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25.09.2014

Iodine deficiency symptoms in humans, natural remedies for tinnitus symptoms - Try Out

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The native iodine content of most foods and beverages is low, and most commonly consumed foods provide 3 to 80 µg per serving (3-7). These studies have demonstrated a significant effect of an iodine deficient diet on the number and distribution of the spines on the pyramidal cells of the visual cortex. Severe iodine deficiency has been produced in the marmoset (Callithrix Jacchus Jacchus) with a mixed diet of maize (60%), peas (15%), torula yeast (10%) and dried iodine deficient mutton (10%). A single intramuscular injection of iodized oil (1 ml = 480 mg iodine) given to the iodine deficient mother at 100 days gestation was followed by partial restoration of the lambs’ brain weight and body weight with restoration of maternal and fetal plasma T4 values to normal (16). The term IDD refers to all the ill-effects of iodine deficiency in a population that can be prevented by ensuring that the population has an adequate intake of iodine (1). Figure 1 shows the time course of the development of the brain and of thyroid function in the human fetus and neonate.
In humans, T4 can be found in the first trimester coelomic fluid from 6 weeks of gestational age, long before the onset of secretion of T4 by the fetal thyroid, which occurs at the 24th week of gestation (29).
The potential adverse effects of mild-to-moderate iodine deficiency during pregnancy are unclear. An increased perinatal mortality due to iodine deficiency has been shown in Zaire from the results of a controlled trial of iodized oil injections alternating with a control injection given in the latter half of pregnancy (34). Apart from mortality, the importance of thyroid function in the neonate relates to the fact that the brain of the human infant at birth has only reached about one third of its full size and continues to grow rapidly until the end of the second year (38). Studies on iodine nutrition and neonatal thyroid function in Europe in the early 1980s confirmed the continuing presence of iodine deficiency affecting neonatal thyroid function and hence a threat to early brain development (39). In developing countries with more severe iodine deficiency, observations have now been made using blood taken from the umbilical vein just after birth. Another important aspect of iodine deficiency in the neonate and child is an increased susceptibility of the thyroid gland to radioactive fall-out. There is cross-sectional evidence that impairment of thyroid function evidenced in mothers and neonates in conditions of mild-to-moderate iodine deficiency affects the intellectual development of their offspring.
A randomized controlled study conducted in Albania in 2006 in a moderately iodine deficient area showed that information processing, fine motor skill and visual problem solving improved in school-children after iodine repletion of the population (46).
In severe iodine deficiency, the frequency distribution of IQ in normal appearing children is shifted towards low values as compared to children who were not exposed to in utero iodine deficiency because of correction of the deficiency in the mothers before or during early gestation (47-49). Data from cross-sectional studies on iodine intake and child growth are mixed, with most studies finding modest positive correlations (60).
Anecdotal reports suggest that there is a high degree of apathy in populations living in severely iodine deficient areas.
Endemic goiter is characterized by enlargement of the thyroid gland in a significantly large fraction of a population group, and is generally considered to be due to insufficient iodine in the daily diet. Although the relation of iodine deficiency to endemic goiter is well established, other factors may be involved.
Selenium deficiency may have profound effects on thyroid hormone metabolism and possibly also on the thyroid gland itself (96-98). Selenium deficiency also leads to a reduction of the selenium containing enzyme glutathione peroxidase. Deficiencies of iron (102,103) and vitamin A (104) may also have a goitrogenic effect in areas of iodine deficiency (Table 5). When iodine intake is abnormally low, adequate secretion of thyroid hormones may still be achieved by marked modifications of thyroid activity. The first functional consequence of iodine deficiency is an increase in the uptake of iodide by the thyroid mediated via a transmembrane protein, the sodium iodide symporter (NIS) (109).
For any adequate adjustment of iodine supply to the thyroid, iodide trapping must fulfill two conditions. Thyroid hyperplasia induced by iodine deficiency is associated with an altered pattern of thyroid hormonogenesis: the abnormal configuration of the poorly iodinated thyroglobulin in the thyroid colloid is accompanied by an increase in poorly iodinated compounds, monoiodotyrosine (MIT) and T3, and a decrease in diiodotyrosine (DIT) and T4. However, efficient adaptation to iodine deficiency is possible in the absence of goiter as demonstrated in nongoitrous patients in endemic goiter areas such as New Guinea (114) and the Congo (115). The characteristic features of neurological endemic cretinism in its fully developed form are extremely severe mental deficiency, together with squint, deaf-mutism and motor spasticity disorders of the arms and legs of a characteristic nature (120-123) (Figure 4). Mental deficiency is characterized by a marked impairment of the capacity for abstract thought but vision is unaffected.
Studies already cited above on the effect of iodine deficiency on brain cell development in the newborn rat, sheep and marmoset suggest that iodine deficiency has an early effect on neuroblast multiplication. Four methods are generally recommended for assessment of iodine nutrition in populations: urinary iodine concentration (UI), the goiter rate, serum thyroid stimulating hormone (TSH), and serum thyroglobulin (Tg) (see overview in Table 6). However, palpation of goiter in areas of mild iodine deficiency has poor sensitivity and specificity; in such areas, measurement of thyroid volume (Tvol) by ultrasound is preferable (137).
In areas of endemic goiter, although thyroid size predictably decreases in response to increases in iodine intake, thyroid size may not return to normal for months or years after correction of iodine deficiency (139). Because >90% of ingested iodine is excreted in the urine, UI is an excellent indicator of recent iodine intake. Because serum thyroid stimulating hormone (TSH) concentration is determined mainly by the level of circulating thyroid hormone, which in turn reflects iodine intake, TSH can be used as an indicator of iodine nutrition. Lemon grass can also be used against the Candida yeasts, causing infection in the human being, due to the presence of antifungal properties. We all know that sugar is not all very good and healthy for the human body if consumed in excess. In many cases, it so has been seen that the deficiency of iodine can cause severe medical conditions which might not get cured for life. The two main diseases or deficiencies which are caused due to lack of iodine are goiter and cretinism. Special emphasis will be put on recent developments such as the role of iodine deficiency in the development of brain damage and mental retardation, assessment of the iodine status of a population and current worldwide epidemiological data, strategies for control and monitoring of the iodine deficiency disorders (IDD), as well as potential side effects of excessive iodine intake. Major dietary sources of iodine in the USA, Europe and Australia are bread, milk and to a lesser extent seafood (3,4).
These dendritic spines can be accurately measured and have been studied in relation to both iodine deficiency and hypothyroidism.
The iodine deficient fetuses at 140 days were grossly different in physical appearance in comparison to the control fetuses.
The consequence of iodine deficiency during pregnancy is impaired synthesis of thyroid hormones by the mother and the fetus.
Iodine treatment of pregnant women in areas of severe deficiency reduces fetal and perinatal mortality and improves motor and cognitive performance of the offspring. There was a substantial fall in infant mortality with improved birth weight following the iodized oil injection. Thyroid hormone, dependent on an adequate supply of iodine, is essential for normal brain development as has been confirmed by the animal studies already cited. A series of 1076 urine samples were collected from 16 centers from 10 different countries in Europe along with an additional series from Toronto, Canada and analyzed for their iodine content. The incidence of permanent congenital hypothyroidism was very similar in the four cities but the rate of transient hypothyroidism was much greater in Freiburg, associated with the lowest level of urine iodine excretion, than in Stockholm, with intermediate findings from Rome and Brussels.
This hypothyroidism persists into infancy and childhood if the deficiency is not corrected, and results in retardation of physical and mental development (42). In a meta-analysis of 19 studies on neuromotor and cognitive functions in conditions of moderate to severe iodine deficiency, Bleichrodt and Born (50) concluded that iodine deficiency resulted in a loss of 13.5 IQ points at the level of the global population.
In five Asian countries, household access to iodized salt was correlated with increased weight-for-age and mid-upper-arm circumference in infancy (61).
Another consequence of longstanding iodine deficiency in the adult (64-67) and child (68) is the development of hyperthyroidism, especially in multinodular goiters with autonomous nodules.


The disease may be seen throughout the Andes, in the whole sweep of the Himalayas, in the European Alps where iodide prophylaxis has not yet reached the entire population, in Greece and the Middle Eastern countries, in many foci in the People’s Republic of China, and in the highlands of New Guinea.
Although goiter was an important problem in many regions of the United States in the past (69), more recent US surveys have shown it in no more than 4-11% of schoolchildren, with evidence of continued adequate iodine nutrition in the country since 1988 (70,71). Almost invariably, careful assessment of the iodine intake of a goitrous population reveals levels considerably below normal. Soybean, an important protein source in many third world countries, interrupts the enterohepatic cycle of thyroid hormone (78) and may cause goiter when iodine intake is limited. A definite role in endemic goiter has only been proved for thiocyanate and sulfurated organics, although substantial and circumstantial evidence favors the view that natural goitrogens, acting in concert with iodine deficiency, may determine the pattern and severity of the condition.
Glutathione peroxidase detoxifies H2O2 which is abundantly present in the thyroid gland as a substrate for the thyroperoxidase that catalyzes iodide oxidation and binding to thyroglobulin, and the oxidative coupling of iodotyrosines into iodothyronines. These adaptive processes include stimulation of the trapping mechanism of iodide by the thyroid as well as stimulation of the subsequent steps of the intrathyroidal metabolism of iodine leading to preferential synthesis and secretion of T3. There is a clear inverse relation between iodine supply and thyroidal uptake of radioiodide. First, it must reduce the amount of iodide excreted in the urine to a level corresponding to the level of iodine intake in order to preserve the preexisting iodine stores.
The shift to increased T3 secretion plays an important role in the adaptation to iodine deficiency because T3 possesses about 4 times the metabolic potency of T4 but requires only 75 % as much iodine for synthesis. Moreover, adequate adaptation to iodine deficiency has been demonstrated in areas of severe iodine deficiency in the absence of endemic goiter (116). As would be expected with a deficiency disease, there is a wide range in the severity of the clinical features in the population affected. Comparative population based neuropsychological assessments of children in areas of iodine deficiency compared with areas of adequate iodine intake confirm a shift of the intelligence curve to the left in apparently normal people living in iodine deficient areas (124). Its role has been suggested in Zaire from the observation that populations in areas with severe but uniform iodine deficiency exhibit cretinism only when a critical threshold in the dietary supply of SCN is reached. Severe selenium deficiency has been reported in Zaire in populations where myxedematous cretinism is endemic (95,98). These indicators are complementary, in that UI is a sensitive indicator of recent iodine intake (days) and Tg shows an intermediate response (weeks to months), whereas changes in the goiter rate reflect long-term iodine nutrition (months to years).
During this transition period, the goiter rate is difficult to interpret, because it reflects both a population’s history of iodine nutrition and its present status. However, in older children and adults, although serum TSH may be slightly increased by iodine deficiency, values often remain within the normal reference range. In prospective studies, dried blood spot Tg has been shown to be a sensitive measure of iodine status and reflects improved thyroid function within several months after iodine repletion (149,150). In iodine-deficient populations, serum T3 increases or remains unchanged, and serum T4 usually decreases. The advantage of iodized salt is that it is used by nearly all sections of a community, irrespective of social and economic status.
The thyroid gland was enlarged with gross reduction in plasma T4 in both mothers and newborns, and was greater in the second pregnancy than in the first, suggesting a greater severity of iodine deficiency. The combination of maternal thyroidectomy (carried out 6 weeks before pregnancy) and fetal thyroidectomy produced more severe effects than that of iodine deficiency, and was associated with greater reduction in both maternal and fetal thyroid hormone levels (17).
Brain damage and irreversible mental retardation are the most important disorders induced by iodine deficiency. The T4 and T3 found in early human fetuses up to mid gestation are likely to be entirely or mostly of maternal origin. Severe iodine deficiency in utero causes a condition characterized by gross mental retardation along with varying degrees of short stature, deaf-mutism, and spasticity that is termed neurological cretinism. In the most severely iodine deficient environments in Northern India, where more than 50% of the population has urinary iodine levels below 25 ug per gram creatinine, the incidence of neonatal hypothyroidism was 75 to 115 per thousand births (40). These observations indicate a much greater risk of mental impairment in severely iodine deficient populations than is indicated by the presence of cretinism.
The apparent thyroidal iodine turnover rate was much higher in young infants than in adults and decreased progressively with age. However, controlled intervention studies of iodized oil alone and iodine given with other micronutrients have generally not found effects on child growth (60).
It is apparent that reduced mental function due to cerebral hypothyroidism is widely prevalent in iodine deficient communities with detrimental effects on their initiative and decision-making. The pathogenesis of this syndrome is discussed later in this chapter in the section on side effects of iodine supplementation. This finding is a testimony to the effectiveness of iodine prophylaxis in preventing endemic goiter.
In attempting to account for the variability in the expression of endemic goiter from one locality to the next, the availability of iodine should be investigated before searching for some other subtle dietary or genetic factors. In the very young, or in older patients who have lived under constant iodine deprivation, the finding is extreme hyperplasia. This clearly indicates that goiter is not required for achieving efficient adaptation to iodine deficiency. Because maternal thyroxine crosses the placenta, it is now envisaged that neurological cretinism is predominantly caused by maternal hypothyroxinemia due to iodine deficiency (123).
In the second panel is an adolescent boy from Tibet from an area of severe iodine deficiency, being supported by his father, and suffering from congenital hypothyroidism, plus the neurological features of cretinism and having an atrophic thyroid gland. SCN crosses the placenta and inhibits the trapping of iodide by the placenta and fetal thyroid (41, 90). Selenium is present in glutathione peroxidase (Gpx) that detoxifies H2O2 produced in excess in thyroid cells hyperstimulated by TSH because of iodine deficiency. However, interpretation of Tvol data requires valid references from iodine-sufficient children. However, several questions need to be resolved before Tg can be widely adopted as an indicator of iodine status. However, these changes are often within the normal reference ranges, and the overlap with iodine-sufficient populations is large enough to make thyroid hormone levels an insensitive measure of iodine nutrition except for severe iodine deficiency (1). By contrast in Delhi, where only mild iodine deficiency is present with low prevalence of goiter and no cretinism, the incidence drops to 6 per thousand. In order to provide the normal rate of T4 secretion, Delange (43) estimated the turnover rate for intrathyroidal iodine must be 25-30 times higher in young infants than in adolescents and adults. In iodine-deficient children, impaired thyroid function and goiter are inversely correlated with IGF-1 and IGFBP-3 concentrations (62). Thus, iodine deficiency can be a major block to the human and social development of communities and constitutes a major teratogen at the community level (63).
An endemic existed in the Great Lakes region in North America until it was corrected by iodized salt in the early 1900s.
The world or regional distribution of goiter was exhaustively reviewed by Kelly and Snedden in 1960 (72) updated in 2005 (73) and the most recent global data on iodine deficiency is discussed later in this chapter. It has been shown that when, in an area of combined iodine and selenium deficiency, only selenium is supplemented, serum T4 decreases (99).
Elevated H2O2 levels in thyrocytes may be more toxic under situations of increased TSH stimulation such as is present in areas with severe iodine deficiency. However, a significantly elevated TSH level in endemic goiter is usually systematically found only in conditions of extreme iodine deficiency. Rather, in these conditions, efficient adaptation to iodine deficiency is possible thanks to a high iodide trapping capacity but with only a slight enlargement of the thyroid.
These data correlate well with the data from the Papua New Guinea trial which indicated that iodine repletion should occur by three months of pregnancy to prevent cretinism (35).


It has been suggested that an autosomal recessive predisposition, besides maternal iodine deficiency, may play an etiological role in neurological cretinism but there is little evidence to support this proposition(121).
In a recent multicenter study, Tvol was measured in 6-12 y-old children (n=3529) living in areas of long-term iodine sufficiency on five continents.
In contrast, TSH is a sensitive indicator of iodine status in the neonatal period (143, 144). One question is the need for concurrent measurement of anti-Tg antibodies to avoid potential underestimation of Tg; it is unclear how prevalent anti-Tg antibodies are in iodine deficiency, or whether they are precipitated by iodine prophylaxis (151,152). However, iodine cycling in many regions is slow and incomplete, and soils and ground water become deficient in iodine. Iodine content in foods is also influenced by iodine-containing compounds used in irrigation, fertilizers, and livestock feed. Goiter was evident from 70 days in the iodine-deficient fetuses and thyroid histology revealed hyperplasia from 56 days gestation, associated with a reduction in fetal thyroid iodine content and reduced plasma T4 values. Thus, iodine deficiency is a leading global cause of preventable mental impairment and other neurocognitive disorders. A reduction of infant mortality has also been reported from China following iodine supplementation of irrigation water in areas of severe iodine deficiency. Some very high values were seen which could be attributed to the use of iodinated contrast media for radiological investigation of the mother during pregnancy. In iodine deficiency a further increase in turnover rate is required to maintain normal thyroid hormone levels.
Recent controlled trials found iodine repletion increased insulin-like growth factor (IGF)-1 and insulin-like growth factor binding protein (IGFBP)-3 and improved somatic growth in children (60). One must also consider the possibility that an observed goiter rate may not reflect current conditions, but rather may be a legacy of pre-existing iodine deficiency that has not yet been entirely resolved by an improvement in the supply of iodine.
All of these substances interfere with the accumulation of thyroidal iodide, an effect that usually can be overcome by an increasing iodine intake.
This effect is explained by restoration of type I deiodinase activity leading to normalization of T4 deiodination while T4 synthesis remains impaired because of continued iodine deficiency. In conditions of mild iodine deficiency, elevated TSH is typically found in only a small fraction of subjects, usually the youngest (110).
Below this critical level of iodine intake, despite a further increase of thyroid iodide clearance, the absolute uptake of iodide diminishes and the iodine content of the thyroid decreases with functional consequences resulting in the development of a goiter (111,112).
In these conditions, iodide is diluted while thyroglobulin is in excess, resulting in a lesser degree of iodization of thyroglobulin and, consequently, in a decrease in iodothyronine synthesis and secretion (118). It has been proposed that the combination of deficiencies in iodine and selenium and SCN overload are required for the occurrence of severe thyroid failure during the perinatal period, and subsequent development of myxedematous cretinism (96). If true, this suggests that to achieve a goiter rate <5% in children may require that they grow up under conditions of iodine sufficiency. Compared to the adult, the neonatal thyroid contains less iodine but has higher rates of iodine turnover.
There are two forms of iodine which can be used to iodize salt: iodide and iodate, usually as the potassium salt. Many people take this wrongly and think that how much of these sugars are consumed they don’t affect the human body and so start consuming is large amounts.
Crops grown in these soils will be low in iodine, and humans and animals consuming food grown in these soils become iodine deficient (1). Iodophors, used for cleaning milking equipment, milk cans and teats in the dairy industry, can increase the native iodine content of dairy products through contamination of iodine containing residues (9).
These differences confirm the need for early treatment of congenital hypothyroidism and prevention of iodine deficiency in the newborn infant in order to prevent brain damage and mental retardation.
These findings demonstrate the significant effects of iodine deficiency on the primate brain. Iodine replacement has probably been an important factor in the national decrease in infant mortality in China (37). This is the reason for the greatly increased susceptibility of the neonate and fetus to iodine deficiency.
In a study of several communities in the Ubangi region of Zaire, a relationship between goiter, thiocyanate and iodide excretion was described. In this formulation, repeated episodes of hyperplasia induced by iodine deficiency are followed by involution and atrophy, the result being a gland containing a mixed bag of nodules, zones of hyperplasia, and involuting, degenerative, and repair elements. It is possible that it is the sensitivity of the thyroid to TSH rather than the TSH level itself that mainly varies with iodide supply.
Hydrolysis of large amounts of poorly iodinated thyroglobulin will result in an important leak of iodide by the thyroid and enhanced urinary loss of iodide, further aggravating the state of iodine deficiency (119).
Finally, elevated hearing thresholds have been reported in children with no other signs of endemic cretinism in conditions of mild iodine deficiency (125).
This is an important finding as it indicates in utero damage from hypothyroxinemia from maternal iodine deficiency does occur in myxedematous cretinism and is followed by severe, irreversible hypothyroidism in infancy and childhood and supports the hypothesis that the expression of this disorder is the outcome of both prenatal and postnatal brain damage (122, 123).
A sustained salt iodization program will decrease the goiter rate by ultrasound to <5% in school-age children and this indicates disappearance of iodine deficiency as a significant public health problem (1).
Particularly when iodine supply is low, maintaining high iodine turnover requires increased TSH stimulation.
Iodate is less soluble and more stable than iodide and is therefore preferred for tropical moist conditions.
If your child shows some symptoms of either of the diseases, then you should go to a doctor immediately. Iodine deficiency also causes an increased uptake of the radioiodide resulting from nuclear radiation. Therefore, large colloid goiters in endemic iodine deficiency represent maladaptation instead of adaptation to iodine deficiency because they may produce a vicious cycle of iodine loss and defective thyroid hormones synthesis.
Serum TSH concentrations are therefore increased in iodine deficient infants for the first few weeks of life, a condition termed transient neonatal hypothyroidism.
Iodine deficient soils are most common in inland regions, mountainous areas and areas of frequent flooding, but can also occur in island states and coastal regions (2). Protection against this increased uptake can be provided by correction of iodine deficiency. The results indicated a reciprocal relationship between iodide and thiocyanate in that increasing amounts of iodide protected increasingly against the thiocyanate derived from the cassava (89).
This arises from the distant past through glaciation, compounded by the leaching effects of snow, water and heavy rainfall, which removes iodine from the soil. The mountainous regions of Europe, the Northern Indian Subcontinent, the extensive mountain ranges of China, the Andean region in South America and the lesser ranges of Africa are all iodine deficient. Also, the Ganges Valley in India, the Irawaddy Valley in Burma, and the Songkala Valley in Northern China are also areas of endemic iodine deficiency. Neonatal TSH is an important measure because it reflects iodine status during a period when the developing brain is particularly sensitive to iodine deficiency. Iodine deficiency in populations residing in these areas will persist until iodine enters the food chain through addition of iodine to foods (e.g. However, there are many pitfalls in the interpretation of neonatal TSH data for monitoring iodine deficiency in a population and further research is required to clarify conflicting data from different countries who have implemented such programs.



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