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close this bookThe Prevention and Control of Iodine Deficiency Disorders - Nutrition policy discussion paper No. 3 (UNSSCN, 1988, 130 p.)
close this folder2.5 ANIMAL MODELS
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View the document2.5.1 IODINE DEFICIENCY IN SHEEP
View the document2.5.3 IODINE DEFICIENCY IN RATS


Studies on rats using diets consumed in two endemic areas in China were carried out. In both instances foetal hypothyroidism was produced.

The most extensive studies were carried out by Li et al. (1985) using the diet consumed by the people of Jixian village in northern Heilongyang province. This village, as already noted (Section 2.4), was severely iodine-deficient with an endemic cretin rate of 11.4 percent. The diet included available main crops (maize, wheat), vegetables from the area with an iodine content of 4.5 mcg/kg (Li et al., 1985) and water (1.0 mcg of iodine per litre). The rats were housed and fed in a specially constructed animal laboratory in the village. Control animals received the same diet with the addition of iodine providing 54.7 mcg iodine/kg. Special attention was paid to the foetal thyroid and brain during gestation (16-20 days) and birth (1-60 days). After the mother had received the diet for four months, there was obvious neonatal goitre (T-4 3.6 mcg percent compared with controls 10.4 mcg percent), and higher 1(125) uptake, with reduced brain weight. The density of brain cells was increased in the cerebral hemispheres. The cerebellum showed delayed disappearance of the external granular layer with reduced incorporation of tritium labelled leucine in comparison with the control group.

Similar effects have been reported with the iodine-deficient diet (mainly rice) being consumed in south China in Guijou province (Zhong et al., 1983).

Extensive studies have also been carried out with mice, using the iodine-deficient diet consumed in Chemeng, Inner Mongolia. There were definite effects on learning capacity observable in over 10 generations (Ma et al., 1983).

So far, in these Chinese models the effects observed are those of foetal hypothyroidism as in sheep and marmosets. In spite of the predominant occurrence of neurological cretinism in the two endemic areas studied in north-east and south China, this condition has not yet been reproduced in rats. This may yet occur in succeeding generations and with more extended observations into the post-natal period. There may, however, be other environmental factors which together with iodine deficiency produce the condition.

Other studies of iodine-deficient rats by Escobar et al. (1986) have demonstrated a decreased reproductive competence in The adult rats, with a reduced number of viable embryos. These findings are consistent with human data indicating reproductive failure (stillbirths) which can be prevented by correction of iodine deficiency (McMichael et al., 1980). The demonstration of cerebral hypothyroidism in iodine-deficient rats has already been cited.

Implications of Results from Animal Models

These results from animal models provide strong support for the human observations of the major effects of iodine deficiency on growth and development. When taken together they have major policy implications.

The implications of these human and animal observations are that iodine deficiency is responsible for a massive problem of reduced mental function due to the lowered level of thyroid resources in the blood affecting the brain. This condition can be reversed by increasing iodine intake, which means that millions of people living in iodine-deficient regions can benefit from removal of this impediment to the achievement of their genetic potential.