Homoeopathic approach in excess iodine

Dr Bharath.M

ABSTRACT
Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, foetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.

INTRODUCTION
Iodine (atomic weight 126.9 g per atom) is a micronutrient that is required for the synthesis of the thyroid hormones. It is a trace element in Earth’s upper crust and is found primarily in or near coastal areas.

For adults, who are not lactating or pregnant, the US Institute of Medicine, and jointly by the WHO, United Nations Children’s Fund (UNICEF) and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), recommend a daily iodine intake of 150 μg and state a tolerable upper level (the approximate threshold below which notable adverse effects are unlikely to occur in the healthy population) of 1,100 μg per day in adults.

In some susceptible individuals, the use of these iodine-containing substances can result in thyroid dysfunction as a result of the high iodine load. In certain circumstances, iodine excess can result in adverse thyroidal effects after only a single exposure to an iodine-rich substance.

Sources of iodine exposure and potential excess

  • Diet: Kelp (per g): 16–8,165 μg36,Bread (per slice): 2.2–587.4 μg,Milk   (per 8   oz): 88–168 μg80,Fish fillet (per g, dry weight): 0.73 μg , Iodized salt(10gms contains 300 μgs )
  • Vitamins (prenatal, labelled content per daily serving): 75–200 μg46
  • Amiodarone (per 200 mg): 75,000 μg
  • Iodinated contrast (free iodine content, per CT scan): 13,500 μg
  • Topical iodine (povidone iodine): variable, usually 1–5% expectorants, mouthwashes, vaginal douches: variable saturated solution of potassium iodide (per drop) 50,000 μg.

THYROIDAL ADAPTATION TO EXCESS IODINE
The acute Wolff–Chaikoff effect was described in 1948 by Drs Jan Wolff and Israel Lyon Chaikoff at the University of California Berkeley, USA. Wolff and Chaikoff observed a transient reduction (lasting ~24 h) in the synthesis of thyroid hormones in rats exposed to high amounts of iodide administered intraperitoneally. The mechanism for the acute Wolff–Chaikoff effect is not completely understood, but is thought to be at least partially explained by the generation of several inhibitory substances (such as intrathyroidal iodolactones, iodoaldehydes and/or iodolipids) on thyroid peroxidase activity. Reduced intrathyroidal deiodinase activity as a result of the increased iodine load might also contribute to decreased synthesis of thyroid hormones.

In most individuals, the decreased production of thyroid hormones is only transient and resumes after adaptation to the acute Wolff–Chaikoff effect. In rats, this adaptation is associated with a marked decrease in expression of the sodium–iodide symporter (NIS) that is present on the basolateral membrane of thyroid follicular cells. NIS is a 13-transmembrane glycoprotein that mediates the active transport of iodine from the circulation into the thyroid. The decrease in expression of the NIS occurs by 24 h after exposure to excess iodine and results in reduced intrathyroidal iodine concentrations. In turn, the reduced iodine levels lead to a decrease in levels of the iodinated substances that inhibit synthesis of thyroid hormones, which results in the resumption of normal production of thyroid hormone.

IODINE INDUCED HYPERTHYROIDISM
In some susceptible patients, an excess iodine load provides a rich substrate for increased production of thyroid hormones. Iodine-induced hyperthyroidism (the Jod–Basedow phenomenon) was first described in the early 1800s, when thyrotoxicosis was observed to be more common among patients with endemic goiter treated with iodine supplementation than in individuals without goiter. Iodine-induced hyperthyroidism might be transient or permanent, and risk factors include nontoxic or diffuse nodular goiter, latent Graves disease and long standing iodine deficiency. In addition, iodine-induced hyperthyroidism in euthyroid patients with nodular goiter in iodine-sufficient areas has also been reported when iodine supplementation is excessive.

IODINE INDUCED HYPOTHYROIDISM
Vulnerable patients with specific risk factors might have an increased risk of failing to adapt to the acute Wolff–Chaikoff effect.Susceptible patients include those with autoimmune thyroid disease; a previous history of surgery, antithyroid drug therapy for Graves disease; subacute thyroiditis; postpartum thyroiditis; type 2 amiodarone-induced thyrotoxicosis (AIT); hemithyroidectomy; IFNα therapy; and concomitant use of potential goitrogens, such as lithium. Failure to escape from the acute Wolff–Chaikoff effect might also be more likely during fetal development, a period when the hypothalamic–pituitary–thyroid axis is still immature, and during neonatal life.

The underlying mechanism of iodine-induced hypothyroidism remains unclear, but could be attributable to failure to adapt to the acute Wolff–Chaikoff effect, probably because of a damaged thyroid as a result of previous pathological insults. Exposure to high concentrations of iodine might also decrease the release of thyroid hormone, as reported in several small studies that show mild decreases in serum levels of thyroid hormone and increases in the serum level of TSH to the upper limit of the normal range.

HOMOEOPATHIC SCOPE

In MURPHY’S repertory under the chapter Toxicity we have few remedies under iodine poisoning which we can consider.

We are considering Toxicity because anything which is in excess has a toxic effect on the human body.

REMEDIES: IODINE, poisoning, ailments from: (23) ant-c. ant-t. Ars. bell. brom. Calc-i. camph. chin. chinin.s. coff. Conv. Hep. hydr. iod. Kali- i. Iycps-v. merc. Op. Phos. sang. Sec. spong. sulph.

When we read the introduction of Phosphorus in Pocket manual of homoeopathic materia medica by Boericke it is mentioned ‘’ILL EFFECTS OF IODINE AND EXCESSIVE USE OF SALT’’’

References:

  • Nature Reviews Endocrinology 10, 136–142 (2014),Published online 17 December 2013 on The National Center for Biotechnology Information.
  • Indian journal of Endocrinology and metabolism for iodine metabolism and    iodine deficiency disorders.
  • Homoeopathic medical repertory by Robin Murphy.
  • Pocket manual of homoeopathic materia medica by Boericke.

Dr.Bharath.M MD Part I
Guide: Dr.Srinath Rao
Dept. Of Homoeopathic Materia Medica
Father Muller homoeopathic medical college and hospital, Derlakatte,
Mangalore 575018
Email:Bharathblr91@gmail.com

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