FAN-Australia Drops a Bombshell on Fluoridation

Media Release: Brisbane, Australia 4 April  2011

 Merilyn Haines, the director of the newly formed group FAN-Australia (Fluoride Action Network Australia), has found some startling statistics buried deep in official research material by ARCPOH (The Australian Research Centre Population Oral Health at the Adelaide Dental School) that could scuttle the water fluoridation program once and for all.

 Haines has found in the ARCPOH statistics that the permanent teeth of children in largely unfluoridated  (<5% before 2009) Queensland were erupting on average two years earlier than the children in the rest of Australia, which is largely fluoridated (see the figure below). A two-year delay would negate all the small reductions in tooth decay claimed by dental researchers since 1990. In other words fluoridation doesn’t work. Any difference in tooth decay claimed to be due to fluoride is simply an artifact of the delayed eruption caused by fluoride.

According to Professor Paul Connett, director of the Fluoride Action Network, who is currently on a fluoride-tour of New Zealand, “Critics of fluoridation, like Dr. Hardy Limeback in Toronto, have long pointed out that any reduced tooth decay touted by promoters could easily be accounted for by the delayed eruption of the teeth. Even when this argument received strong experimental support from Komarek et al. in 2005, this has still has been ignored by those promoting fluoridation. But they cannot ignore it any longer: the figures of the dental department research team most associated with the promotion of fluoridation in Australia (and beyond) demonstrate that this delay is real.”

Less teeth erupted for any given age would mean less surfaces available for tooth decay to have taken place. A delayed eruption of one – two years would account for the small reductions claimed in ALL the US and Australian studies published since 1990 (Brunelle and Carlos, 1990; Slade et al., 1996; Spencer et al., 1996; Armfield et al., 2009; Armfield, 2010). These studies have found reductions ranging from 0.12 of one permanent tooth surfaces saved in Western Australia (Spencer et al., 1996) to 0.6 permanent tooth surface saved in the largest survey ever conducted in the US (Brunelle and Carlos, 1990). This is not very much when you consider that there are five surfaces to the chewing teeth and four to the cutting teeth, and by the time all the child’s teeth have erupted there are a total of 128 tooth surfaces. One tooth surface saved amounts to less than 1% of all the surfaces in a child’s mouth. Now even this small benefit has evaporated.

 More on the history

In 1999, the National Health and Medical Research Council, Australia’s peak Medical Research body, stated that, “evidence exists that tooth eruption is delayed in fluoridated areas. It has been suggested that a proper comparison of caries rates should involve children one year older in fluoridated areas than in non- fluoridated areas.”

 In 2000, the York Review pointed out that none of the studies that they had reviewed had controlled for “the number of erupted teeth per child” (McDonagh et al., 2000, p.24).

 In 2005, Komarek et al.  did control for eruption of teeth and reported no difference in decay between children living in Belgium receiving fluoride supplements (and those who weren’t) that was relatable to fluoride exposure (as measured by the severity of dental fluorosis).

 In 2009, Peiris et al. reported that children in largely fluoridated Australia had a delay in “dental age” of 0.82 years compared to children in largely unfluoridated UK. However, the authors did not discuss the possible reasons for this delay and the number of children involved in the study (about 80 in each country) was not very large.

 2011. Now the bombshell – the delay has been found and it is in the official statistics.   ARCPOH has failed to respond to several inquiries on this matter.  According to Haines, “Surely, this must end water fluoridation. If it doesn’t work what’s the point of putting this toxic substance into the drinking water and what reason can they possibly have for forcing it on people who don’t want it?”

 However, this isn’t just about teeth. The finding could be even more significant than that. If fluoride causes a delayed eruption of the teeth then the most likely mechanism for doing so is fluoride’s ability to lower thyroid function (see chapter 8 in the 2006 National Research Council review, “Fluoride in Drinking Water.” According to Connett,   “Lowered thyroid function in infants would mean slower growth of their tissues and could explain the 24 studies that have found an association between lowered IQ in children and exposure to moderate levels of fluoride in China, India, Iran and Mexico.”

 It also raises the possibility that millions of people in fluoridated countries suffering from hypothyroidism have had this condition caused, or exacerbated, by exposure to fluoridated water.  Haines’ asks “If ingesting fluoride delays tooth eruption for 1 to 2 years what other effects is it having on our bodies?”

 Meanwhile, if swallowing fluoride does not reduce tooth decay, why would any reasonable person, decision maker or regulatory official continue to sanction adding fluoride to the public water supply? 

  Source – Published and unpublished data from 2003- 2004 Australian Child Dental Health Surveys
Media Release sent by Queenslanders For Safe Water on behalf of Fluoride Action Network Australia Inc.

FAN-Australia Drops a Bombshell on Fluoridation

Media Release: Brisbane, Australia 4 April  2011

Merilyn Haines, the director of the newly formed group FAN-Australia (Fluoride Action Network Australia), has found some startling statistics buried deep in official research material by ARCPOH (The Australian Research Centre Population Oral Health at the Adelaide Dental School) that could scuttle the water fluoridation program once and for all.

Haines has found in the ARCPOH statistics that the permanent teeth of children in largely unfluoridated  (<5% before 2009) Queensland were erupting on average two years earlier than the children in the rest of Australia, which is largely fluoridated (see the figure below). A two-year delay would negate all the small reductions in tooth decay claimed by dental researchers since 1990. In other words fluoridation doesn’t work. Any difference in tooth decay claimed to be due to fluoride is simply an artifact of the delayed eruption caused by fluoride.

According to Professor Paul Connett, director of the Fluoride Action Network, who is currently on a fluoride-tour of New Zealand, “Critics of fluoridation, like Dr. Hardy Limeback in Toronto, have long pointed out that any reduced tooth decay touted by promoters could easily be accounted for by the delayed eruption of the teeth. Even when this argument received strong experimental support from Komarek et al. in 2005, this has still has been ignored by those promoting fluoridation. But they cannot ignore it any longer: the figures of the dental department research team most associated with the promotion of fluoridation in Australia (and beyond) demonstrate that this delay is real.”

Less teeth erupted for any given age would mean less surfaces available for tooth decay to have taken place. A delayed eruption of one – two years would account for the small reductions claimed in ALL the US and Australian studies published since 1990 (Brunelle and Carlos, 1990; Slade et al., 1996; Spencer et al., 1996; Armfield et al., 2009; Armfield, 2010). These studies have found reductions ranging from 0.12 of one permanent tooth surfaces saved in Western Australia (Spencer et al., 1996) to 0.6 permanent tooth surface saved in the largest survey ever conducted in the US (Brunelle and Carlos, 1990). This is not very much when you consider that there are five surfaces to the chewing teeth and four to the cutting teeth, and by the time all the child’s teeth have erupted there are a total of 128 tooth surfaces. One tooth surface saved amounts to less than 1% of all the surfaces in a child’s mouth. Now even this small benefit has evaporated.

More on the history

In 1999, the National Health and Medical Research Council, Australia’s peak Medical Research body, stated that, “evidence exists that tooth eruption is delayed in fluoridated areas. It has been suggested that a proper comparison of caries rates should involve children one year older in fluoridated areas than in non- fluoridated areas.”

In 2000, the York Review pointed out that none of the studies that they had reviewed had controlled for “the number of erupted teeth per child” (McDonagh et al., 2000, p.24).  

In 2005, Komarek et al.  did control for eruption of teeth and reported no difference in decay between children living in Belgium receiving fluoride supplements (and those who weren’t) that was relatable to fluoride exposure (as measured by the severity of dental fluorosis).  

In 2009, Peiris et al. reported that children in largely fluoridated Australia had a delay in “dental age” of 0.82 years compared to children in largely unfluoridated UK. However, the authors did not discuss the possible reasons for this delay and the number of children involved in the study (about 80 in each country) was not very large. 

2011. Now the bombshell – the delay has been found and it is in the official statistics.   ARCPOH has failed to respond to several inquiries on this matter.  According to Haines, “Surely, this must end water fluoridation. If it doesn’t work what’s the point of putting this toxic substance into the drinking water and what reason can they possibly have for forcing it on people who don’t want it?”

However, this isn’t just about teeth. The finding could be even more significant than that. If fluoride causes a delayed eruption of the teeth then the most likely mechanism for doing so is fluoride’s ability to lower thyroid function (see chapter 8 in the 2006 National Research Council review, “Fluoride in Drinking Water.” According to Connett,   “Lowered thyroid function in infants would mean slower growth of their tissues and could explain the 24 studies that have found an association between lowered IQ in children and exposure to moderate levels of fluoride in China, India, Iran and Mexico.”

It also raises the possibility that millions of people in fluoridated countries suffering from hypothyroidism have had this condition caused, or exacerbated, by exposure to fluoridated water.  Haines’ asks “If ingesting fluoride delays tooth eruption for 1 to 2 years what other effects is it having on our bodies?”

Meanwhile, if swallowing fluoride does not reduce tooth decay, why would any reasonable person, decision maker or regulatory official continue to sanction adding fluoride to the public water supply? 

 Source – Published and unpublished data from 2003- 2004 Australian Child Dental Health Surveys

Media Release sent by Queenslanders For Safe Water on behalf of Fluoride Action Network Australia Inc.

Occupational Metal Exposures and the Risk of Parkinson’s Disease

Occupational exposure to specific metals (manganese, copper, lead, iron, mercury, zinc, aluminum and others) appears to be a risk factor for Parkinson’s disease (PD) in some, but not all, case-control studies. These epidemiological studies are reviewed. Several methodological issues that may account for the lack of unanimity of findings are discussed, and suggestions for improved case-control methodology are offered. The study of the neurological disease outcome of workers who have had long-term, well-defined occupational exposure to one or more metals is also urged, with collaborative work including industrial hygienists, occupational toxicologists, neurologists, epidemiologists and biostatisticians. Such efforts, employing state-of-the-art case and control ascertainment and enrollment from suitable population bases, neurological diagnostic rigor and exposure assessment, will help to further define the potentially important roles played by metals in PD and other neurodegenerative disorders.

Gorell JM, Rybicki BA, Cole Johnson C, Peterson EL. Neuroepidemiology. 1999; 18(6):303-8. 10545782 PubMed.

Effects of Metals on the Nervous System of Humans and Animals

Several metals have toxic actions on nerve cells and neurobehavorial functioning. These toxic actions can be expressed either as developmental effects or as an increased risk of neurodegenerative diseases in old age. The major metals causing neurobehavioral effects after developmental exposure are lead and methylmercury. Lead exposure in young children results in a permanent loss of IQ of approximately 5 to 7 IQ points, and also results in a shortened attention span and expression of anti-social behaviors. There is a critical time period (<2 years of age) for development of these effects, after which the effects do not appear to be reversible even if blood lead levels are lowered with chelation. Methylmercury has also been found to have effects on cognition at low doses, and prenatal exposure at higher levels can disrupt brain development. Metals have also been implicated in neurodegenerative diseases, although it is unlikely that they are the sole cause for any of them. Elevated aluminum levels in blood, usually resulting from kidney dialysis at home with well water containing high aluminum, result in dementia that is similar to but probably different from that of Alzheimer’s disease. However, there is some epidemiological evidence for elevated risk of Alzheimer’s in areas where there is high concentration of aluminum in drinking water. Other metals, especially lead, mercury, manganese and copper, have been implicated in amvotrophic lateral sclerosis and Parkinson’s disease.

Carpenter DO. Int J Occup Med Environ Health. 2001; 14(3):209-18. 11764847 PubMed.

Mercury Linked to Alzheimer’s Disease

Research conducted at the University of Calgary Faculty of Medicine has demonstrated that trace amounts of mercury can cause the type of damage to nerves that is characteristic of the damage found in Alzheimer’s Disease. The level of mercury exposure is consistent with those levels found in humans with mercury/silver amalgam dental fillings. The exposure to mercury caused the formation of “neurofibrillar tangles,” which are one of the two diagnostic markers for Alzheimer’s Disease. The scientists found that other metals, including aluminum, did not cause the damage. Previous research has shown that mercury can cause the formation of the other Alzheimer’s Disease diagnostic marker, “amyloid plaques.” In 2000, researchers at the Neurobiology Laboratory, Psychiatric University Hospital in Basel, Switzerland using neuroblastoma cells exposed to mercury demonstrated an increase in production of amyloid protein that makes up the amyloid plaques as well as significantly increasing the phosphorylation of Tau protein.

Leong CW, Syed NI, Lorscheider  FL. University of Calgary Medical School. 26-Mar-2001.