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PREGNANCY~ Can you give me some info on iodine&pregnancy?

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Iodine & pregnancy   by wombat   13 year 1 of 1 (100%)


//www.curezone.org/forums/fm.asp?i=869832#i


Hey Moms & Moms to be:) Here's some info I've been able to gather on the importance of Iodine during pregnancy and the importance of Iodine on child development. The USA RDA for Iodine is set at 150 MCG and that amount is that needed in order to prevent a most obvious manifestation of deficiency, goiter.The RDA for pregnant women is 220 mcg.. The average suggested daily amount of iodine needed by(non-pregnant) women I've seen in my reading(Abraham, Flescha, Brownstein, et al) is 12 mg. I have not been able to find info on how much iodine is needed during pregnancy according to our Gurus...
When bringing our bodies to sufficiency, the thyroid is saturated first, then the iodine goes to other areas of the body. Any excess iodine is excreted in the urine....pregnant women need more iodine to nurture the growing child within.......

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A little background info on this next link...in the 1950's, atmospheric testing in Nevada released a great amount of radioactive iodine 131 into the environment. When folks downwind of the testing sites were tested, they were found to have a great deal of the radioactive(cancer-causing) iodine in their thyroids. So our government mandated that each and every slice of commercially prepared bread in this country had to contain 150 mcg. of iodine as iodine displaces radioactive iodine 131. This was absolutely a cover-your-ass move on the part of our government. The iodine supplementation of baked products continued until around 1980, at which point it was mysteriously discontinued...



http://www.lewisford.info/files/The_Basic_Program_from_Feeling_Young_and_In_Love3.pdf


"Later, I will go over this again in more extensive
detail, but for now let me just assert that in addition to
helping to block the absorption of Iodine-131, the Iodide
supplementation program of the 1960’s also ended up
delivering other, unexpected health benefits. Among other
things, it helped to reverse the growing rate of obesity that
had developed among Americans during the 1950’s. It
delayed the onset of puberty in adolescents. During the
1960’s the puberty of American pre-teens ended up
occurring years later than it had occurred during the 1950
and 40’s, and also occurred 2 - 5 years later, on average,
than puberty occurs today. During the 1960s female high
school seniors grew about 1 inch taller, and weighed about
25 pounds less, on average, than our female high school
seniors do today. Also during the 1960’s American high
school students achieved higher SAT scores than they ever
achieved before or afterwards. Our classrooms were much
more orderly and learning oriented, during the 1960’s, than
they are today. During the 1960’s, the highest proportion
ever, of American teenagers, graduated from high school,
and went on to college. Also, the highest proportion of
young adults ever ended up graduating from college.
During the 1960’s American elementary students enjoyed
the highest average intelligence scores ever. During the
decades since the 1960’s, on-the-other-hand, the IQ tests
used in this country have had to be re-calibrated downward
several times, so that the “Average Student” could still
score an IQ of 100. With the adjustments, American
students now score lower on the non-verbal IQ tests than
children from most of the other developed countries in the
world. For example, an extensive international study
conducted during the 1980’s found that 77% of the
Japanese population scored better on IQ tests than the
“average” American scored. By American standards they
had an average IQ of 111, vs. 100 for the average
American. Since then the Japanese have continued
extending their lead. On non-verbal IQ tests their 18 year
olds now score, on average, a full standard deviation
(depending on the test used, 12 or 16 points) higher than
our 18 year olds."

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http://www.childinfo.org/areas/idd/



The past decade has seen dramatic progress in the campaign to eliminate iodine deficiency, the world's leading cause of preventable mental retardation and impaired psychomotor development in young children. In its most extreme form, iodine deficiency causes cretinism. It also significantly raises the risks of stillbirth and miscarriage for pregnant women. Most commonly and visibly associated with goitre, iodine deficiency takes its greatest toll in impaired mental growth and development, contributing in turn to poor school performance, reduced intellectual ability, and impaired work performance.

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Iodine stimulates apoptosis, programmed cell death, a natural occurrence:



http://iodine4health.com/overviews/summaries/iodinesource.htm



"Iodine and Pregnancy

During pregnancy the placenta captures iodine to the point of raising the levels in the fetal circulation to five times the mother's level. As there are a huge number of cells dying by apoptosis during fetal growth, so iodine is of importance to the fetal development. The brain has more apoptosis going on during development than most other organs, so it follows that low iodine can cause abnormal brain development. Early fetal development is partly under the guidance of maternal thyroid hormones that have crossed the placenta, but it is theorized that the primitive cells at the beginning of fetal development still have the ability to make thyroid hormone themselves for their own use as in the early evolution of eukaryotes.

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"Mental retardation from iodine deficiency is not limited to the extreme form of cretinism, but instead extends over a broad continuum to mild intellectual blunting that may go unrecognized unless carefully investigated."



http://jcem.endojournals.org/cgi/content/full/86/6/2360




The most vulnerable target for iodine deficiency is the developing brain. Iodine is critical to maturation of the central nervous system, particularly its myelination. DeLong et al. (22) have carefully examined the effects at different stages of pregnancy. Correction of iodine deficiency during the second trimester reduced neurological abnormalities, increased head growth, and improved the development quotient in a severely iodine-deficient area of western China. Correction at a later period did not improve neurological development, although there was a trend toward slightly larger mean head circumference and higher development quotients than in untreated individuals. The principal effects of T4 are on somatogenesis, neuronal differentiation, and formation of neural processes, particularly active for the cerebral cortex, cochlea, and basal ganglia during the second trimester; brain growth and differentiation are more active in the third trimester (22, 23, 24). In iodine deficiency, maternal T4, which must cover fetal needs during the first trimester before the fetal thyroid makes its own, is low, so the fetus is exposed to inadequate T4 throughout gestation.

The most extreme clinical result is cretinism, defined by severe mental retardation, associated defects (e.g. deaf mutism, spasticity, and stunted growth), and iodine deficiency as the causal agent. Historically, cretins were separated phenotypically into neurological and myxedematous types, but the division is not rigid and the entity is better described as a spectrum. The neurological type typically has the features mentioned above, whereas the myxedematous has, in addition, hypothyroidism, attributed to thyroid exhaustion in the third trimester and early postnatal period (2).

Mental retardation from iodine deficiency is not limited to the extreme form of cretinism, but instead extends over a broad continuum to mild intellectual blunting that may go unrecognized unless carefully investigated. Thus, iodine deficiency puts virtually everyone in the affected population at some risk for brain damage. Many studies have compared performance of iodine-deficient children with that of iodine-sufficient peers on standardized intelligence tests. A meta-analysis of 18 such studies, comprising 2214 subjects, concluded that iodine deficiency lowered a mean intelligence quotient by 13.5 points (25). In view of the many people living in iodine-deficient areas and their vulnerability to its effects on the developing brain, these numbers indicate a staggering public health problem. This and neonatal mortality, rather than goiter, have become the main reasons for advocating urgent correction of iodine deficiency.

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http://www.accessmylibrary.com/coms2/summary_0286-16254252_ITM



The developing foetus does not possess a functioning thyroid gland until 13 to 15 weeks gestation and therefore relies solely on the mother to ensure neuropsychological development.

Children of mothers whose iodine intake is low are at risk of not reaching their total intellectual potential.

Low levels of iodine in the womb can also lead to a higher risk of Attention Deficit and Hyperactivity Disorder (ADHD).

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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11396705&dopt=Abstract



Pregnancy, therefore, represents one of the environmental factors that may help explain the higher prevalence of goiter and thyroid disorders in women compared with men. An iodine-deficient status in the mother also leads to goiter formation in the progeny and neuropsycho-intellectual impairment in the offspring. When adequate iodine supplementation is given early during pregnancy, it allows for the correction and almost complete prevention of maternal and neonatal goitrogenesis.

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http://www.nature.com/ejcn/journal/v58/n7/full/1601933a.html



Mild-to-moderate iodine deficiency during pregnancy adversely affects thyroid function of the mother and newborn and mental development of the offspring and these adverse effects can be prevented or minimized by supplementation.

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Prevention of cretinism by iodine supplementation during pregnancy - adapted from the New England Journal of Medicine, December 29, 1994
Nutrition Research Newsletter, Feb, 1995

Endemic cretinism, caused by severe iodine deficiency during pregnancy, is a major cause of mental retardation in some parts of the world. Despite iodine supplementation programs, endemic cretinism is still found in southern and eastern Europe and is common in Asia, Africa, and Latin America; the prevalence may be as high as 10% in some communities. In 1990, the World Health Organization estimated that 20 million people in the world had preventable brain damage due to the effects of iodine deficiency on fetal brain development.

Endemic cretinism can be prevented by iodine supplementation before conception. Previous studies have not established, however, whether supplementation during pregnancy or in early childhood would be of value in reducing the risk.

In a new study conducted in a severely iodine-deficient area of the Xinjiang region of China, iodine was administered to women in various stages of pregnancy and to children from birth to age three years. The treated children and offspring of treated women were followed for two years. Three independent measures of neural development were assessed.
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Iodine supplementation during the second trimester of pregnancy was clearly beneficial in reducing the prevalence of moderate and severe neurologic abnormalities. Iodine supplementation during the first trimester may have been effective as well, but difficulties in administering the required dose to this group of women prevented definitive conclusions from being reached. Iodine administration during the third trimester or after birth was less valuable; it did not improve neurologic status, but head growth and developmental quotients improved slightly.

These findings indicate that supplementation with iodine before the end of the second trimester of pregnancy can protect the fetal brain from the effects of iodine deficiency. "It is obviously preferable to start providing iodine before pregnancy and to provide it continuously." However, supplementation during early pregnancy would be of value in instances where adequate iodine intake cannot be ensured before conception.

Cao Xue-Yi, Jiang Xin-Min, Dou Zhi-Hong et al, Timing of Vulnerability of the Brain to Iodine Deficiency in Endemic Cretinism, New England J Medicine 331(26):1739-1744 (29 Dec 1994) [Reprints: G Robert DeLong, MD, Division of Pediatric Neurology, Duke University Medical Center, Box 3936, Durham NC 277101

Basil S Hetzel, Iodine Deficiency and Fetal Brain Damage [Editorial], New England J Medicine 331(26):1770-1771 (29 Dec 1994) [Correspondence: Basil S Hetzel, MD, International Council for Control of Iodine Deficiency Disorders, North Adelaide, SA 5006, Australia]

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http://jcem.endojournals.org/cgi/content/full/86/6/2360



During lactation, the mother must obtain enough iodine for her own thyroid plus that of her growing infant. Calculations from the EAR for nonpregnant adult women (95 µg/day) and from an average loss in human breast milk (about 114 µg/day) lead to an EAR during lactation of 209 µg iodine/day and a RDA of 290 µg/day. The IOM report also includes "adequate intake" (AI) estimates (used when an EAR cannot be calculated) and RDAs for other population groups (8). The AI is less exact and, therefore, reaches higher levels than those derived by the EAR/RDA methodology, which is based largely on balance studies. The IOM sets the AI at 110 µg iodine/day for infants 0–6 months old and at 130 µg/day for those 7–12 months old; the RDA is 90 µg/day for children 1–8 yr old, 120 µg/day for those 9–13 yr, and 150 µg/day for older ages. These values correspond fairly closely to those recommended by WHO, ICCIDD, and other groups and provide a reasonable target in considering iodine nutrition for mother and child. Positive iodine balance for the neonate and young infant, which is required to accommodate the increasing stores of the thyroid, is achieved only when the iodine intake is at least 15 µg/kg·day in full term and 30 µg/kg·day in preterm infants (10). This corresponds to an iodine intake of approximately 90 µg/day and is the present recommendation by WHO/UNICEF/ICCIDD for infants and children aged 0–59 months (9).

Effects of iodine deficiency on the mother

Hypothyroxinemia, elevated serum TSH, enlargement of the thyroid (by 10–50%), and goiter are the most obvious consequences for the pregnant woman. They can be prevented by adequate iodine supplementation (14, 15). Because the increased demands for iodine continue during lactation, an iodine-deficient woman may face several years of exaggerated iodine loss and consequent goiter. Even after she stops lactation and the iodine demand decreases, her thyroid may not return to its previous size and she risks multinodular goiter and hyperthyroidism later. In iodine-sufficient countries like the United States, goiter is rarely found in pregnancy and unlikely to be related to iodine.

Iodine deficiency poses additional reproductive risks, including overt hypothyroidism, infertility, and increased abortions. Hypothyroidism causes anovulation, infertility, gestational hypertension, increased first trimester abortions, and stillbirths; all are common in iodine deficiency. Lack of iodine also has cultural and socioeconomic consequences for the mother. Infertility and fetal wastage may compromise her quality of life and her role in the family and community. If she produces a defective child, she will most likely be responsible for its long-term care, diverting her time and resources from other needs.

Effects of maternal iodine deficiency on the fetus and neonate

Iodine deficiency increases neonatal mortality. We emphasize this statement so that iodine deficiency can take its proper place among the disorders that kill children; "child survival" is something of a buzzword in international aid circles, and showing its relation to iodine deficiency helps direct resources toward its correction. Here, we briefly cite supporting evidence.

In one study, DeLong et al. (16) added KIO3 to irrigation water in western China over several years. In three treated villages, infant mortality decreased to half the average of the previous 5 years (e.g. from 58.2 to 28.7 per 1000 for one village). In comparison with untreated villages, the odds of neonatal death were reduced by about 65%. An investigation from an iodine-deficient region of Indonesia found the mortality in infants treated at 6–10 weeks with oral iodized oil to be only half that of an untreated group (17). In Congo, women with a median pregnancy stage of 28 weeks received iodized oil im; their offspring had lower neonatal mortality and higher birth weights than those from untreated controls (18). A long-range follow-up of women treated with im iodized oil in an iodine-deficient area of Papua, New Guinea, showed that their offspring had a significantly greater 15-yr survival than those from an untreated control group (19). Investigations from several other countries support these conclusions. In addition, a large older literature documents the adverse effects of iodine deficiency on reproduction in farm animals, especially abortions and neonatal mortality. As just one example, "hairless pig malady" from iodine deficiency killed one million pigs annually in Montana in the early part of the 20th century (20).

The epidemiologic studies in humans do not directly address the causes of the increased mortality. Undoubtedly, many factors are at play, and other nutritional and health problems usually accompany iodine deficiency in most of its geographic and sociocultural settings. Infectious diseases are the usual immediate cause of childhood death. Iodine deficiency may impair the immune response and, thus, lower the child’s defense against infection (21). More generally, the iodine-deficient child is poorly equipped to deal with his harsh environment and its many threats. Birth weights are lower, and development is less advanced. Whatever the roles of other factors, the available data clearly show that correction of iodine deficiency per se substantially decreases neonatal and infant mortality.

The most vulnerable target for iodine deficiency is the developing brain. Iodine is critical to maturation of the central nervous system, particularly its myelination. DeLong et al. (22) have carefully examined the effects at different stages of pregnancy. Correction of iodine deficiency during the second trimester reduced neurological abnormalities, increased head growth, and improved the development quotient in a severely iodine-deficient area of western China. Correction at a later period did not improve neurological development, although there was a trend toward slightly larger mean head circumference and higher development quotients than in untreated individuals. The principal effects of T4 are on somatogenesis, neuronal differentiation, and formation of neural processes, particularly active for the cerebral cortex, cochlea, and basal ganglia during the second trimester; brain growth and differentiation are more active in the third trimester (22, 23, 24). In iodine deficiency, maternal T4, which must cover fetal needs during the first trimester before the fetal thyroid makes its own, is low, so the fetus is exposed to inadequate T4 throughout gestation.

The most extreme clinical result is cretinism, defined by severe mental retardation, associated defects (e.g. deaf mutism, spasticity, and stunted growth), and iodine deficiency as the causal agent. Historically, cretins were separated phenotypically into neurological and myxedematous types, but the division is not rigid and the entity is better described as a spectrum. The neurological type typically has the features mentioned above, whereas the myxedematous has, in addition, hypothyroidism, attributed to thyroid exhaustion in the third trimester and early postnatal period (2).

Mental retardation from iodine deficiency is not limited to the extreme form of cretinism, but instead extends over a broad continuum to mild intellectual blunting that may go unrecognized unless carefully investigated. Thus, iodine deficiency puts virtually everyone in the affected population at some risk for brain damage. Many studies have compared performance of iodine-deficient children with that of iodine-sufficient peers on standardized intelligence tests. A meta-analysis of 18 such studies, comprising 2214 subjects, concluded that iodine deficiency lowered a mean intelligence quotient by 13.5 points (25). In view of the many people living in iodine-deficient areas and their vulnerability to its effects on the developing brain, these numbers indicate a staggering public health problem. This and neonatal mortality, rather than goiter, have become the main reasons for advocating urgent correction of iodine deficiency.

Screening for congenital hypothyroidism offers a useful index of community iodine nutrition and of the risk of brain damage in the developing infant (26). Neonates are more sensitive than children and adults to the effects of iodine deficiency because they have a very small intrathyroidal iodine pool with markedly accelerated turnover. Iodine deficiency, even of a degree that does not affect adult thyroid function, elevates neonatal TSH values so that more than 5% (the upper limit of the normal distribution in iodine sufficiency) exceed the critical cutoff point of 5 mU/L. This shift can increase the number of neonates recalled for suspected congenital hypothyroidism in areas of moderate to severe iodine deficiency and increase the appearance of overt, although transient, hypothyroidism. The long-term effects of transient neonatal hypothyroidism are not established, but the potential for damage should be respected, and every effort made to ensure adequate iodine (27). Screening programs are already in place in most developed countries, and the results should be regularly examined to detect signs of iodine deficiency.


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