Fluoride: The dumbing-down of a generation

New studies from China show that an excessive intake of fluoride can accumulate in the brain, permanently reducing a child’s intelligence.

Two suburban villages in Shanxi Province in China are very much alike – except for the level of calcium fluoride in their water supply.

Xinghua’s water contains 0.91 parts per million (ppm; equal to mg/L) of fluoride, and 14 per cent of the population have dental fluorosis – mottling, softening, and increased porosity and brittleness of tooth enamel – but no cases of bone fluorosis. In contrast, Sima has fluoride levels four times higher than its neighbour, or 4.12 ppm. In this town, 86 per cent show clear evidence of dental fluorosis, and 9 per cent have clinically diagnosed skeletal fluorosis (Fluoride, 1996; 29: 190-2).

In each village, 160 randomly selected children (excluding those with congenital or acquired diseases not related to fluoride) took a standard IQ test lasting 40 minutes. Each child’s mother had lived in the study village during pregnancy.

The two studies came to extra-ordinary and identical conclusions: exposure to high fluoride lowers intelligence, as measured by IQ test scores (Chin J Control Endem Dis Suppl, 1991).

The mean IQ in high-fluoride Sima was 97.7 whereas, in lower-fluoride Xinghua, it was 105.2 – 7.5 points or 7.7 per cent higher, a statistically significant difference (Fluoride, 1996; 29: 190-2).

Indeed, the entire range of IQs was lower in high-fluoride Sima, giving that village’s bell-shaped IQ curve a distinctly flattened shape (Alive Can J Health Nutr, 1998; 191: 67-8).

Among the 160 children selected for the study, the number of children from Sima with IQs of 69 or below was six times that of those in lower-fluoride Xinghua, and 26 per cent fewer children in Sima had IQ scores of 120 or above (Chung Hua Liu Hsing Ping Hsueh Tsa Chih, 1994; 5: 296-8).

A separate Chinese study looked at the IQs of 907 children aged 8-13 years from four areas of Guizhou Province (Chung Hua Liu Hsing Ping Hsueh Tsa Chih, 1994; 5: 296-8). This study compared the degree of fluorosis in the population, rather than the fluoride content of the water. In some areas, fluorosis was worsened by inhalation of fluoride-containing soot from China’s low-quality coal.

The maximum IQ among the low-fluorosis students was 140, a good score. However, in students with moderate-to-severe fluorosis, the maximum IQ scores were only 110.

The very large difference in mean IQ scores between the high- and low-fluorosis areas appears to be caused in part by exposure to lead as well as fluoride. Another study in a coal-burning area found that excessive fluoride lowered mental work capacity and zinc content of the blood (Hua His I Ko Ta Hsueh Hsueh Pao, 1994; 25: 188-91).

How fluoride harms IQ
How does high fluoride reduce a child’s intelligence? Sadly, many of our early clues are from animal studies, which may not apply to humans. Those laboratory studies that we do have strongly suggest that fluoride causes motor dysfunction, IQ deficits and/or learning disabilities, and a generalised pattern of disruptive behaviour. Phyllis Mullenix, PhD, then head of toxicology at Forsyth Dental Center, Boston, carried out major studies in the early 1990s (Neurotoxicol Teratol, 1995; 17: 169-77).

In her tests on rats, the results indicated that fluoride is a powerful central nervous system toxin (Pharmacol Biochem Behav, 1987; 27: 559-64).

[WDDTY is opposed to animal studies, but we cite these here because of the tendency of pro-fluoridationists to quote studies using rats. This is because of their supposed far higher resistance to toxins than other species. Rats also lack a vomit reflex (Section 2, Health effects: Comparative toxicokinetics, Abstracts from USPHS [Public Health Service] Toxicological Profile on Fluorides, p 16). In other words, rat studies are used to show that fluoride is harmless.]

Before Mullenix, no one had ever considered – much less studied – the subtle effects of fluoride exposure on the developing brain. At the time, she was unaware of the ongoing tests in China.

Although rats are supposed to resist fluoride (which ironically started life as a rat poison), Mullenix’s tests showed that exposure prenatally, as weanlings or adults caused subtle, but real, sex- and dose-specific behavioural deficits with a common pattern. The fluoride accumulating in important regions of the rat brain, especially the hippocampus, increased the more fluoridated water they drank.

The hippocampus is considered to be the central processor which integrates input from the environment, memory and motivational stimuli to produce behavioural decisions and modify memory.

It appears that fluoride accumulates in brain tissue, and younger animals and people are more vulnerable than older ones (Neurotoxicol Teratol, 1995; 17: 169-77). We also know that children excrete fluoride less efficiently than adults and so retain more of it (Aust Trad Med Soc Newslett, 1993/94; Summer).

In these studies, researchers discovered that fluoride caused behavioural problems not unlike hyperactivity as well as learning deficits (Neurotoxicol Teratol, 1995; 17: 169-77). What was also surprising is how little exposure was needed before subtle brain damage was seen. Also, the brain effects were measurable at a lower level of exposure than that required to damage bones.

The researchers also discovered subtle differences between the sexes in the timing of exposure required to cause damage. Males were most sensitive to prenatal exposure while females were more likely to be damaged if exposed as weaned babies or as adults.

The behavioural problems were also different, depending on time of exposure. Rats exposed prenatally tended to be hyperactive whereas those exposed as young rats or adults tended to have cognitive (mental-processing) deficits.

The level of exposure required to cause damage, and the apparent differences between male and female tolerances to exposure corresponded to those found in other studies of hippocampal brain damage.

Although animal studies don’t necessarily apply to humans, they provide important clues concerning the damage wreaked by fluoride in the Chinese towns. Fluoride blood levels in this rat model (0.059-0.640 ppm) were similar to those reported in children one hour after receiving topical fluoride treatment of their teeth.

A few mechanisms have been suggested as to how fluoride affects brain function. These include influencing calcium currents, altering enzyme structure, inhibiting brain hormone activity and increasing phosphoinositide (needed for cell and calcium activation) breakdown (Fluoride, 1996; 29: 187). In guinea pigs, which like primates, including humans, cannot synthesise their own vitamin C, intracellular fluoride alters calcium currents from hippocampal neurons (J Neurosci, 1986; 6: 2915).

The fluoride ion also affects amide binding such as occur in proteins. This may explain how fluoride is able to disrupt key sites in biological systems (J Am Chem Soc, 1981; 103: 24-8; Int Clin Psychopharmacol, 1994; 9: 79-82).

Another study found that fluoride binding induced significant disorders in the structure of the cytochrome-c peroxidase enzyme (Chem Eng News, 1988; Aug 1: 26-42). Indeed, over 100 enzymes are affected by fluoride binding to enzyme cofactors such as magnesium, manganese and phosphate, thus preventing the appropriate coenzyme from activating its enzyme (Lee L, The Enzyme Cure, Tiburon, CA: Future Medicine Publishing, 1998; p 211).

Fluoride from any type of exposure destroys 66 out of 83 known enzymes (Judd GF, Good Teeth Birth to Death, Glendale, AR: Research Publications, 1997; pp 19, 53). Fluoride attacks enzymes at their weakest links – hydrogen bonds surrounding the active site. For every enzyme inhibited or destroyed, a major metabolic function is stopped, as they are required in every bodily process.

Prenatal exposure
The human nervous system develops throughout gestation and in the early postnatal period; higher cognitive functions develop toward the end of gestation, when brain nerve cells become differentiated and brain development is particularly rapid, and soon after delivery. Slowly and with some difficulty, fluoride penetrates the fetal blood-brain barrier (Fluoride, 1986; 19: 108-12; Chin J Epidemiol, 1993; 2: 97-8) to accumulate in the brain tissue (Chin J Control Epidem Dis, 1989; 4: 136-7).

The draconian Chinese one-child-per-family rule has given us more evidence of the deadly effects of fluoride on the developing fetal brain. China has persisted with abortions in families who already have one child. In those areas with elevated fluoride and fluorosis due to coal-burning, fluoride has been found in brain tissue obtained from aborted embryos. Stereological and ultramicroscopy studies of this developing brain tissue show poor differentiation of brain nerve cells and delayed brain development (J Fluoros Res Commun, 1991; 138 [in Chinese]).

One of the dangers of fluoride is that this damage to a developing fetus occurs with levels far lower that those considered dangerous to adults. Fluoride effects on intelligence in utero occur at levels not toxic to the mother. In one study, fluoride concentration was higher in a typical mother’s placenta than in her blood (Gedalia et al., 1961; Abstracts from USPHS Toxicological Profile on Fluorides). Umbilical cord levels do not accurately reflect fetal fluoride status, suggesting that the placenta somehow isolates the fluoride as an innate protective measure (J Perinat Med, 1995; 23: 279-82). Eventually, however, enough fluoride crosses the placenta and reduces the available fluoride-binding sites in the newborn (Pediatrics, 1975; 55: 517-22).

The US Public Health Service reported in 1991 that millions of women in ‘optimally’ fluoridated cities ingest from all sources – and expose their embryos and fetuses to – as much as 6.6 mg of fluoride per day (US PHS, Review of Fluoride Benefits and Risks, 1991). While the women themselves may not have symptoms or problems, such levels could be deadly to the brain of their developing babies.

Damage as adults
Do IQs drop still lower if high exposure to fluoride continues? Studies do not answer this directly, but there is some evidence that continued exposure does worsen mental problems.

High fluoride exposure appears to weaken mental function in a dose-related manner in adults as well as in children. Declassified 1944 documents show that one year before USPHS epidemiological ‘testing’ of fluoridation was to start in Grand Rapids, Michigan, and Newburgh, New York, the military/industrial complex had already acquired evidence that fluorides affect memory and cognitive skills.

The Manhattan Uranium Project concluded: ‘Clinical evidence suggests . .. . mental confusion, drowsiness and lassitude as the conspicuous features. It seems most likely that the fluoride component is the causative factor’ (US Medical Corps document, 4/29/44). Much of the evidence of adverse fluoride effects was censored out of the document, and later, related documents are ‘missing’ or have been made to disappear by the US government (Griffiths J, Bryson C, Fluoride, teeth and the atomic bomb, Waste Not, 1997; Sept: 1-8).

Researcher Dr Bruce Spittle has cited examples of fluoride affecting adult mental function (Int Clin Psychopharmacol J, 1994; 9: 79-82). As he concluded: ‘The late George L. Waldbott, MD, in 1979 studied 23 persons living within three miles of an enamel factory that emitted hydrogen fluoride into the air. Symptoms included a distinct decline in mental acuity, poorer memory, inability to coordinate thoughts and reduced ability to write. Those living further away from the factory were less affected and had lower urinary fluoride’ (Vet Hum Toxicol, 1979; 21: 4-8).

In 1981 after a fluoride overfeed to the water of Annapolis, Maryland, Waldbott wrote: ‘Six [out of 112 who suffered ill effects] reported deterioration of their mental acuity, lethargy, loss of memory . . .’ (Clin Toxicol, 1981; 18: 537-49).

In another study of 60 aluminium smelter workers, 97 per cent had skeletal fluorosis and 22 per cent had psychiatric disturbances, including depression, mental sluggishness and forgetfulness (Fluoride, 1977; 10: 12-6).

In other studies by Waldbott and colleagues, psychiatric symptoms such as lethargy, memory impairment, and difficulties with concentration and thinking, began after fluoride exposure. This usually occurred with fluoridated drinking water, though three cases involved industrial exposure.

Dr Spittle concludes, ‘There is suggestive rather than definitive evidence that chronic toxicity affecting cerebral functioning can follow exposure to fluoride’ (Int Clin Psychopharmacol, 1994; 9: 79-82).

In light of the findings in China, however, the conclusions are moving toward certainty, and fluoride damage to intelligence may be worse in the UK and US than in China. Millions of embryos and infants receive daily fluoride at doses known to cause crippling skeletal fluorosis in adults (US PHS, Review of Fluoride Benefits and Risks, 1991).

Furthermore, fluoride intake may increase two- to fourfold or more during hard physical work in a hot climate – and even more if the water used in cooking and in beverages is also fluoridated. About 3 per cent of the US population drinks at least four litres of water a day, and more where the climate is hotter.

Boiling water evaporates chlorine while concentrating fluoride. If the water contains 4 ppm of fluoride, a person may ingest 16 mg of fluoride a day or more, in addition to the fluoride from other sources like toothpaste, food and air – enough to produce crippling skeletal fluorosis within a few years.

China is sensibly protecting the intelligence of its unborn children by defluoridating its water supply (J Orthomolec Med, 1993; 8: 149-53). We can all learn from their example.

This was adapted from material for an article that first appeared in the Journal of Orthomolecular Medicine.

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