What Is the Role of Iodine in Thyroid Health - Research Paper Example

What is the Role of Iodine in Thyroid Health? Introduction Iodine is an important mineral that is known to play a pivotal role in various environmental processes such as in the terrestrial ecosystem, and most importantly in the marine coastal environment (LeBlanc et al, 2006). However, when it comes to human health, iodine is just as important as a vital micronutrient, and is therefore crucial for an individual’s health and vitality. The sole source of iodine is from the diet. Iodine is found in iodide form in various foods such as cod, shrimp, tuna, and other seafood. It can also be found in dairy products such as grains, fruits, and vegetables. Iodized table salt is one of the major sources of the nutrient. The recommended dietary intake of iodine for an average adult is 150 micrograms per day. The thyroid gland is one of the major endocrine glands of the human body. The gland secretes two major hormones - thyroxine (T4) and triiodothyronin (T3). Both of these hormones are important for normal growth and development and have an effect on many metabolic processes. Thus, both hyposecretion and hypersecretion of the hormones can lead to disorders of overall endocrine function. (Nussey and Whitehead, 2001) Iodine metabolism in the human body occurs through various stages and involves the hypothalamus, pituitary gland, thyroid gland, and blood. Iodine is also a major component of the thyroid hormones, and the thyroid gland plays the most important role in the metabolism of the nutrient. The gland consists of follicles filled with colloid thyroglobulin. An active transport system assists in the uptake of the mineral into the follicles followed by production of thyroglobulin which contains 140 tyrosine residues. The iodide form is then oxidized to iodine and iodination of the tyrosine residues of thyroglubulin occurs. Iodination occurs at the 3’ position forming monoiodotyrosine (MIT), followed by iodination at the 5’ position resulting in formation of diiodotyrosine (DIT). This is followed by a coupling reaction leading to formation of T3 and T4 hormones. The thyroglobulin is fused with lysosome containing proteolytic enzymes which digest the thyroglobulin molecule and release the hormones. These hormones then circulate in the blood stream. MIT and DIT get de-iodinated thereby recycling the iodide (Ahad and Ganie, 2010). Being an important mineral for human health, a deficiency in iodine is likely to affect the thyroid system which could lead to several adverse effects on the overall health of an individual at each and every stage of his/her life - from the fetus to adulthood. However, in some cases excessive iodine can also be detrimental. Therefore, balanced intake of iodine from the diet is absolutely essential for the prevention of thyroid related disorders. Iodine and Thyroid Related Problems Iodine is an important nutrient for development and overall health, and appropriate intake is important for maintaining the function of the thyroid system. Thus, an imbalance in iodine intake (either in the form of excess of decreased intake) could lead to thyroid related diseases. Problems associated with iodine deficiency are prevalent in many countries, especially those which are developing and are under-developed. One of the main signs of iodine deficiency is the enlargement of the thyroid gland, also referred to as goiter. Before the 1990s, only a handful of countries such as the USA, Canada, Australia, and Switzerland were iodine sufficient; whereas most other countries in the world lacked iodine in their everyday diet. Statistics show that on a yearly basis more than 17 million babies are born in Asia with considerable brain damage as a result of iodine deficiency (Zimmermann et al, 2008). The main problem has been availability of iodized salt in both rural and urban areas. A similar situation has been seen in African countries. As a result, most governments have initiated fortification programs to combat the growing problem of iodine deficiency. Aweke et al. conducted a study across Ethiopia to understand the magnitude and causes of goiter in the region. Five hundred and thirteen school children and their biological mothers were questioned and clinically examined for presence of goiter. The study was conducted in areas of cultivation, where surplus crops such as legumes, oils, chilies etc. were grown. Urinary iodine analysis was carried out according to international standards to estimate the amount of iodine in the bodies of the participants. The results showed that the goiter rate among school children was much higher than that recorded during the last national survey in 2005. In 2014, it stands at 54.5%, and girls are more affected than boys. Also, in women of reproductive age, the prevalence of goiter was found to be 31.7%. The main reason for this was that the area of cultivation had increased their use of pesticides such as DDT, malathion, aluminum phosphate, and 2,4-D acid for crop protection. Previous studies have shown the negative effects of chemical usage on crops and uptake of iodine. This study also successfully showed that iodine availability is affected by both dietary and environmental factors (Aweke et al., 2014). It is well established that iodine deficiency impairs thyroid function, however, some studies have also shown that excess intake of iodine can also lead to the inhibition of thyroid hormone synthesis and the development of hypo- and hyperthyroidism. Teng et al. conducted a cohort study in China to study the impact of different concentrations of iodine intake on thyroid disorders (Teng et al, 2006). Since 1996, China has fortified their salt with iodine and this has led to an increase in iodine intake all across the country. The authors compared three different populations consuming different amounts of iodine: mildly deficient, more than adequate, and excessive. The iodine deficient population hailed from Pashan, where inhabitants consumed local salt, which lacked iodine and thus caused the development of chronic iodine deficiency among a number of individuals in the community. Residents of Zhangwu represented the population that consumed a more than adequate amount of iodine, while the population that consumed an excessive amount of iodine consisted of residents from Huanghua. These particular residents consumed drinking water, which had very high levels of iodine. In both the baseline, as well as the five-year follow up study, the levels of thyrotropin, thyroglobulin antibody, thyroglobulin level, and level of thyroid peroxidase antibody in each of the subjects were measured. Statistical analysis was conducted, and results showed that an increase in iodine uptake was associated with elevated instances of hypothyroidism. Therefore, it was deduced that above adequate and excessive intake of iodine leads to the development of hypothyroidism and autoimmune thyroiditis. In addition to China, where several regions have water rich in iodine content, several other regions in Japan and Korea are rich in natural dietary iodine. Investigations show that a dietary pattern rich in iodine is associated with thyroid cancer and autoimmune thyroid disease (Luo et al., 2014). Several other investigations have been conducted in different parts of the world in order to understand the association between excessive iodine intake and thyroid malfunctions. In a study initially meant to investigate iodine deficiency in the northern province of Iran, Dalili et al. instead found the youth population to be at risk for development of hyperthyroidism. The prevalence of iodine deficiency disorder (IDD) was investigated in neonates and school children in Guilan, Iran. Neonates born between 2006 and 2010 were screened for congenital hypothyroidism, while biochemical analysis for urinary iodine level was conducted in 1200 school children. The results showed that the study area was in fact a non-IDD endemic area, as the incidence rate of congenital hypothyroidism was only 1/625. However, the authors found that the median urine iodine level in the school children group was 200-299 μg/l. They thus concluded that the health care systems should pay more attention to the excess iodine consumption and in turn the increased risk of iodine induced hyperthyroidism in this population (Dalili et al., 2012) Medani et al. (2013) conducted a nationwide study on the prevalence of goiter in Port Sudan City, located on the western bank of the Red Sea. Previous studies had found that in spite of high iodine output in urine, high prevalence of goiter was observed among individuals in the region. Male and female school children aged 6-12 years were recruited as study subjects. Blood and urine samples were collected from 31 students from Port Sudan City, and also from 329 students hailing from other Sudanese cities. Since excessive iodine has the potential to block the synthesis of the thyroid hormone, depression in levels of T3 and T4 could be employed for detection. The serum samples were therefore analyzed for T4, T3, TSG, and thyroglobulin. Statistical analysis was conducted and it was seen that the prevalence of goiter in Port Sudan was about 34.86%. Twenty-four of the 31 Sudan City pupils were found to have urinary iodine concentrations greater than 30mg/dl. Thus, it was deduced that in contrast to other cities, in which goiter is prevalent because of iodine deficiency, the cases of goiter in Port Sudan City were a result of excessive iodine intake. The results of the study therefore showed that excessive intake of iodine could produce far greater negative effects than could iodine deficiency. Iodine deficiency can be tolerated and even overcome by the thyroid gland, however no such resistance is seen in the case of excess iodine concentration in the body (Medani et al., 2013). Some researchers believed that those with excess iodine-induced hypothyroidism had underlying problems with their thyroid function. However according to a study conducted by Hwang et al. it was seen that changes in iodine intake can also affect individuals with normal thyroid function. The researchers studied 337 Korean subjects who had normal thyroid functioning, without a history of autoimmune thyroid disease, and obtained normal levels of thyroglobulin antibodies and thyroid peroxidise antibodies from urine samples. These subjects were known to have a very high intake of iodine from food due to the Korean peninsula being surrounded by iodine-rich water on three sides. Statistical analysis showed that urinary iodine had a negative correlation with FT4 and positive correlation with TSH. It was established that high intake of iodine had adverse effects on the thyroid hormones even in individuals with normal thyroid function overall (Hwang et al, 2011). Effects of Salt Fortification At the global level, almost 2 billion people suffer from iodine deficiency and related problems. Most parts of Asia and Sub-Saharan Africa fall under the region known as the iodine deficiency belt. Salt fortified with iodine is one of the major sources of iodine, and since the introduction of fortification in different parts of the world, a reduction in iodine deficiency induced disorders has been observed. However, sudden change in iodine intake has some impacts on human health as well. A prospective population study was conducted by Pederson et al. who investigated the increase in overt hypothyroidism after iodine fortified salt was introduced in Denmark (Pederson et al, 2007). The investigation was carried out between 1997-2005 and comprised of four stages: iodine fortification (IF), voluntary IF, mandatory IF, and late mandatory IF. The study populations included two populations representing two distinctly different parts of Denmark, an iodine-deficient region – Aalborg, and a mildly deficient region - Copenhagen. The results showed that the overall instances of hypothyroidism increased during the study period. The increase was most visible in the young and the middle aged adults. The results initially were not unusual. Denmark had a stable low intake of iodine for a relatively long period of time. The low intake was associated with several problems of thyroid malfunction among the population. However, since fortification in 1998, an increase in the incidence of hypothyroidism cases was observed. This showed that a sudden introduction of iodine can lead to iodine-induced hypothyroidism as well (Pederson et al, 2007). Salt fortification can however be very effective. The success of salt fortification was recently investigated in Iran by Khajedaluee et al. Iran had almost 2 million people whose dietary intake of iodine was far below the required amount, and therefore many individuals in the population suffered from severe deficiency complications such as brain damage. Iodine was added to the country’s salt in an effort to remove this deficiency and ensure better public health. The study was conducted in two stages. One was done before the introduction of fortification, and the other was conducted after fortification began. The study sample consisted of 2150 school students aged between 6-18 years. In 1995 (before fortification) the children were evaluated for goiter. In 2002, the same study sample was analyzed again. The results showed that in seven years, the prevalence of goiter had decreased from 34% to 25.7%. The prevalence of thyroid related diseases had also fallen from 35.8 to 23.5 percent in the urban regions, and from 35.6 to 28.5 in the rural areas. Statistically it was seen that variables such as socioeconomic background and education were also related to goiter prevalence in Iran. Thus the authors also concluded that an increase in number of Iranian students in higher education over the seven year period was in part a result of fortification, supporting that adequate iodine status has an impact on mental function (Khajedaluee et al, 2013). Iodine Intake in Mother and Implications for the Fetus Iodine deficiency in mothers, during and after pregnancy, has severe implications on the fetus and the newborn child. However, awareness of such implications is lacking since most pregnant women do not have a sufficient amount of iodine in their bodies even to this day. Kibirige et al, measured urinary iodide to estimate iodine intake in both pregnant and non-pregnant conditions and established that in the U.K. alone, 3.5% of pregnant women suffered from iodine deficiency while almost 40% were borderline deficient (Kibirige et al, 2004). A fetus growing within an iodine deficient mother is at risk of several damaging diseases such as still birth, cretinism, neurological problems, and retarded brain development. Proper thyroid function is entirely dependent on the availability of dietary iodine in the system, and iodine deficiency has a negative impact on the neural development of the fetus. In 2010, Gong et al, studied the role of doublecortin and NCAM-180 in neural development impairment as a result of iodine deficiency in rats. During the developmental period of the fetus, the mother is the sole source of iodine and therefore iodine deficiency in the mother affects the offspring as well. The rat offspring are unable to synthesize their own thyroid hormone till birth and are therefore depend on the mother. T3 and T4 are major contributors towards the development of the brain especially the hippocampal region. Neural plasticity is a characteristic of the hippocampus where new neurons are added continuously. Doublecortin and NCAM-180 are involved in the various aspects of the hippocampal plasticity. The researchers divided rats into two groups: a control group that was given iodine in their diet, and an experimental group that was fed an iodine-deficient diet. The offspring were sacrificed and histochemical studies were conducted. The results showed that mother rats who were fed iodine deficient food gave birth to pups who had impaired nerve fibers (CA1, CA3, and DG) in the hippocampus and expressed lower levels of doublecortin and higher levels of NCAM-180 when compared to the control pups obtained from pregnant rats fed the iodized diet. Thus, it was deduced that properly functioning thyroid hormones were necessary for various brain processes and for the development of nerve fibers (Gong et al, 2010). A similar study was conducted by Wang et al. in 2011 and showed that iodine deficiency and hypothyroidism affected normal development of the cerebellum. The study supported the fact that thyroid hormones were necessary for normal and proper development of the cerebellum, and that iodine deficiency during both gestation and the post-natal period can result in developmental hypothyroidism leading to problems with cerebellar development. The study also linked up-regulation of Caveolin-1 and down-regulation of Synaptotagmin-1 to impaired neuronal development during deficiency of the mineral element (Wang et al, 2011). Excessive iodine intake, can also be detrimental to infant health and thyroid function. Post-partum women who consume excessive amounts of iodine secrete excess iodine in their breast milk, which in turn affects the thyroid function of pre-term infants. Chung et al. studied the impact of excessive iodine intake and the consequent impact on infants in Korea (Chung et al, 2009). During gestation, fetuses receive iodine from their mothers through the placenta, and after birth the major source of iodine for neonates is breast milk. Preterm infants are highly sensitive to thyroid suppression due intake of high amounts of iodine through the mother’s milk. The authors conducted a study with 31 pre-term infants. Thyroid function was tested, and the results showed high iodine concentration coming from the breast milk of the Korean mothers. This was attributed to consumption of brown seaweed (Undaria pinnatifida) soups, which are very rich in iodine. The daily intake of iodine among these post-partum women was above 2000 micrograms. This iodine was found to be secreted in the breast milk, which reached the infants directly during breast-feeding. (Chung et al, 2009). Conclusion Iodine is an essential element for the development and maintenance of normal thyroid function, and iodine deficiency has become an important public health concern around the world. Aweke et al presented the situation in Ethiopia where iodine deficiency led to increased goiter. Excess iodine is also a major cause of hypo- and hyperthyroidism among many populations. Dalili et al. 2012, showed that children in Iran were at risk of developing hyperthyroidism as a result of excess iodine intake. Teng et al’s study in China showed that people consuming iodine rich foods presented with more thyroid problems. Medani et al. 2013, also conducted a similar study in Port Sudan City and found that excess intake of iodine led to increased cases of goiter. Salt fortification has been implemented around the world to combat iodine deficiency. However, sudden introduction of iodine, particularly in places where iodine deficiency is prevalent, can have negative impacts as well. Pederson et al. 2007, conducted their study in Denmark and concluded that the sudden change in iodine intake led to an increase in hypothyroidism cases. Salt fortification has however been beneficial, as could be seen in Iran, where after seven years of consuming fortified salt, goiter prevalence had deteriorated and the sample population exhibited fewer cases of brain damage. It is well known that iodine is necessary for development, especially development of the brain, and the diet of the mother plays a key role in this. Gong et al. 2010, used a mouse model to show that iodine deficiency during gestation resulted in offspring with brain damage. The role of the mother’s diet was also studied by Chung et al. 2009, and excess intake of iodine by mothers was shown to cause the development of hypothyroidism in their suckling infants. Thus, by now we have understood the important role of iodine in the normal function of the human thyroid system. Iodine is an indispensable element, and is required at every stage of life. However, both deficiency and excess of the mineral can cause problems with thyroid function. Therefore, iodine intake should be balanced to regulate and maintain normal functioning of the thyroid system. References Ahad,F., and Ganie.,S.(2010). Iodine, Iodine metabolism and Iodine deficiency disorders revisited. 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