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Iodine Research

Resource Network of The Iodine Movement

                               Iodine and the Body


Green Tea and Fluoride
Derry D (Interview with Mary Shomon)

Although, we do have fluoride in our bodies there is no normal physiological function for it. In
higher amounts it is toxic. Iodine is the most important element in our bodies by far. But what is
important is fluoride is in the same chemical family as iodine and can replace iodine in the body if
the iodine is deficient. But ideally one never wants to do that as fluoride is a toxin and should not
be used to replace normal iodine functions."

"Some countries are fluoridating their water supply for the theoretical benefits of fluoride helping
to prevent cavities. What is happening is the ingested fluoride takes the place of iodine that
should be there in the teeth, especially growing teeth. Iodine and thyroid for example have
complete control of tooth growth along with some help from growth hormone. (6-8) It is only
because our iodine intake has been decreasing over the years that fluoride has been mistakenly
added to our water with the idea of helping children's teeth. It would have made more scientific
sense to have added more iodine."

"Fluoride has also been used against osteoporosis with beneficial results. This again is just
replacing what iodine should be doing. The minor problems of osteopenia (minor loss of calcium)
seen in some patients put on thyroid is related to the fact that the same patients are low in iodine.
The low iodine causes the hypothyroidism and also the inappropriate short term bone response. If
iodine is given with the thyroid hormone this abnormal response can be avoided. So persons
taking adequate daily iodine will unlikely to ever develop osteoporosis."

"Radioactive iodine injected into patients shows a full outline of the bones on a total body scan.
This means one of the places iodine goes to immediately is bones. Thyroid hormone makes
bones grow, mature and remodel, when necessary. Together thyroid hormone, iodine and growth
hormone maintain a healthy bone structure. As vertebrates (animals with backbones) are the only
animals with thyroid glands it makes sense that iodine and thyroid control bone structure and

Bone Disorder Linked to Iodine Deficiency
Mercola J

Kashin-Beck disease, a bone disorder most commonly found in central Asia, may be caused by
chronic iodine deficiency, researchers report. Kashin-Beck disease is a debilitating bone disorder
which slows bone growth and triggers a gradual stiffening of the major joints. Disease onset
typically begins at between 5 and 15 years of age, with those having varying degrees of joint
deformation and limited joint mobility. The illness is especially prevalent in areas of central Asia
and central Africa where the usual diet often lacks two essential nutrients: iodine and selenium.
Until now, most experts have assumed that Kashin-Beck is caused by selenium deficiency. The
researchers believe that iodine deficiency impairs thyroid activity, which in turn slows bone growth
and causes joints to stiffen."
The New England Journal of Medicine October 15, 1998;339:1112-1120.

COMMENT: It is interesting to note how all the hormones are interconnected and that by
decreasing iodine one can damage the bone. Iodine is not a mineral one would normally associate
with decreased bone density.

Nutritional epidemiology and thyroid hormone metabolism.
Vanderpas J.
Annu Rev Nutr. 2006;26:293-322. Review.
[abstract only]

Severe iodine deficiency was the main cause of endemic goiter and cretinism. Most of the
previously iodine-deficient areas are now supplemented, mainly with iodized salt. The
geographical distribution of severe endemic areas has been progressively reduced, and at
present, approximately 200 million people living in remote places are still at risk of severe iodine
deficiency. International public health programs should be focused first on reaching these
populations, and second on auditing and monitoring the operational work of supplementation
programs. This second point is essential to prevent iodine-induced hyperthyroidism or
interruptions of iodine supplement distribution, which could be catastrophic for the fetus and the
young infant. Echography brings a complementary tool to clinical assessment of goiter by
palpation. Inductively coupled plasma-mass spectrometry brings at least a definitive gold standard
for iodine measurement and thyroid hormone measurement. Thiocyanate overload has been
clearly documented as a goitrogen in Central Africa, and when associated with selenium
deficiency, it may be included as risk factor for endemic myxedematous cretinism. Variable
exposure to different environmental risk factors is likely the explanation of the variable distribution
of two types of endemic cretinism (neurological and myxedematous), and the clinical overlap of
the pathogeny of both syndromes is more important than previously described. It is possible that
Kashin-Beck osteoarthropathy is another evanescent endemic disease that will disappear with the
correction of iodine deficiency.

Selenium and iodine supplementation of rural Tibetan children affected by Kashin-Beck
Moreno-Reyes R, Mathieu F, Boelaert M, Begaux F, Suetens C, Rivera MT, Neve J, Perlmutter N,
Vanderpas J.
Am J Clin Nutr. 2003 Jul;78(1):137-44.

BACKGROUND: Kashin-Beck disease is an osteoarthropathy endemic in selenium- and iodine-
deficient areas around Lhasa, Tibet.

OBJECTIVE: We assessed the efficacy of selenium supplementation on disease progression.

DESIGN: A double-blind, randomized controlled trial of selenium supplementation was carried out
in 324 children aged 5-15 y who had Kashin-Beck disease. Two hundred eighty children received
iodized oil before being randomly assigned to receive selenium or placebo, and a control group of
44 subjects was not supplemented at all. Clinical and radiologic signs, selenium status, urinary
iodine, and thyroid function were evaluated at baseline and at 12 mo.

RESULTS: The frequencies of joint pain, decreased joint mobility, and radiologic abnormalities
were not significantly different between the 3 groups at 12 mo. Height-for-age z scores increased
significantly in the subjects who received placebo and iodine or selenium and iodine. In contrast,
unsupplemented control subjects did not recover from growth retardation. Serum selenium
concentrations at 12 mo were within the reference range and were significantly greater in the
selenium-iodine group than in the placebo-iodine group. Serum thyroid hormone concentrations
were within the reference ranges after the administration of iodine, and these values were not
significantly affected by selenium supplementation.

CONCLUSIONS: The results of this study do not rule out the possibility that selenium may help to
prevent the occurrence of Kashin-Beck disease. However, selenium supplementation had no
effect on established Kashin-Beck disease, growth, or thyroid function once iodine deficiency was
corrected. These results suggest that iodine, but not selenium, deficiency should be corrected in
Tibetan children with Kashin-Beck disease.

Selenium, iodine and fungal contamination in Yulin District (People's Republic of China) endemic
for Kashin-Beck disease.
Zhang WH, Neve J, Xu JP, Vanderpas J, Wang ZL.
Int Orthop. 2001;25(3):188-90.
[abstract only]

We studied the status of selenium, iodine and fungal contamination in 353 school children (age 5-
14 years) from four rural villages in the District of Yulin. In three villages Kashin-Beck disease
(KBD) was endemic, whereas there were no cases of KBD in the fourth village. Clinical, biological
and radiological examinations (right hand) were performed and KBD was established by X-ray
diagnosis. The prevalence rate of KBD was 30.2%, 44.2% and 45.3% in the three endemic
villages. Mean hair selenium and urine iodine concentrations were lower in affected than in
unaffected children and fungal contamination in cereal grains stored in families with KBD was
more elevated than in families without KBD. Low hair selenium concentration and presence of
fungal cereal contamination were significantly associated with an increased risk of KBD, but low
urine iodine was not.

Epidemiological support for a multifactorial aetiology of Kashin-Beck disease in Tibet.
Suetens C, Moreno-Reyes R, Chasseur C, Mathieu F, Begaux F, Haubruge E, Durand MC, Neve
J, Vanderpas J.
Int Orthop. 2001;25(3):180-7.

We carried out a cross-sectional study in 12 rural villages in order to identify the risk factors for
Kashin-Beck disease in Tibet. Children aged 5-15 years (n=575) were examined and their
corresponding houses were visited. Samples were collected in order to study fungal contamination
of stored grain and the organic matter content of drinking water. Multivariate analysis was
performed using logistic regression and population attributable fractions were computed to
estimate the impact of each factor. The following variables were independently associated with the
disease: age, gender, low socio-economic status, indicators of a poorly diversified diet, iodine
deficiency and small water container size (with higher organic matter levels in small containers).
Selenium deficiency was severe in all study subjects. The degree of fungal contamination of
barley grain was related to the highest percentage of cases (65%) in a sample of the study
population. Higher urinary iodine levels were not associated with decreasing prevalence rates
when Alternaria sp. was isolated. The data that we report supports the hypothesis that Kashin-
Beck disease occurs as a consequence of oxidative damage to cartilage and bone cells when
associated with decreased antioxidant defence. Another mechanism that may coexist is bone
remodelling stimulated by thyroid hormones whose actions can be blocked by certain mycotoxins.

Kashin-Beck disease and iodine deficiency in Tibet.
Moreno-Reyes R, Suetens C, Mathieu F, Begaux F, Zhu D, Rivera T, Boelaert M, Neve J,
Perlmutter N, Vanderpas J.
Int Orthop. 2001;25(3):164-6.
[abstract only]

We evaluated iodine and selenium status in 575 children between 5 and 15 years with Kashin-
Beck disease from endemic and non-endemic areas. Of these 267 (46%) children had goiter. The
proportion of subjects with goiter was higher in the villages with Kashin-Beck disease than in the
control village. In the villages with Kashin-Beck disease, 105 (23%) of the subjects had a serum
thyrotropin greater than 10 mU/l as compared with 3 (4%) in the control village. The percentages
of low serum thyroxine values and low serum tri-iodothyronine were greater in the villages where
Kashin-Beck disease was endemic than in the control village. The percentages of low urinary
iodine concentration were significantly greater in the subjects with Kashin-Beck disease. The
results suggest that in areas where severe selenium deficiency is endemic, iodine deficiency is a
risk factor for Kashin-Beck disease.

[Kashin-Beck disease in China: osteochondrodysplasia related to nutrition and environment]
Vanderpas J, Neve J.
Bull Mem Acad R Med Belg. 1999;154(3-4):177-84; discussion 184-9. French.
[abstract only]

Kashin-Beck disease is a endemic juvenile osteochondrodysplasy, whose association with
selenium deficiency and/or mycotoxin toxicity has been corroborated by epidemiological studies in
China, including Tibet. Iodine deficiency appears to be a new etiological factor. Together with the
geographical and epidemiological exploration of the disease, scientific multidisciplinary
investigations (clinics, radiological imaging, histology, environmental and molecular biology)
should afford to understand the cause of the disease before it disappears as a consequence of
the evolution of the Chinese Society, including in Tibet.

Kashin-Beck osteoarthropathy in rural Tibet in relation to selenium and iodine status.
Moreno-Reyes R, Suetens C, Mathieu F, Begaux F, Zhu D, Rivera MT, Boelaert M, Neve J,
Perlmutter N, Vanderpas J.
N Engl J Med. 1998 Oct 15;339(16):1112-20.

BACKGROUND AND METHODS: Kashin-Beck disease is a degenerative osteoarticular disorder
that is endemic to certain areas of Tibet, where selenium deficiency is also endemic. Because
selenium is involved in thyroid hormone metabolism, we studied the relation among the serum
selenium concentration, thyroid function, and Kashin-Beck disease in 575 subjects 5 to 15 years
of age in 12 villages around Lhasa, Tibet, including 1 control village in which no subject had
Kashin-Beck disease. Clinical, radiologic, and biochemical data were collected.

RESULTS: Among the 575 subjects, 280 (49 percent) had Kashin-Beck disease, 267 (46 percent)
had goiter, and 7 (1 percent) had cretinism. Of the 557 subjects in whom urinary iodine was
measured, 66 percent had a urinary iodine concentration of less than 2 microg per deciliter (157
nmol per liter; normal, 5 to 25 microg per deciliter [394 to 1968 nmol per liter]). The mean urinary
iodine concentration was lower in subjects with Kashin-Beck disease than in control subjects (1.2
vs. 1.8 microg per deciliter [94 vs. 142 nmol per liter], P<0.001) and hypothyroidism was more
frequent (23 percent vs. 4 percent, P=0.01). Severe selenium deficiency was documented in all
villages; 38 percent of subjects had serum concentrations of less than 5 ng per milliliter (64 nmol
per liter; normal, 60 to 105 ng per milliliter [762 to 1334 nmol per liter]). When age and sex were
controlled for in a multivariate analysis, low urinary iodine, high serum thyrotropin, and low serum
thyroxine-binding globulin values were associated with an increased risk of Kashin-Beck disease,
but a low serum selenium concentration was not.

CONCLUSIONS: In areas where severe selenium deficiency is endemic, iodine deficiency is a risk
factor for Kashin-Beck disease.

PIP: Selenium is involved in thyroid hormone metabolism. Kashin-Beck disease is a degenerative
osteoarticular disorder endemic to certain areas of Tibet, where selenium deficiency is also
endemic. Findings are reported from an investigation of the relationship among serum selenium
concentration, thyroid function, and Kashin-Beck disease in 575 subjects aged 5-15 years in 12
villages around Lhasa, Tibet, including 1 control village in which no one had Kashin-Beck disease.
Clinical, radiologic, and biochemical data were collected. 280 (49%) subjects had Kashin-Beck
disease, 267 (46%) had goiter, and 7 (1%) had cretinism. Of the 557 subjects in whom urinary
iodine was measured, 66% had a urinary iodine concentration of less than 2 mcg/dl. Mean urinary
iodine concentration was lower in subjects with Kashin-Beck disease than in control subjects and
hypothyroidism was more frequent. Severe selenium deficiency was documented in all villages,
with 38% of subjects having serum concentrations of less than 5 ng/ml. When age and sex were
controlled for in a multivariate analysis, low urinary iodine, high serum thyrotropin, and low serum
thyroxine-binding globulin values were associated with an increased risk of Kashin-Beck disease,
but a low serum selenium concentration was not."

Kashin-Beck disease: from etiology to prevention or from prevention to etiology?
Sudre P, Mathieu F.
Int Orthop. 2001;25(3):175-9. Review.
[abstract only]

"The aetiology of Kashin-Beck disease (KBD) remains elusive. Four factors have been
convincingly associated with the disease: selenium deficiency, iodine deficiency, grain
contamination with mycotoxin-producing fungi, and water pollution with organic material and fulvic
acid. The most credible studies from a scientific standpoint, i.e. randomised placebo controlled
trials and observational cohort studies have either not been conducted or did not provide
unequivocal demonstration in favour of any of these hypotheses. Many studies such as case-
control, cross-sectional, "before-after", and even more so, ecological studies have been
conducted. They merely produced weak evidence and fail to support any single factor to the
exclusion of the others. The most scientifically sound studies have included animal models,
laboratory experiments and pathology studies; however, these have only provided indirect
evidence. Although none of the competing theories prevails when they are compared using a
predefined and standard set of causality criteria (temporality, strength of the association,
biological gradient, experimental evidence, biological plausibility, coherence, specificity and
analogy), none should be discounted. This is an indication that a comprehensive and unifying
theory is most likely to be multifactorial. Because the ultimate goal of those who are compelled by
the challenge of KBD is to prevent its occurrence, a perfect understanding of its mechanisms is
not indispensable for action. Well-conducted randomised intervention should be the priority of
researchers as well as public health professionals to demonstrate what works and what does not.

Beijing conference reviews Kashin-Beck disease.
Tomlinson R.
BMJ. 1999 Feb 20;318(7182):485.

Life is hard for Tibetan farmers in the impoverished, remote regions of the Himalayan plateau, and
a little understood, disabling osteoarticular disorder-Kashin-Beck disease-is causing even greater
economic difficulties for some rural inhabitants. A recent international symposium in Beijing,
organised by Médecins Sans Frontiàres (MSF) and the Chinese government, brought together
experts from various scientific fields to review likely causes of this mysterious disease and plan
research for the future.

"The disease affects people in a crescent shaped region through Tibet, northern China, Mongolia,
Siberia, and North Korea. In China, about 30 million people live in areas where the disease is
endemic, and at least 2-3 million people are estimated to be affected. Many of them live in the
poorest parts of Tibet, where the disease is known as “big bone disease.” There is no cure, and
no clear preventive measures exist, so prevalence can be as high as 80-90%in some small

"The debilitating disorder starts in childhood, with symptoms occurring from the age of about 4
years. The disease attacks the growth of joint cartilage, with the worst forms resulting in dwarfism,
very short upper limbs, and deformed, painful joints with mobility as low as 30 degrees in the case
of elbows. The most frequently affected joints are ankles, knees, wrists and elbows, leading to
atrophied muscles, making manual farming work difficult and painful, especially in Tibet's cold
climate. Franåoise Mathieu, who leads MSF's project on the disease in Tibet, described showing
an x ray film of a Tibetan patient's joints to colleagues in Europe. “They thought I was showing an
x ray of a person aged 70-80, not a 15 year old,” she said.

"Kashin-Beck disease was first identified in 1849 by a Russian doctor, Nikolai Ivanovich Kashin,
but its causes remain unknown. In Tibet, the risk factors seem to include selenium deficiency in
the soil, fungal contamination of barley (the staple grain), organic matter in the water, and iodine
deficiency. These create an environment in which mycotoxins enter the rural food supply, but the
precise cause is still a mystery.

"Since 1992, MSF has run a physiotherapy project in Tibet which includes the training of 90 local
doctors, in order to ease the pain and immobility of people with Kashin-Beck disease. Long term
progress depends on identifying the cause of the disease, so a three year research project
covering 1026 children in 22 Tibetan villages was started in 1998. This entails distributing
selenium and iodine supplements, providing fungicide for use on barley, supervising better
storage conditions for the grain, and establishing clean drinking water supplies.

Kashin-Beck disease--expanding the spectrum of iodine-deficiency disorders.
Utiger RD.
N Engl J Med. 1998 Oct 15;339(16):1156-8.

These findings suggest that Kashin-Beck disease results from the combination of selenium and
iodine deficiency.  The Kashin-Beck type of osteoarthropathy is not a feature of endemic goiter,
hypothyroid cretinism, or sporadic hypothyroidism in children....

"How might combined iodine and selenium deficiency affect cartilage?  One possibility is that
growth-plate cartilage is not only especially dependent on locally produced triiodothyronine but
also sensitive to oxidative damage.  Thus, deficiency of iodothyronine deiodinase and glutathione
peroxidase might result in a combination of local thyroid hormone deficiency and cellular injury
that could cause chondronecrosis.  The combined deficiency may affect other tissues as well, but
if it does, the changes are less obvious than those of Kashin-Beck disease or of endemic

Long-term Effects of Various Iodine and Fluorine Doses on the Thyroid and Fluorosis in Mice.
Zhao W, Zhu H, Yu Z, Aoki K, Misumi J, Zhang X.
Endocr Regul. 1998 Jun;32(2):63-70.
[abstract only]

OBJECTIVE: To elucidate the participation of the independent and combined long term effect of
various concentrations of iodine and fluorine on the pathogenesis of goiter and fluorosis in mice.

METHODS: Nine drinking water supplies with different iodine and fluorine content were prepared
by combination of potassium iodate and sodium fluoride solutions in bidistilled water. The
concentrations of iodide were: 1. iodine deficiency (ID): 0.0; 2. iodine normal (IN): 20.0; 3. iodine
excess (IE) 2500.0 ug/l; and these of fluoride were: 1. fluoride deficiency (FD) 0.0; 2. fluoride
normal 0.6; 3. fluoride excess (FE), 30.0 mg/l. A total of 288 Kunmim mice was divided into 9
groups consisting of 32 animals each and each group, in addition to basal diet, received one of
following iodide/fluoride mixtures: ID+FD, ID+FN, ID+FE, IN+FD, IN+FN, IN+FE, IE+FD, IE+FN,
IE+FE. By such manner, one half of the animals of each group was treated for 100 days and the
other half for 150 days.

RESULTS: It was found that ID only and IE only could both induce the goiter. FE induced dental
fluorosis and increased fluorine content in the bone. In addition, fluorine also affected the thyroid
changes induced by ID or IE. After 100 days of treatment, fluorine showed some stimulatory effect
on the thyroid in ID conditions and inhibitory effect in IE conditions. After 150 days, however, the
effects of fluorine on the thyroid reversed as compared with that of 100 days. On the other hand,
difference of iodide intake could also increase the toxic effects of FE on the incisors and bones.
The rate and degree of the incisor fluorosis, the fluorine contents in the bone were significantly
higher in the ID+FE group than those in the IN+FE and IE+FE groups.

CONCLUSIONS: Both iodine deficiency and excess induced goiter as well as other functional and
histopathological changes in the mouse thyroid. Excessive fluorine caused fluorosis of incisors
and limb bones. In addition, iodine and fluorine do have mutually interacting effects on both goiter
and fluorosis in the experimental mice.