The Iodine Group

powered by FreeFind
     

Home | Orthoiodosupplementation | Body | Disease | Special | Overviews

Overviews

Summaries

 

UK: Expert Group on Vitamins & Minerals

 

Risk Assessment:  Iodine

UK, Expert Group on Vitamins and Minerals

2003

 

"High levels of iodine are present in marine fish (up to 2.5 mg/kg), shellfish (up to 1.6 mg/kg) and sea salt (up to 1.4 mg/kg). Levels in cereals and grains vary depending on the iodine content of the soil. The food colour erythrosine is also rich in iodine. In the UK, iodine is also present in cows’ milk (average level 0.15 mg/kg), probably as a result of the use of supplemented cattle feeds and iodophors as teat sterilants. The content of iodine in raw food is reduced by cooking. Iodine, as iodide, is present in multivitamin

and mineral supplements (providing up to 0.49 mg iodine/day) and is a component of kelp products. It is also present in licensed medicines, topical antiseptics and radiographic contrast agents."

 

"Iodine is claimed to assist with weight loss, rheumatism, ulcers, hair loss and the maintenance of healthy arteries, nervous tissue and nails."

 

"A variety of mechanisms exist to compensate for low levels of iodine intake. These include enlargement of the thyroid gland (goitre). Only when these mechanisms fail do the clinical signs of hypothyroidism (also known as myxoedema) develop. Symptoms and signs of hypothyroidism include lethargy, weakness, weight gain, poor concentration, oedema, myalgia, dry skin, delayed tendon reflexes and slow heart rate. In pregnancy, iodine deficiency is associated with an increased risk of miscarriage, stillbirth and congenital abnormality. Cretinism is the result of iodine deficiency in the developing foetus, and is characterised by mental retardation, deaf mutism, and spastic diplegia. A less common form of cretinism is the myxoedematous type, which is characterised by hypothyroidism and dwarfism."

 

"Iodine interacts with selenium and possibly with vanadium."

 

"Inorganic iodine (generally in the form of iodide) is readily absorbed, largely from the small intestine. It can also be absorbed through the skin, absorption being increased when the skin is damaged."

 

"Once absorbed, iodine is distributed rapidly throughout the extracellular fluid, secreted into saliva, and enters the gastrointestinal system, from where it is reabsorbed. Iodine can cross the placenta and is secreted into human breast milk."

 

"Iodine is largely excreted in the urine, mainly in the form of iodine. Very small amounts of iodine may be excreted in sweat, feces and exhaled air."

 

"Several biological mechanisms protect against iodine toxicity; these include reduced iodine uptake and preferential production of the more heavily iodinated thyroid hormones. Not all exposed subjects will react to excess iodine.

 

"Clinical features of acute iodine toxicity that have been produced following accidental or deliberate ingestion, or medical procedures such as wound irrigation, include gastrointestinal disturbance (vomiting and diarrhea), metabolic acidosis, seizure, stupor, delirium and collapse. Sensitivity reactions, such as iodide mumps, iododerma and iodide fever may also occur following treatment with iodine-containing drugs, or the use of radiographic contrast media. Chronic and sub-chronic toxicity have also been identified.

 

"Excess iodine or iodide intake may disrupt thyroid function, resulting in the induction of hypothyroidism with or without goitre, hyperthyroidism (thyrotoxicosis) and changes in the incidence and types of thyroid malignancies. Responses of this type frequently occur where there is general high iodine intake or where intervention has taken place to correct iodine deficiency. The pattern of effects changes over time as iodine exposure in the population changes. For example, in the UK, the possibility of iodine induced hyperthyroidism associated with prior iodine deficiency appears to be less common due to recent increases in the iodine intake of the population as a whole.

 

"No data have been identified on the carcinogenicity of iodine. Both iodine deficiency and excess can promote tumor formation in animals pre-exposed to known carcinogens. Metaplasia of the thyroid was reported in rats given potassium iodide in drinking water for two years. This was thought to occur via a non-genotoxic proliferation dependent mechanism. Human epidemiological studies have shown variations in the incidence of thyroid cancer, depending on the levels of iodine available in water supplies in these areas. The type of cancer appears to differ depending on whether iodine levels are deficient or excess. Changes to the pattern of thyroid tumours have been noted after prophylaxis. The mutagenicity data for iodine are generally negative."

 

 

Revised Review of Iodine

Expert Group on Vitamins and Minerals Secretariat

August 2002

 

Summary

183. Iodine is a halogen. At room temperature it is a blue-black solid which sublimes into a gaseous form. Iodine is present in seaweed, igneous rocks and some soils.

 

184. In the diet, iodine is naturally present in marine fish, shell fish and sea salt. Levels in cereals and grains vary depending on the soil content. The food colour erythrosine is also rich in iodine. In the UK, iodine is also present in cows’ milk probably as a result of the use of supplemented cattle feeds and iodophors as  sterilants. Iodine is present in food supplements both in its elemental from and as a component of kelp products. It is also present in licensed medicines, topical antiseptics and radiographic contrast agents.

 

185. In the UK, the mean adult intake of iodine from food is estimated to be 0.219 mcg/day. High level (97.5th percentile) intake in adults is estimated to be 0.434 mcg/day. On a body weight basis, iodine intakes in children are higher than those in adults as a result of the larger proportion of milk consumed. Iodine intake from water is estimated to be generally less than 30 mcg/day. The LRNI and RNI for iodine is 70 and 140 mcg/day respectively.

 

186. Iodine interacts with selenium and possibly vanadium. Natural goitrogens in the diet derived from plants such as cassava, maize, potato, cauliflower and broccoli as well as ions present in drinking water interfere with iodine metabolism.

 

187. Iodine is readily absorbed, largely from the small intestine. It can also be absorbed dermally, particularly when the skin is damaged. Once absorbed, iodine is distributed rapidly throughout the extracellular fluid. Iodine can be secreted into saliva or gastric juices and reabsorbed. It can cross the placenta and is secreted into human milk.

 

188. The thyroid gland is the only significant store of iodine. Uptake of iodine by the thyroid is determined by need, a process mediated by thyroid stimulating hormone (TSH). It is then incorporated into thyroid hormones within a large protein, thyroglobulin; this protein is then stored in the colloid of the thyroid gland.

 

189. Iodine is largely excreted in the urine with all circulating iodine being cleared regardless of the circulating concentrations. Very small amounts may be excreted in sweat and in faeces.

 

190. Thyroid hormones are involved in the maintenance of metabolic rate, cellular metabolism and cellular integrity. In the developing foetus and infant, thyroid hormones are necessary for the development of the nervous system. A variety of mechanisms exist to compensate for low levels of iodine intake. These include enlargement of the thyroid gland a condition known as goitre. Only when these mechanisms fail do the clinical signs of hypothyroidism (also known as myxoedema) become apparent. Symptoms include lethargy, weakness, weight gain, poor concentration, oedema, muscle ache, dry skin, delayed reflexes and slow cardiac rhythm. In pregnancy, iodine deficiency is associated with in an increased risk of miscarriage, still birth and congenital abnormalities. In the developing foetus, the major feature of deficiency is endemic cretinism, characterised by mental retardation, deaf mutism and spastic diplegia. A less common form of cretinism, due to hypothyroidism persisting post-natally, is the myxoedematous type, which is characterised by hypothyroidism and dwarfism.

 

191. As with iodine deficiency, a number of mechanisms exist to protect the thyroid against iodine excess. These include reduced iodide uptake by the thyroid, a switch towards the production of the iodine-richer hormones and reduced secretion of thyroid hormones. In humans, the effects of excess iodine can be divided into three types (though not all exposed subjects will react). These are 1) disturbance of thyroid function, resulting in the induction of hypothyroidism and/or goitre, or hyperthyroidism (thyrotoxicosis). These types of responses may occur where there is general high iodine intake or where intervention has taken place to correct iodine deficiency. The patterns of thyroid malignancy may also be altered. 2) Sensitivity reactions, such as iodide mumps, iododerma and iodide fever. These tend to occur following treatment with iodine-containing drugs, or radiographic contrast media. 3) Iodine poisoning. This may occur following accidental or deliberate ingestion, medical procedures such as wound irrigation.

 

192. In animals, symptoms of acute iodine toxicity include diarrhea, alternating periods of hyperactivity, weakness, prostration, convulsions and death. In subchronic toxicity studies, reduced weight gain and haemolysis have been reported in addition to specific effects on the thyroid. BB/W rats are susceptible to the development of lymphocytic thyroiditis and have been used to investigate the mechanism for this condition. No data have been identified on the carcinogenicity of iodine in laboratory animals per se, however, both iodine deficiency and excess can promote tumour formation is animals pre-treated with known carcinogens. Metaplasia has been identified in one chronic study. The available genotoxicity data are negative. Adverse effects on reproduction and development have been reported, but the data are sparse.

 

 Home | Orthoiodosupplementation | Body | Disease | Special Topics | Overviews  
The Iodine Group | Books | Disclaimers | Contact Us | Search  
  Copyright: Zoe, 2006.