Iodine deficiency ! - falling intakes - goitregens - competition bromine and fluorine

[R.B.]

And this paper http://www.google.com/url?sa=t&rct=j...55123115,d.Yms powerfully makes the point that water flouride levels of 1.4 and 1.6 mg/l can result in significant levels of fluorosis 62.96% and 76.49% respectively - they also noted the water was low in zinc and selenium - so maybe there is a cautionary tale here;

The determination of a safe fluoride intake should have regard to wider mineral intake

High fluoride levels may ? reduce mineral availability, which is particularly relevant in those who are already mineral deficient.


Given many in the west are mineral deficient in one or more minerals this may be of particular significance.

[R.B.]

It occurred to me after writing the above post that I had previously seen a paper linking thyroid dysfunction / goitre with areas know to be low in selenium.

Logically this risk will be greater in areas of high flouride in water and food, the level of other goitrogens in the diet, on the basis that the fluoride may bind with some of the limited available selenium so exacerbating the deficiency.

Selenium is widely recognised as essential to thyroid function, and its absence leads to dysfunction.

http://www.ncbi.nlm.nih.gov/pubmed/12487769

http://www.ncbi.nlm.nih.gov/pubmed/12487769

and

J Pediatr Endocrinol Metab. 2002 Jul-Aug;15(7):1027-31.
Iodine and selenium deficiency in school-children in an endemic goiter area in Turkey.
Aydin K, Kendirci M, Kurtoğlu S, Karaküçük EI, Kiriş A.
Source

Selcuk University Medical Faculty, Konya, Turkey. kursaday@hotmail.com
Abstract

Endemic goiter is one of the most important health problems in Turkey. However, there are not enough studies associated with iodine and selenium status. This study was carried out to establish the effects of iodine and selenium levels on thyroid gland size and thyroid functions in 73 healthy school-children, 7-12 years old (mean 9.56 +/- 1.77 years), 38 girls (52%) and 35 boys (48%), living in an endemic goiter area. Goiter was found in 32 of the children (43.8%) by palpation, and 56 of the children (76.7%) by ultrasonography. Mean serum T3 and TSH levels were in the upper limit of normal, and mean serum T4 levels were within the normal limits, but mean serum thyroglobulin levels were higher than the normal limits. Mean serum selenium level was 30.84 +/- 23.04 microg/l, and mean urinary iodine level was 3.91 +/- 3.77 microg/dl, appropriate for moderate iodine and selenium deficiency. Thyroid volumes of the children were negatively correlated with serum selenium levels, but there was no correlation with urinary iodine levels and thyroid hormones. In conclusion, school-children in this area had significant goiter problems, probably due to the iodine and selenium deficiencies.

[R.B.]

Of the flouride we ingest a proportion is retained in the body mainly in the bones, and some in organs that calcify like arteries. If intake is significantly lowered some, a limited amount, of the deposited fouride will leave the body. Much as yet is unknown but it appears in general the amount of fluoride in bone increases throughout life.

This paper http://www.google.com/url?sa=t&rct=j...55123115,d.Yms used radioactive fluoride for a pet scan. It is very clear from the PET scan image in the paper where most of the fluoride ends up, the spine, and interestingly some is evidently taken up by the blood vessels.



The effects at flouride intakes in the particular background circumstances that lead to fluorosis of the bone are devastating as clearly evident from this video. http://fluoridealert.org/fan-tv/crippling-waters/

High fluoride in bones is associated with more brittle bones etc. What the effects of a lifetimes accumulation of fouride are in more 'normal' circumstances is much less clear.

It appears that fluoride intake from our youngest moments is in a sense 'for life', and it is probably only in the long term that we will have a better understanding of the effects of our increasing intake from a range of sources including water, and how other factors such as iodine and mineral intake effect fluoride metabolism .

Association of vascular fluoride uptake with vascular
calcification and coronary artery disease
Yuxin Lia, Gholam R. Berenjia, Wisam F. Shabaa, Bashir Taftia, Ella Yevdayeva
and Simin Dadparvarb

Conclusion sodium [18F]fluoride PET/CT might be
useful in the evaluation of the atherosclerotic process in
major arteries, including coronary arteries. An increased
fluoride uptake in coronary arteries may be associated with
an increased cardiovascular risk.

[R.B.]

Anemia and iodine metabolism

It appears that iron deficiency will exacerbate the effect of low iodine.

Iron deficiency is also an issue in 'western' countries

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5140a1.htm

Iron Deficiency --- United States, 1999--2000

Iron deficiency, the most common nutritional deficiency worldwide, has negative effects on work capacity and on motor and mental development in infants, children, and adolescents, and maternal iron deficiency anemia might cause low birthweight and preterm delivery (1--3). Although iron deficiency is more common in developing countries, a significant prevalence was observed in the United States during the early 1990s among certain populations, such as toddlers and females of childbearing age (4).


Persistence of goiter despite oral iodine supplementation in goitrous children with iron deficiency anemia in Côte d'Ivoire1,2,3

Michael Zimmermann,
Pierre Adou,
Toni Torresani,
Christophe Zeder, and
Richard Hurrell


http://ajcn.nutrition.org/content/71/1/88.long

"The findings in this study suggest that iron deficiency anemia in children may limit the effectiveness of an iodine intervention program. If confirmed, this result will have broad public health implications for the control of IDDs. More than 2 billion people—mainly young women and children, most in developing countries—are iron deficient (44). Children and pregnant women are also highly vulnerable to iodine deficiency and are the main target groups for iodine-supplementation programs (1, 3). Of the 419 children screened in this study, nearly 1 in 5 had both goiter and iron deficiency anemia. If iron deficiency is a nutritional factor that influences the pathogenesis of IDDs, iron deficiency may have a greater effect on IDDs than do previously described goitrogens because of its high prevalence in vulnerable groups."

[R.B.]

Iodine deficiency as a cause of brain damage is a fascinating editorial paper which may be of wider interest and has wider implications for the individual and society particularly in respect of extremely preterm infants.

"Identifying the appropriate indications for supplementation may alleviate individual pain and distress due to disability for several hundred extremely low birth-weight neonates each year in the US alone, and save society a pro-rated lifetime cost of nearly $US1 million per child." (see below) http://www.ncbi.nlm.nih.gov/pubmed/17107219

Iodine deficiency as a cause of brain damage

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1741987/

Abstract
This editorial reviews the impact of iodine deficiency
(1) on thyroid function in pregnant women and
neonates and (2) on the neurointellectual development
of infants and children.
All degrees of iodine deficiency (mild: iodine
intake of 50–99 μg/day, moderate: 20–49 μg/day, and
severe: <20 μg/day) affect thyroid function of the
mother and the neonate as well as the mental development
of the child. The damage increases with the
degree of the deficiency, with overt endemic cretinism
as the severest consequence. Maternal hypothyroxinaemia
during early pregnancy is a key factor in
the development of the neurological damage in the
cretin. Selenium deficiency combined with iodine
deficiency partly prevents the neurological damage
but precipitates severe hypothyroidism in cretins.
Iodine deficiency results in a global loss of 10–15
IQ points at a population level and constitutes the
world’s greatest single cause of preventable brain
damage and mental retardation.

A large series of investigations conducted in areas with
moderate iodine deficiency have demonstrated the presence
of definite abnormalities in the psychoneuromotor
and intellectual development of children and adults who
are clinically euthyroid and who do not exhibit the other
signs and symptoms of endemic cretinism, that is, the most
severe form of brain damage caused by iodine deficiency.
The psychometric tests used to find evidence for these
abnormalities are various and include locally adapted
“culture free” intelligence tests. The findings include low
visual-motor performances, motor skill, perceptual and
neuromotor abilities, and low development quotients and
intellectual quotients (IQ).11 12 20


The paper also make the points

Iodine is important to fetal development. Thyroxine is apparently found in fetal related fluid from the 6th week; the fetus does not start to make its own until the 24th week, (Is this logically a potential issue in extreme prematurity - is thyroxine provided to premature infants ? - It appears the issue is recognised but still under research. http://www.ncbi.nlm.nih.gov/pubmed/17107219 http://clinicaltrials.gov/show/NCT01306227 ).

Thyroid volume increases in iodine deficient women in pregnancy.

Globally iodine deficiency is a huge issue.

Food based thiocyanates may aggravate iodine deficiency in pregnancy, with different consequences in different circumstances.

As previously discussed there are a number of other increasingly common place blockers of iodine metabolism which have been greatly increased by human action or activity including fluoride, nitrates, chlorination, many soy based foods, bromination, dioxins . . .

[R.B.]

This is a well regarded extensive UK study . . .


http://www.thejournal.ie/iodine-defi...19382-May2013/


‘Children of the 90s’ research

Researchers used samples and data from Bristol-based Avon Longitudinal Study of Parents and Children (ALSPAC), also known as ‘Children of the 90s’. This is a long-term project involved more than 14,000 pregnant women in 1991 and 1992, and the health and development of their children has been followed by scientists ever since.

Researchers measured the iodine concentration in urine samples taken in the first trimester from 1,040 pregnant women. Referring to World Health Organisation (WHO) guidelines on recommended concentrations of iodine during pregnancy, they classified women who had an iodine-to-creatinine ratio [1] of less than 150 μg/g as being iodine deficient, and those with a ratio of 150 μg/g or more as iodine sufficient. Over two thirds (67 per cent) of the women fell into the category of “iodine deficient”.

The babies born underwent mental development assessments which involved measuring child IQ at age eight and reading ability at age nine. Adjusting the results for external factors likely to affect these scores, such as parental education and breast-feeding, the researchers found that children of women in the iodine-deficient group were “significantly” more likely to have low scores (lower quartile) of verbal IQ, reading accuracy, and reading comprehension. The research, published in the Lancet medical journal, found that the lower the mother’s concentration of iodine, the lower were the average scores for IQ and reading ability in the children.

[R.B.]

The effect of thiocyanates may extend to blocking the incorporation of iodine / iodide into breast milk.

The reduction of iodine in dairy is also of relevance as diary foods are an important source of iodine.

Thiocyanate in Food and Iodine in Milk: From Domestic Animal Feeding to Improved Understanding of Cretinism

To cite this article:
Peter Laurberg, Stig Andersen, Nils Knudsen, Lars Ovesen, Susanne B. Nøhr, and Inge Bülow Pedersen. Thyroid. October 2002, 12(10): 897-902. doi:10.1089/105072502761016520.


Transport of iodine in the mammary gland into breast milk plays a central role in various fields of prevention of thyroid diseases. First, a sufficient content of iodine in the mother's milk is necessary for normal brain development in the breastfed child. This is attained by expression during lactation in the mammary gland of the sodium iodide symporter (NIS), also responsible for iodine transport in the thyroid. Milk iodine content varies with the iodine intake of the mother, and urinary iodine excretion in groups of mothers seems to be a valuable indicator of the iodine status of their breastfed children. Second, iodine in dairy products provides a considerable part of iodine intake in many populations. Thiocyanate from rapeseed feeding of cows decreases milk iodine content, probably by competitive inhibition of NIS in the mammary gland. Alterations in feeding of dairy cows may alter the iodine content of consumer milk, and this may influence the risk of thyroid diseases in the population. Thiocyanate inhibition of iodine transport into milk may also be operative in humans with a high thiocyanate intake. This could further impair iodine status in breastfed children in low-iodine intake areas of the world. It can be speculated that a low-iodine content of mother's milk because of inhibition of NIS in the mammary gland may be one factor of importance for development of myxedematous cretinism.