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

[R.B.]

I have also included this in part in the summary as I think these papers are important.

The presence of selenium and other minerals in fish may explain why fish intake that is likely high in fluoride (eg whole fish such as sardines) is not generally associated with thyroid conditions etc.

The Chinese paper starkly demonstrates that higher iodine alone will not necessarily prevent the inhibition by excess or imbalance of fluoride of thyroid function and the induction of goiter or indeed fluorosis.


Importantly this http://www.google.com/url?sa=t&rct=j...55123115,d.Yms Chinese study of a population with both high fluoride 3mg per litre (approx) and relatively high iodine 1mg per liter (approx) in their water observed "In high iodine and high fluorine areas, the goiter and dental fluorosis rates of children aged from 8 to 12 were 29.8% and 72.98%.", which suggests that higher iodine alone may not mitigate high fluoride intake. It looks as if the picture is more complex and also involves mineral intake; likely all of the 'elements' (as in pieces of the nutritional jigsaw - no pun intended ) need to be in place to minimise the risk of fluorosis / wider iodine / thyroid dysfunction.

Does high fluoride intake in whole marine foods have the same effect is a question I raise, as we have always associated fish intake with healthy populations. Fish would also contain important minerals such as selenium and zinc.

Fluoride apparently actively binds with selenium which interestingly may be protective against the effects of fluoride. http://www.ncbi.nlm.nih.gov/pubmed/20143719 Apparently it also bind with other minerals, so could part of the effect of fluoride be to inactivate minerals, which are often already in short supply in the western diet, but are provided in marine foods. This mechanism would in nutritional terms be a double edged sword;

- protection against excess fluoride by deactivation of fluoride by binding to minerals good.

- deactivation of important minerals that are already deficient in many diets bad.


An unreferenced comment here http://www.healthyshopping.com/OlaLoa/autism.asp by Richard A. Kunin, M.D. said interestingly

" Fluoride forms insoluble complexes with selenium. Since selenium is strongly electropositive, it combines with fluoride preferentially, with even greater avidity than calcium, magnesium, iron, zinc, sodium, potassium. The total adult body content of selenium is less than 100 mg, so little as to be vulnerable to sodium fluoride intakes of 3 to 5 mg per day, which are usual in this country because of fluoridation and fluoridated toothpaste. Consider that vital trace minerals, such as selenium, chromium and molybdenum, are ingested on average only about 50 mcg per day. Fluoride intake is 100 times more and fluoride complexes are likely to inactivate these trace minerals by rendering them insoluble--even in the presence of calcium, magnesium, boron or aluminum salts, which also bind with fluoride. Sodium fluoride, the relatively soluble fluoride used in water fluoridation, preferentially binds to the trace minerals, selenium and chromium."


This paper refers to possible links between calcium and magnesium deficiences and populations at risk of fluorosis. http://www.google.com/url?sa=t&rct=j...55123115,d.Yms

[R.B.]

Flourine contamination from industrial sources may be a significant issue if this paper from the 1950s still holds. It contains a powerful image of a leg bone of a cow with fluorosis, which resembles a knobbly tree branch in texture.


PS if you have got this far without falling asleep; very well done


http://www.google.com/url?sa=t&rct=j...55123115,d.Yms

"The problem of fluorosis in farm animals in Britain
is not due to the high fluorine content of rock phosphate
deposits, volcanic soils, or water supplies, but
arises from the emission of fluorine containing gases
and dusts from industrial plants. If the density of our
industrial areas is considered in relation to the relatively
small area of the whole country, it can be readily
understood that a great deal of agricultural land must
be adjacent to industrial works.
The chief sources of fluorine contamination of
grassland and crops are: (1) steel and metal works
when the method of production involves the use of
large amounts of fluorspar as a flux ; (2) brickworks,
where the source is usually the local clay, although coal
is sometimes a contributory factor; (3) production of
aluminium by the electrolytic reduction of alumina;
(4) glass, enamel, and colour works where fluorine
compounds are often added to facilitate melting and to
give the finished products certain properties ; (5) the
calcining of iron-stone where the sourtie is mainly the
fluorine-rich ore itself; (6) potteries and other ceramic
industries where the materials used in manufacture are
high in fluorine; (7) collieries, power stations and
other industries which consume large quantities of
pulverised low-grade coal with a high fluorine content.

It is generally accepted that the fluorine content
of most plants, with the exception of the roots, is
not readily affected by the amount of fluorine in the
soil. There seem to be a few exceptions to this, notably
the tea plant. and the camellia, which appear to
be fluorine collectors, but common fluorine values for uncontaminated animal foodstuffs lie between 1 and
10 p.p.m. on a dry matter basis. Excessively high
values’ up to 2000 p.p.m. have been reported (Green
1946) on herbage near sources of emission of fluorine
compounds. "

and a paper called The Emerging Medical and Geological Association from The American Clinical and Climatological Association http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473139/ states


"The health problems caused by fluorine volatilized during domestic coal use are far more extensive than those caused by arsenic. More than 10 million people in Guizhou Province and surrounding areas suffer from various forms of fluorosis. Typical symptoms of fluorosis include mottling of tooth enamel (dental fluorosis) and various forms of skeletal fluorosis including osteosclerosis, limited movement of the joints, and outward manifestations such as knock-knees, bow legs, and spinal curvature. Fluorosis combined with nutritional deficiencies in children can result in severe bone deformation.

The etiology of fluorosis is similar to that of arseniasis in that the disease is derived from foods dried over coal-burning stoves. Adsorption of fluorine by corn dried over unvented ovens burning high ([greater than, closed by curve, equal, slanted]200 ppm) fluorine coal is the probable cause of the extensive dental and skeletal fluorosis in southwest China. The problem is compounded by the use of clay as a binder for making briquettes. The clay used is a high-fluorine (mean value of 903 ppm) residue formed by intense leaching of a limestone substrate."

In the west we do not have the same level of exposure but it is clear that coal could be a significant source of flourine emissions

[R.B.]

Two further papers suggesting mineral deficiency as well as fluoride plays a part in fluorosis

http://en.cnki.com.cn/Article_en/CJF...F200802013.htm

http://en.cnki.com.cn/Article_en/CJF...W200204035.htm

[R.B.]

Another and particularly powerful fluoridealert video; a heartrending plea from a pediatrician.

Iodine / fluoride problems have their largest effect in the young.

Fluoride is accumulated over time in bone and calcified tissue, and provides a background reserve, so even once fluoride intake is reduced there will continue to be releases from calcified tissue and bone.

As I keep stressing to the iodine blocking effects of fluoride in water we can add chlorination, perchlorate, nitrates, bromide, fluoride in tooth paste (a real issue if you do not rinse really well it appears), fluoride in foods . . .

However it is important to keep in mind that fluoride and iodine whilst of the same family have very different sizes and characteristic, so will overall have lots of effects in pathways that are not common. Very high levels of fluoride have been shown to affect a raft of important pathways including reducing energy production, oxidation stress, and affecting immune function. The question is at what intake level do these effects become significant; we do not know, and it is all very complicated because for example you cannot entirely separate the effects of fluoride excess from iodine deficiency.

http://fluoridealert.org/fan-tv/dr-whyte/

[R.B.]

. . . And this made me howl with laughter at the irony of it . . . this paper recommends that goats with chronic fluorosis should receive mineral supplementation copper iron manganese and nickel . . . they did not look at selenium.

http://www.google.com/url?sa=t&rct=j...55123115,d.Yms

I found it ironic that I can find a paper on mineral deficiency and fluorosis in goats but not people, and in many hours of hunting for information have not seen anybody suggest the possible need for mineral supplementation in those with fluorosis !


But tary a moment the paper above references another Turkish paper looking at mineral deficiencies in humans and this is what it said - looks like we have more in common with goats than we would care to admit

http://www.google.com/url?sa=t&rct=j...55123115,d.Yms

In conclusion, our findings indicate that chronic fluorosis is associated with reduced levels of serum Cu, Zn, Mn, and Mg. However, more studies are needed to verify and clarify the relationship between serum mineral status and chronic fluorosis.

(that is copper zinc manganese and magnesium)

[R.B.]

Is iodine accumulated in fat tissue is a question I have wanted the answer to for a while. This is the first paper I have found that confirms iodine is accumulated in fatty muscle tissue (albeit in pigs).

Six months after an initial single dosage of 480mg dorsal fatty muscle tissue contained over 2 mg per kilo which was way more than the amount in liver skin or lean meat (fig 4).

The accumulation of iodine in fatty tissue for me raises the question if those who have significant fat tissue will require a higher iodine intake, because a greater proportion of any intake will be taken up by the fatty tissue. This is what is seen with vitamin D. The obese will have a lower level of vitamin D in the blood for the same intake compared to a slim person; as a result a greater number of obese people are vitamin D deficient.

In the pigs the measures of iodine such as concentration in urine, blood and thyroid were still higher after 6 months, which begs the question if the iodine is being released from the fat tissue to sustain higher iodine levels.

It also raises the issue of what role does iodine play in fat tissue; for example does it have antioxidant roles.

These are important questions but so far I have failed to find any research looking at these issues in humans.

The intramuscular delivery may have been a slightly more effective vehicle than oral delivery.


Iodine concentrations in porcine blood, urine, and tissues after
a single dose of iodised oil

http://www.google.com/url?sa=t&rct=j...55819444,d.Yms

[R.B.]

This paper recognises it is important to bear in mind the additive effects of iodine blockers as they may well have cumulative effect especially where iodine intake is low.

As discussed to perchlorate, and thiocyantes (from brassica type foods) we can add chlorination, nitrates, some chlorine products, other foods blockers such as agents in soy . . .


Combined effects of perchlorate, thiocyanate, and iodine on thyroid function in the National Health and Nutrition Examination Survey 2007–08

http://www.sciencedirect.com/science...13935113000091


Abstract

Perchlorate, thiocyanate, and low iodine intake can all decrease iodide intake into the thyroid gland. This can reduce thyroid hormone production since iodide is a key component of thyroid hormone. Previous research has suggested that each of these factors alone may decrease thyroid hormone levels, but effect sizes are small. We hypothesized that people who have all three factors at the same time have substantially lower thyroid hormone levels than people who do not, and the effect of this combined exposure is substantially larger than the effects seen in analyses focused on only one factor at a time. Using data from the 2007–2008 National Health and Nutrition Examination Survey, subjects were categorized into exposure groups based on their urinary perchlorate, iodine, and thiocyanate concentrations, and mean serum thyroxine concentrations were compared between groups. Subjects with high perchlorate (n=1939) had thyroxine concentrations that were 5.0% lower (mean difference=0.40 μg/dl, 95% confidence interval=0.14–0.65) than subjects with low perchlorate (n=2084). The individual effects of iodine and thiocyanate were even smaller. Subjects with high perchlorate, high thiocyanate, and low iodine combined (n=62) had thyroxine concentrations 12.9% lower (mean difference=1.07 μg/dl, 95% confidence interval=0.55–1.59) than subjects with low perchlorate, low thiocyanate, and adequate iodine (n=376). Potential confounders had little impact on results. Overall, these results suggest that concomitant exposure to perchlorate, thiocyanate, and low iodine markedly reduces thyroxine production. This highlights the potential importance of examining the combined effects of multiple agents when evaluating the toxicity of thyroid-disrupting agents.
Highlights

► Recent data suggest that essentially everyone in the US is exposed to perchlorate. ► Perchlorate exposure may be associated with lower thyroid hormone levels. ► Some groups may be more susceptible to perchlorate than others.

[R.B.]

A paper looking at development and intelligence in areas including of modest fluoride in water and low iodine.

There is no wider detail as to diet or mineral intake, so much we do not know in terms of potential relevance and comparability to Europe and America.

None the less the paper does indicate potential serious effects on development where fluoride intake is modest and iodine intake low, whcih in light of the figures above as to the iodine status of adolescent and pregnant females in the UK is scary in its possible implications.




http://www.slweb.org/IDD.html



Discussion

One hundred and four children with mental retardation were detected in all. Area A had 25%, area B 16%, and area C 8%. The significant differences in IQ among these regions suggests that fluoride can exacerbate central nervous lesions and somatic developmental disturbance caused by iodine deficiency. This may be in keeping with fluoride's known ability to cause degenerative changes in central nervous system cells and to inhibit the activities of many enzymes, including choline enzymes, causing disturbance of the nerve impulse (5). We found significant differences among the three areas, indicating that lack of iodine in children results in disturbance of the process of growth and ossification and that high fluoride intake can further disturb bone development (6,7). Also, the auditory threshold was significantly different among the three areas, with severe loss of hearing in high fluoride and low iodine areas. Severe iodine deficiency in early fetal life has adverse effects on the development and differentiation of the acoustic organ, and we suggest that high fluoride intake may also promote hearing loss. . . MORE

Summary

We studied a total of 769 schoolchildren of 7-14 years in three areas, characterized by intakes of (A) low iodine, high fluoride; (B) low iodine, normal fluoride; and (C) iodine supplemented, normal fluoride. Results for the following parameters for areas A, B, and C, respectively were: (a) average IQ: 71, 77, 96; (b) average auditory threshold (in dB): 24, 20, 16; (c) bone age retardation (%): 28, 13, 4; (d) thyroid 131I uptake (%): 60, 50, 24; and (e) serum TSH (mU/ml): 21, 11, 6. Statistically significant differences existed between these areas, suggesting that a low iodine intake coupled with high fluoride intake exacerbates the central nervous lesions and the somatic developmental disturbance of iodine deficiency. The detection rate of subclinical endemic cretinism in children with mental retardation was 69%, and the total attack rate of subclinical endemic cretinism 9%.

[R.B.]

Iodine overload - how much is too much ?

Whilst there appears to be significant amount of material suggesting benefits in some from high iodine intake, possibly in those where there has been historic imbalance, or deficiency, and suggestions that some populations have a high intake, there are equally indications that high iodine intake can have adverse consequences.

Daily recommended intakes are in micro grams rather than milligrams. Is this enough given uncertainties as to the level of iodine blockers and competitors such as bromine in our diet. Clearly some think not, and sadly it appears that many are not even getting the minimum requirements in their diet, and that is before the potential blocking of iodine uptake may inhibit their usage of an already very low intake. http://lpi.oregonstate.edu/infocenter/minerals/iodine/

There is much we do not know, for example exactly how other dietary factors interact with iodine intake. The Japanese whatever their historic intake was got their intake from natural food based sources mainly seaweed which would also have been mineral rich and interestingly likely contained significant amounts of bromine (seaweed contains quite high levels of bromine generally).

Iodine contents of seaweeds vary considerably, and iodine is lost in processing and drying, which makes iodine intake through seaweed a bit of a lottery, and clearly if somebody has a lot of bromine in their system from artificially brominated foods then intuitively a food source potentially rich in bromide may not be ideal (although it is possible some of the bromine will also be lost in processing)

Bromine in foods is more of a problem in the US than UK due to brominated soft drinks and flour; but bromine may be used in other products viz the fumigation of dried foods such as nuts; nuts contain quite high amounts of bromine it appears. It seems potentially lots of foods are fumigated with bromine. Whilst there may be some restriction on fumigation with bromine in the west with foods being sourced all round the world and complex regulations I suspect sadly the reality is overall we do not know what our food contains.

I have no idea if the relatively high levels of bromine found in nut products is from the soil or fumigation, but would guess it is probably largely from fumigation in the county of origin.

Also as previously mentioned bromine/bromide may be used in the brewing industry. Does it reach the beer; I have not been able to find a definitive answer to the question.

http://www.fao.org/docrep/x5042e/x5042e08.htm "Almost invariably, nuts and shelled nuts are fumigated in the country of origin before export, often with methyl bromide. If more than one fumigation is required after importation, there may be danger of taint and a trial treatment should be made."

Methyl bromide may be particularly well absorbed because it is in an organic form (and differently ? metabolised) - oh dear that raises a whole heap of new questions - as ever things are rarely straight forward - it appears marine organisms produce it and some will end up in the atmosphere. Some plants including the brassicas produce it in small quantities. Large amounts can kill you and do kill customs officers opening containers. http://en.wikipedia.org/wiki/Bromomethane What effect does the sort of levels found in food have? I have no idea but clearly based on the forgoing a bromine iodine imbalance in the metabolic pathways is a potential health issue.

Back to iodine intake; a Japanese Radiological society paper suggest current intake of iodine was around 1mg with their parents consuming more, but exactly how much we do not know. Higher intakes may be problematic particularly for those with other dietary deficiencies including selenium and other minerals.

The paper below looked at a group of Peace Corp staff who had high iodine intake possibly 50mg a day or more for 32 months. The core conclusion is that those using iodination to decontaminate water need regular medical checks. Interestingly the paper does not recommend that sanitisation of water with iodine should not be used, only that regular checks should take place and particular care should be taken in pregnancy. It is a shame the information is not more comprehensive, and does not look at any longer term implications of high dose iodine intake if any.


Effects of Chronic Iodine Excess in a Cohort of Long-Term American Workers in West Africa

http://jcem.endojournals.org/content/87/12/5499.long

The body of the text contains the following comment; if it means this was the result of examination prior to iodine exposure it adds a further dimension to the results.

There was a high prevalence of goiter among Peace Corps volunteers in this study at baseline in both euthyroid and hypothyroid individuals. . .

Abstracts from text

As the arid climate in Niger results in the daily consumption of 5–9 liters water, the volunteers consumed at least 50 mg iodine daily, which is approximately 300 times the daily U.S. Recommended Dietary Allowance (2). Urinary iodine excretion in this iodine-enriched population ranged from 392–153,780 μg/liter (median, 5,048 μg/liter). Volunteers used the water purification devices described above for up to 32 months.

The findings in this study have significant public health implications. In 1998, an estimated 60,000 iodine resin devices and 300,000 bottles of iodine tablets were sold to U.S. civilians for water disinfection (24). In addition, iodine-based water purification systems are routinely used by the military, in international relief efforts, and by other government-sponsored programs. In this regard we have recently reported that excess iodine ingestion by American astronauts from water treated with iodine for purification in space resulted in a small transient rise in serum TSH values upon return to earth (25). Since 1998, the iodine has been removed from astronauts’ potable water by an anion exchange resin just before the water is consumed, and no rise in serum TSH values has been observed. It is probably inadvisable for pregnant women, individuals with a history or a strong family history of thyroid disease, especially autoimmune thyroid disease, or individuals residing in areas of endemic iodine deficiency to use iodine-based methods of water purification unless extremely careful monitoring of the iodine content is carried out. Any individual anticipating prolonged ingestion of excess amounts of iodine in medications or as a byproduct of a water purification system should see a physician for a baseline physical exam to exclude the presence of preexisting goiter and to measure thyroid function tests and serum thyroid antibody levels to rule out abnormalities. Repeat thyroid function tests should then be repeated at intervals until excess iodine ingestion is eliminated.

[R.B.]

This is an interesting paper on estimated Japanese iodine intake which ties in with another report I have seen.

"By combining information from dietary records, food surveys, urine iodine analysis (both spot and 24-hour samples) and seaweed iodine content, we estimate that the Japanese iodine intake--largely from seaweeds--averages 1,000-3,000 μg/day (1-3 mg/day)."
See below

The report also recognises that pre 1950 Japanese ate a lot more kelp (Kombu) "elders ate up to four times more than those under the age of 29" so their intake figures could have been significantly higher.

It is also recognised in the paper that intakes of iodine will vary considerably on a day to day basis, which is reflected in urine output. So on some days Japanese may be consuming many grams of iodine. "Urine iodine levels can increase from 100 μg/L to 30,000 μg/L in a single day and return to 100 μg/L within a couple of days, depending on seaweed intake [39]. This is somewhat expected when varying amounts and types of seaweeds are consumed on a day-to-day basis."

An analysis of studies of iodine in urine incontrovertibly shows the Japanese have much higher iodine levels than we do in the west, the data in the paper shows at least historically they had a much lower level of many western medical conditions.

It is also clear from the report that a variety of dietary seaweeds are very much part of the Japanese life, and that the seaweeds in food vary in iodine content for a wide variety of reasons.

The full paper is free and the implications are thought provoking, both in terms of recommended western daily recommended intake, and the use of iodine at higher intakes as a medicine to correct historic imbalances.


"Japanese health statistics linked to high seaweed intake

The Japanese are considered one of the world's longest living people, with an extraordinarily low rate of certain types of cancer. A major dietary difference that sets Japan apart from other countries is high iodine intake, with seaweeds the most common source. Here are some astonishing Japanese health statistics, which are possibly related to their high seaweed consumption and iodine intake:

-Japanese average life expectancy (83 years) is five years longer than US average life expectancy (78 years) [41].

-In 1999 the age-adjusted breast cancer mortality rate was three times higher in the US than in Japan [42].

-Ten years after arriving in the US (in 1991), the breast cancer incidence rate of immigrants from Japan increased from 20 per 100,000 to 30 per 100,000 [43].

-In 2002 the age-adjusted rate of prostate cancer in Japan was 12.6 per 100,000, while the US rate was almost ten times as high [44].

-Heart related deaths in men and women aged 35-74 years are much higher in the US (1,415 per 100,000) as they are in Japan (897 per 100,000) [45].

-In 2004, infant deaths were over twice as high in the US (6.8 per 1,000) as they were in Japan (2.8 per 1,000) [46]."


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204293/


Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis

Abstract

Japanese iodine intake from edible seaweeds is amongst the highest in the world. Predicting the type and amount of seaweed the Japanese consume is difficult due to day-to-day meal variation and dietary differences between generations and regions. In addition, iodine content varies considerably between seaweed species, with cooking and/or processing having an influence on iodine content. Due to all these factors, researchers frequently overestimate, or underestimate, Japanese iodine intake from seaweeds, which results in misleading and potentially dangerous diet and supplementation recommendations for people aiming to achieve the same health benefits seen by the Japanese. By combining information from dietary records, food surveys, urine iodine analysis (both spot and 24-hour samples) and seaweed iodine content, we estimate that the Japanese iodine intake--largely from seaweeds--averages 1,000-3,000 μg/day (1-3 mg/day).

[R.B.]

A while ago I posted this link to a paper looking at the accumulation of iodine in various tissues in pigs.

http://www.vri.cz/docs/vetmed/46-6-153.pdf

A the moment I am wading my way through the 1000 pages plus of this not inexpensive text book on iodine http://books.google.com/books?id=7v7...iodine&f=false

I am again struck that the majority position still seems to be that most of the iodine in the body is found in the thyroid, despite the claims of some that this is not the case. I have not found any papers that definitively clarify this point.

From my reading I would suggest the relative proportions of iodide in the thyroid and wider tissue depends on the iodine intake status.

The linked paper Fig 3 and 4 clearly show that the amount of iodine in wider body tissue increases dramatically as intake increases; for example from a few micorgrams to in excess of 2mg per Kg in dorsal fat. For a 90kg pig, given the amounts of iodine found in other tissues based on the figures in the graph, the amount of iodine in a 90kg pig would mount up.

The amount in the thyroid at the highest intake is about 6 milligrams total, based on their figures.

The data in the above would suggest that at least in pigs where iodine intake is on the higher side, significantly more iodine will be found in the wider body tissues than the thyroid, which is what Venturi claims in the paper on the first page. The wider role of iodine in the body, and the examination of optimal requirements of tissues in addition to those of the thyroid may well result in the redefinition of the western guidelines on the optimal uptake of iodine.

The role of iodine / iodide / iodine in all its forms in many of the body's tissues including in female reproductive tissues remains to varying degrees to be clarified, and does not get much research funding because you cannot patent iodine, and iodine is very cheap in comparative terms. . .

[R.B.]

In the UK the Government recently asked the body responsible for setting national nutritional standards called SACN to look at iodine intake. In their consequent position statement (linked below) SACN declined to look at maternal iodine intake due to a lack of 'robust' evidence. There is a huge amount of non randomized control evidence (RCTs) as to the importance of iodine in development, and RCTs to look at the neurological impact of iodine deficits in pregnancy can never happen due to ethical implications. The refusal of SACN to look at the issue begs the question who is responsible. I put the issues below in questions to a director of NICE and Health for England (HFE) (UK health regulatory agencies) and made this delegate submission at a recent forum held by an excellent organization called the Westminster Forums. http://www.westminsterforumprojects.co.uk/ (the size of allowed submissions is limited). Importantly there is growing evidence that nutrient deficiency in the first trimester may lead to irreversible sub-optimal brain formation, for example incomplete neuron migration. There is also some evidence that fundamental factors such as abstract thought, empathy, musicality and higher human function generally may be compromised, which factors help define our humanity. Motor and more basic function is less sensitive to degradation. In a resource pressured world higher human function arguably including empathy and abstract thought is of fundamental importantance to the avoidance of conflict.


SUBMISSION

Optimal neurological development including IQ is crucial to individuals, society, and nations. Cell development in common with all cellular function, indeed life itself, is nutrient dependent. Is Health for England (HFE) ultimately responsible for national dietary and consequent nutrient intake; if not who is?

SACN reports to HFE but appears to restrict considerations to specific nutrient issues where science is ‘robust’; who then is responsible for assessment of health risks relating to significant population insufficiencies, where ‘evidence’ of risk is ‘weak’ e.g. no RCTs, but the overview fairly compelling? Further who is tasked to design and implement corrective strategies for existing identified nutritional insufficiencies.

For example SACN’s ‘Position Statement’ on iodine intake during pregnancy stated “The Subgroup advised that without further evidence it would not be possible to carry out a robust review of the UK DRV ”; although it is widely accepted very low iodine causes cretinism, and significant if ‘non-robust’ evidence suggests mild to moderate iodine deficiency may, starting in the first trimester, incrementally increase risks of irreversible sub-optimal brain formation, lower IQ 5-10 points, impair abstract thought, and lower other life-chance related developmental outcomes. (Maternal thyroxin supplies early foetus needs. Hypothyroxinemia is commonly associated with low iodine.) Accumulating evidence indicates growing iodine insufficiencies in adolescent females and pregnant women . Low income arguably increases deficiency risks. Further, DHA , and vitamin D deficiencies inter alia, likely also incrementally irreversibly compromise brain structure and function; examples of insufficiency and its effects include:

• DHA – 500 mg daily after week 22 reduced low birth weight babies by 35%, and very early pre-term deliveries by 50% (par 2.32) 7
• Iodine – 85% of adolescent females in a Belfast sample (par 5.1.1) 7 and 61% of pregnant women were classed as iodine deficient (par 5.1.5.2) 7
• Vitamin D – 75-96% of pregnant women were vitamin D insufficient 12

Iodine and vitamin D insufficiencies present particular challenges; realistically population based intake normalisation is only achievable through fortification or supplementation:

• Vitamin D food sources are limited compared to sun exposure production, which in modern day life is limited. The problem is particularly acute in the dark skinned.
• Iodine is only found in significant amounts in marine and particularly estuarine foods including seaweeds. Dairy foods are the next best source, but primarily because of cattle supplementation rather than pasture content . Other food sources of iodine are limited. Use of iodised salt, and idophors as food-industry disinfectants are falling. Iodine is lost during food preparation and storage, complicating intake assessments. Significant amounts are lost during intensive exercise. Iodine is stored in fat, so likely a greater issue in the obese. Thyroid iodide uptake is inhibited by a wide range of increasingly common foods including brassicas, perchlorates, and competing halides (bromine and chlorine), which group can partially be mitigated by higher iodine intake. Other rising factors that decrease thyroid function include high fluoride, nitrates, PCBs, chlorination, lithium, smoking, and likely polyunsaturated fat imbalances and excesses.

DHA is also mainly found in marine food, but livestock DHA could be increased somewhat by appropriate intervention. Inattention to dietary needs of livestock leads to large falls in DHA content.

In summary evidence grows of UK population wide insufficiencies in fertile and pregnant females of inter alia Omega 3 DHA, vitamin D, and iodine. Realistically addressing increasing pre and post-natal neurodevelopmental national nutrient insufficiency risks of particular relevance to the disadvantaged, including crucially iodine, vitamin D, and DHA, in fertile and pregnant females, can only be achieved by food supplementation; this will require bringing together health agricultural and food sectors in a quest for optimal solutions; the question is by whom?


1. SACN position statement on iodine and health - February 2014 – par. 122 http://www.sacn.gov.uk/pdfs/sacn_pos...and_health.pdf
2. Comprehensive Handbook of Iodine: Nutritional, Biochemical, Pathological and Therapeutic Aspects - Victor R. Preedy, Gerard N. Burrow, Ronald Ross Watson - Academic Press, 17 Mar 2009 - Medical - 1334 pages – in part on line - multiple references e.g - (FYO I purchased a copy and have read it twice from cover to cover)
http://books.google.com/books?id=7v7...gnancy&f=false
3. Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC) - Sarah C Bath PhD, Colin D Steer MSc, Prof Jean Golding FMedSci, Pauline Emmett PhD, Prof Margaret P Rayman DPhil, - The Lancet, Volume 382, Issue 9889, Pages 331 - 337, 27 July 2013 - http://www.thelancet.com/journals/la...436-5/abstract
4. Section IV - The Scientific Basis for the Elimination of Brain Damage due to Iodine Deficiency – F Delange and B S Hetzel - http://www.iccidd.org/cm_data/hetzel-e-section4.pdf
5. Mild iodine deficiency in pregnancy in Europe and its consequences for cognitive and psychomotor development of children: A review – Caroline Trumpff, Jean De Schepper, Jean Tafforeau, Herman Van Oyen,
Johan Vanderfaeillie, Stefanie Vandevijvere – J Trace Elem Med Biol (2013) - http://www.iccidd.org/cm_data/2013_T...evelopment.pdf
6. Chapter 20 - The Iodine Deficiency Disorders - Creswell J. Eastman, M.D Michael Zimmermann, M.D – Thyroid Disease Manager - http://www.thyroidmanager.org/chapte...ncy-disorders/
7. Benefits of Docosahexaenoic Acid, Folic Acid, Vitamin D and Iodine on Foetal and Infant Brain Development and Function Following Maternal Supplementation during Pregnancy and Lactation. - Nancy L. Morse - Nutrients. Jul 2012; 4(7): 799–840 - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407995/
8. Recommendations; UK 150mcg; WHO 250mcg; American Paediatrics 220 - 290mcg, Japan 3000mcg.
9. Dietary (n-3) Fatty Acids and Brain Development – Sheila M. Innis - J. Nutr. April 2007 vol. 137 no. 4 855-859
http://jn.nutrition.org/content/137/4/855.full
10. Omega-3 Fatty Acid Deficiency in Infants before Birth Identified Using a Randomized Trial of Maternal DHA
Supplementation in Pregnancy - Kelly A. Mulder, D. Janette King, Sheila M. Innis - LoS ONE 9(1): e83764. doi:10.1371/journal.pone.0083764 - http://www.plosone.org/article/fetch...esentation=PDF
11. DHA Deficiency and Prefrontal Cortex Neuropathology in Recurrent Affective Disorders – Robert K McNamara - J Nutr. Apr 2010; 140(4): 864–868. - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2838627/
12. Vitamin D deficiency and insufficiency in pregnant women: a longitudinal study - Valerie A. Holmes, Maria S. Barnes, H. Denis Alexander, Peter McFaul and Julie M. W. Wallace - British Journal of Nutrition / Volume 102 / Issue 06 / September 2009, pp 876-881 http://journals.cambridge.org/action...07114509297236
13. Vitamin D deficiency in pregnancy - still a public health issue. - McAree T1, Jacobs B, Manickavasagar T, Sivalokanathan S, Brennan L, Bassett P, Rainbow S, Blair M.- Matern Child Nutr. 2013 Jan;9(1):23-30. doi: 10.1111/mcn.12014.- http://www.ncbi.nlm.nih.gov/pubmed/23230904
14. Vitamin D3 and brain development - D Eyles, J Brown, A Mackay-Sim, J McGrath, F Feron http://www.direct-ms.org/pdf/VitDGen...evelopment.pdf
15. Developmental vitamin D deficiency causes abnormal brain development. - Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH. - Psychoneuroendocrinology. 2009 Dec; 34 Suppl 1:S247-57. doi: 10.1016/j.psyneuen.2009.04.015. - http://www.ncbi.nlm.nih.gov/pubmed/19500914
16. The geochemistry of iodine and its application to environmental strategies for reducing the risks from iodine deficiency disorders http://nora.nerc.ac.uk/10724/1/CR03057N.pdf
17. To refine and confirm the level of selenium and iodine supplementation for breeding ewes http://www.eblex.org.uk/wp/wp-conten...ort-190214.pdf
18. POLICY STATEMENT Iodine Deficiency, Pollutant Chemicals, and the Thyroid: New Information on an Old Problem – COUNCIL ON ENVIRONMENTAL HEALTH – American Academy of Pediatrics - DOI: 10.1542/peds.2014-0900 ; originally published online May 26, 2014; Pediatrics http://pediatrics.aappublications.or....full.pdf+html
19. http://her2support.org/vbulletin/showthread.php?t=53928 I am R.B.
20. Modern organic and broiler chickens sold for human consumption provide more energy from fat than protein. Wang Y, Lehane C, Ghebremeskel K, Crawford MA. - Public Health Nutr. 2010 Mar;13(3):400-8. doi: 10.1017/S1368980009991157. - http://www.ncbi.nlm.nih.gov/pubmed/19728900

[R.B.]

This paper is full of thought provoking material including these two references to the use of iodine for water purification in prison populations.

It makes the point in the introduction that cooking losses of iodine can be significant, which is both of relevance to us in the west and in assessing Japanese iodine intakes.

"The iodine content of raw food is reduced by cooking (WHO, 1996). For example, the iodine loss on boiling or grilling/frying fish was 50-82 and 20% respectively (Harrison et al., 1965)."

It also suggest that absorption of iodine in food may only be 50%.

"22. Inorganic iodine is readily absorbed from the gut, generally as iodide (Nordic Project Group, 1995). However, probably only 50% of iodine present in organic compounds in foods is absorbed (Bender and Bender 1997). Though some absorption occurs in the stomach, the small intestine appears to be the principal site of absorption in both humans and rats (Riggs, 1952, Small et al., 1961)."

I have been looking for but unable to find any papers looking at the effect of thiocyantes / perchlorate / nitrates etc on the iodine importers in the gut (if any)

Logically losses in the gut and in food preparation need to be considered in making any dietary recommendations.

Vegans are reported to be at particular risk of low iodine levels.

"40. It has been reported that vegans and vegetarians can consume inadequate intakes of dietary iodine. A controlled experimental diet (performed in Germany, a classical iodine deficient country until the mid 1990s) used a repeated measure method (Remer et al., 1999). It exposed six adult volunteers to a 5 day dietary intervention in which isoenergetic lactovegetarian and non vegetarian diets were
consumed. The strict vegetarian diet produced both an extremely low iodine intake (<20 μg/d) and urinary output (36.6 (SD 8.8) μg/d). The authors concluded that strict vegetarians are possibly at risk of developing iodine defciency disorders."

The risks associated with low intake could possibly be added to increased thiocyanate intake in basicas by virtue of higher vegetable intake, and increased goitrogens in soy by virtue of a higher intake of soy products

Could the high levels of hypothyroidism in Whickham (UK) Par 65 be maybe due to high fluoride intake from sources unknown - industry or water etc









EXPERT GROUP ON VITAMINS AND MINERALS

http://www.google.co.uk/url?sa=t&rct...56146854,d.d2k


EVM/00/06.REVISEDAUG2002
__________________________________________________ _______________________________33
This paper has been prepared for consideration by the Expert Group on Vitamins and Minerals and
does not necessarily represent the final views of the Group.

136.The health and thyroid function of representative subjects of a prison population
(initially 133 euthyroid prisoners though due to discharge this number was
gradually reduced to 70) was assessed before and during usage of iodinated water
for 9 months (Freund et al., 1966). Water containing 1 mg/l iodine induced a
marked decrease in the uptake of radioactive iodine to 7% but protein bound
iodine levels did not change significantly until the iodine concentration was
increased to 5 mg/l for 2 months (following 7 months exposure at the lower
level), resulting in a decrease of radioactive iodine to 2%. Serum thyroxine
concentration did not change regardless of the iodine concentration. No
information on actual intake is provided but it can be assumed that water
consumption would be approximately 2 litres/day. The authors noted that
prisoners continued to receive iodine from the diet including the use of iodised
salt. It was also noted that no effects on thyroid function were found in nonprison
personnel who swam in water iodinated at a level of 5 mg/l. No evidence
of iodine allergy was apparent. Two of fifteen male inmates who had had
consumed water containing 1 mg I/l for at least 3 months, had impaired iodine
organification (as measured by the change in thyroidal 131I concentration
following administration of perchlorate). The clinical significance of this effect is
unclear as individual T4 concentrations remained unchanged throughout the
study i.e. no patients demonstrated iodine-induced hypothyroidism.


137. As a continuation of the study discussed above, iodination of a prison water
supply at a concentration of 0.5 to 0.75 mg/l (estimated intake 1-1.5 mg/day) for
up to15 years did not result in any change to serum thyroxine level (Thomas, et
a., 1978). During the same period, 177 women in the prison gave birth to 181
full term infants without any enlargement of the thyroid being noted in the infants
(Stockton and Thomas, 1978). The mothers of 101 infants had been in prison for
≥122 days, whilst 80 mothers had been incarcerated for < 118 days (10-118).
However, the symptoms of 4 women who were hyperthyroid before entering,
worsened.

[R.B.]

Thyroid peroxidase activity as toxicity target for fluoride in patients with thyroid dysfunction

https://www.google.com/search?q=flou...icial&start=20 (free full paper PDF)

Swati Singla and Shashi A*
Department of Zoology, Punjabi University, Patiala- 147002, Punjab, India
* Corresponding author: Shashi Aggarwal, email: shashiuniindia@yahoo.co.in


ABSTRACT
The present study aimed to assess the effects of drinking water fluoride (F) on the activity of thyroid peroxidase (TPO) enzyme involved in thyroid hormone synthesis. 840 fluorotic patients affected with thyroid hypo and
hyper function and 140 euthyroid without fluorosis representing control were randomly selected from high endemic fluoride areas of Bathinda district, Punjab, India. The findings indicate significant (P<0.001) increase in the levels of serum F, urinary F and Urinary iodine (I) in fluorotic patients affected with thyroid disease.
Significant (P<0.001) inhibition was recorded in activity of TPO in fluorotic patients with thyroid hypofunction and the activity was elevated in hyperthyroid fluorotic patients. Pearson’s bivariate correlation revealed strong positive correlation between water F and serum F (r= 0.98, P<0.01). Negative correlation existed between serum F vs TPO (r= -0.93, P<0.003), urinary I vs TPO (r = -0.95, P<0.002) and serum TSH vs TPO (r = -0.8876, P<0.001). The activity of TPO showed positive correlation with T3 (r = 0.963, P<0.01) as well as with T4 (r = 0.965, P<0.001). From the present study it may be concluded that the ingestion of drinking water with high concentration of fluoride leads to stress of the mechanism of biosynthesis of thyroid hormones, as evidenced by depletion in the activity of TPO, which may be produced by the attraction of fluoride with oxidized form of iodide and/or with the iodide site on the TPO molecule. This tends to decrease in concentration of T3, T4 and increase production of TSH in the serum.

INTRODUCTION
Over the past decade there has been an increasing focus
on the effects of hazardous chemicals on human
endocrine systems. Exposure to specific environmental
toxins has been shown to interfere with the production,
transportation and metabolism of thyroid hormones
(TH) by a variety of mechanisms or in modifying the
metabolism of thyroid hormones. Environmental
endocrine disruptors are exogenous substances that
can interfere with TH synthesis, deiodinase function in
peripheral tissues, proteins in the blood, and the
agonistic or antagonistic actions of certain chemicals on
target tissue receptors [1]. Fluorine containing
compound have been listed among the most significant
endotoxins that appear in natural environment as after
effects of industrial activity of humans. The high cell
membrane penetrating power, bioaccumulation, and
biodegradable property of fluoride cause it to have a
major impact on ecotoxicology [2].

The U.S National Research Council [3] states fluoride is
an endocrine disruptor and has the potential to disrupt
the function of many tissues that require iodine. Studies
that have examined human populations with adequate
intake of iodine have reported mixed results about
fluoride’s ability to produce goiter [4]. The research has
been more consistent, however, where the examined
populations had either excessive iodine intakes [5], or
deficient iodine intakes [6]. Thyroid disruptors can
affect thyroid physiology in many phases of thyroid
regulation. The complex system of iodine uptake,
thyroid hormone production, interconversion of
thyroid hormones and hormone degradation and
elimination can be directly altered by thyroid
disruptors [7].


And in the body of the text

Fluoride had significant effect on TPO activity, and
decreases T3 and T4 levels and increases TSH. This
disruption of TPO activity could be a sensitive TH end
point for various concentrations of water fluoride.
Several chlorinated POPs disrupt the TH axis, including
polychlorinated biphenyls, polychlorinated dibenzo-pdioxins,
and dibenzofurans [25,26]. In animal studies,
Boas et al. [27] reported that fluorinated compounds
such as PFOS and PFOA also inhibited TPO activity in
the rats, with reductions in T4 and T3.

PFOS http://en.wikipedia.org/wiki/Perfluo...esulfonic_acid

PFOA http://en.wikipedia.org/wiki/Perfluorooctanoic_acid

and there is a great table showing urine and serum fluorine levels for various intakes of fluorine ; they rise "significantly" as does iodine excretion !

The increase level of urinary iodine with increasing fluoride intake is striking. They do not record the iodine intakes, but this raises some interesting questions as to why more iodine is being excreted in those with a high fluoride intake - if intakes of iodine are already low would this be a double high fluoride intake whammy?

Should all thyroid function assessments also look at flouride levels ? I have no idea to what extent the issue is on the wider public health adgenda. This is the NHS UK information of fluoride that I found http://www.nhs.uk/Conditions/Fluorid...roduction.aspx makes no mention of flouride and potential impact on thyroid function on this page.

[R.B.]

This 'in full' paper on Fluoride Alert raises some interesting questions and information. I found it whilst trying to better understand the role of fluorine in hyperthyroidism.

Is fluoride-induced hyperthyroidism a cause of psychosis among East African immigrants to Scandinavia?
http://fluoridealert.org/studies/zac...-2009/?print=1

Viz local waters in some parts of Africa can contain 10 -40ppm of fluoride which raises the question what levels of fluorosis and thyroid problems do these groups have; one of the attached papers looks at fluorosis in Africa, which I will read and link here later.

This video clip http://www.youtube.com/watch?v=UkJuWLMaoG0 is intriguing (but has no details as to the speaker or occasion). If correct the information would seem to be of importance; viz that fluoride can substitute for iodine in T3 and T4, and tests for them will not differentiate between the iodine and fluorine content of T3 and T4, which would surely have a raft of implications. For example could a fluoride rich T4 result in higher activity in a still healthy thyroid because it fails to satisfy the body's demand for iodine?

It is also suggested soy is high in fluorine. I have seen this suggested before but not a paper as yet; if correct is high fluoride an inherent property of soy or a consequence of the type of the land it has been grown on?

[R.B.]

This is the paper I mention above.

It is fascinating because it suggests that calcium in the diet through milk can mitigate the effect of fluorine intake, it is presumed by reducing the uptake of fluorine by the gut.

Further those that drank from well where the water was higher in calcium also appear protected, even though they had relatively high intakes of fluorine. Those that had higher fluoride plus low calcium saw a high incidence of dental fluorosis.

There is no information on selenium zinc magnesium iron etc.

Seaweed is apparently in relative terms very high in calcium; might calcium in seaweed explain why there is no widespread suggestion that fluorosis was an problem in Hokkaido. Would this also explain why fish such as sardines are not associated with fluorosis or thyroid issues, because the bones which are high in fluoride are also high in calcium.

Apparently other studies has suggested vitamin D may also be a factor in fluorosis.

The paper states it was unable to show a direct association between fluoride intake and the occurrence of fluorosis.

Poor absorption of fluoride may explain why its effects are limited in other high fluoride areas.

All of which suggests it is important in fluoride studies to look at urinary fluoride, (so uptake as well as intake is known) and it would also be informative if iodine in the diet and in urine was measured too (to help tease out the roots of hyperthyroidism).

So as usual in human biology it appears that mechanisms are multifaceted and widely interconnected.





Groundwater quality and its health impact: An assessment of dental fluorosis in rural inhabitants of the Main Ethiopian Rift
Tewodros Rango a,⁎, Julia Kravchenko b, Behailu Atlaw c, Peter G. McCornick d, Marc Jeuland e, Brittany Merola a, Avner Vengosh a

PDF full version

http://www.google.com/url?sa=t&rct=j...TKiKToDzS3Lm2Q




PS. I have spent quite a while searching for papers on the displacement in the body of iodine by fluorine in T3 and T4 without much success so far. It does appear at least the first step can be created in the lab.

[R.B.]

This paper adds to the evidence that fluoride is actively prevented from incorporation in breast milk.


Eur J Clin Nutr. 1991 Jan;45(1):37-41.
Intake of fluoride and excretion in mothers' milk in a high fluoride (9 ppm) area in Kenya.
Opinya GN, Bwibo N, Valderhaug J, Birkeland JM, Lökken P.
Source

Department of Dental Surgery, University of Nairobi, Kenya.
Abstract

In 27 nursing mothers a study was made on breast milk fluoride (F) levels and the 24-h intake of F through foods and beverages. The daily F intake averaged 22.1 mg (range 9.5-37.2 mg); cooked food contributed 11.7 mg, water 4.5 mg and tea 5.8 mg. The breast milk F concentration averaged 0.033 mg/l (range 0.011-0.073 mg/l). No significant correlation could be established between the milk F level and the intake of F. The milk F level was, however, correlated positively to mothers' age and negatively to mothers' weight. It is concluded that the milk fluoride level was only moderately increased by the high intake of F, and that the children's intake of F through mothers' milk was negligible compared to the very high F intake through complementary foods and beverages.

[R.B.]

This is a very useful slide presentation which I found today that contains lots of thought provoking information by Abraham, Brownstein, Eskin, Flechas and Shevin

http://www.slideshare.net/MedicineAndHealth14/iodine

[R.B.]

Effect of Sodium Fluoride on Calcium Absorption and Balances in Man1,2

HERTA SPENCER, M.D., Chief3,
ISAAC LEWIN, M.D., Associate Chief4,
JOSEPHINE FOWLER, M.S., Research Dietitian5, and
JOSEPH SAMACHSON, PH.D., Chief Chemist6


The crunch

(47Ca = radioactive calcium so it can be traced)

http://ajcn.nutrition.org/content/22/4/381.abstract


3) In the majority of patients the plasma levels of 47Ca were lower during the intake of sodium fluoride than in the control studies indicating decreased absorption of 47Ca. The average decrease of the 47Ca plasma levels was 30% and the average decrease in 47Ca absorption, determined from fecal 47Ca excretions, was 23%.

which from the conclusion is not what they were anticipating . . .

4) These studies have shown that the intestinal absorption of calcium and the calcium balances did not improve during an intake of 20.6 mg sodium fluoride/day given for 22-42 days.

somewhat of an understatement

[R.B.]

It appears that fluoride may also inhibit magnesium uptake and re-uptake, and that conversely magnesium may inhibit fluoride uptake. The first abstract points out the importance of magnesium, the rising fluoride intake and falling magnesium intake and discusses possible implications.

http://www.mgwater.com/fl2.shtml

FLUORIDE-MAGNESIUM INTERACTION (Guest Editorial)
by A Machoy-Mokrzynska (Institute of Pharmacology and Toxicology, Pomeranian Medical Academy, Szczecin, Poland)
Fluoride (J. of the International Society for Fluoride Research), Vol. 28 No. 4; November, 1995, pp 175-177

In summary, it can be stated that in intoxication with fluorine compounds, magnesium plays a protective role by countering and reducing the toxic effects of F-.


http://jn.nutrition.org/content/117/3/496.long

Influence of Dietary Magnesium on Fluoride
Bioavailability in the Rat1'2
FLORIAN L. CERKLEWSKl
Department of Foods and Nutrition, College of Home Economics, Oregon State University,
Corvallis, OR 97331

Enhancement of fluoride bioavailability
in rats fed diets containing low magnesium,
and depressed fluoride bioavailability in rats fed diets
containing high levels of magnesium, can be explained
by the ability of magnesium to form an insoluble com
plex with fluoride in the intestinal tract.