3), T(4), and iodine were measured in thyroglobulin (Tg) from controls and patients with Graves' disease who had been treated either with propranolol only or with antithyroid drugs plus iodide before surgery. To avoid possible artifacts associated with pulse labeling and chromatography, T(3) and T(4) were determined by radioimmunoassay of Pronase hydrolysates of purified Tg. Results of analyses of Tg from six control patients and seven with Graves' disease, not receiving thiourea drugs or iodide, showed that the iodine content of Graves' disease Tg was not different from normal. Both contained 3.4 residues of T(4)/molecule Tg, but there was 0.39+/-0.08 (mean+/-SD) residue of T(3)/molecule Tg in Graves' Tg as opposed to 0.23+/-0.07 residue T(3) molecule Tg in controls matched for iodine content (P < 0.01). This difference resulted in a significantly lower T(4)/T(3) molar ratio (9+/-2) in Graves' Tg as opposed to control (15+/-2, P < 0.001). In Tg from patients with treated Graves' disease, iodine, T(3), and T(4) were reduced, but the reduction in the latter was more substantial, resulting in a T(4)/T(3) molar ratio of 3.4+/-1. Fractionation of Tg from all groups by RbCl density gradient ultracentrifugation indicated that at physiological levels of Tg iodination, the molar ratio of T(3)/Tg was consistently higher in Graves' disease. The specific mechanism for this difference is not known, but it is not due to iodine deficiency. If T(3) and T(4) are secreted in this altered ratio in patients with Graves' disease, the magnitude of the difference could explain the relative T(3) hyperproduction which is characteristic of this state.

New Zealand Views on Goitre

            (Jones 1928) Download

Simple goitre is highly prevalent in New Zealand, and there is considerable incidence of toxic goitre. The aetiology of simple goitre seems fairly well established, and an attempt is being made to apply the data from simple goitre to the problems of toxic goitre.Endemic goitre is of great antiquity among the Maoris, and has been described among Europeans for about fifty years. It occurs in both men and animals. At five years its incidence is similar in boys and girls, later it decreases in boys but increases greatly in girls. It is often hereditary, and many children are born goitrous. In children it is generally small, but may enlarge and cause pressure, myxoedema and toxicity. Its incidence varies greatly in different districts.The only cause found consistent with this variation in distribution is lack of iodine in the soil. An inverse ratio has been demonstrated between the iodine content of the soil and the incidence of goitre in school children in thirty-three districts. The iodine content of the soil is reflected in the food raised upon it.The daily iodine intake was estimated at 35 microgrammes in a non-goitrous, and at 20 microgrammes in a goitrous district.The amount of iodine involved is infinitesimal, and its intake can be ensured by the use of salt for ordinary consumption, which contains four parts per million of potassium iodide.TOXIC GOITRE IS ALSO FREQUENT: in this connexion, the influence of iodine on the thyroid has been investigated. If starved of iodine the thyroid adapts itself either by increasing its colloid or by a diffuse hyperplasia, both may occur in different parts of the same gland. Simple goitre is the response of the healthy thyroid to iodine deficiency, the responding areas may be diffuse or adenomatous, and degenerations may occur. Such goitres may be treated with iodine, in children re-adjustment to the increased intake is readily made, but in adults long accustomed to a low intake, excess often causes too great hormone production, with toxic symptoms, hence the minimal dose alone is permissible in iodized salt.Goitre stored with iodine at low pressures may become toxic under stress, and this may be precipitated by iodine. The prevalence of toxic goitre may be partly due to the prescription of iodides in therapeutic doses for common ailments.Diffuse colloid goitre may subside under physiological iodine, the adenomatous is more prone to toxic symptoms and may go on to secondary Graves' disease or to myxoedema. Diffuse hyperplasia is a possible manifestation of iodine deficiency as primary Graves' disease. Lugol's solution probably allows of a temporary storage in this condition. Iodine has certainly some bearing on the problems of toxic goitre.

Iodine intake as a determinant of thyroid disorders in populations

            (Laurberg, Cerqueira et al. 2010) Download

Depending on the availability of iodine, the thyroid gland is able to enhance or limit the use of iodine for thyroid hormone production. When compensation fails, as in severely iodine-deficient populations, hypothyroidism and developmental brain damage will be the dominating disorders. This is, out of all comparison, the most serious association between disease and the level of iodine intake in a population. In less severe iodine deficiency, the normal thyroid gland is able to adapt and keep thyroid hormone production within the normal range. However, the prolonged thyroid hyperactivity associated with such adaptation leads to thyroid growth, and during follicular cell proliferation there is a tendency to mutations leading to multifocal autonomous growth and function. In populations with mild and moderate iodine deficiency, such multifocal autonomous thyroid function is a common cause of hyperthyroidism in elderly people, and the prevalence of thyroid enlargement and nodularity is high. The average serum TSH tends to decrease with age in such populations caused by the high frequency of autonomous thyroid hormone production. On the other hand, epidemiological studies have shown that hypothyroidism is more prevalent in populations with a high iodine intake. Probably, this is also a complication to thyroid adaptation to iodine intake. Many thyroid processes are inhibited when iodine intake becomes high, and the frequency of apoptosis of follicular cells becomes higher. Abnormal inhibition of thyroid function by high levels of iodine is especially common in people affected by thyroid autoimmunity (Hashimoto's thyroiditis). In populations with high iodine intake, the average serum thyroid-stimulating hormone (TSH) tends to increase with age. This phenomenon is especially pronounced in Caucasian populations with a genetically determined high tendency to thyroid autoimmunity. A small tendency to higher serum TSH may be observed already when iodine intake is brought from mildly deficient to adequate, but there is at present no evidence that slightly elevated serum TSH in elderly people leads to an increase in morbidity and mortality. Conclusion: Even minor differences in iodine intake between populations are associated with differences in the occurrence of thyroid disorders. Both iodine intake levels below and above the recommended interval are associated with an increase in the risk of disease in the population. Optimally, iodine intake of a population should be kept within a relatively narrow interval where iodine deficiency disorders are prevented, but not higher. Monitoring and adjusting of iodine intake in a population is an important part of preventive medicine.

The Use of Lugol's Solution in the Treatment of Exophthalmic Goitre

            (Mason 1924) Download

The Effect of Combined Feeding of Potassium Iodide and Anterior Lobe of the Pituitary upon the Thyroid Gland

            (McCordock 1929) Download

Iodine status and its correlations with age, blood pressure, and thyroid volume in South Indian women above 35 years of age (Amrita Thyroid Survey)

            (Menon, Chellan et al. 2011) Download

BACKGROUND: Thyroid disorders are more commonly seen among females and the prevalence increases with age. There is no population data from India focusing on iodine levels and their correlations with thyroid volume and other factors in adult women. AIM: This study was designed to establish the iodine status and its relation with various factors including thyroid volume measured by ultrasound among the females of Kerala. MATERIALS AND METHODS: This was a cross sectional house to house survey among the females above 35 years of age in a randomly selected urban area in Cochin Corporation, Kerala State, India. Selected subjects were interviewed, examined and blood and urine tests were done. Thyroid volume was calculated using ultrasound. RESULTS: Among the 508 subjects who participated in the checkup, 471 subjects were included for analysis. Mean age was 50.3 + 10.7 years and 53.2% were postmenopausal. A total of 98% of the subjects were using iodized salt and median urinary iodine excretion (UIE) was 162.6 mcg/l. UIE had negative correlation with age and systolic blood pressure (BP), but had no correlation with thyroid volume (TV), thyroid nodularity, free thyroxine 4 (FT4), thyroid stimulating hormone (TSH) or anti thyroid peroxidase (TPO) levels. Iodine deficiency was more commonly seen in subjects with hypertension and also among postmenopausal females. CONCLUSIONS: This study showed that females > 35 years were iodine sufficient, though one third of the subjects had UIE levels less than the recommended level. Iodine levels had significant negative correlation with age and systolic BP and no correlation with thyroid volume or biochemical parameters. Iodine deficiency was significantly higher in subjects with new and known hypertension and this relation merits further evaluation.


Recent Contributions in Diseases of the Thyroid and Diabetes

            (Palmer 1931) Download

The Fractionation of the Iodine of the Blood in Thyroid Disease

            (Perkin and Hurxthal 1939) Download

The Effects of Iodine Treatment, with and without Vitamins, on the Basal Metabolic Rate in Exophthalmic Goitre

            (Rabinowitch 1929) Download

IODINE STUDIES: I. The Avidity of the Thyroid Gland for Various Iodine Compounds in Vitro

            (Rabinowitch and Frith 1925) Download

The Treatment of the Thyroid Crisis

            (Snowden 1936) Download

Evaluation of Potassium Iodide as a Thyroid Suppressive Agent and Its Comparison with Triiodothyronine (Cytomel)

            (Spring 1964) Download

Serum Iodine in Hypothyroidism before and during Thyroid Therapy

            (Winkler, Riggs et al. 1945) Download


References

Abrams, G. M. and P. R. Larsen (1973). "Triiodothyronine and thyroxine in the serum and thyroid glands of iodine-deficient rats." J Clin Invest 52(10): 2522-31.

Bernecker, C. (1969). "Potassium iodide in bronchial asthma." Br Med J 4(5677): 236.

Byers, S. O., M. Friedman, et al. (1956). "An evaluation of potassium iodide as a therapeutic agent in the treatment of experimental hypercholesteremia and atherosclerosis." J Clin Invest 35(9): 1015-24.

Curtis, G. M. and M. B. Fertman (1945). "Blood Iodine Studies : VII. The Relation of the Basal Metabolic Rate to the Blood Iodine in Thyroid Disease." Ann Surg 122(6): 963-72.

Edward, J. F. (1948). "Iodine deficiency disease." Can Med Assoc J 58(2): 210.

Frazier, C. H. (1932). "The Use of Potassium Iodide in Hyperthyroidism." Ann Surg 95(4): 517-24.

Frazier, C. H. and W. B. Mosser (1929). "The Effect of Iodine and Thyroid Feeding on the Thyroid Gland." Ann Surg 89(6): 849-56.

Gray, S. H. (1929). "The Effect of Potassium Iodide, Thyroid Extract and Anterior Pituitary Extract Upon Regeneration and Early Compensatory Hypertrophy of the Thyroid Gland." Am J Pathol 5(4): 415-23.

Gray, S. H. and J. Rabinovitch (1929). "The Effect of Combined Potassium Iodide and Thyroid Substance Upon the Thyroid Gland." Am J Pathol 5(5): 485-90.

Hoption Cann, S. A. (2006). "Hypothesis: dietary iodine intake in the etiology of cardiovascular disease." J Am Coll Nutr 25(1): 1-11.

Izumi, M. and P. R. Larsen (1977). "Triiodothyronine, thyroxine, and iodine in purified thyroglobulin from patients with Graves' disease." J Clin Invest 59(6): 1105-12.

Jones, D. W. (1928). "New Zealand Views on Goitre." Proc R Soc Med 21(7): 1217-30.

Laurberg, P., C. Cerqueira, et al. (2010). "Iodine intake as a determinant of thyroid disorders in populations." Best Pract Res Clin Endocrinol Metab 24(1): 13-27.

Mason, E. H. (1924). "The Use of Lugol's Solution in the Treatment of Exophthalmic Goitre." Can Med Assoc J 14(3): 219-21.

McCordock, H. A. (1929). "The Effect of Combined Feeding of Potassium Iodide and Anterior Lobe of the Pituitary upon the Thyroid Gland." Am J Pathol 5(2): 171-178 5.

Menon, V. U., G. Chellan, et al. (2011). "Iodine status and its correlations with age, blood pressure, and thyroid volume in South Indian women above 35 years of age (Amrita Thyroid Survey)." Indian J Endocrinol Metab 15(4): 309-15.

Palmer, W. W. (1931). "Recent Contributions in Diseases of the Thyroid and Diabetes." Bull N Y Acad Med 7(10): 807-25.

Perkin, H. J. and L. M. Hurxthal (1939). "The Fractionation of the Iodine of the Blood in Thyroid Disease." J Clin Invest 18(6): 733-7.

Rabinowitch, I. M. (1929). "The Effects of Iodine Treatment, with and without Vitamins, on the Basal Metabolic Rate in Exophthalmic Goitre." Can Med Assoc J 21(2): 156-60.

Rabinowitch, I. M. and A. B. Frith (1925). "IODINE STUDIES: I. The Avidity of the Thyroid Gland for Various Iodine Compounds in Vitro." J Clin Invest 1(5): 473-81.

Snowden, R. R. (1936). "The Treatment of the Thyroid Crisis." Trans Am Clin Climatol Assoc 52: 225-33.

Spring, M. (1964). "Evaluation of Potassium Iodide as a Thyroid Suppressive Agent and Its Comparison with Triiodothyronine (Cytomel)." J Nucl Med 5: 281-96.

Winkler, A. W., D. S. Riggs, et al. (1945). "Serum Iodine in Hypothyroidism before and during Thyroid Therapy." J Clin Invest 24(5): 732-41.