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Resource Network of The Iodine Movement
IODINE AND HYPOTHYROIDISM pg 3
Inhibition by iodine of the release of thyroxine from the thyroid glands of patients with thyrotoxicosis.
Wartofsky L, Ransil BJ, Ingbar SH.
J Clin Invest. 1970 Jan;49(1):78-86.
A method has been devised which is free of many of the shortcomings of serial epithyroid counting
techniques as an index of the rate of thyroid hormone secretion. By means of this method, the
effect of treatment with Lugol's iodine on the rate of thyroidal secretion of thyroxine (T4) has been
assessed in eight patients with thyrotoxicosis due to diffuse or multinodular goiter. The technique
involves administration of a tracer dose of inorganic 125I followed several days later by an
intravenous tracer dose of 131I-labeled T4. Serial observations of serum protein-bound (PB) 125I
and 131I are accompanied by frequent measurements of endogenous serum T4 (T4-127I)
concentration. Regardless of whether or not its administration was anteceded and accompanied by
the administration of large doses of methimazole, iodine induced a rapid decrease in serum T4-
127I concentration which could not be explained by an increase in the peripheral turnover of T4,
as judged from the metabolism of the 131I-labeled hormone. Hence, the decreased serum T4
concentration could only have resulted from decreased secretion of the hormone by the gland.
Analyses of specific activity relationships between PB125I or T4-127I and PB131I made possible
estimations of the extent to which iodine had decreased the rate of secretion of T4. From such
analysis, and in view of other considerations, it is concluded that the rapid decrease in T4
secretion induced by iodine is not the result of an acute, sustained inhibition of T4 synthesis, but
rather results from an abrupt decrease in the fractional rate of thyroidal T4 release.
Fradkin JE, Wolff J.
Medicine (Baltimore). 1983 Jan;62(1):1-20. Review.
Iodide-induced thyrotoxicosis (IIT) occurs in patients with: 1) endemic goiter; 2) nonendemic goiter;
3) no previous thyroid disease. Iodine prophylaxis for endemic goiter caused transient increase of
0.01-0.04% over the basal incidence of hyperthyroidism peaking at 1-3 years and normalizing in 3-
10 years despite continued iodide exposure. Elderly subjects with large nodular goiters of long
standing are at greater risk. In nonendemic areas, iodine-containing drugs such as amiodarone,
radiographic contrast media or iodochlorhydroxyquinoline are implicated in IIT more often than
iodides. With nonendemic goiter, IIT occurs more commonly in women whereas, in the absence of
preexisting thyroid disease, men are more often affected. In both groups, exophthalmos and
antithyroid antibodies are absent, radioiodine uptake is low, there is no thyroid tenderness or pain,
and the hyperthyroidism is self-limited (1-6 months) and should thus be treated conservatively. IIT
occurs more frequently in areas of marginal iodine intake (Europe) than in the U.S. In view of the
extensive exposure to iodine, it is a rare complication in this country. It is postulated that defective
autoregulation of hormone biosynthesis may contribute to IIT.
Chronic iodine excess does not increase the incidence of hyperthyroidism: a prospective
community-based epidemiological survey in China.
Yang F, Shan Z, Teng X, Li Y, Guan H, Chong W, Teng D, Yu X, Fan C, Dai H, Yu Y, Yang R, Li J,
Chen Y, Zhao D, Mao J, Teng W.
Eur J Endocrinol. 2007 Apr;156(4):403-8.
OBJECTIVE: An increasing incidence of hyperthyroidism has been observed when iodine
supplementation has been introduced to an iodine-deficient population. Moreover, the influence of
chronic more than adequate or excessive iodine intake on the epidemiological features of
hyperthyroidism has not been widely and thoroughly described. To investigate the influences of
different iodine intake levels on the incidence of hyperthyroidism, we conducted a prospective
community-based survey in three communities with mild-deficient, more than adequate (previously
mild deficient iodine intake), and excessive iodine intake.
SUBJECTS AND METHODS: In three rural Chinese communities, a total of 3761 unselected
inhabitants aged above 13 years participated in the original investigation and 3018 of them
received identical examinations after 5 years. Thyroid function, levels of thyroid peroxidase
antibody (TPOAb), thyroglobulin antibody and urinary iodine excretion were measured and thyroid
ultrasound examination was also performed.
RESULTS: In three communities, median urinary iodine excretion was 88, 214, and 634 mug/l (P<0.
05) respectively. The cumulative incidence of hyperthyroidism was 1.4, 0.9, and 0.8% (P>0.05)
respectively. Autoimmune hyperthyroidism was predominant in thyroid hyperfunction in all the
three cohorts. Either positive TPOAb (>50 U/ml) or goiter in original healthy participants was
associated with the occurrence of unsuspected hyperthyroidism in 5 years (logistic regression,
OR=4.2 (95% CI 1.7-8.8) for positive TPOAb, OR=3.1 (95% CI 1.4-6.8) for goiter).
CONCLUSION: Iodine supplementation may not induce an increase in hyperthyroidism in a
previously mildly iodine-deficient population. Chronic iodine excess does not apparently increase
the risk of autoimmune hyperthyroidism, suggesting that excessive iodine intake may not be an
environmental factor involved in the occurrence of autoimmune hyperthyroidism.
Effect of different iodine intake on the prevalence of hypothyroidism in 3 counties in China.
Shan ZY, Li YS, Wang ZY, Jin Y, Guan HX, Hu FN, Teng XC, Yang F, Gao TS, Wang WB, Shi XG,
Tong YJ, Chen W, Teng WP.
Chin Med J (Engl). 2005 Nov 20;118(22):1918-20.
In this study, we found that the prevalence of hypothyroidism varied from 0% to 1.8% in the entire
population, 0.3%-1.8% in women and 0%-0.7% in men. The prevalence of hypothyroidism
increased with increasing iodine supply.［2-4］ The prevalence of hypothyroidism in the elderly
increased from 0.8% to 1.5% and 7.6% with the urinary iodine level increasing from 72 μg/g
creatinine to 100 μg/g creatinine and 513 μg/g creatinine, respectively.［2］
Elevated level of TSH is regarded as an early index to assess impaired thyroid function. Subclinical
hypothyroidism is a definite risk factor for overt hypothyroidism and coronary heart diseases. The
reported prevalence of subclinical hypothyroidism is 2.5%-10.4% in general population, 4%-17% in
women, and 2%-7% in men.［5］ In this study, the effect of iodine on the prevalence of subclinical
hypothyroidism was similar to that of hypothyroidism, and the prevalence of subclinical
hypothyroidism in the elderly was significantly higher in the area with 150 μg/L of UI than that with
38 μg/L UI.［6］
Epidemiological survey on the relationship between different iodine intakes and the prevalence of
Yang F, Teng W, Shan Z, Guan H, Li Y, Jin Y, Hu F, Shi X, Tong Y, Chen W, Yuan B, Wang Z, Cui
B, Yang S.
Eur J Endocrinol. 2002 May;146(5):613-8.
OBJECTIVE: To investigate the effect of different levels of iodine intake on the prevalence of
hyperthyroidism and the impact of universal salt iodization on the incidence of hyperthyroidism.
DESIGN: A comparative cross-sectional and longitudinal survey was conducted in three areas with
borderline iodine deficiency, mild iodine excess (previously mild iodine deficiency) and severe
iodine excess. Universal salt iodization had been introduced 3 years previously except in the area
with borderline iodine deficiency.
METHODS: In total 16 287 inhabitants from three areas answered a questionnaire concerning the
history of thyroid disease. Among them 3761 unselected subjects received further investigations
including thyroid function, thyroid autoantibodies, thyroid ultrasonography and urinary iodine
RESULTS: Among areas with median urinary iodine excretion of 103 microg/l, 375 microg/l and
615 microg/l (P<0.05), the prevalence of hyperthyroidism did not differ significantly (1.6%, 2% and
1.2%). The prevalence of subclinical hyperthyroidism was higher in areas with borderline iodine
deficiency and mild iodine excess than in the area with severe excess iodine intake (3.7%, 3.9%
and 1.1%, P<0.001). The prevalence of Graves' disease and its proportion in hyperthyroidism did
not differ among areas. The incidence of hyperthyroidism did not significantly increase after the
introduction of universal salt iodization.
CONCLUSION: Different iodine intakes under a certain range do not affect the prevalence and
type of hyperthyroidism. Subclinical hyperthyroidism is more prevalent in the iodine deficient area
than in the severe iodine excessive area. In the area with mild iodine deficiency, the introduction of
universal salt iodization may not be accompanied by an increased incidence of hyperthyroidism.