Fluoride and the Brain |
Have you seen the research from China and the USA showing that fluoride is toxic, can damage the central nervous system, and is linked with Alzheimer’s disease and low IQ?
BFS suggested answer
Fluoridation is both safe and beneficial. There is no evidence whatsoever to support such claims.
BFS suggested answer refuted
The presence of low levels of fluoride in the drinking water, equal to the amount found in fluoridated water, caused damage to the tissue of the brain similar to Alzheimer’s and other forms of dementia, as well as kidney damage.
Dr J.A. Varner et al.10
It has been known for many years that fluoride inhibits the enzyme acetylcholinesterase, which is involved in transmitting signals along nerves.1 Clinical and physiological studies from Russia published in 1974 demonstrated that patients with occupational fluorosis exhibited disturbed nervous activity and brain dysfunction.2 China, like India, has areas with high levels of endemic fluorosis. Not surprisingly, a great deal of research into other possible adverse effects of fluorides has been conducted in those two countries. The first suggestions that fluoride could affect the brain were published in China in 1982.3 Since then, many studies have been conducted into the role of fluoride in brain development and its effects on intelligence.
Because it is unethical to subject children to substances known to be toxic, most of the clinical studies with fluorides have been conducted on rats, mice and hamsters. A landmark study was published by Dr Phyllis Mullenix and colleagues in 1995.4
Mullenix worked in the Department of Psychiatry at Children’s Hospital in Boston and the Department of Neuropathology at Harvard University Medical School. Her studies focussed on neurotoxicity of therapeutic agents: radiation, lead, amphetamine, phenytoin and nitrous oxide, and so on. In 1982 Mullenix was invited by the Director of Forsyth’s Dental Infirmary for Children in Boston, Dr John Hein, to conduct research at Forsyth and to apply it to substances used in dentistry. Among those substances, fluoride was prominent.
Until that time, the effects of fluoride on the developing brain had not been considered. Dr Mullenix was to rectify that omission. It was a subject in which she had little interest at the time.
It took until 1986 to complete the computer program they needed for accurate measurement of behaviour in an animal model. The finished program was so perfect that the Forsyth Dental Center was noted for this achievement in the Wall Street Journal and the Boston Herald.
Mullenix and her team investigated the ‘safe and effective’ treatment for dental caries by exposing the rats to different concentrations of sodium fluoride (NaF) during late gestation, at weaning and as adults, and by comparing the rats’ behaviour and body weight with fluoride levels in their blood and brains. Mullenix expected that rats drinking fluoride-treated water would behave the same as matched, untreated controls – they did not. She had been led to expect that fluoride would not cross the blood/brain barrier, and that if the mothers were fluoridated, the fluoride would not affect the unborn foetus – but in both cases it did. Mullenix says: ‘Like walking into quicksand, our confidence that brain function was impervious to fluoride was sinking.’5
Published in 1995, the paper by Mullenix and colleagues was the first laboratory study to demonstrate in living animals that the brain was vulnerable to fluoride. They demonstrated that:
•The effects on behaviour depended on the age at exposure.
•Fluoride accumulated in brain tissues.
•The severity of the effect on behaviour increased directly as fluoride levels rose in the blood and the brain.
•Fluoride exposures caused sex- and dose-specific behavioural deficits with a common pattern: males were most sensitive to prenatal exposure, whereas females were more sensitive to weaning and adult exposures.
The fluoride levels used were less than one-tenth the amount found in children one hour after receiving topical applications of dental fluoride gels. Mullenix concluded: ‘Thus, humans are being exposed to levels of fluoride we know alters behaviour in rats’, levels that ‘flagged potential for motor dysfunction, IQ deficits and/or learning disabilities in humans’.
A review by Dr Bruce Spittle of Dunedin School of Medicine, New Zealand, published in 1994,6 found confirmation in Mullenix’s study. Spittle listed case reports that spanned almost sixty years of central nervous system effects in humans excessively exposed to fluoride.
Fluoride and children’s IQ
Measuring the intelligence of children aged eight to thirteen years living in areas with no, slight, medium and serious fluorosis, Chinese scientists showed in 1995 that IQ scores were 5–19 points lower for the children in the severe fluorosis area compared with those in the non-fluorosis area.7 This was confirmed by a second study of children aged seven to fourteen in two areas, one of which had a fluoride level in water four times that of the other (0.91 ppm versus 4.12 ppm).8 These data, displayed in Figure 1, show a 6–12 point lower IQ in those children from the high-fluoride area compared with those from the low-fluoride area.
Source: Zhao et al. Fluoride 1996; 29: 190–2.
Figure 1. Comparisons of average IQ by age in Sima and Xinhua
In this study, intelligence was significantly impaired at a fluoride concentration in drinking water of 4.12 ppm but was not impaired at 0.91 ppm, which is close to the recommended ‘optimal’ dose. In a study of 8-year-old children, Dr Spittle and colleagues also found no difference in IQ between those drinking water fluoridated at 1 ppm and those whose water contained less than 0.1 ppm. They say: ‘Thus a threshold effect for fluoride toxicity may be present with demonstrable effects being present with water containing 4–10 ppm but not 1 ppm of fluoride.’9
So should we be worried about water that is fluoridated at 1 ppm? It seems we should if the fluoride comes with other minerals – and in fluoridated tap water, it does. Recent work by Varner and colleagues suggests that fluoride may have the potential to cause neurotoxicity at a level of 1 ppm if present with aluminium ions at a concentration of 0.5 ppm.10
Fluoride, aluminium and Alzheimer’s disease
For many years, researchers have noticed that elderly people suffering from Alzheimer’s disease (senile dementia) have high levels of aluminium in their brains. A large percentage of cookware these days is made of aluminium, and aluminium compounds are frequently added to the water supply as clarifying agents. Are these to blame for the dementia? It’s hard, at first sight, to see how, because on its own aluminium is not readily absorbed by the body.
However, add fluoride to the equation, and all that changes: when fluoride is present, it combines with any aluminium to form aluminium fluoride, which is easily absorbed.
After population studies showed a higher incidence of Alzheimer’s disease among people who lived in fluoridated areas, Dr Robert Isaacson of the State University of New York added aluminium fluoride to rats’ food. He found that the rats lost their sense of smell, developed short-term memory problems and other characteristics of Alzheimer’s disease.11 Dr Mullenix had studied only sodium fluoride. Dr Isaacson’s studies compared aluminium fluoride with sodium fluoride to determine if fluoride’s effect on aluminium cookware, or its effect when combined with the aluminium sulphate added to some water as a flocculent, had an impact on the development of Alzheimer’s disease. It did. The aluminium fluoride was more toxic to the brain than sodium fluoride. This finding has great significance, as Alzheimer’s disease was unknown until people started using aluminium cookware.
In January 1987, experiments performed at the Medical Research Endocrinology Department, Newcastle upon Tyne, England, and the Physics Department of the University of Ruhana, Sri Lanka, showed that water ‘optimally’ fluoridated at 1 ppm, when used in cooking with aluminium cookware, concentrated the aluminium to up to 600 ppm.12 Fluoridated tap water in Antigo, Wisconsin, in conjunction with aluminium cookware, increased aluminium concentration by 833 times, and the fluoride content doubled.13
The maximum aluminium content of water allowed by the World Health Organization is 200 μg per litre. Antigo water, when cooked in aluminium, was seventy-five times over the limit. Dr I. Jansen, who conducted the Antigo study, writes that to ‘chance exchanging a hole in a tooth – which can be repaired at a nominal fee – for dementia in later years, for which there is no remedy at any price, hardly seems to be a good bargain’.
Let us also not forget that a large proportion of modern aluminium cookware is lined with a non-stick substance such as Teflon or Tefal, which, made from PTFE (poly-tetra-fluoroethane) is another significant source of fluoride.
Fluoride and lead
In 1999 Professor Roger D. Masters of Dartmouth Medical College, and Myron Coplan, a chemical engineer, in a study of 280,000 Massachusetts children found that levels of lead in the blood were significantly higher in communities whose water was fluoridated.14 Heavy metals compromise normal brain development and neurotransmitter function, leading to long-term deficits in learning and social behaviour. At the individual level, earlier studies revealed that hyperactive children and criminals had significantly elevated levels of lead, manganese or cadmium, compared with controls. High levels of lead in the blood at age seven predicts both juvenile delinquency and adult crime. Surveys of children’s blood lead across the United States show that where silicofluorides are used, risk ratios for blood lead over the danger level of 10 µg/dL are up to two and a half times as high as where silicofluorides are not used.
Not surprisingly, communities using silicofluorides report higher rates of learning disabilities, attention deficit disorder (ADD), hyperactivity and violent crime. Data from the US Third National Health and Nutrition Evaluation Survey (NHANES III), and a survey of over 120,000 children in New York towns, corroborate this effect. Masters and Coplan reported that minorities are at particular risk: African-American and Mexican-American children in fluoridated communities have significantly higher levels of lead in their blood than such children in unfluoridated communities.
Ironically, NHANES III also found that children with higher lead levels had more tooth decay.15 ‘So water fluoridation may prove to cause tooth decay rather than prevent it’, says lawyer Paul Beeber, president of the New York State Coalition Opposed to Fluoridation.
Lead has long been recognised as having a deleterious effect on the brain. It is for precisely this reason that leaded petrol has been phased out – yet some still insist on adding silicofluorides to drinking water!
Fluoride and hypothyroidism
Fluoride was used for decades as an anti-thyroid medication to treat hyperthyroidism (overactive thyroid). Fluoride is very effective in this context, as it has the ability to mimic the action of TSH – thyroid-stimulating hormone, or thyrotropin. It is highly significant that fluoride was frequently used at levels below the current ‘optimal’ intake of 1 mg/day to suppress the action of the thyroid gland. It should come as no surprise, then, that of the more than 150 symptoms of hypothyroidism (underactive thyroid), almost all are also symptoms of fluoride poisoning.
Canadian thyroid researcher Andreas Schuld, head of a global organisation, Parents of Fluoride-Poisoned Children, found that excessive fluoride intakes correlate with other thyroid-related issues such as iodine deficiency, which is recognised as the most common cause of preventable brain damage and mental disability in the world today.
Fluorine and iodine, both members of the halogen group of elements, have an antagonistic relationship. When there is an excess of fluoride in the body, fluoride competes with iodine and interferes with the function of the thyroid gland. Such interactions affect brain development in the unborn child. Mullenix’s observation that those exposed to fluorides before birth were born hyperactive and remained so throughout their lives fits very neatly with existing research on hypothyroidism.
In 1994 another thyroid/fluoride connection was seen in Jennifer Luke’s data, which showed that fluoride accumulates in the pineal gland at least as much as, if not more than, in bones and teeth.16 The pineal gland synthesises melatonin, a hormone that regulates our sleep patterns. Luke showed that melatonin production was inhibited by fluoride in test animals. She also found that this inhibition caused an earlier onset of sexual maturity, an effect already reported in humans in 1956 as part of the Kingston/Newburgh study in New York State. Girls living in fluoridated Newburgh began menstruating significantly earlier than in unfluoridated Kingston.17
This early onset of sexual puberty is well established as a 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 gonadotrophins LH and FSH, which stimulate puberty and reproduction, and ACTH, which is necessary for cortisol and hydrocortisone secretion by the adrenal gland.18 In this context, it should be noted that aluminium fluoride also mimics the inhibitory action of melatonin.19
It is possible that the most common cause of brain damage and mental disability in the world, ‘iodine deficiency’, could be reduced dramatically simply by reducing fluoride intake.
Fluoride interactions with drugs
Fluoridated pharmaceuticals increase our total fluoride exposure. Antacids, used to treat heartburn and stomach upsets, and probably the world’s most prescribed drugs, are aluminium-based. Drugs such as Prozac, designed to act upon the central nervous system, are usually fluoride-based. Both types of drug are so commonly used that they are likely to be taken together, which could have disastrous results in later life. But fluoride in foods and water can also interact with prescribed drugs, with undesirable consequences. With some, fluorides have a synergistic effect, increasing the action of prescribed drugs, while their action on other drugs may have the opposite effect, that of reducing their effectiveness.
Fluoride drugs and violent deaths
Many anti-depressive drugs contain fluoride because of its profound effect on mood. Fluanxol, Motipress, Motival, Parstelin and the biggest seller, Prozac, are all highly fluorinated. Hypothyroidism, which they produce, can induce almost any psychiatric symptom or syndrome, including rage, fear ranging from mild anxiety to frank paranoia, mood swings and aggression.
Recently, the USA has seen an alarming rise in apparently motiveless killings, where individuals – usually men, but also children – have taken a gun and shot several people before shooting themselves.
The number of people, including preschool children, prescribed anti-depressants and stimulants rose in the mid-1990s despite limited knowledge about the effects of such drugs on young children. The reasons for prescribing such medications for young children include pain relief, anxiety associated with medical, pre-surgery and dental procedures, bed-wetting and attention-deficit/hyperactivity disorder in children aged three years and older.
The University of Maryland looked at 200,000 patients in three areas of the country. It found that use of stimulants and anti-depressants rose in all the areas between 1991 and 1995. Julie Zito, principal author of the study, said that some of the drugs’ uses are not included in warnings on drug packages. While this is not uncommon with some drugs for adults, there is no information about how these psychotropic drugs work on children: ‘Unresolved questions involve the long-term safety of psychotropic medications, particularly in light of earlier ages of initiation and longer durations of treatment.’20
In an early case, a young defendant was found not guilty because he committed a murder ‘in the course of a hypothyroid psychosis . . . He was later judged to be not guilty by reason of insanity, although he was clearly sane at the time of his trial.’21
In a recent rampage, of a kind that has become frighteningly familiar in the USA, Kip Kinkel, a 15-year-old student in Springfield, Oregon, murdered his parents, and the next day ran through a crowded school cafeteria firing his rifle from the hip. He killed two classmates and critically wounded several others. The Associated Press headline read:
Oregon shooting: Yet another warning of the dangers of Prozac and its clones.22
This was disturbingly similar to a violent episode that took place in Louisville, Kentucky, in 1989. Joseph Wesbecker stepped out of an elevator at work, firing an AK-47 semi-automatic assault rifle. Twelve people were wounded and eight killed before Joseph Wesbecker took his own life. One victim described him as ‘totally devoid of human element and human soul’.
Kip Kinkel was restrained before he could take his life, but begged others to shoot him when they tackled him. Both he and Wesbecker were taking Prozac at the time of their rampages.
Prozac’s manufacturer, Eli Lilly, has repeatedly claimed that Prozac is safe. The International Coalition for Drug Awareness (ICFDA), a non-profit group that warns of potential serious adverse reactions to prescription medications, reports that there is abundant evidence in medical literature showing a link between Prozac and violence, as well as suicide.
Dr Ann Blake Tracy, director of ICFDA, and author of Prozac: Panacea Or Pandora?, has testified as an expert witness since 1992 in criminal cases involving Prozac and other anti-depressants. Dr Tracy poses the question: ‘How many patients have ever been warned that even something as simple as mixing most major cough syrups with their use of these medications can produce PCP (‘angel dust’)-like reactions?’ ‘We are sitting in the middle of this nation’s most dangerous drug problem and have not yet awakened to the seriousness of this situation.’23
Wesbecker and Kinkel are only two of a growing number of people who commit violent crimes while taking Prozac or one of its clones:
•A mother on Prozac in San Francisco smothered her three small daughters by wrapping their hands and faces with duct tape, and attempted to take her own life.
•A man in Los Angeles on Prozac committed suicide in front of TV cameras.
•A lottery employee taking Luvox (a Prozac clone) in Connecticut shot and killed four fellow workers before taking his own life.
•A man in Wyoming taking Paxil (another Prozac clone) shot and killed his wife, daughter and baby granddaughter before he took his own life.
Many more people have died in similar rampages, and Kinkel is facing a life without his parents and several classmates. He also faces spending the rest of his life in prison while he slowly comes to a realisation of what he did in this drug-induced stupor.
According to internal company documents made public in court cases filed against Eli Lilly, in 1990 they attempted to protect their ‘golden goose’ (Prozac was bringing in over $6 million per day). Dr Leigh Thompson went ‘against the advice of his staff’ and told the Board of Directors that suicide and hostile acts committed by Prozac users were, in all probability, caused by the patients’ underlying disorders rather than Prozac. On 7 November 1990 he asked, ‘What are our priorities?’
Of course priority number one for Eli Lilly was to protect Prozac.
In December 1993 the world heard that Prozac had been found ‘not guilty’ in the murderous rampage and suicide of Joseph Wesbecker. But in fact, Eli Lilly had paid millions of dollars to settle out of court. The judge was so upset about the secrecy and deception surrounding the case that he called for an additional hearing to force Lilly to admit this publicly. He succeeded, and Lilly and the plaintiffs were forced to admit that this was indeed a settlement and not a ‘not guilty’ verdict for Prozac.
In another Prozac case against Lilly (Forsyth v. Lilly) currently being tried in Federal District Court in Hawaii, Judge Alan C. Kay ruled:
•‘Lilly falsified reports of side effects of suicide attempts by reporting them as overdoses.’
•‘Material issues of fact exist as to whether Lilly deliberately suppressed adverse studies.’
•‘The Court finds that Plaintiffs have presented sufficient evidence to show that Lilly may have acted wantonly, oppressively, or with such malice as implies a spirit of mischief or criminal indifference.’
Conclusion
Despite the BFS’s denial, there is no doubt that fluoride affects the brain. Why would it be used in drugs that are designed to affect the central nervous system, if it did not? While some effects are considered beneficial, others clearly are not.
These facts alone should be sufficient to limit any individual’s exposure to fluoride. Ad libitum, unregulated intakes of fluoridated water must pose a risk to the brain.
1.Waldbott GL, in collaboration with Burgstahler AW, McKinney HL. Fluoridation: The great dilemma. Lawrence, KS: Coronado Press, 1978: 150.
2.Popov LI, Filatova R, Shershever AS. Gig Tr Prof Zabol 1974; 5: 25–7. Cited in Chem Abstr 1974; 14: 271.
3.Shung-Guan CM et al. The non-skeletal lesions of endemic fluorosis. Chin J Intern Med 1982; 21: 217–9. See also: Hu YH. Direct damage on nervous system by fluorosis. Compilation of First Conference on Neuropsychiatric Diseases in Xinjian, China, 1982: 86–8.
4.Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. Neurotoxicity of sodium fluoride in rats. J Neurotoxicol Teratol 1995; 17:169–77.
5.Mullenix PJ. Central nervous system damage from fluorides. 14 September 1998. http://www.cadvision.com/fluoride/brain2.htm. Accessed 13 April 2000.
6.Spittle B. Psychopharmacology of fluoride: a review. Int Clin Psychopharmacol 1994; 9: 79–82.
7.Li XS, Zhi JL, Gao RO. Effect of fluoride exposure in intelligence in children. Fluoride 1995; 28 (4): 189–92.
8.Zhao LB, Liang G, Zhang D, Lu-Liang XW. Effect of high fluoride water supply on children’s intelligence. Fluoride 1996; 29 (4): 190–2.
9.Spittle B, Ferguson D, Bouwer C. Intelligence and fluoride exposure in New Zealand children. Abstracts of papers to be presented at the XXIInd Conference of the International Society for Fluoride Research, Bellingham, Washington, USA, 24–27 August 1998: S13.
10.Isaacson RL, Varner JA, Jensen KF. Toxin-induced blood vessel inclusions caused by the chronic administration of aluminium and sodium fluoride and their implications for dementia. Neuroprotective agents. Ann NY Acad Sci 1997; 825: 152–66. See also: Varner JA, Jensen KF, Horvath W, Isaacson RL. Chronic administration of aluminium fluoride or sodium fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res 1998; 784: 284–98.
11.Isaacson, R. Rat studies link brain cell damage with aluminium and fluoride in water. State University of New York, Binghamton, NY. Wall Street Journal article by Marilyn Chase, 28 October 1992: B-6.
12.Sci News 1987; 131: 73.
13.Jansen I. J Natl Acad Res Biochem 1990; Jan/Feb: http://www.halcyon.com/wfrazier/fluoride.htm.
14.Children’s Health and the Environment. 17th International Neurotoxicology Conference, Little Rock, Arkansas, USA, 17–20 October 1999. See also: Masters RD, Coplan MJ. Water treatment with silicofluorides and lead toxicity. Int J Environ Studies 1999; 56: 435–49.
15.Moss ME, Lanphear BP, Auinger P. Association of dental caries and blood lead levels. J Am Med Assoc 1999; 281: 2294–8.
16.Luke, JA. Effect of fluoride on the physiology of the pineal gland. Caries Res 1994; 28: 204.
17.Schlesinger ER, Overton DE, Chase HC, Cantwell KT. Newburgh–Kingston caries–fluorine study. XIII: Pediatric findings after ten years. J Am Dent Assoc 1956; 52: 296–306.
18.Foley, Jr TP. University of Pittsburgh and Children’s Hospital of Pittsburgh, Pennsylvania, the MAGIC Foundation Clinical Hypothyroidism Division. http://www.magicfoundation.org/clinhypop.html. Accessed 24 April 2000.
19.Morgan PJ, Hastings MH, Thompson M et al. Intracellular signalling in the ovine pars tuberalis: an investigation using aluminium fluoride and melatonin. J Mol Endocrinol 1991; 7: 137–44.
20.Magno Zito, Safer DJ, dosReis S et al. Trends in the prescribing of psychotropic medications to preschoolers. J Am Med Assoc 2000; 283: 1025–30.
21.Easson WM. Myxedema psychosis – insanity defense in homicide. J Clin Psychiatry 1980; 41: 316–8.
22.http://www.drugawareness.org/oregon.html. Accessed 15 April 2000.
23.Source as in ref. 22.