Did you know that there is Fluoride & Aluminum in Black & Green Tea? Recently I came across an article that states that green, black & a few other teas does more harm then benefits… it’s very high in fluoride content! Fluoride in tea is much higher than the Maximum Contaminant Level (MCL) set for fluoride in drinking water. Also contains Aluminum! Green tea is known to be a miracle drink that offers a host of health benefits to those who drink it. However, some worry that green teas simply have too much fluoride and should be avoided. The difficulty in this argument is separating fact from fiction, true science from theories. There is lots of information available on green tea and fluoride, but most of it mangles the facts and mixes in theory or even personal opinion without clarifying the difference. The tea plant, Camellia sinensis, naturally absorbs fluoride from the environment more effectively than other plants. And as it ages, more fluoride is absorbed by the leaves, so the younger leaves have less fluoride than the older leaves. In practical terms, this means white tea (which is only very young leaves) has less fluoride than green, black or oolong teas, which include older leaves (Herbal teas do not contain any Camellia sinensis leaves and have almost no fluoride to speak of). In addition, the younger the leaves make a higher quality tea. Tea dust (in tea bags) and tea bricks (made from older leaves) have much higher levels of fluoride than high quality tea. This study explored the difference between high quality teas and low quality in terms of fluoride: high quality teas had significantly less fluoride. The main teas to avoid with high content of Fluoride is: instant tea, low quality teas w/loose powder content, Oolong, Black, Green, Tibetan Milk Teas, Kukicha or Bancha twig tea, be aware of its aluminum and fluoride levels. Please remember to purchase only high quality organic teas, herbal teas, grain teas – i.e. Genmaicha Tea (organic toasted brown rice tea), Buckwheat tea, Herbal teas, Milk Thistle, Yerba Mate, Comfrey, Chickweed, & Dandelion tea … plus do a little more research on line. This here article provides insightful information and it’s a bit lengthy but well worth reading…
OPEN LETTER TO: Susan Cameron-Block
Host – Current Health Issues
I am writing this letter with the intent to inform on various issues associated with the use of fluorides, especially as it relates to green and black teas, and to voice our concern about the continued promotion of green tea as a drink”beneficial to one’s health” on your radio show “Current Health Issues”.
Tea is very high in fluoride content. Fluoride in tea is much higher than the Maximum Contaminant Level (MCL) set for fluoride in drinking water.
Tea leaves accumulate more fluoride (from pollution of soil and air) than any other edible plant (1,2,3). Fluoride content in tea has risen dramatically over the last 20 years, as has tea consumption (4).
While in 1976 a Belgian analysis showed content of between 50 and 125 ppm fluoride in 15 varieties of tea (3), a Polish study in 1995 found fluoride content of up to 340 ppm in 16 varieties of black tea (5). A major Canadian study published in 1995 reports average fluoride content in tea to be 4.57 mg/l in the 1980’s (6).
A website by a pro-fluoridation infant medical group lists a cup of black tea to contain 7.8 mgs of fluoride (7), which is roughly the same amount as if one were to drink 7.8 litres of water in an area fluoridated at 1ppm. It is well known that fluoride in tea gets absorbed by the body similarly as the fluoride in drinking water (1,8).
Some British and African studies from the 1990’s showed a daily fluoride intake of between 5.8 mgs and 9 mgs a day from tea alone (9,10,11).
In order to understand a dose/concentration relationship properly, one needs to realize that the level of fluoride at 1 part-per-million (ppm) = 1 mg/l was set in the 40’s when TOTAL intake was considered to be only about 1 mg/day in areas with fluoridated water. It was thought that the fluoridation of water supplies at 1 ppm (1 mg/l) would duplicate this intake, assuming that people would drink 4 glasses of water a day. However, average current total intake of fluorides is approaching the 8mg/day range, according to the last official data available from the US PHS (1991) and other publications (12).
TOTAL intake from ALL sources is the amount to be considered for any adverse health effect evaluation (13,14,15).
The fact that fluorides accumulate in the body is the reason why a MCL (Maximum Contaminant Level) for fluoride content in water needs to be set by the US Environment Protection Agency (EPA) – by law under the US Surgeon General. This is to be done specifically to avoid a condition known as Crippling Skeletal Fluorosis (CSF).
The MCL is set so as to only avoid the third and crippling stage of this disease. It is set at 4ppm => 4mg/liter, assuming that people will retain half of this amount (2mg), and therefore be at a “safe” level. The EPA scientists, whose job and legal duty it is to set the MCL, declared that this level was set fraudulently by outside forces, and that 90% of the data showing the mutagenic properties of fluoride were omitted (16).
Virtually every company selling green tea advertises it’s high fluoride content as “beneficial” in preventing cavities, promulgating the misleading and false data supplied for the last 50 years by the ADA/CDA and other dental health trade organizations, as well as various public health agencies. There are NO double-blind studies anywhere proving the efficacy of fluoride as a caries preventative (17). There ARE double-blind studies proving adverse health effects, at the level of 1ppm (1mg/l) in water.(18) There are no studies documenting safety at any intake level.
Drinking a cup of tea with fluoride content as mentioned above (7.8mg) would mean a fluoride intake much higher(!) than amounts which were actually given as medication to treat hyperthyroidism (-> over-functioning thyroid) for numerous decades – in several countries – specifically to reduce thyroid activity! [(2 -10 mg NaF/day => 0.9mg – 4.5mg F-)] (19,20,21,22)
In the 1930’s May reported having _successfully_ treated 1,158 hyperthyroid patients within 6 years with either sodium fluoride or fluorothyrosine, given per mouth. Among products later released on the market were Pardinon and Tyrosin (23, 24). Checking an older Merck Index will verify this information (25). Gorlizer von Mundy treated patients for more than 30 years in baths containing HF (30ccHF in 200 l water). Later fluorides were deemed not “reliable enough” to be recommended as an antithyroid (26).
RE: CANCER AND GREEN TEA
While there can be no doubt as to the beneficial effects of individual antioxidants found in green tea, the same cannot be said about green tea as a beverage. Existing studies tend to concentrate on active ingredients of green tea, such as epigallocatechin gallate (EGCG), a compound that belongs to a family of antioxidants known as polyphenols. EGCG and other polyphenols are constituents of tea – especially of green tea.
However, no studies exist investigating the effects of fluorides on these anti-oxidants. Existing studies involving other antioxidants and fluoride compounds give evidence that fluorides can adversely affect the action of antioxidants(27). Thus, while isolated antioxidants may slow down the development of some forms of cancer in experimental studies, their effect may be annihilated in their complex natural environment (as a sum of the action of all the substances present).
Several reviews of available data seem undecided in their conclusions as to the inhibition of carcinogenesis in experimental animals by tea or tea compounds. Data reviewed by Blot et al. (28) suggest “at most a modest benefit, since there is considerable international variation in tea consumption but generally small differences in cancer rates…More relevant case-control and cohort studies show mixed results.”
Other epidemiological and human studies have also shown varying results. In a review by Bushman (29) thirty-one human studies and four reviews were examined. Among five studies reporting on colon cancer, three found an inverse association and one reported a positive association.
For rectal cancer, only one of four studies reported an inverse association; increased risks were seen in two of the studies. An inverse association was suggested for urinary bladder cancer in two of two studies.
While lung cancer studies have shown an inverse effect with Okinawan tea, a tentatively increased risk was shown in another study, clearly indicating that more research into this matter is needed. In a recent study on Finnish men, published in 1998 by Terryl Hartman and others, again a positive correlation between colon cancer and tea intake was found. Colon
cancer occurrence increased with higher intake (30).
Many available green tea/cancer studies last only a few months, and do not take into account the cumulative effects of fluoride, which is a known cancer promoter, and has the ability to transform healthy cells into cancerous ones (1,17,35,36). For any conclusive evidence to be obtained this must be considered, for long time fluoride ingestion has been shown to _cause_
cancer, especially osteosarcomas and uterine cancer (31,32).
Dean Burk, for many decades Chief Chemist at the National Cancer Institute, testified at congressional hearings in 1981 stating that over 40,000 cancer deaths in that year were attributable to fluoridation (33). He has said that no chemical causes as much cancer, and faster, than fluorides (34).
Public health officials are quick to say that this data is not verified, which is entirely untrue, for international research as well as congressional hearings and court proceedings HAVE verified this information (1,2,16,17,31,32,33,34,35,36,37,38).
Dental fluorosis (mottled teeth) is the first visible sign of fluoride poisoning.
Studies conducted on tea consumption in Tibetan children by Cao et al. found both dental (51.2%) and skeletal (32.83%) fluorosis, mainly as a result rom drinking brick tea, also known as milk tea (39). More studies by Cao and others reported similar results (40,41) as did a study from Chile showing dental fluorosis risks in 22.1% of the children consuming tea as a main beverage (42). Many similar studies on tea as well as other beverages have been published in the journals of the American Dental Association (ADA) or American Medical Association (AMA) themselves.
Studies on hydrofluoric-acid workers from an electronics company documented that, among the influences of fluorine-containing foodstuff on fluoride content in the biological fluids, the effect of black tea and/or green tea intake was “particularly remarkable”. Measuring the urine and serum levels of fluorine ion, in the case of the non-hydrofluoric-acid workers, the concentration increased to about double of the control value. Similarly in a diet test on volunteers, the concentration increased about six times (43).
There are several other factors to consider regarding fluoride content in tea. One is the amount of fluoride leeching over time. Chinese teas continue to release F- throughout the first hour of infusion, whereas release of F- from Ceylon/Indian teas is essentially completed after 5 minutes (44).
The first study to investigate fluoride content in decaffeinated teas found an even higher fluoride content in those teas as compared to their caffeinated counterparts (45). It is thought that this is due to the high fluoride content in the water involved in the de-caffeination process, which then would also make coffee similarly decaffeinated high in fluoride content.
In addition, the caffeine in tea has a great augmentative effect on the bio-availability of fluoride. In 1990 researchers at the University of Texas even theorized that “the rise in incidence of dental fluorosis in North America is mainly due to the replacement of water intake by caffeine-containing beverages among the young population” (46). In 1990 German researchers wrote that “continuous intake of black tea rich in fluorides leads to distinct increase of fluoride content of temporary teeth. This is to consider analogous a caries prophylaxis.” (47)
Considering this, and tea market statistics which report that, “on any given day, nearly 127 million people — half of all Americans — are drinking tea”, and that tea is available in 80% of US households (4), one must seriously ask why anyone in their right mind would want to add to the already existing load by adding fluorides to the public water supply.
Fluoride and Aluminum in Tea
To make matters much worse for human health, fluorides in teas are found together with aluminum. The combination of aluminum and fluorides in tea is of urgent concern, due to the increased damage done by fluorides when in the presence of aluminum, especially neurological and renal damage)(17).
A study by Wei and others reported a high correlation (r = 0.81) found between the released F and Al in all tested Chinese, Indian and herbal teas (48).
Nabrzyski and Gajewska (49) report: “..In the 16 samples of commercially available brands of black teas, the levels of aluminum and fluoride ranged from 445 to 1552 ppm (mean = 897 +/- 264 ppm) and from 30 to 340 ppm (mean 141 +/- 85 ppm), respectively. In six herbal teas, the mean levels of aluminum and fluoride were lower, and amounted to 218.9 +/- 150.7 ppm and 6.0 +/- 6.9 ppm, respectively…”
That the aluminum present is indeed resorbed in the simultaneous presence of fluoride is shown in a study by Drs. Klaus R. Koch and Colleagues at the University of Cape Town. They examined the urinary excretion of aluminum (which is an indicator of its resorption) in healthy male volunteers after drinking equal volumes (1.2 litres) of tea, coffee or tap water on separate days.
In every case the amount of aluminum excreted over the 12-hour period increased on the day when tea was taken. Their results indicate that tea consumption must be considered in any assessment of the total dietary intake of aluminum in human beings (50).
A most important study from 1998 conducted at the Nanchang University in China showed that in older rats fed green tea water extract or green tea leaves, the cerebrum calcium contents were significantly decreased and aluminum contents increased. Zinc contents in the cerebrum were also gradually decreased with the increase of tea leaves dose and tea concentration (51). The cerebrum is the portion of the brain (frontal lobes) where thought and higher function reside (52).
The fluoride/aluminum association is of particular importance as it relates to Alzheimer’s Disease. Aluminum by itself is not readily absorbed by the body. However, in the presence of fluoride ions, the fluoride ions combine with the aluminum to form aluminum fluoride, which is absorbed by the body. In the body, the aluminum eventually combines with oxygen to form aluminum oxide or alumina (53). Alumina is the compound of aluminum that is found in the brains of Alzheimer’s disease.
In the brain, protein binds to the alumina, and “that is the key to the plaques and tangles which are the hallmarks of this terrible disease” (54). In a study by Dr. Robert Isaacson at the State University of New York, aluminum fluoride was added to the rats diet. This, contrary to normal expectations, passed through the brain barrier and gave the rats short term memory, smell sensory loss, unsteady gait, and loss of structures of the neo-cortex and hippocampus, all symptoms of Alzheimer’s (53,54,55,56). A Varner and Jensen study conducted with Isaacson confirmed this in 1998 (57).
Free fluorine ions and traces of aluminum form a complex, fluoroaluminate, which stimulates cellular G proteins. Such a complex can form in food, drinking water, in the organism after fluoride ingestion or absorption, or after administration of a vaccine. Susa (58,59) reports that “fluoroaluminate crosses the cell membrane and directly binds to the membrane-associated inactive Ga protein subunits. Within the Ga subunit, fluoroaluminate occupies the position next to GDP.
The resulting Ga-GDP-AlF4- complex assumes an active state conformation, which resembles that of Ga-GTP complex. Under physiological conditions, Ga-GTP complex is formed upon activation of seven transmembrane receptors that couple to heterotrimeric G proteins…Both fluoroaluminate-activated and receptor-activated Ga subunits are capable of transmitting intracellular signals that lead to cellular responses.”
There are hundreds of G protein-coupled receptors (60). The thyroid stimulating hormone (TSH) receptor is also coupled to the G protein. The TSH receptor is densely expressed in the thyroid gland and mediates the production and secretion of thyroid hormones. (61) To presume that the fluoroaluminate will not interfere here is simply naive.
There have been hundreds of scientific studies using aluminum/fluoride complexes in the last ten years. A review of the literature by Strunecká and Patocka reveals that aluminofluoride complexes influence all cells and tissues of the human body with “powerful pharmacological efficacy.”(62,63)
This MEDLINE search will return approx. 100 fluoroaluminate-related items: http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&uid=9917518&dopt=m&dispmax=20
Neurological Effects of Fluoride
Other numerous studies in the late 1990’s have been published documenting the effects of fluoride on the neurological system (65,66,67,68,69).
They are briefly addressed here in an excerpt from a paper published by the National Treasury Employees Union (NTEU) Local 280, formerly National Federation of Federal Employees Local 2050, representing the approximately 1500 scientists, lawyers, engineers and other professional employees at EPA Headquarters in Washington, D.C.:
“Why EPA’S Headquarters Union of Scientists Opposes Fluoridation” Issued May 1, 1999 (17):
“In 1995, Mullenix and co-workers showed that rats given fluoride in drinking water at levels that give rise to plasma fluoride concentrations in the range seen in humans suffer neurotoxic effects that vary according to when the rats were given the fluoride – as adult animals, as young animals, or through the placenta before birth.
Those exposed before birth were born hyperactive and remained so throughout their lives. Those exposed as young or adult animals displayed depressed activity. Then in 1998, Guan and co-workers gave doses similar to those used by the Mullenix research group to try to understand the mechanism(s) underlying the effects seen by the Mullenix group. Guan’s group found that several key chemicals in the brain – those that form the membrane of brain cells – were substantially depleted in rats given fluoride, as compared to those who did not get fluoride.
Another 1998 publication by Varner, Jensen and others reported on the brain- and kidney damaging effects in rats that were given fluoride in drinking water at the same level deemed “optimal” by pro-fluoridation groups, namely 1 part per million (1ppm). Even more pronounced damage was seen in animals that got the fluoride in conjunction with aluminum. These results are especially disturbing because of the low dose level of fluoride that shows the toxic effect in rats – rats are more resistant to fluoride than humans.
This latter statement is based on Mullenix’s finding that it takes substantially more fluoride in the drinking water of rats than of humans to reach the same fluoride level in plasma. It is the level in plasma that determines how much fluoride is ‘seen’ by particular tissues in the body. So when rats get 1 ppm in drinking water, their brains and kidneys are exposed to much less fluoride than humans getting 1 ppm, yet they are experiencing toxic effects. Thus we are compelled to consider the likelihood that humans are experiencing damage to their brains and kidneys at the ‘optimal’ level of 1 ppm.”
(“Optimum intake” = 1mg/day)
Toothpaste also contains a significant quantity of Al, more so, when packed in Al tubes (70). That children frequently ingest too much toothpaste is well established and the reason why since April 1997 a poison warning is to be placed on all fluoride-containing toothpastes in the US. It is an absolute disgrace that this is not the same in Canada, especially when the US FDA has issued several Import Alerts and customs detention orders, documenting fluoride amounts double that of permissable content originating in Canada! (71)
Thyroid hormones are extremely important in the regulation of metabolic processes and brain development. Every cell in the body depends upon thyroid hormones for regulation of their metabolism.
Many of the symptoms documented in the vast literature on the subject of chronic or low-grade fluoride poisoning can be directly related to thyroid functions and disorders. One of the most prominent features of preskeletal fluorosis is the extraordinary general fatigue experienced by most sufferers, a marked weakness usually linked to low activity of the thyroid gland (2).
This has been reported since the classic 1930’s Roholm study on cryolite workers exposed to fluorides, a study which still serves as the basis for occupational fluoride exposure regulations (73). At the time of Roholm’s work the specialized field of “endocrinology” was yet to be recognized as a reputable discipline. Thyroid diseases were poorly understood. From 1940 to 1970, the application of radioiodine improved this understanding immeasurably.
Fragu (74) writes:”The main transformations brought about by this tool were the knowledge of radioiodine uptake mechanisms, basis of its therapeutic effect, complete identification of thyroid hormonosynthesis, serum transport of thyroid hormones and thyroid imaging. More recently immunological and molecular paradigms changed the understanding of thyroid diseases.”
It is only in the last two decades during which endocrinology has progressed so rapidly, that now over 150 symptoms and associations can be identified in hypothyroidism. Almost all correlate with known symptoms of fluoride poisoning.(74) Most of the double-blind test results of fluoride poisoning found in Moolenburgh’s study on water containing 1ppm of fluoride – which led to the ban of fluoridation in Holland – are now recognized symptoms of hypothyroidism (75).
The effects of fluoride on the thyroid gland have been studied so extensively, that it baffles the mind how experts on thyroid disease from Harvard or the University of Toronto can claim that fluorides do not affect thyroid gland function, especially when it has been used as medication to do just that! (76)
This stance just defies all knowledge properly gained in the last 70 years of related research. One cannot find any mention of fluorides in ANY current “official” thyroid disease related literature. And this at fluoride intake levels and at dental fluorosis rates as high as they are!
Already in 1940 authors Robert H. Wilson and Floyd DeEds from the United States Department of Agriculture (discussing the role of fluorine in pesticide sprays), wrote:
“Should a spray residue tolerance limit for fluorine be set to protect the normal, the hyperthyroid, or the hypothyroid individual? … should the tolerance limit take into consideration that in certain areas the public is already exposed to a fluorine intake in the drinking water?”(77)
We have posted over 100 studies documenting the adverse effects of fluoride on the thyroid gland from the last 70 years or so in the Virtual Library on Fluoride Research (78)at:
Thyroid, SIDS and Down Syndrome
A toxicologist in the United Kingdom recently found that perinatal deaths in a fluoridated area was 15% higher than in neighboring non-fluoridated areas. The fluoridated area had a higher socio-economic status and would have been expected to have less perinatal deaths.
The fluoridated area also had a 30% higher rate of Down’s Syndrome (79a). Down’s Syndrome is a disease associated with thyroid pathology (79b). Chile banned fluoridation because of research by the world-reknowned researcher Dr. Albert Schatz, which showed a link to infant deaths due to fluoridation (80). Already in the 1950s, Ionel Rapaport published studies showing links between Down’s Syndrome and natural fluoridation (81).
[In this context an article should be noted which appeared in the October1995 issue of the “Monitor”, a publication by the American Psychological Association, which reported of the similarity in neurological signs in Down’s Syndrome and Alzheimer’s disease.
The link between the two dates back to the 1940s when George Jervis, who later became the first director of New York State Institute for Basic Research in Developmental Disabilities, conducted autopsies on people with Down’s syndrome and found they had the same neuropathology as people with Alzheimer’s disease. People with Down’s syndrome tend to age faster than the general population and suffer a wide range of accompanying health problems–many of which mimic or mask the presence of Alzheimer’s disease(82).]
Thyroid and Learning Disorders
Learning disorders such as Attention Deficit Hyperactivity Disorder (ADHD) did not knowingly exist before the fluoridation of public water supplies began.
In the 1950’s ADHD spread rapidly among school children and gained much exposure in the medical science and health literature. In 1963 the US PHS listed dozens of symptoms associated with hyperactivity and officially changed the name to “minimal brain dysfunction”.
By the the 1970’s some leading authorities noted that this disorder appeared to lie at the root of nearly every type of childhood behaviour problem, and had become the most commonly diagnosed illness among childhood counsellors (83,84).
In 1987 the American Medical Association acknowledged that minimal brain damage had become the leading disability reported by elementary schools, and “one of the most common referral problems to psychiatry outpatients clinics” (85).
Many studies on thyroid hormones have shown that attention deficit and/or hyperactivity disorders in children are linked to changes in the levels of thyroid hormone in the blood, and that irritability and aggressive behaviour are linked to thyroid hormone levels and hypothyroidism (86,87,88,89,90,91, 92,93,94,95,96,97).
Behaviour disorders have been associated with thyroid function for over 100 years.
In 1997 Aronson and Dodman wrote, “the hypothyroid human patient has been reported to show a wider range of behavioral symptoms. Particularly in the early stages of the disease reduced cognitive function and concentration together with impaired short-term memory may be confused with attention deficit-hyperactivity disorder, and in one study 66% of patients diagnosed with ADBD were found to be hypothyroid. Supplementing their thyroid levels was largely curative. Visual and auditory hallucinations may result from altered perception and have been misdiagnosed as schizophrenia or psychosis. Other behavioral symptoms have included fear – ranging from mild anxiety to frank paranoia, mood swings and aggression.”(98)
Many psychoactive drugs including Prozac, Paxil and Luvox (Littleton) are fluorinated medications. Rohypnol, the infamous date-rape drug, is fluorinated Valium, which is about 20-30 times more potent than Valium alone. In essence, these drugs effect enzyme functions in certain areas of the brain to achieve the desired effect (99).
Thyroid hormone disorders may induce almost any psychiatric symptom or syndrome, including rage.
Peter Whybrow (100), of the University of Pennsylvania, writes:
“An intimate association between disturbances of thyroid hormone homeostasis and behavior has been recognized for a long time already: Hyper- and hypothyroidism can induce disturbances of mood and intellectual function (in severe cases even psychosis can be mimicked). Reciprocally many psychiatric disturbances, such as major depression and manic depressive disease have associated with them disturbances of peripheral thyroid hormone metabolism.”
Whybrow reports on the successful treatment of psychiatric disorder by supplementing T4 and T3, both of which are reduced in plasma of rats after two months of fluoride administration of 0.1 – 1mg/day (101).
Recent Chinese studies show that the influence of a high fluoride environment on intelligence can occur early in development such as during the stages of embryonic life or infancy when differentiation and growth are more rapid. Ultramicroscopic study of embryonic brain tissue obtained from termination of pregnancy operations in endemic fluorosis areas showed “differentiation of brain nerve cells were poor, and brain development was delayed.”(102,103)
Highly alarming studies and reviews in the last few years have documented the high accumulation of fluorides in the fetus in countries all over the world (104,105,106,107).
Fluoride tends to fransfer freely and immediately through the placenta, as has been shown in numerous publications (108,109).
It is important to note that mother’s milk passes on neglible amounts of fluoride in very high fluoride-intake areas, as if “nature” meant to protect the infant (110).
Thyroid Florine Iodine Anatagonism
Additionally, a most important factor to consider is the role of fluoride in iodine deficiency disorders (IDD). The antagonistic relationship between fluoride and iodine, being at opposite ends in the halogen group, has been observed in many studies ever since Wagner von Jauregg began a mass iodine-supplementation program in Austrian areas endemic with goiter (enlargement of the thyroid gland) in the 1920’s (112). The late George Waldbott (2) wrote that when the total iodine pool in the body is low, fluoride interferes with the function of the thyroid gland and thereby produces a fluoride-iodine antagonism, a view shared and documented by numerous others (113,114).
However, it has become clear within the last decade that fluoride excess, combined with iodine excess also exert “severe damage to the human body” (115, 116). In the study by Yang et al.(116) on children’s intelligence in high iodine and fluorine regions, the percentage of low-intelligence children was 16.7% at dental fluorosis rates of 72.9%. This is comparable to fluorosis rates we see in North America, some of which are up to 80% (117).
A study published this year on endemic goiter occurrences in the absence of iodine deficiency again showed higher goiter rates in high-fluoride areas in South Africa (118).
Could it be that the world-wide “iodine deficiency” is actually fluoride excess? By comparing IDD data supplied by the WHO (119) with fluorosis data found on MEDLINE an answer may be found. You may judge for yourself:
While it is well known that goiter and hypothyroidism occur more often in mountainous areas, the same has now been shown for dental fluorosis (120,121).
[Note:While checking for IDD/Goiter data for the US, we discovered that a national survey has never been conducted. The only Canadian data available dates back 30 years, and mentions earlier goiter occurences in the Great Lakes area. [Brantford (Great Lakes) was the first Canadian city to be fluoridated.)]
Meanwhile, “iodine deficiency” is now recognized as the most common cause of preventable brain damage and mental disability in the world today. It affects the brain development of the fetus. All thyroid disorders, including hypothyroidism, can develop already in the fetus.
Regarding the findings by Dr. Phyllis Mullenix (65), and her observation that those exposed to fluorides before birth were born hyperactive and remained so throughout their lives, it fits very neatly with existing research on hypothyroidism:
“Hypothyroidism that is present from birth is referred to as congenital hypothyroidism (CH). In North America, CH occurs in about 1 in 4000 live-born babies. The majority (over 90%) of affected babies in North America have a permanent, life-long type of CH”.(122)
Another thyroid/fluoride connection can be seen in Jennifer Luke’s data (123) which has shown that fluoride accumulates in the pineal gland and inhibits its production of melatonin. Luke showed in test animals that this inhibition causes an earlier onset of sexual maturity, an effect already reported in humans as well in 1956, as part of the Kingston/Newburgh study. In fluoridated Newburgh, young girls experienced earlier onset of menstruation than girls in non-fluoridated Kingston (124).
The early onset of sexual puberty is a well established symptom of thyroid hormone dysfunction. Usually patients with low thyroid hormones also have deficient secretion of growth hormone, and may have deficient secretion of the gonadotropins, called LH and FSH, which stimulate puberty and reproduction, and ACTH, which is necessary for cortisol and hydrocortisone secretion by the adrenal gland (125).
[In the above context it should be noted, that aluminum fluoride also mimicks the inhibitory action of melatonin (126).]
Another symptom of an underactive thyroid condition (or iodine deficiency?) – severe growth disturbances – was observed in 1935 by DeEds and Thomas in children in areas where the water contained F- at 1-2 ppm (127).
Osteoporosis, Arthritis, and Other Bone Disorders
Left undetected and untreated, thyroid disorder can elevate cholesterol levels, cause long-term organ complications and may lead to irregular menstrual cycles, infertility and worsening osteoporosis (128,129,130).
Fluorides accumulate in your body. For this reason, as mentioned before, a MCL (Maximum Contaminant Level) must be set for fluoride in the drinking water to avoid Crippling Skeletal Fluorosis (CSF).
The US PHS wrote in 1991 that “fluoride increases the stability of the crystal lattice in bone, but makes bone more brittle… the total quantity of fluoride ingested is the single most important factor in determining the clinical course of skeletal fluorosis; the severity of symptoms correlates directly with the level and duration of exposure.”(131)
On page 6 of the same report it states:”Fluoride in the drinking water may increase the risk of elderly men and women breaking bones”..pages 56-57:
“The weight of evidence from these experiments suggests that fluoride added to water can increase the risk of hip fracture in both elderly women and men…If this effect is confirmed, it would mean that hip fracture in the elderly would replace dental fluorosis as the most sensitive endpoint of fluoride exposure”.
Since then several more studies have been published, all showing greater incidence of hip fractures among the elderly in fluoridated areas (132,133,134). The elderly are also the population suffering greatest from hypothyroidism.
To understand the implications of fluoride in bone disorders:
If you drink 1 cup of green/black tea a day, with F- content of 5mg, you can expect Chronic Skeletal Fluorosis to appear as follows (135):
Comparing intake levels as high as they are (12) with statistical data, it must become clear that this is already happening to a significant portion of the population.
As argued by Dean Burk and the attorneys who established the connection between cancer deaths and fluoridation, there is a premise in logic which states that the most obvious cause of an event must be taken as face value while one searches for alternative possibilities.
Because it can be documented that fluorides were given as medication for hyperthyroid patients it should be considered the OBVIOUS cause for hypothyroidism and other thyroid-hormone function-related disorders, including ADHD, arthritis, osteoporosis, etc., especially at intake levels as high as they are.
Fluoride poisoning can be observed in large groups of the population, in the form of hypothyroidism. In 1995 one publication (see 127) on hypothyroidism reported that 41 percent of women had fatigue for no obvious reason in the past year. Of these women, 57 percent said they experience fatigue three or more times a week. More than half of women (51 percent) had experienced three or more symptoms commonly associated with hypothyroidism over the past year.
Other symptoms/associations of hypothyroidism include loss of libido, carpal tunnel syndrome, arthritis, lupus, fibromyalgia, memory loss, etc. [For a more complete list, please see (74)]
Dental fluorosis is the first visible indicator that severe thyroid hormone dysfunction has occurred and is occurring. It is NOT a mere cosmetic effect as the dental profession would like us to believe. The evidence is staggering.
We must take immediate action to protect our children’s mental and physical health from the ever-increasing fluoride intake. Water fluoridation must be halted, all foods must be labelled for F- content, and emissions by industry must be strictly regulated.
Overall fluoride intake must be radically reduced!
PLEASE advise responsibly regarding green tea; choice organic young leaves and reliable sources when purchasing.
Resource: Green Tea, Fluoride & the Thyroid
Website: PFPC The Fluoride Education Project
Parents of Fluoride Poisoned Children (PFPC)
Vancouver, B.C., Canada
- Fluoride Content in Black Tea, White Tea, Green Tea, and Oolong Tea ~ Loose Leaf Tea Health Benefits and Tea Dangers
- FLUORIDE IN NEWER TEA COMMODITIE
- Tea Travesty
- Fluoride in Herbal Teas
- Tea Summary Research
- Green Tea and Fluoride
- Green Tea Side Effects from Caffeine, Fluoride and Aluminum
- Harmful Fluoride Levels Found in Instant Iced Tea
- FLUORIDE IN FOOD
- FLUORIDE ACTION NETWORK – Sources of Fluoride
- 2004 USDA National Fluoride Database of Selected Beverages and Foods
- Safely Detox Fluoride From Your Body
- Detoxing from Radiation, Heavy Metals, Cleansing & Restoring Your Body – Naturally
- The cleansing & health benefits of lemon
1)Meiers, P. – “Zur Toxizität von Fluorverbindungen, mit besonderer Berücksichtigung der Onkogenese”, Verlag für Medizin Dr. Ewald Fischer, Heidelberg (1984)
2)Waldbott, GL; Burgstahler, AW; McKinney, HL – “Fluoridation:The Great Dilemma” Coronado Press (1978)
3)Srebnik-Friszman, S; Van der Miynsbrugge, F.-“Teneur en Fluor de quelques thés prélevés sur le Marché et de leurs Infusions” Arch Belg Med Soc Hyg Med Trav Med Leg 33:551-556, (1976)
4)Press Releases/Market Figures – Tea Council
5)Nabrzyski M, Gajewska R – “Aluminium and fluoride in hospital daily diets and in teas” Z Lebensm Unters Forsch 201(4):307-10 (1995)
6)Dabeka, WD; McKenzie,AD – “Survey of lead, cadmium, fluoride, nickel, and cobalt in food composites and estimation of dietary intakes of these elements by Canadians in 1986-1988” Journal of AOAC International 78 :4, 897-909 (1995)
7)BabyCenter Editorial Team w/ Medical Advisory Board
8)Rüh, K – “Resorbierbarkeit und Retention von in Mineralwässern und Erfrischungsgetränken enthaltenem Fluorid bei Mensch und Laboratoriumsratte” Diss. Würzburg 1968
9)Jenkins GN – “Fluoride intake and its safety among heavy tea drinkers in a British fluoridated city” Proc Finn Dent Soc 87(4):571-9 (1991) Department of Oral Biology, Dental School, Newcastle upon Tyne, United Kingdom.
10)Opinya GN, Bwibo N, Valderhaug J, Birkeland JM, Lokken P – “Intake of fluoride and excretion in mothers’ milk in a high fluoride (9ppm) area in Kenya” Eur J Clin Nutr 45(1):37-41 (1991) Department of Dental Surgery, University of Nairobi, Kenya
11)Diouf A, Sy FO, Niane B, Ba D, Ciss M – “Dietary intake of fluorine through of tea prepared by the traditional method in Senegal” Dakar Med 1994;39(2):227-30
12)”Documentation of Rising Intake of Fluorides” – 26 Official Documents compiled by Darlene Sherrell, Dental Fluorosis Prevention Program http://www.rvi.net/~fluoride/riseinta.htm
13)The problem of providing optimum fluoride intake for prevention of dental caries, Food and Nutrition Board, Division of Biology and Agriculture, National Academy of Sciences, National Research Council, Pub.#294, November 1953
1953:”.. a person drinking fluoridated water may be assumed to ingest only about 1 milligram per day from this source … the development of mottled enamel is, however, a potential hazard of adding fluorides to food. The total daily intake of fluoride is the critical quantity.”
14)World Health Organization, International Drinking Water Standards, 1971.
1971: “In the assessment of the safety of a water supply with respect to the fluoride concentration, the total daily fluoride intake by the individual must be considered. Apart from variations in climatic conditions, it is well known that in certain areas, fluoride containing foods form an important part of the diet. The facts should be borne in mind in deciding the concentration of fluoride to be permitted in drinking water.”
15)Review of Fluoride Benefits and Risks, Department of Health and Human Services, February 1991, p.45
1991: “The total quantity of fluoride ingested is the single most important factor in determining the clinical course of skeletal fluorosis; the severity of symptoms correlates directly with the level and duration of exposure.”
16)”Applying the NAEP code of ethics to the Environmental Protection Agency and the fluoride in drinking water standard”. Carton, R.J. and Hirzy, J.W. Proceedings of the 23rd Ann. Conf. of the National Association of Environmental Professionals. 20-24 June, 1998. GEN 51-61
17) NTEU – “Why EPA’s Headquarters Union of Scientists Opposes Fluoridation” Prepared on behalf of the National Treasury Employees Union Chapter 280 by Chapter Senior Vice-President J. William Hirzy, Ph.D. For more information please call Dr. Hirzy at 202-260-4683. His E-mail address is firstname.lastname@example.org
18)Grimbergen, G.W. -“A Double Blind Test for Determination of Intolerance to Fluoridated Water (Preliminary Report)”, Fluoride 7:146-152 (1974)
19)Galetti, PM;Joyet, G – “Effect of Fluorine On Thyroidal Iodine Metabolism in Hyperthyroidism” J Clin Endocrinol 18:1102-1110 (1958)
20)May, W – “Antagonismus zwischen Jod und Fluor im Organismus” Klin Wochenschr 14:790-792 (1937)
21)May, W – “Behandlung der Hypothyreosen einschließlich des schweren genuinen Morbus Basedow mit Fluor” Klin Wochenschr 16:562-564 (1937)
22)Gorlitzer von Mundy – “Einfluss von Fluor und Jod auf den Stoffwechsel, insbesondere auf die Schilddrüse” Münch Med Wochenschrift 105:234-247 (1963)
23)Conference On Fluorides And Fluorocarbons – Department of the Navy, January
27 and 28, 1949; Navy Research Section, Science Division, Reference Department, Library, AD B221473
24)Gordonoff, T. – Fluor und die Schilddrüse, Toxikology des Fluors Basel/Stuttgart, pp.111-123 (1964)
25)1968 Merck Index, pg.959
26)Bürgi, H.; Siebenhüner, L; Miloni, E. – “Fluorine and Thyroid Gland Function: A Review of the Literature” Klin Wochenschr 62:564-569 (1984)
27)Sztarbala T, Gos R, Kedziora J, Blaszczyk J, Sibinska E, Goralczyk M – “Changes in the antioxidant system of the vitreous in rabbits after administration of sulfur hexafluoride” Klin Oczna 100(2):69-71 (1998)
28)Blot WJ, Chow WH, McLaughlin JK – “Tea and cancer: a review of the epidemiological evidence.” Eur J Cancer Prev 5(6):425-38 (1996) International Epidemiology Institute, Rockville, MD 20850, USA.
29)Bushman JL – “Green tea and cancer in humans: a review of the literature” Nutr Cancer 1998;31(3):151-9
30)Hartman,TJ; Joseph A. Tangrea,JA; Pietinen;Malila,PN; Virtanen,M;Taylor,PR Albanes, D – “Tea and Coffee Consumption and Risk of Colon and Rectal Cancer in Middle-Aged Finnish Men” Nutrition and Cancer 31(1):41-48, (1998)
31)Tohyama, E. – “Relationship between fluoride concentration in drinking water mortality rate from uterine cancer in Okinawa prefecture” Japan. J Epidemiol (CL8); 6 (4): 184-91 (1996)
32)Cohn, P.D. “A brief report on the association of drinking water fluoridation and the incidence of osteosarcoma among young males” New Jersey Department of Health (1992)
33)Burk, D.: Statement Regarding Fluoridation Facts. Hearings before a subcommittee of the Committee on Appropriations, House of Representatives, 97th Congress, 1st session, Part 8, Washington, D.C. (1981)
34)Yiamouyiannis, J. – “Fluoride – The Aging Factor”, 3rd. Edition, Health
Action Press, 6439 Taggart Road, Delaware, Ohio (1993)
35)Takeki Tsutui, et al. – Sodium Fluoride-induced Morphological and Neoplastic Transformation, Chromosome Aberrations, Sister Chromatid Exchanges, and Unscheduled DNA Synthesis in Cultured Syrian Hamster Embryo Cells”, Cancer Research, Volume 44, pp.938-941 (1984)
36)C.A. Jones, et al. – Sodium Fluoride Promotes Morphological Transformation of Syrian Hamster Embryo Cells, Carcinogenesis, Volume 9, pp.2279-2284 (1988)
37)Yiamouyiannis, J; Burk, D.: Public Water Fluoridation Hearings before a subcommittee of the Committee on Appropriations, House of Representatives, 94th Congress, 1st session, Washington, D.C. (1976)
38)Pennsylvania Judge Rules: Fluoride Is Carcinogenic. National Health Federation Bulletin 25 (1979)
39)Cao J, Bai X, Zhao Y, Liu J, Zhou D, Fang S, Jia M, Wu J – “The relationship of fluorosis and brick tea drinking in Chinese Tibetans” Environ Health Perspect 104(12):1340-3 (1996)
40)Cao J, Zhao Y, Liu J – “Brick tea consumption as the cause of dental fluorosis among children from Mongol, Kazak and Yugu populations in China” Food Chem Toxicol 35(8):827-33 (1997)
41)Cao J, Zhao Y, Liu JW – “Safety evaluation and fluorine concentration of Pu’er brick tea and Bianxiao brick tea” Food Chem Toxicol 36(12):1061-3 (1998)
42)Sergio Gomez S, Weber A, Torres C – “Fluoride content of tea and amount ingested by children” Odontol Chil 37(2):251-5 (1989)
43)Toyota S – “Fluorine content in the urine and in the serum of hydrofluoric acid workers as an index of health administration” Sangyo Igaku 21(4):335-48 (1979)
44)Gulati P, Singh V, Gupta MK, Vaidya V, Dass S, Prakash S – “Studies on
the leaching of fluoride in tea infusions” Sci Total Environ.138(1-3):213-21 (1993)
45)Chan J.T.; Koh, S.H. -“Fluoride content in caffeinated, decaffeinated and herbal teas” Caries Res 30(1):88-92 (1996)
46)Chan J.T.; Yip, T.T.; Jeske, A.H. – “The role of caffeinated beverages in dental fluorosis” Med Hypotheses 33(1):21-2 (1990)
47)Schmidt, C.W.; Leuschke, W. – “Fluoride content of deciduous teeth after
regular intake of black tea” Dtsch Stomatol 40(10):441 (1990)
48)Wei, S.H.; Hattab, F.N., Mellberg, J.R. – “Concentration of fluoride and selected other elements in teas” Nutrition 5(4):237-40 (1989)
49)Nabrzyski M, Gajewska R – “Aluminium and fluoride in hospital daily diets and in teas” Z Lebensm Unters Forsch 201(4):307-10 (1995)
50)Koch K. R., Pougnet B., De Villiers S.: “Increased urinary excretion of Al after drinking tea”; Nature 333 (May 12, 1988)
51)Zeyuan D, Bingying T, Xiaolin L, Jinming H, Yifeng C- “Effect of green tea and black tea on the metabolisms of mineral elements in old rats.” Biol Trace Elem Res 65(1):75-86 (1998)
52)Graylab Medical Dictionary
53)Ronsivalli, LJ -“Addenda to Fluoridation Of Public Water Supplies”, Mermakk Publications, 5 West Bedford Street, Methuen, MA 01844 (1999)
54)Frech, F.- “Alzheimer’s Disease:Solving The Mystery”. In a speech before a health care workers conference at Shawnee-Mission, Kansas, Medical Centre, September 14, 1993. (Population Renewal Office, 36 West 59th Street, Kansas City, MO 64113-1246)
55) Judd, G – “Good Teeth Birth To Death”, Research Publications, Glendale Arizona (1997)
56)Isaacson, R – “Rat studies link brain cell damage with aluminum and fluoride in water” State Univ. of New York, Binghampton, NY 1-607-777-2000 (Wall Street Journal article by Marilyn Chase; Oct.28, 1992, p.B-6)
57)Varner, J.A., Jensen, K.F., Horvath, W. And Isaacson, R.L. – “Chronic administration of aluminum- fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity” Brain Research 784 284-298 (1998)
58)Susa M – “Heterotrimeric G proteins as fluoride targets in bone (Review)” Int J Mol Med 3(2):115-126 (1999)
59)Susa M, Standke GJ, Jeschke M, Rohner D-” Fluoroaluminate induces pertussis toxin-sensitive protein phosphorylation: differences in MC3T3-E1 osteoblastic and NIH3T3 fibroblastic cells.” Biochem Biophys Res Commun 235(3):680-4 (1997)
60)Gilman, A.G. -“G proteins, transducers of receptor-generated signals.” Annu Rev Biochem 56, 615-649 (1987)
61)Bockmann J, Winter C, Wittkowski W, Kreutz MR, Bockers TM -“Cloning and expression of a brain-derived TSH receptor” Biochem Biophys Res Commun 238(1):173-8 (1997)
62)Strunecká, A; Patocka, J – “Aluminofluoride complexes: new phosphate analogues for laboratory investigations and potential danger for living organisms” Charles University, Faculty of Sciences, Department of Physiology and Developmental Physiology, Prague/Department of Toxicology, Purkynì Military Medical Academy, Hradec Králové, Czech Republic
63)Strunecká A, Patocka J – “Aluminum and fluoride: a new, deadly duo in Alzheimer’s Disease” Cesk Fysiol 48(1):9-15 (1999)
64)National Library of Health:PUBMED/MEDLINE
65)Mullenix, P.J.;Denbesten, P.K.;Schunior, A; Kernan, W.J. – “Neurotoxicity of Sodium Fluoride In Rats”. Neurotoxicology and Teratology, 17(2):169-177 (1995) also see Letter by Dr. Phyllis Mullenix, September 14, 1998
66)Z.Z. Guan, Y.N. Wang, K.Q. Xiao, D.Y. Dai, Y.H. Chen, J.L. Liu, P. Sindelar and G. Dallner -“Influence of chronic fluorosis on membrane lipids in rat brain Neurotoxicology and Teratology” 20;537-542 (1998).
67)Zhao, L.B., Liang, G.H., Zhang, D.N., and Wu, X.R. – “Effect of high fluoride water supply on children’s intelligence” Fluoride 29; 190-192 (1996)
68)Li, X.S., Zhi, J.L., and Gao, R.O. “- Effect of fluoride exposure on intelligence in children” Fluoride 28 (1995)
69)Varner, J.A., Jensen, K.F., Horvath, W. And Isaacson, R.L. – “Chronic administration of aluminum- fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity” Brain Research 784 284-298 (1998)
70)Rajwanshi, P.; Singh,V.; Gupta, M.K.; Kumari, V; Shrivastav, R.; Ramanamurthy, M; Dass, S. – “Studies on aluminium leaching from cookware in tea and coffee and estimation of aluminium content in toothpaste, baking powder and paan masala” Sci Total Environ 193(3):243-9 (1997)
71)IA #63-01, 5/1/97 – REVISED IMPORT ALERT #63-01, “DETENTION WITHOUT PHYSICAL EXAMINATION OF COLGATE FLUORIDE TOOTHPASTE FROM CANADA AND MEXICO AND GUIDANCE FOR ALL OTHER FLUORIDE TOOTHPASTE PRODUCTS”
If link should become unavailable, please contact author at email@example.com
72)Roholm, K.; Fluorine Intoxication – A Clinical Hygiene Study, With A Review Of the Literature And Some Experimental Investigations. H.K. Lewis & Co., London (1937)
73)Fragu P -“The history of science with regard to the thyroid gland (1800-1960)” Ann Endocrinol (Paris) 60(1):10-22 (1999)
74)Schuld A – “Over 150 common symptoms and associations: Fluoride poisoning and hypothyroidism” PFPC, Vancouver, BC, Canada (1999) (contact author at firstname.lastname@example.org)
75)Grimbergen, G.W. -“A Double Blind Test for Determination of Intolerance
to Fluoridated Water (Preliminary Report)”, Fluoride 7:146-152 (1974)
76)Schuld, A. – “The Thyroid Gland And Truth Decay” http://www.bruha.com/fluoride/html/thyroid_fluor.htm
77)Wilson, RH; DeEds, F – “The Synergistic Action Of Thyroid On Fluorine Toxicity” Endocrinology 26:851 (1940)
78)Fluoride Virtual Research Library – PFPC
79a)Woffinden, B – “Clear And Present Danger”, The Guardian Weekend, June 7,1997
79b)Mattheis, P – “Thyroid Disease in Down syndrome: Clinical perspectives, and directions of research” Originally presented at the 2nd International Symposium on Biomedical and Psychoeducational Aspects on Down Syndrome, Mexico City, April 24,1997.
80)Schatz, A -“Low-level fluoridation and low-level radiation –Two case histories of mis-conduct in science” by Albert Schatz, Ph.D,1996, Philadelphia, Pennsylvania
81)Rapaport, I -“Nouvelles recherches sur le mongolisme. A propos du role pathogénique du fluor. Bull Acad Nat Med (Paris)143:367-370 (1959)
82)Sleek S – “What constitutes dementia vs. normal aging?” American Psychological Association (APA Monitor) – October 1995
83)Ross, D.M.;Ross, S.A. -“Hyperactivity:Research, Theory and Action” New York:John Wiley, (1982)
84)American Psychiatric Association – “Diagnostic and Statistical Manual of Mental Disorders” Third Edition Revised, pp36-37 (1987)
85)Cowart, V.S. -“Attention-Deficit Hyperactivity Disorder:Physicians Helping Parents Pay More Heed” JAMA 259:18, p.2647 (1988)
86)Cameron, D.L. Crocker, A.D. “The hypothyroid rat as a model of increased sensitivity to dopamine receptor agonists” Pharm Biachem & Behav 37:627-632 (1990)
87)Dluhy, R.J.- “The adrenal cortex in hypothyroidism” In: Braverman, L.E; Utiger, R.D (eds) Werner and Ingbar’s “The thyroid, a fundamental and clinical text” (7th edition). Philadelphia. Lippincott-Raven, 841-844 (1996)
88)Hauser, P; Zametkin, A.J; Martinez, P- “Attention deficit-hyperactivity disorder in people with generalized resistance to thyroid hormone” NE JMed, 328:997-1001(1993)
89)Dodman, N.H; Mertens, P.A; Aronson, L.P.- “Aggression in two hypothyroid dogs – behavior case of the month” J Am Vet Med Assoc 207:1168-1171(1995)
90)Denicoff, K.D.; Joffe, R.T;Lakschmanan, M.C; Robbins, J; Rubinow, D.R. – “Neuropsychiatric manifestations of altered thyroid state” Am J Psychiatry, 147:94-99 (1990)
91)Joseph, R.J; Peterson, M.E. -“Review and comparison of neuromuscular and central nervous system manifestations of hyperthyroidism in cats and humans” Prog Vet Neurol 3:114-119 (1992)
92)Herman, J.P, Cullina, W.E. “Neurocircuitry of stress: central control of the hypothalamo- pituitary-adrenocortical axis” TINS 20:78-84 (1997)
93)Henley, W.N.; Chen, X; Klettner, C; Bellush, L.L; Notestine, M.A. – “Hypothyroidism increases serotonin turnover and sympathetic activity in the adult rat” Can J Physiol Pharmacol 69-.205-210(1991)
94)Uchida, Y; Dodman, N; DeNapoli, J; Aronson, L. – “Characterization and
treatment of 20 canine dominance aggression cases” J Vet Med Sci 59:397-399 (1997)
95)Whybrow, P.C. – “Behavioral and psychiatric aspects of thyrotoxicosis” In Braverman LE, Utiger RD (eds) Werner and Ingbar’s “The thyroid: a fundamental and clinical text” (7th edition). Philadelphia. Lippincott-Ravm 696-700(1996)
96)Baumgartner, A -“Thyroid hormones and depressive disorders–critical overview and perspectives. Part 1: Clinical aspects” Nervenarzt 64(1):1-10 (1993)
97)Whybrow, P.C.-“Behavioral and psychiatric manifestations of hypothyroidism” In Braverman LE, Utiger RD (eds) Werner and Ingbar’s “The thyroid: a fundamental and clinical text” (7th edition). Philadelphia, Lippincott-Raven,866-870(1996)
98)”Thyroid Dysfunction as a Cause of Aggression in Dogs and Cats” L.P. Aronson DVM & N.H. Dodman RVMS – Presented at the 43. Jahrestagung der Deutschen Veterinarmedizinischen Gesellschaft Fachgruppe Kleintierkrankheiten 29-31 August 1997 in HCC Hannover, Germany
99)Glasser, G. – “Mental Fluorosis: Brain Damage from Exposure to Fluorides” Sarasota ECO Report (1995)
100)Whybrow, P.C.-“The therapeutic use of triiodothyronine and high dose thyroxine in psychiatric disorder” Acta Med Austriaca 21(2):47-52 (1994) Department of Psychiatry, University of Pennsylvania, Philadelphia 19104.
101)Bobek, S; Kahl, S.; Ewy, Z. – “Effect Of Long Term Fluoride Administration on Thyroid Hormone Levels In Rats” Endocrinol Exp (Bratisl)10:289-295 (1976) PMID:1087230
102)Li, X.S., Zhi, J.L., Gao, R.O., – “Effect of Fluoride Exposure on Intelligence of Children” Fluoride 28; 4; 189-192 (1995)
103)Foulkes, RG-“Fluoride and the Placental Barrier” Townsend Letter for Doctors and Patients (1998)
104)Chlubek D, Mokrzynski S, Machoy Z, Olszewsk M – “Fluorides in the body of the mother and in the fetus. III. Fluorides inamniotic fluid” Ginekol
Pol 66(11):614-7 (1995)
105)Montherrat-Carret L, Perrat-Mabilon B, Barbey E, Bouloc R, Boivin G, Michelet A, Magloire H – “Chemical and X-ray analysis of fluoride, phosphorus, and calcium in human foetal blood and hard tissues” Arch Oral Biol 41(12):1169-78 (1996)
106)Mokrzynski S, Chlubek D, Machoy Z, Samujlo D – “Fluoride in the organism of mother and fetus. II. Fluoride cumulation in the organism of the fetus” Ginekol Pol 65(12):678-81 (1994)
107)Brambilla E, Belluomo G, Malerba A, Buscaglia M, Strohmenger L – “Oral administration of fluoride in pregnant women, and the relation between concentration in maternal plasma and in amniotic fluid.” Arch Oral Biol 39(11):991-4 (1994)
108)”Trace Elements In Human and Animal Nutrition” U.S. Dept. of Agriculture, p.382 (1987)
“This study confirms that a placental barrier does not exist for fluoride and that the latter passes through the placenta to the fetus in significant amounts.”
109)”Trace Elements In Human and Animal Nutrition”, U.S. Dept. of Agriculture,p.383 (1987)
“… fluorine from the anesthetic methoxyflurane crossed the placental barrier when administered to pregnant women. The transfer to the fetus was immediate.”
110)Opinya GN, Bwibo N, Valderhaug J, Birkeland JM, Lokken P – “Intake of fluoride and excretion in mothers’ milk in a high fluoride (9ppm) area in Kenya” Eur J Clin Nutr 1991 Jan;45(1):37-41
111)Villa AE, Guerrero S, Icaza G, Villalobos J, Anabalon M – “Dental fluorosis in Chilean children: evaluation of risk factors” Community Dent Oral Epidemiol 26(5):310-5 (1998)
112)Gordonoff, T. – Fluor und die Schilddrüse, Toxikology des Fluors Basel/Stuttgart, pp.111-123 (1964)
113)Day, TK;Powell-Jackson,PR -“Fluoride, Water Hardness, and Endemic Goitre” Lancet 1:1135-1138 (1972) A study on 648 people in 13 mountaineous regions in Nepal where the iodine content in the water was low found a close relationship between fluoride intake and the incidence of goiter.
114)Siddiqui, A.H. – “Incidence of Simple Goiter in Areas of Endemic Fluorosis in Nalgonda District, Andra Pradesh, India” Fluoride 2:200-205 (1969)
In India, small visible goiters have been connected directly to high fluoride concentrations in drinking water in persons 14 to 17 years of age.
115)Zhao, W;Zhu, H; Yu, Z;Aoki, K; Misumi, J; Zhang, X -“Long-term Effects of Various Iodine and Fluorine Doses on the Thyroid and Fluorosis in Mice” Endocr Regul 32(2):63-70 (1998)
116)Yang Y, Wang X, Guo X – “Effects of high iodine and high fluorine on children’s intelligence and the metabolism of iodine and fluorine” Chung Hua Liu Hsing Ping Hsueh Tsa Chih 15(5):296-8 (1994)
117)Health Effects of Ingested Fluoride, Subcommittee on Health Effects of Ingested Fluoride, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission on Life Sciences, National Research Council pp.37,48 (1993)
118)Jooste PL, Weight MJ, Kriek JA, Louw AJ – “Endemic goitre in the absence of iodine deficiency in schoolchildren of the Northern Cape Province of South Africa” Eur J Clin Nutr 53(1):8-12 (1999)
119)IDD by COUNTRY
120)Yoder KM, Mabelya L, Robison VA, Dunipace AJ, Brizendine EJ, Stookey GK “Severe dental fluorosis in a Tanzanian population consuming water with negligible fluoride concentration” Community Dent Oral Epidemiol
121)Rwenyonyi C, Bjorvatn K, Birkeland J, Haugejorden O- “Altitude as a Risk Indicator of Dental Fluorosis in Children Residing in Areas with 0.5 and 2.5 mg Fluoride per Litre in Drinking Water.” Caries Res 33(4):267-274 (1999)
122)CONGENITAL HYPOTHYROIDISM – The Thyroid Society
123)Luke, J.A.- “Effect of fluoride on the physiology of the pineal gland” Caries Research 28 204 (1994)
124)Schlesinger, E.R., Overton, D.E., Chase, H.C., and Cantwell, K.T.- “Newburgh-Kingston caries-fluorine study XIII. Pediatric findings after ten years” JADA 52 296-306 (1956)
125)Thomas P. Foley, Jr; M.D.; Professor of Pediatrics University of Pittsburgh and Children’s Hospital of Pittsburgh, Pennsylvania, The MAGIC Foundation Clinical Hypothyroidism Divison
126)Morgan, P.J; Hastings, M.H; Thompson, M; Barrett, P; Lawson, W; Davidson, G. – “Intracellular signalling in the ovine pars tuberalis: an investigation using aluminium fluoride and melatonin” J Mol Endocrinol 7(2):137-44 (1991)
127)DeEds,F; Thomas,O.- Chem Zbl 3542 (1935)
128)Press Releases – Thyroid Federation International
129)Press Release – Gland Central
130)Wood, Lawrence C., David S. Cooper, and E. Chester Ridgway. “Your Thyroid, A Home Reference,” New York: Ballantine Books, 1995
131)Review of Fluoride: Benefits and Risks, Department of Health and Human Services, Public Health Service, February 1991
132)Jacobsen, S.J., Goldberg, J., Miles, ,T.P. et al. – “Regional variation in the incidence of hip fracture: U.S. white women aged 65 years and older” JAMA 264 500-502 (1990)
133)Danielson, C., Lyon, J.L., Egger, M., and Goodenough, G.K. – “Hip fracture and fluoridation in Utah’s elderly population” JAMA 268 746-748 (1992).
134)Jacobsen, S.J., Goldberg, J., Cooper, C. and Lockwood- “The Association between water fluoridation and hip fracture among white women and men aged 65 years and older: a national ecological study , S.A. Ann. Epidemiol.2 617-626 (1992)
135)Toxicological Profile for Fluorides, Hydrogen Fluoride and Fluorine, ATSDR/U.S. Public Health Service, 1993, page 46