Fluoride Debate: Why I support fluoridation – 2nd response from Connett
This is Paul Connett’s second response to Ken Perrott’s original article – Fluoride debate: Why I support fluoridation In it he is responding to Ken’s article Fluoride Debate: Why I support fluoridation – response to Connett.
I am going to ignore most of the personal criticisms in Ken’s response to my critique of his opening statement and focus largely on the science and scientific studies in question.
Had Ken taken advantage of my sending him the full pdf text of our book he would have quickly seen that the charge he levels at me of selectively using the Li et al (2001) text on bone fractures from China is grossly inaccurate.
Instead of relying on the misleading commentary of pro-fluoridation activist Kurt Ferre, he could have read Chapter 17 of our book (The Case Against Fluoride, CAF), where we covered both parts of Li’s paper. The part Ken and Ferre cover, shows a U-shaped curve for all fractures combined. This shows a minimum for fracture rate at the village at 1 ppm. It could be argued – as Ken does – that at 1 ppm fluoride may confer some benefit in strengthening of elderly bones after a lifetime of exposure. However, such an argument is somewhat muted by the second part of Li’s paper that deals with hip fractures, which is the most critical bone fracture for elderly people, since about half of the elderly never regain an independent existence after such a fracture. In this part of the study there is no U-shape – i.e. no apparent protection offered by fluoride against hip fracture – and the hip fracture prevalence appears to increase in a linear fashion above 1 ppm (actually maybe from 0.25 ppm).
This systematic increase becomes more apparent when one checks our re-plot of the data– see Figure 17.2 on p.179.
Please note I say replot because the graphs provided by Li et al (2001), including the one used by Ken, are not real plots at all. They are only illustrative. The points on the x-axis neither represent an average of the fluoride concentration in each village nor the estimated dose (mg/day) calculated by the authors, the six data points are simply evenly spaced out to illustrate which village is being represented for the fracture data on the y-axis. In the case of Figure 17.1 it makes little difference when one puts in the average dose in mg/day, but in the case of Figure 17.2 it makes a big difference and shows up this “apparent” linear trend more clearly.
While Ken is correct when he says that the only individual village to show a statistically significant increase in hip fractures is village 6, based on our replot the increases in villages 4 and 5 appear to be “real,” even though they are not statistically significant individually. In fact, the data for the whole set of villages appear consistent with a linear regression. Statistical significance is not the final word on whether a data point or data set is real or not. In our view, a linear increase in fracture rate for villages 3 through 6 (and maybe even villages 1-6) looks a more reasonable interpretation of the data than a threshold (i.e. a sudden tripling of the hip fracture rates) at village 6, the interpretation that Ken prefers.
It is unfortunate that Ken uses an inaccurate commentary from Ferre to mischaracterize what we did here.
Nor is it just the bones of the elderly that is in question. I am still waiting to see Ken’s response to the finding in the Schlesinger et al (1956) study of the second fluoridation trial (Newburgh-Kingston, NY, 1945-55) in which they reported a statistically significant increase in the prevalence of cortical bone defects (the ratio was about 2 to 1) in children in the fluoridated community versus the non-fluoridated community. The cortical bone is the outside lamellar structure of the bone whose integrity is important in resisting fractures. We discuss Schlesinger’s work in CAF (p.96).
I am not aware of any health agency in any fluoridated country comparing fracture rates in children in fluoridated versus non-fluoridated communities or even examining fracture rates in children as a function of the severity of dental fluorosis. Scientists did this in Mexico (Alarcón-Herrera et al., 2001) and found an increase in fractures as the severity of dental fluorosis increased (see P.169, CAF). No attempt has been made to reproduce this result or conduct a similar study in any of the fluoridated countries.
As the CDC states the concentration of fluoride delivered by the saliva gland “is not likely to affect cariogenic activity.” However, if it is the fluoride levels reached when fluoridated water has entered the mouth that is the key dynamic for fighting tooth decay, then I think this weakens the need to force people to drink fluoridated water. Maybe we should be suggesting that people swish with fluoridated bottled-water and then spit it out! I also have to wonder why we are giving fluoridated water to babies before their teeth have erupted.
Let me ask for the third time how Ken feels about an alternative delivery system for fluoridated water. This would involve using fluoridated bottled-water in one-liter bottles at 0.7 – 1.2 ppm. These could be made freely available in dental offices (supermarkets, pharmacies or clinics). With this approach one could a) use pharmaceutical grade sodium fluoride; b) could control the dose and c) avoid not forcing it on people who don’t want it. Nor does it involve giving up the central paradigm of the fluoridation program.
As far as the rest of the 2001 CDC quote is concerned I think the Oral Health Division is using a slight of hand here by mixing up a discussion of fluoride in food and water with the fluoride in toothpaste. That 100-1000 fold increase might take place when toothpaste containing 1000 or even 1500 ppm is used but is hardly likely with water at 0.7- 1.2 ppm.
I think the CDC put the “cat among the pigeons” among both fluoridation opponents and proponents when it admitted in 1999 that:
“Fluoride’s caries-preventive properties initially were attributed to changes in enamel during tooth development… However, laboratory and epidemiologic research suggest that fluoride prevents dental caries predominantly after eruption of the tooth into the mouth, and its actions primarily are topical…” (CDC, 1999).
It maybe that the CDC Oral Health Division in its 2001 paper was scrambling to salvage some kind of role for fluoridated water, sufficient to justify continuing its long-time support and promotion of the fluoridation program, despite its admission of the predominance of a topical effect. However, It would have been better if, in 1999, the CDC had changed the focus of its efforts from delivering fluoride systemically to delivering it topically, as well as addressing other key issues of diet, regular brushing and providing early interventions for children of low-income families.
In the latter respect I do not understand why Ken completely ignored the exciting news that I provided from unfluoridated Scotland, where they are having great success with teaching toothbrushing to infants as well providing better diets and earlier interventions.
As far as the mechanisms that Ken offers for a topical benefit derived from fluoridated water directly to the saliva in the mouth (and not via systemic exposure), he discussed “fluoride ions transferring from the water (or food) to saliva (and biofilms on the teeth).”
My experience when drinking water is that it hits the tongue, the back of the top front teeth and the palate before it swiftly goes down the gullet (unless it is deliberately swished). It seems to me that the fluoride ions have little opportunity to form a biofilm on any teeth other than the back of the front teeth. Nor is there much time to mix with the saliva. But this is only conjecture based on simple personal observations on my part and if Ken has a study that shows the level of fluoride in the saliva is dramatically increased immediately after someone has swallowed a glass of water that would be very helpful.
Yes, there are weaknesses in many of these IQ studies but the greatest “weakness” is the fact that countries that practice water fluoridation have made virtually no attempt to reproduce them or pursue the matter in any way. That is why, as Ken complains, I have not quoted studies from a wider range of countries: apart from a small early study in NZ (Shannon et al., 1986) and small behavioral study in the US (Warren et al., 1998) there aren’t any. At the very least these studies from China, India, Iran and Mexico represent a serious red flag on this practice and the health agencies in fluoridated countries are ignoring this red flag.
In his further attempt to downplay Xiang’s 2003 study Ken asks
“Why did the authors choose to publish in the journal “Fluoride?” It is certainly not considered of high quality. It is actually rather suspect because of the ideological committment of the editors. This gives the impression that even suspect papers will be published if the story is right.”
I discuss these derogatory comments about Fluoride and its editors, and the double standard that Ken and other proponents of fluoridation exercise on this matter below, here I would like to discuss more about Xiang’s work.
That being said if Ken is going to make judgments based on what journal the article appears in, then he might be interested by the fact that in 2010 Xiang et al submitted an updated version of their work to one of the leading environmental health journals, Environmental Health Perspectives, which is published by the National Institute of Environmental Health Sciences (NIEHS) a division of the National Institute of Health (NIH). After peer review this journal agreed to publish Xiang’s work and posted a pre-publication copy on the internet (see Xiang et al., 2010).
However, Xiang was asked to withdraw his article for the technical reason that some of the material had already been published by this team (and that was the Fluoride article from 2003). But the key fact from the point of view of this discussion is that despite Ken’s criticisms Xiang’s work was peer-reviewed by this prestigious journal and was found acceptable for publication.
The update from Xiang was very important for this discussion and it is a pity that this was withheld from the mainstream scientific community. Xiang found that the lowering of IQ in his study correlated with the fluoride levels in the children’s plasma. This greatly strengthens Xiang’s finding by moving from a population (or ecological) study closer to a study based on individual exposure. Xiang finally published this part of his finding in Fluoride (Xiang et al., 2011).
Despite all of this, Ken considers Xiang’s paper “a minor piece of evidence” and argues that,
So when Ken argues that “Papers are selected and then values are pulled out of them to make assertions or claims that really are not warranted – and certainly not by a balanced reading of the literature.”
I must ask Ken what “balanced reading of the literature” on fluoride’s potential to damage the brain are you talking about? I have cited a large body of work and it almost all goes in one direction: fluoride is a potent neurotoxicant. Can you cite an extensive body of literature Ken that points in the opposite direction?
In fact the scientist who published one of the earliest animals studies on fluoride and animal behavior, Dr. Phyllis Mullenix, was fired after her paper was accepted for publication (Mullenix et al., 1995). Mullenix was the chairperson of the first toxicology department in any dental school in the US. She was hired specifically to look at the neurological effects of the chemicals used in dentistry. However, when she found changes in animal behavior related to fluoride exposure and published it, she was told that her work was “no longer relevant to dentistry.” I would argue that her work conflicted with dental establishment’s determination to continue the fluoridation program at all costs. The treatment meted out to Mullenix did not go unnoticed by members of the research community, who have treated doing research on fluoride like touching the third rail as far their careers were concerned.
In addition to their lack of interest in pursuing the lowering of IQ, neither health agencies nor those “highly qualified scientists” Ken talks about, have been inclined to fully investigate many other serious concerns such as lowered thyroid function, accumulation in the pineal gland (Luke 1997, 2001), arthritis rates in fluoridated populations, bone fractures in children (discussed above), earlier onset of puberty, behavioral problems in children and the plight of those who claim to be highly sensitive to fluoride’s toxicity.
All these concerns cry out for attention and certainly the attention of those critical of the epidemiology of studies conducted in those countries that are investigating some of these issues because they are legitimately concerned about what naturally fluoridated water is doing to their citizens. I have expressed my own thoughts on the reason for this lack of attention, but I would be interested in Ken’s thoughts on this overwhelming lack of scientific interest in investigating fluoridation’s potential health effects in the many years since the US Public Health Service endorsed fluoridation in 1950? Why in fluoridated countries are we getting an endless stream of studies on teeth but virtually none on other tissues in the body?
“A few epidemiologic studies of Chinese populations have reported IQ deficits in children exposed to fluoride at 2.5 to 4 mg/L in drinking water. Although the studies lacked sufficient detail for the committee to fully assess their quality and relevance to U.S. populations, the consistency of the results appears significant enough to warrant additional research on the effects of fluoride on intelligence.” p.8
(Note from PC: this comment was based on a review of only five of these IQ studies, there have now been 42.)
“On the basis of information largely derived from histological, chemical, and molecular studies, it is apparent that fluorides have the ability to interfere with the functions of the brain and the body by direct and indirect means.” p.222
“histopathological changes similar to those traditionally associated with Alzheimer’s disease in people have been seen in rats chronically exposed to AlF.” p.212
“Fluorides also increase the production of free radicals in the brain through several different biological pathways. These changes have a bearing on the possibility that fluorides act to increase the risk of developing Alzheimer’s disease.” p.222
“More research is needed to clarify fluoride’s biochemical effects onthe brain.” p.222
“The possibility has been raised by the studies conducted in China that fluoride can lower intellectual abilities. Thus, studies of populations exposed to different concentrations of fluoride in drinking water should include measurements of reasoning ability, problem solving, IQ, and short- and long-term memory.” p.223
“Studies of populations exposed to different concentrations of fluoride should be undertaken to evaluate neurochemical changes that may be associated with dementia. Consideration should be given to assessing effects from chronic exposure, effects that might be delayed or occur late-in-life, and individual susceptibility.” p.223
EPA researchers listed fluoride among those chemicals for which there was “substantial evidence of developmental neurotoxicity” (W. Mundy et al. http://www.epa.gov/ncct/toxcast/files/summit/48P%20Mundy%20TDAS.pdf
The EPA headquarters scientists made this request to the U.S. Senate in 2000 (Hirzy 2000):
“We ask that you order an epidemiology study comparing children with dental fluorosis to those not displaying (fluoride) overdose during growth and development years for behavioral and other disorders.”
And according to Dr. Philippe Grandjean, one of the authors of the Choi et al (2012) study:
Meanwhile, according to my son Michael Connett, who is the special project director at FAN, and compiled FAN’s Health Database, research on fluoride and the brain in animals has been rolling in at a steady pace over the past year — with over a dozen new studies, including some at notably low doses. One such study that is worthy to have on the radar is a study on mice by Liu et al, 2013. It reports that exposure to fluoride in drinking water (at 5 and 10 ppm) 4 weeks after weaning not only impaired cognition, but caused “anxiety- and depression-like behavior” as well. Here’s an excerpt from the discussion:
Even if this had been a strong animal study, it is one of a small minority that found no evidence of neurotoxicity of fluoride. So, taking the scientific evidence on this topic as a whole, the weight of evidence from both animal and human studies is that fluoride is a developmental neurotoxicant.
Why is it Ken you see proponents’ support of fluoridation as being “scientific” and opponents’ opposition to fluoridation as being “ideological”? Isn’t it possible that opponents of fluoridation are opposed for scientific reasons?
Fluoride is the only journal in the world, which is completely devoted to research on fluoride in many different areas of study (geological, biological, biochemical, toxicological, epidemiological, medical and dental to name a few). To its discredit the US National Institute of Health (NIH) has refused to cover the contents of this journal in PubMed, thus depriving many researchers valuable information on fluoride’s toxicity. This has been particularly true of depriving the mainstream medical community (many of whom use PubMed as their primary research tool) knowing about the extensive database indicating that fluoride is a neurotoxicant. It has done this despite covering the contents of far lesser journals and even trade magazines.
There have been three editors of Fluoride since it began its quarterly publication in 1968: Dr. George Waldbott, Dr. John Colquhoun and Dr. Albert Burgstahler (who passed away a few weeks ago). You would be correct in asserting that each of these editors was opposed to fluoridation, however that opposition was rooted in science not some ill-defined ideology. I think you can get a glimpse of the caliber of both Dr. George Waldbott and Professor Albert Burgstahler in the book they co-authored “Fluoridation: The Great Dilemma.” (Coronado Press, Lawrence, Kansas, 1978).
I met Dr. John Colquhoun (briefly before he died in 1998) and videotaped an interview with him during to trip to NZ. I count this interview one of the great moments of my scientific career. Never have I been more impressed by someone’s character than I was by John. He had been an avid promoter of fluoridation both as the chief dental officer of Auckland and as a city councilor. When during a world tour in 1980 (he went to Australia, Asia, North America and Europe) he found that talking behind the scenes to leading dental researchers that they were not finding much of difference between tooth decay in fluoridated and non-fluoridated communities and found the same in “confidential reports” from the NZ dental authorities on his return, he had the enormous courage and scientific integrity to come out publicly against water fluoridation and spent the rest of his life trying to right the wrong he had done. But while he was at the reins he never hesitated to allow pro-fluoridation voices and articles to be published in Fluoride.
I worked with professor Albert Burgstahler for many years and I can vouch for his scientific integrity. In fact for me he represented one of the pinnacles of scientific integrity and that is why FAN named an annual award in his name.
I never met Dr. Waldbott, but I know that his position was that neither the journal nor its supporting organization (the International Society for Fluoride Research, ISFR) should adopt a formal opposition to fluoridation (and its membership included both pro and anti-fluoridation scientists), but to publish as much science as they could on the subject – and as far as water fluoridation was concerned from both sides – and to let the chips fall where they may. He and his successors also believed that if the science was aired fully and openly it would lead most independent scientists to an anti-fluoridation position.
I should also point out that there have been several occasions where dental journals have gone out of their way to publish papers that have provided an “ideological” as opposed to a “scientific” support for one side of a controversial matter. Take the example of osteosarcoma. In 1991, shortly after the 1990 NTP animal study had found an association in male rats between fluoride exposure and osteosarcoma, the Journal of the American Dental Association (JADA) rushed to give prominence (i.e. the front cover was devoted to it) to an article, in which the authors clearly reveal their bias in favor of fluoridation. In this very small epidemiological study they proposed that far from causing osteosarcoma fluoride was actually protective against it (see P.187 in The Case Against Fluoride, CAF).
I think the following comments reveal a greater sensitivity to the need to protect the fluoridation program than protecting a few young boys from a life threatening disease:
“An incorrect inference implicating systemic fluoride carcinogenicity and its removal from our water systems would be detrimental to the oral health of most Americans, particularly those who cannot afford to pay for increasingly expensive restorative dental care . . .Because of its strengthening action, fluoride has been widely accepted as the responsible agent for the dramatic declines in the tooth decay rates of U.S. children and adolescents . . . A disruption in the delivery of fluoride through municipal water systems would increase decay rates over time . . . Linking of fluoride ingestion and cancer initiation could result in a large-scale defluoridation of municipal water systems under the Delaney clause. (McGuire et al., 1991, quoted on p. 187, CAF).
In my view the commentary (above) plus the JADA editors’ choice to give it this article full-front page coverage is an example of “ideology” not science at work. The authors and the journal both had a need to protect the fluoridation program at all costs – even if it meant downplaying the concerns about the fate of the young boys in question. I will pick up the osteosarcoma story again in a later submission.
http://www.fluorideresearch.org/342/files/FJ2001_v34_n2_p139-149fig.pdf
CDC, 1999. Centers for Disease Control and Prevention, “Achievements in Public Health, 1900–1999: Fluoridation of Drinking Water to Prevent Dental Caries,” Mortality and Morbidity Weekly Review 48, no. 41 (October 22, 1999): 933–40, http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4841a1.htm
CDC, 2001. Centers for Disease Control and Prevention, “Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States,” Morbidity and Mortality Weekly Report 50, no. RR14 (August 17, 2001): 1–42, http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5014a1.htm
Choi AL, Sun G, Zhang Y, Grandjean P. 2012. Developmental fluoride neurotoxicity: a systematic review and meta-analysis. Environ Health Perspect 120:1362–1368.
Connett, P., Beck, J and Micklem HS. The Case Against Fluoride. Chelsea Green, White River Junction, Vermont, 2010.
Harvard School of Public Health. (2012). Impact of fluoride on neurological development in children. July 25. Available online at: http://www.hsph.harvard.edu/news/features/fluoride-childrens-health-grandjean-choi/
Hirzy, 2000. Statement of Dr. J. William Hirzy, National Treasury Employees Union Chapter 280 before the Subcommittee on Wildlife,
Fisheries and Drinking Water, United States Senate. June 29, 2000.
Li, Y et al., 2001. “Effect of Long-Term Exposure to Fluoride in
Drinking Water on Risks of Bone Fractures,” Journal of Bone and Mineral Research 16, no. 5 (2001): 932–39.
Liu F. et al., 2013 (online) (hard copy 2014). “Fluoride exposure during development affects both cognition and emotion in mice.” Physiology & Behavior 124 (2014) 1–7.
Luke, J, 1997, “The Effect of Fluoride on the Physiology of the Pineal Gland,” PhD thesis, University of Surrey, Guildford, UK, 1997. Excerpts at http://fluoridealert.org/studies/luke-1997/ and a complete copy of Dr. Luke’s dissertation can be downloaded at http://www.fluoridealert.org/wp-content/uploads/luke-1997.pdf (with the author’s permission).
Luke, J, 2001. “Fluoride Deposition in the Aged Human Pineal Gland,” Caries Research 35, no. 2 (2001): 125–28.
McDonagh et al., 2000. “Systematic Review of Water Fluoridation,” British Medical Journal 321, no. 7265 (2000): 855–59, http://www.bmj.com/cgi/content/full/321/7265/855 Note: The full report that this paper summarizes is commonly known as the York Review and is accessible at http://fluoridealert.org/re/york.review.2000.pdf
McGuire et al, 1991. “Is There a Link between Fluoridated Water and Osteosarcoma?” Journal of the American Dental Association 122, no. 4 (1991): 38–45.
Mullenix, PJ et al., 1995. “Neurotoxicity of Sodium Fluoride in Rats,” Neurotoxicology and Teratology 17, no. 2 (1995): 169–77.
Morgan, L. et al. 1998, “Investigation of the Possible Associations between Fluorosis, Fluoride Exposure, and Childhood Behavior Problems,” Pediatric Dentistry 20, no. 4 (1998): 244–52.
NRC, 2006. Fluoride in Drinking Water: A Scientific Review of EPA’s Standards (2006) http://www.nap.edu/catalog.php?record_id=11571
NTP, 1990. National Toxicology Program, “NTP Technical Report on the Toxicology and Carcinogenesis Studies of Sodium Fluoride (CAS no. 7682-49-4) in F344/N Rats and B6C3F1 (Drinking Water Studies),” Technical Report 393, NIH publ. no. 91-2848, National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services, Research Triangle Park, NC, 1990.
E. R. Schlesinger, D. E. Overton, H. C. Chase, and K. T. Cantwell, “Newburgh-Kingston Caries-Fluorine Study XIII. Pediatric Findings After Ten Years,” Journal of the American Dental Association 52, no. 3 (1956): 296–306.
Shannon, FT et al., 1986. “Exposure to Fluoridated Water Supplies and Child Behaviour,” New Zealand Medical Journal 99, no. 803 (1986):416–18.
Waldbott, GL, Burgstahler,AW and H. L. McKinney, Fluoridation: The Great Dilemma (Lawrence, Kansas: Coronado Press, 1978).
Whitford, GM et al. 2009. “Appetitive-based Learning in Rats: Lack of Effect of Chronic Exposure to Fluoride,” Neurotoxicology and Teratology 31, no. 4 (2009): 210–15.
Q. Xiang, Y. Liang, L. Chen, et al., “Effect of Fluoride in Drinking Water on Children’s Intelligence,” Fluoride 36, no. 2 (2003): 84–94, http://www.fluorideresearch.org/362/files/FJ2003_v36_n2_p84-94.pdf
Q. Xiang, Y. Liang, M. Zhou, and H. Zang, “Blood Lead of Children in Wamiao-Xinhuai Intelligence Study” (letter), Fluoride 36, no. 3 (2003):198–99, http://www.fluorideresearch.org/363/files/FJ2003_v36_n3_p198-199.pdf
Xiang, Q. et al., 2010. “Serum Fluoride Level and Children’s Intelligence Quotient in Two Villages in China.” Environmental Health Perspectives. EHPonline.org
Xiang, Q. et al. 2011. “Analysis of children’s serum fluoride in relation to intelligence scores in a high and low fluoride village in China.” http://www.fluorideresearch.org/444/files/FJ2011_v44_n4_p191-194_sfs.pdf
Anyone wanting to follow the debate and/or check back over previous articles in the debate can find the list of articles at Fluoride Debate.
See also:
Similar articles on fluoridation
Making sense of fluoride Facebook page
I am going to ignore most of the personal criticisms in Ken’s response to my critique of his opening statement and focus largely on the science and scientific studies in question.
1. Different interpretations of the Li et al. (2001) paper
I am very familiar with the Li et al. (2001) paper on bone fractures in the elderly in six Chinese villages with fluoride concentrations in well water ranging from about 0.25 to 8 ppm. In fact, I reviewed a pre-publication copy of this paper sent to me by the lead author as part of my invited peer review of the York Report (McDonagh et a., 2000).Had Ken taken advantage of my sending him the full pdf text of our book he would have quickly seen that the charge he levels at me of selectively using the Li et al (2001) text on bone fractures from China is grossly inaccurate.
Instead of relying on the misleading commentary of pro-fluoridation activist Kurt Ferre, he could have read Chapter 17 of our book (The Case Against Fluoride, CAF), where we covered both parts of Li’s paper. The part Ken and Ferre cover, shows a U-shaped curve for all fractures combined. This shows a minimum for fracture rate at the village at 1 ppm. It could be argued – as Ken does – that at 1 ppm fluoride may confer some benefit in strengthening of elderly bones after a lifetime of exposure. However, such an argument is somewhat muted by the second part of Li’s paper that deals with hip fractures, which is the most critical bone fracture for elderly people, since about half of the elderly never regain an independent existence after such a fracture. In this part of the study there is no U-shape – i.e. no apparent protection offered by fluoride against hip fracture – and the hip fracture prevalence appears to increase in a linear fashion above 1 ppm (actually maybe from 0.25 ppm).
This systematic increase becomes more apparent when one checks our re-plot of the data– see Figure 17.2 on p.179.
Please note I say replot because the graphs provided by Li et al (2001), including the one used by Ken, are not real plots at all. They are only illustrative. The points on the x-axis neither represent an average of the fluoride concentration in each village nor the estimated dose (mg/day) calculated by the authors, the six data points are simply evenly spaced out to illustrate which village is being represented for the fracture data on the y-axis. In the case of Figure 17.1 it makes little difference when one puts in the average dose in mg/day, but in the case of Figure 17.2 it makes a big difference and shows up this “apparent” linear trend more clearly.
While Ken is correct when he says that the only individual village to show a statistically significant increase in hip fractures is village 6, based on our replot the increases in villages 4 and 5 appear to be “real,” even though they are not statistically significant individually. In fact, the data for the whole set of villages appear consistent with a linear regression. Statistical significance is not the final word on whether a data point or data set is real or not. In our view, a linear increase in fracture rate for villages 3 through 6 (and maybe even villages 1-6) looks a more reasonable interpretation of the data than a threshold (i.e. a sudden tripling of the hip fracture rates) at village 6, the interpretation that Ken prefers.
It is unfortunate that Ken uses an inaccurate commentary from Ferre to mischaracterize what we did here.
2. Other studies of fluoride and the bone
However, there is a great deal of literature available on fluoride’s impact on the bone (see the references to Chapter 17, CAF). Ken will need more than the Li et al (2001) paper to establish that there is an overall benefit to the elderly bone when people are exposed for a lifetime to an approximate ten-fold increased exposure to fluoride via artificially fluoridated water. This is especially true for people with poor kidney function and high water drinkers (miners in Western Australia drink between 10 and 12 liters of water a day). Can you provide more studies that support the possibility that fluoride protects the elderly bone Ken?Nor is it just the bones of the elderly that is in question. I am still waiting to see Ken’s response to the finding in the Schlesinger et al (1956) study of the second fluoridation trial (Newburgh-Kingston, NY, 1945-55) in which they reported a statistically significant increase in the prevalence of cortical bone defects (the ratio was about 2 to 1) in children in the fluoridated community versus the non-fluoridated community. The cortical bone is the outside lamellar structure of the bone whose integrity is important in resisting fractures. We discuss Schlesinger’s work in CAF (p.96).
I am not aware of any health agency in any fluoridated country comparing fracture rates in children in fluoridated versus non-fluoridated communities or even examining fracture rates in children as a function of the severity of dental fluorosis. Scientists did this in Mexico (Alarcón-Herrera et al., 2001) and found an increase in fractures as the severity of dental fluorosis increased (see P.169, CAF). No attempt has been made to reproduce this result or conduct a similar study in any of the fluoridated countries.
3. Fluoride’s topical action and saliva
As far as the mechanism of fluoride’s topical mechanism on the teeth is concerned, Ken quotes the CDC from 2001,” . . drinking fluoridated water, brushing with fluoride toothpaste, or using other fluoride dental products can raise the concentration of fluoride in saliva present in the mouth 100-to 1,000-fold. The concentration returns to previous levels within 1–2 hours but, during this time, saliva serves as an important source of fluoride for concentration in plaque and for tooth remineralization.”I went back to this CDC Oral Health Division statement from 2001 and found the sentences that preceded Ken’s quote most revealing. These preceding sentences read:
“Saliva is a major carrier of topical fluoride. The concentration of fluoride in ductal saliva, as it is secreted from salivary glands, is low – approximately 0.016 parts per million (ppm) in areas where drinking water is fluoridated and 0.006 ppm in nonfluoridated areas (27). This concentration of fluoride is not likely to affect cariogenic activity. However, drinking fluoridated water, brushing with fluoride toothpaste…These few sentences further strengthen Ken’s arguments that it is fluoride delivered directly into the mouth that provides the saliva with concentrations, which may or may not do something and not, the meager concentrations reached systemically through the salivary gland, a position I erroneously attributed to him. My apologies.
As the CDC states the concentration of fluoride delivered by the saliva gland “is not likely to affect cariogenic activity.” However, if it is the fluoride levels reached when fluoridated water has entered the mouth that is the key dynamic for fighting tooth decay, then I think this weakens the need to force people to drink fluoridated water. Maybe we should be suggesting that people swish with fluoridated bottled-water and then spit it out! I also have to wonder why we are giving fluoridated water to babies before their teeth have erupted.
Let me ask for the third time how Ken feels about an alternative delivery system for fluoridated water. This would involve using fluoridated bottled-water in one-liter bottles at 0.7 – 1.2 ppm. These could be made freely available in dental offices (supermarkets, pharmacies or clinics). With this approach one could a) use pharmaceutical grade sodium fluoride; b) could control the dose and c) avoid not forcing it on people who don’t want it. Nor does it involve giving up the central paradigm of the fluoridation program.
As far as the rest of the 2001 CDC quote is concerned I think the Oral Health Division is using a slight of hand here by mixing up a discussion of fluoride in food and water with the fluoride in toothpaste. That 100-1000 fold increase might take place when toothpaste containing 1000 or even 1500 ppm is used but is hardly likely with water at 0.7- 1.2 ppm.
I think the CDC put the “cat among the pigeons” among both fluoridation opponents and proponents when it admitted in 1999 that:
“Fluoride’s caries-preventive properties initially were attributed to changes in enamel during tooth development… However, laboratory and epidemiologic research suggest that fluoride prevents dental caries predominantly after eruption of the tooth into the mouth, and its actions primarily are topical…” (CDC, 1999).
It maybe that the CDC Oral Health Division in its 2001 paper was scrambling to salvage some kind of role for fluoridated water, sufficient to justify continuing its long-time support and promotion of the fluoridation program, despite its admission of the predominance of a topical effect. However, It would have been better if, in 1999, the CDC had changed the focus of its efforts from delivering fluoride systemically to delivering it topically, as well as addressing other key issues of diet, regular brushing and providing early interventions for children of low-income families.
In the latter respect I do not understand why Ken completely ignored the exciting news that I provided from unfluoridated Scotland, where they are having great success with teaching toothbrushing to infants as well providing better diets and earlier interventions.
As far as the mechanisms that Ken offers for a topical benefit derived from fluoridated water directly to the saliva in the mouth (and not via systemic exposure), he discussed “fluoride ions transferring from the water (or food) to saliva (and biofilms on the teeth).”
My experience when drinking water is that it hits the tongue, the back of the top front teeth and the palate before it swiftly goes down the gullet (unless it is deliberately swished). It seems to me that the fluoride ions have little opportunity to form a biofilm on any teeth other than the back of the front teeth. Nor is there much time to mix with the saliva. But this is only conjecture based on simple personal observations on my part and if Ken has a study that shows the level of fluoride in the saliva is dramatically increased immediately after someone has swallowed a glass of water that would be very helpful.
4. The work of Xiang et al (2003) on IQ
Ken suggests that I am “cherry picking” the data by “singly pulling out the Xiang et al. study from 2003.” In actuality, I gave that as a specific example of a human study where effects were found at concentrations very close to the level at which we artificially fluoridate (0.7 to 1.2 ppm). This was in response to Ken’s claim that he was not impressed by all the high concentration animal studies that have found fluoride causes harm. I cited Xiang in the larger context of 37 (out of 46 human studies that have found an association between fluoride exposure and lowered IQ.) These studies come from India, Iran, Mexico and China, with the majority coming from China. 27 of them were reviewed by a Harvard team (Choi et al., 2012). Of these 27 studies 26 found a lowering of IQ (average of 7 IQ points). These results are remarkably consistent even though they have been performed in several different countries and many different parts of China. However, proponents of fluoridation have dismissed them on the basis that in two of these studies the range in the high fluoride village went up to 11.5 ppm. However, I pointed out that nine of the studies found a lowering of IQ at or less than 3 ppm, which offers no adequate margin of safety for a whole population drinking water in the range 0.7 to 1.2 ppm. So I wasn’t cherry picking here. We have to see Xiang’s work in the context of all these other studies as well as the other studies that show that fluoride is a neurotoxicant (discussed below). I chose Xiang’s study because it is one of the better studies. It controlled for more potential co-founders than others (including lead and iodine intake). Recently, Xiang has confirmed that as far as arsenic was concerned there were higher levels in the low fluoride village, so clearly arsenic was not a factor in the lower IQs found in the high fluoride village.Yes, there are weaknesses in many of these IQ studies but the greatest “weakness” is the fact that countries that practice water fluoridation have made virtually no attempt to reproduce them or pursue the matter in any way. That is why, as Ken complains, I have not quoted studies from a wider range of countries: apart from a small early study in NZ (Shannon et al., 1986) and small behavioral study in the US (Warren et al., 1998) there aren’t any. At the very least these studies from China, India, Iran and Mexico represent a serious red flag on this practice and the health agencies in fluoridated countries are ignoring this red flag.
In his further attempt to downplay Xiang’s 2003 study Ken asks
“Why did the authors choose to publish in the journal “Fluoride?” It is certainly not considered of high quality. It is actually rather suspect because of the ideological committment of the editors. This gives the impression that even suspect papers will be published if the story is right.”
I discuss these derogatory comments about Fluoride and its editors, and the double standard that Ken and other proponents of fluoridation exercise on this matter below, here I would like to discuss more about Xiang’s work.
5. Xiang and the journal Environmental Health Perspectives
Xiang almost certainly chose to publish in the journal Fluoride because it has probably given more coverage to the possibility that fluoride affects the brain of animals and lowers IQ in humans than any other journal in the world.That being said if Ken is going to make judgments based on what journal the article appears in, then he might be interested by the fact that in 2010 Xiang et al submitted an updated version of their work to one of the leading environmental health journals, Environmental Health Perspectives, which is published by the National Institute of Environmental Health Sciences (NIEHS) a division of the National Institute of Health (NIH). After peer review this journal agreed to publish Xiang’s work and posted a pre-publication copy on the internet (see Xiang et al., 2010).
However, Xiang was asked to withdraw his article for the technical reason that some of the material had already been published by this team (and that was the Fluoride article from 2003). But the key fact from the point of view of this discussion is that despite Ken’s criticisms Xiang’s work was peer-reviewed by this prestigious journal and was found acceptable for publication.
The update from Xiang was very important for this discussion and it is a pity that this was withheld from the mainstream scientific community. Xiang found that the lowering of IQ in his study correlated with the fluoride levels in the children’s plasma. This greatly strengthens Xiang’s finding by moving from a population (or ecological) study closer to a study based on individual exposure. Xiang finally published this part of his finding in Fluoride (Xiang et al., 2011).
Despite all of this, Ken considers Xiang’s paper “a minor piece of evidence” and argues that,
“it should be objectively considered together with all other publications in this area of research. The fact that it is taken in isolation (except for a few other low quality Chinese studies), and nothing of higher quality or from different regions is considered, makes me suspicious. After all, a number of countries with highly qualified scientists (and activists claiming negative effects) have had many years to look at possible health effects from fluoridation. The fact that more credible papers are not produced is hardly good evidence for the claims made by anti-fluoride activists. Why would they rely on low quality research if better research supporting their claims was available?”First of all, I argue that this study by Xiang is part of a large body of work that indicates that fluoride can damage the brain and I have summarized this large body of work previously (and it can be found at www.FluorideAlert.org/issues/health/brain )
So when Ken argues that “Papers are selected and then values are pulled out of them to make assertions or claims that really are not warranted – and certainly not by a balanced reading of the literature.”
I must ask Ken what “balanced reading of the literature” on fluoride’s potential to damage the brain are you talking about? I have cited a large body of work and it almost all goes in one direction: fluoride is a potent neurotoxicant. Can you cite an extensive body of literature Ken that points in the opposite direction?
6. Fluoridated countries are not doing studies on key health concerns
Sadly, as I have already indicated the health agencies in those countries that support and promote fluoridation show absolutely no inclination to study their populations with respect to this effect, i.e. lowered IQ.In fact the scientist who published one of the earliest animals studies on fluoride and animal behavior, Dr. Phyllis Mullenix, was fired after her paper was accepted for publication (Mullenix et al., 1995). Mullenix was the chairperson of the first toxicology department in any dental school in the US. She was hired specifically to look at the neurological effects of the chemicals used in dentistry. However, when she found changes in animal behavior related to fluoride exposure and published it, she was told that her work was “no longer relevant to dentistry.” I would argue that her work conflicted with dental establishment’s determination to continue the fluoridation program at all costs. The treatment meted out to Mullenix did not go unnoticed by members of the research community, who have treated doing research on fluoride like touching the third rail as far their careers were concerned.
In addition to their lack of interest in pursuing the lowering of IQ, neither health agencies nor those “highly qualified scientists” Ken talks about, have been inclined to fully investigate many other serious concerns such as lowered thyroid function, accumulation in the pineal gland (Luke 1997, 2001), arthritis rates in fluoridated populations, bone fractures in children (discussed above), earlier onset of puberty, behavioral problems in children and the plight of those who claim to be highly sensitive to fluoride’s toxicity.
All these concerns cry out for attention and certainly the attention of those critical of the epidemiology of studies conducted in those countries that are investigating some of these issues because they are legitimately concerned about what naturally fluoridated water is doing to their citizens. I have expressed my own thoughts on the reason for this lack of attention, but I would be interested in Ken’s thoughts on this overwhelming lack of scientific interest in investigating fluoridation’s potential health effects in the many years since the US Public Health Service endorsed fluoridation in 1950? Why in fluoridated countries are we getting an endless stream of studies on teeth but virtually none on other tissues in the body?
7. What other authorities are saying about fluoride as a neurotoxicant
Meanwhile, I am not the only scientist who is expressing concerns about fluoride’s neurological affects. According to the report by US National Research Council (NRC, 2006):“A few epidemiologic studies of Chinese populations have reported IQ deficits in children exposed to fluoride at 2.5 to 4 mg/L in drinking water. Although the studies lacked sufficient detail for the committee to fully assess their quality and relevance to U.S. populations, the consistency of the results appears significant enough to warrant additional research on the effects of fluoride on intelligence.” p.8
(Note from PC: this comment was based on a review of only five of these IQ studies, there have now been 42.)
“On the basis of information largely derived from histological, chemical, and molecular studies, it is apparent that fluorides have the ability to interfere with the functions of the brain and the body by direct and indirect means.” p.222
“histopathological changes similar to those traditionally associated with Alzheimer’s disease in people have been seen in rats chronically exposed to AlF.” p.212
“Fluorides also increase the production of free radicals in the brain through several different biological pathways. These changes have a bearing on the possibility that fluorides act to increase the risk of developing Alzheimer’s disease.” p.222
“More research is needed to clarify fluoride’s biochemical effects onthe brain.” p.222
“The possibility has been raised by the studies conducted in China that fluoride can lower intellectual abilities. Thus, studies of populations exposed to different concentrations of fluoride in drinking water should include measurements of reasoning ability, problem solving, IQ, and short- and long-term memory.” p.223
“Studies of populations exposed to different concentrations of fluoride should be undertaken to evaluate neurochemical changes that may be associated with dementia. Consideration should be given to assessing effects from chronic exposure, effects that might be delayed or occur late-in-life, and individual susceptibility.” p.223
EPA researchers listed fluoride among those chemicals for which there was “substantial evidence of developmental neurotoxicity” (W. Mundy et al. http://www.epa.gov/ncct/toxcast/files/summit/48P%20Mundy%20TDAS.pdf
The EPA headquarters scientists made this request to the U.S. Senate in 2000 (Hirzy 2000):
“We ask that you order an epidemiology study comparing children with dental fluorosis to those not displaying (fluoride) overdose during growth and development years for behavioral and other disorders.”
And according to Dr. Philippe Grandjean, one of the authors of the Choi et al (2012) study:
“Fluoride seems to fit in with lead, mercury, and other poisons that cause chemical brain drain. The effect of each toxicant may seem small, but the combined damage on a population scale can be serious, especially because the brain power of the next generation is crucial to all of us.” (Harvard Press Release)As such it seems reckless to me – and many others – that we should knowingly increase the whole population’s exposure to this neurotoxicant by putting it into the public water supply.
Meanwhile, according to my son Michael Connett, who is the special project director at FAN, and compiled FAN’s Health Database, research on fluoride and the brain in animals has been rolling in at a steady pace over the past year — with over a dozen new studies, including some at notably low doses. One such study that is worthy to have on the radar is a study on mice by Liu et al, 2013. It reports that exposure to fluoride in drinking water (at 5 and 10 ppm) 4 weeks after weaning not only impaired cognition, but caused “anxiety- and depression-like behavior” as well. Here’s an excerpt from the discussion:
“Almost all existing epidemiological surveys on areas with high-fluoride drinking water have focused on cognition; however, our data suggest the need for a large-scale epidemiological survey to investigate whether drinking water with high levels of fluoride can lead to human emotional behavior changes. In summary, we found developmental fluoride exposure through drinking water 1) caused cognitive impairment and 2) led to anxiety- and depression-like behavior in adult mice. Therefore, consideration should be given to the neurotoxicity of fluoride used to combat dental caries, and attention should be paid to the concentration and dosage of fluoride, especially in young children. Our data suggest that excessive fluoride intake should be avoided to prevent its adverse effects.”So the weight of evidence that fluoride impacts both the brain of animal and humans keeps piling up. About the only animal study that proponents can produce that has not found an effect is one performed by Whitford et al., 2009, who used behavioral tests on rats. They found no neurotoxic effects in their study setting. The study is limited because the rats were not dosed in utero or even during earliest post-natal development, but only after they had been weaned, which roughly translates to adolescence in rats.
Even if this had been a strong animal study, it is one of a small minority that found no evidence of neurotoxicity of fluoride. So, taking the scientific evidence on this topic as a whole, the weight of evidence from both animal and human studies is that fluoride is a developmental neurotoxicant.
8. The journal Fluoride and the ISFR
In his commentary on Xiang’s IQ paper Ken chose to do what a number of proponents of fluoridation do and that is to try and trash the journal Fluoride. He claims that Fluoride “is certainly not considered of high quality. It is actually rather suspect because of the ideological commitment of the editors.”Why is it Ken you see proponents’ support of fluoridation as being “scientific” and opponents’ opposition to fluoridation as being “ideological”? Isn’t it possible that opponents of fluoridation are opposed for scientific reasons?
Fluoride is the only journal in the world, which is completely devoted to research on fluoride in many different areas of study (geological, biological, biochemical, toxicological, epidemiological, medical and dental to name a few). To its discredit the US National Institute of Health (NIH) has refused to cover the contents of this journal in PubMed, thus depriving many researchers valuable information on fluoride’s toxicity. This has been particularly true of depriving the mainstream medical community (many of whom use PubMed as their primary research tool) knowing about the extensive database indicating that fluoride is a neurotoxicant. It has done this despite covering the contents of far lesser journals and even trade magazines.
There have been three editors of Fluoride since it began its quarterly publication in 1968: Dr. George Waldbott, Dr. John Colquhoun and Dr. Albert Burgstahler (who passed away a few weeks ago). You would be correct in asserting that each of these editors was opposed to fluoridation, however that opposition was rooted in science not some ill-defined ideology. I think you can get a glimpse of the caliber of both Dr. George Waldbott and Professor Albert Burgstahler in the book they co-authored “Fluoridation: The Great Dilemma.” (Coronado Press, Lawrence, Kansas, 1978).
I met Dr. John Colquhoun (briefly before he died in 1998) and videotaped an interview with him during to trip to NZ. I count this interview one of the great moments of my scientific career. Never have I been more impressed by someone’s character than I was by John. He had been an avid promoter of fluoridation both as the chief dental officer of Auckland and as a city councilor. When during a world tour in 1980 (he went to Australia, Asia, North America and Europe) he found that talking behind the scenes to leading dental researchers that they were not finding much of difference between tooth decay in fluoridated and non-fluoridated communities and found the same in “confidential reports” from the NZ dental authorities on his return, he had the enormous courage and scientific integrity to come out publicly against water fluoridation and spent the rest of his life trying to right the wrong he had done. But while he was at the reins he never hesitated to allow pro-fluoridation voices and articles to be published in Fluoride.
I worked with professor Albert Burgstahler for many years and I can vouch for his scientific integrity. In fact for me he represented one of the pinnacles of scientific integrity and that is why FAN named an annual award in his name.
I never met Dr. Waldbott, but I know that his position was that neither the journal nor its supporting organization (the International Society for Fluoride Research, ISFR) should adopt a formal opposition to fluoridation (and its membership included both pro and anti-fluoridation scientists), but to publish as much science as they could on the subject – and as far as water fluoridation was concerned from both sides – and to let the chips fall where they may. He and his successors also believed that if the science was aired fully and openly it would lead most independent scientists to an anti-fluoridation position.
9. The double standard
Unfortunately, none of the dental journals have adopted the same openness on this issue. By and large they do not entertain any anti-fluoridation editorial or even a review that conflicts with their mantra that fluoridation is “safe and effective.” So I think Ken is exercising a double standard here.I should also point out that there have been several occasions where dental journals have gone out of their way to publish papers that have provided an “ideological” as opposed to a “scientific” support for one side of a controversial matter. Take the example of osteosarcoma. In 1991, shortly after the 1990 NTP animal study had found an association in male rats between fluoride exposure and osteosarcoma, the Journal of the American Dental Association (JADA) rushed to give prominence (i.e. the front cover was devoted to it) to an article, in which the authors clearly reveal their bias in favor of fluoridation. In this very small epidemiological study they proposed that far from causing osteosarcoma fluoride was actually protective against it (see P.187 in The Case Against Fluoride, CAF).
I think the following comments reveal a greater sensitivity to the need to protect the fluoridation program than protecting a few young boys from a life threatening disease:
“An incorrect inference implicating systemic fluoride carcinogenicity and its removal from our water systems would be detrimental to the oral health of most Americans, particularly those who cannot afford to pay for increasingly expensive restorative dental care . . .Because of its strengthening action, fluoride has been widely accepted as the responsible agent for the dramatic declines in the tooth decay rates of U.S. children and adolescents . . . A disruption in the delivery of fluoride through municipal water systems would increase decay rates over time . . . Linking of fluoride ingestion and cancer initiation could result in a large-scale defluoridation of municipal water systems under the Delaney clause. (McGuire et al., 1991, quoted on p. 187, CAF).
In my view the commentary (above) plus the JADA editors’ choice to give it this article full-front page coverage is an example of “ideology” not science at work. The authors and the journal both had a need to protect the fluoridation program at all costs – even if it meant downplaying the concerns about the fate of the young boys in question. I will pick up the osteosarcoma story again in a later submission.
10. A request to Ken
Finally, Ken I think it would save us all a lot of time if – putting the rhetoric and your general disdain for the opponents of fluoridation to one side – you would be kind enough to list the primary studies that you have read that have most convinced you that fluoridation is both safe for the bottle-fed baby and for the adult over lifelong exposure.References
Alarcón-Herrera et al., 2001. “Well Water Fluoride, Dental Fluorosis, Bone Fractures in the Guadiana Valley of Mexico,” Fluoride 34, no. 2 (2001): 139–49http://www.fluorideresearch.org/342/files/FJ2001_v34_n2_p139-149fig.pdf
CDC, 1999. Centers for Disease Control and Prevention, “Achievements in Public Health, 1900–1999: Fluoridation of Drinking Water to Prevent Dental Caries,” Mortality and Morbidity Weekly Review 48, no. 41 (October 22, 1999): 933–40, http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4841a1.htm
CDC, 2001. Centers for Disease Control and Prevention, “Recommendations for Using Fluoride to Prevent and Control Dental Caries in the United States,” Morbidity and Mortality Weekly Report 50, no. RR14 (August 17, 2001): 1–42, http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5014a1.htm
Choi AL, Sun G, Zhang Y, Grandjean P. 2012. Developmental fluoride neurotoxicity: a systematic review and meta-analysis. Environ Health Perspect 120:1362–1368.
Connett, P., Beck, J and Micklem HS. The Case Against Fluoride. Chelsea Green, White River Junction, Vermont, 2010.
Harvard School of Public Health. (2012). Impact of fluoride on neurological development in children. July 25. Available online at: http://www.hsph.harvard.edu/news/features/fluoride-childrens-health-grandjean-choi/
Hirzy, 2000. Statement of Dr. J. William Hirzy, National Treasury Employees Union Chapter 280 before the Subcommittee on Wildlife,
Fisheries and Drinking Water, United States Senate. June 29, 2000.
Li, Y et al., 2001. “Effect of Long-Term Exposure to Fluoride in
Drinking Water on Risks of Bone Fractures,” Journal of Bone and Mineral Research 16, no. 5 (2001): 932–39.
Liu F. et al., 2013 (online) (hard copy 2014). “Fluoride exposure during development affects both cognition and emotion in mice.” Physiology & Behavior 124 (2014) 1–7.
Luke, J, 1997, “The Effect of Fluoride on the Physiology of the Pineal Gland,” PhD thesis, University of Surrey, Guildford, UK, 1997. Excerpts at http://fluoridealert.org/studies/luke-1997/ and a complete copy of Dr. Luke’s dissertation can be downloaded at http://www.fluoridealert.org/wp-content/uploads/luke-1997.pdf (with the author’s permission).
Luke, J, 2001. “Fluoride Deposition in the Aged Human Pineal Gland,” Caries Research 35, no. 2 (2001): 125–28.
McDonagh et al., 2000. “Systematic Review of Water Fluoridation,” British Medical Journal 321, no. 7265 (2000): 855–59, http://www.bmj.com/cgi/content/full/321/7265/855 Note: The full report that this paper summarizes is commonly known as the York Review and is accessible at http://fluoridealert.org/re/york.review.2000.pdf
McGuire et al, 1991. “Is There a Link between Fluoridated Water and Osteosarcoma?” Journal of the American Dental Association 122, no. 4 (1991): 38–45.
Mullenix, PJ et al., 1995. “Neurotoxicity of Sodium Fluoride in Rats,” Neurotoxicology and Teratology 17, no. 2 (1995): 169–77.
Morgan, L. et al. 1998, “Investigation of the Possible Associations between Fluorosis, Fluoride Exposure, and Childhood Behavior Problems,” Pediatric Dentistry 20, no. 4 (1998): 244–52.
NRC, 2006. Fluoride in Drinking Water: A Scientific Review of EPA’s Standards (2006) http://www.nap.edu/catalog.php?record_id=11571
NTP, 1990. National Toxicology Program, “NTP Technical Report on the Toxicology and Carcinogenesis Studies of Sodium Fluoride (CAS no. 7682-49-4) in F344/N Rats and B6C3F1 (Drinking Water Studies),” Technical Report 393, NIH publ. no. 91-2848, National Institutes of Health, Public Health Service, U.S. Department of Health and Human Services, Research Triangle Park, NC, 1990.
E. R. Schlesinger, D. E. Overton, H. C. Chase, and K. T. Cantwell, “Newburgh-Kingston Caries-Fluorine Study XIII. Pediatric Findings After Ten Years,” Journal of the American Dental Association 52, no. 3 (1956): 296–306.
Shannon, FT et al., 1986. “Exposure to Fluoridated Water Supplies and Child Behaviour,” New Zealand Medical Journal 99, no. 803 (1986):416–18.
Waldbott, GL, Burgstahler,AW and H. L. McKinney, Fluoridation: The Great Dilemma (Lawrence, Kansas: Coronado Press, 1978).
Whitford, GM et al. 2009. “Appetitive-based Learning in Rats: Lack of Effect of Chronic Exposure to Fluoride,” Neurotoxicology and Teratology 31, no. 4 (2009): 210–15.
Q. Xiang, Y. Liang, L. Chen, et al., “Effect of Fluoride in Drinking Water on Children’s Intelligence,” Fluoride 36, no. 2 (2003): 84–94, http://www.fluorideresearch.org/362/files/FJ2003_v36_n2_p84-94.pdf
Q. Xiang, Y. Liang, M. Zhou, and H. Zang, “Blood Lead of Children in Wamiao-Xinhuai Intelligence Study” (letter), Fluoride 36, no. 3 (2003):198–99, http://www.fluorideresearch.org/363/files/FJ2003_v36_n3_p198-199.pdf
Xiang, Q. et al., 2010. “Serum Fluoride Level and Children’s Intelligence Quotient in Two Villages in China.” Environmental Health Perspectives. EHPonline.org
Xiang, Q. et al. 2011. “Analysis of children’s serum fluoride in relation to intelligence scores in a high and low fluoride village in China.” http://www.fluorideresearch.org/444/files/FJ2011_v44_n4_p191-194_sfs.pdf
Anyone wanting to follow the debate and/or check back over previous articles in the debate can find the list of articles at Fluoride Debate.
See also:
Similar articles on fluoridation
Making sense of fluoride Facebook page
This entry was posted in Health and Medicine, SciBlogs, science, Science and Society and tagged Connett, debate, fluoridation, fluoride, fluoride debate, Perrott, SciBlogs. Bookmark the permalink.
7 Responses to Fluoride Debate: Why I support fluoridation – 2nd response from Connett
Leave a Reply
Subscribe
Subscribe to Open Parachute
Subscribe by Email
Open Parachute is syndicated at
Recent Comments
Ken on Fluoride debate: Why I support… alison on Fluoride Debate: Why I support… Fred Norris on Fluoride debate Part 1a… Peter Daniel on Fluoride debate: Why I support… Kurt Ferre DDS, Port… on Fluoride Debate: Why I support… chris on Fluoride Debate: Why I support… Steve Slott on Fluoride Debate: Why I support… Richard Christie on Fluoride Debate: Why I support… socialbeverageguy on Fluoride Debate: Why I support… Ken on From dental neglect to child… ChristopherAtkinson on From dental neglect to child… Johnny Johnson, DMD,… on Fluoride Debate: Why I support… chris on From dental neglect to child… Cedric Katesby on From dental neglect to child… scrag12345 on From dental neglect to child… 
NZ Science Blogs- An error has occurred; the feed is probably down. Try again later.
-
Add to Favourites
per Paul Connett:
“I am not aware of any health agency in any fluoridated country comparing fracture rates in children in fluoridated versus non-fluoridated communities or even examining fracture rates in children as a function of the severity of dental fluorosis. Scientists did this in Mexico (Alarcón-Herrera et al., 2001) and found an increase in fractures as the severity of dental fluorosis increased (see P.169, CAF). No attempt has been made to reproduce this result or conduct a similar study in any of the fluoridated countries.”
Alarcón-Herrera’s report was on NATURALLY HIGH OCCURRING LEVELS OF FLUORIDE in the water in Mexico, NOT on optimally fluoridated. There is a distinct difference Paul.
and on the subject, If we were to set a base level of exposure at 0.7ppm it would take not less than one mediocre cup of tea to push the individual in questions risk of chronic exposure to fluoride into a higher risk band.
Therefore, these studies looking at higher micro-molar exposure levels are of importance to this debate.
Please allow me to be of assistance:
NATURALLY HIGH (caps in original)
vs
optimally fluoridated [levels]
Too, Paul needs to cease cluttering the discussion with his unsubstantiated opinions and conjecture on why this organization did this, why that person was fired, all the conspiracies occurring at this level or that, and so on and so on. That kind of irrelevant nonsense serves no useful purpose in a scientific debate such as this.
So, okay…….Where is the evidence of the disorders Paul keeps trying to link to water fluoridation? This public health initiative has been in place for 68 years. There have been tens of millions of people ingesting fluoride at the optimal level, continuously for decades.
Osteosarcoma:
“No significant association between bone fluoride levels and osteosarcoma risk was detected in our case-control study, based on controls with other tumor diagnoses.”
An assessment of bone fluoride and osteosarcoma.
Kim FM, Hayes C, Williams PL, Whitford GM, Joshipura KJ, Hoover RN, Douglass CW; National Osteosarcoma Etiology Group.
Collaborators (9)
Source
Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
The United States has a population of 315 million with 73% fluoridation. Given this, there should be astronomical numbers of osteosarcoma each year, were there the associations with water fluoridation that Paul so desperately keeps trying to establish. However:
“Osteosarcoma is not a common cancer. Each year, about 800 new cases of osteosarcoma are diagnosed in the United States. About 400 of these are in children and teens.”
—http://www.cancer.org/cancer/osteosarcoma/detailedguide/osteosarcoma-key-statistics
Hip Fractures:
“Overall, we found no association between chronic fluoride exposure and the occurrence of hip fracture. The risk estimates did not change in analyses restricted to only low-trauma osteoporotic hip fractures. Chronic fluoride exposure from drinking water does not seem to have any important effects on the risk of hip fracture, in the investigated exposure range.”
——Estimated Drinking Water Fluoride Exposure and Risk of Hip Fracture
A Cohort Study
P. Näsman, J. Ekstrand, F. Granath, A. Ekbom, C.M. Fored
JDR October 1, 2013
The Ever-present 27 Chinese IQ studies:
Once again………The Harvard Review was of 27 Chinese studies found in obscure Chinese scientific journals, of the effects of high levels of naturally occurring fluoride in the well water of various Chinese, Mongolian, and Iranian village. The concentration of fluoride in these studies was as high as 11.5 ppm. By the admission of the Harvard researchers, these studies had key information missing, used questionable methodologies, and had inadequate controls for confounding factors. These studies were so seriously flawed that the lead researchers, Anna Choi, and Phillippe Grandjean, were led to issue the following statement in September of 2012:
“–These results do not allow us to make any judgment regarding possible levels of risk at levels of exposure typical for water fluoridation in the U.S. On the other hand, neither can it be concluded that no risk is present. We therefore recommend further research to clarify what role fluoride exposure levels may play in possible adverse effects on brain development, so that future risk assessments can properly take into regard this possible hazard.”
–Anna Choi, research scientist in the Department of Environmental Health at HSPH, lead author, and Philippe Grandjean, adjunct professor of environmental health at HSPH, senior author
As it seems there have been no translations of these studies into English by any reliable, objective source, it is unclear as to whether they had even been peer-reviewed, a basic for credibility of any scientific study. These studies were flawed that NOTHING could be “concluded” from them.
And the “Journal Fluoride”:
“There are some periodicals that pose as peer-reviewed scientific journals but are not. One such is the journal “Fluoride.” This quarterly publication, which is also available also on the Internet, appears biased toward anti-fluoridation opinion and presents experimental work of questionable quality. Whereas their instructions to authors (found at http://www.fluoride-journal.com/papers.htm) suggest a review process, an examination of a few dozen articles reveals that the same authors appear repeatedly (and tend to cite each other) and the experimental work is poorly describe
and executed. There may be quality science aired in this journal, but ALL articles we examined have an anti-fluoride theme, and many contained significant technical or scientific errors.
For example one study (Chlubek et al., 1998) attempted to assess the fluoride levels of maternal plasma, and the marginal- and central-placentas of 30 pregnant women, ages ranging from 19 to 40 years old, living in an area with relatively low water and air fluoride (fluorine) content. They concluded that the placenta could accumulate fluoride in healthy women who are exposed in pregnancy to relatively low fluoride concentrations in water and in the air. However, an examination of their data show that in Table 1 and Table 2, they shift units between “m M/L” (a meaningless unit: it should be either m mol/L or m M) and m g fluoride/g of tissue ash (a unit that is not comparable to exposure data in their publication) makes their findings meaningless, and makes one wonder whether these workers are competent in elementary chemistry. Moreover, their study included no controls that are critical to interpreting the results as they intended.”
Impact of Fluoridation of the Municipal Drinking Water Supply:
Review of the Literature
Prepared for:
Escambia County Utilities Authority
Prepared by:
The Center for Environmental Diagnostics and Bioremediation
University of West Florid
Joe Eugene Lepo & Richard A. Snyder. May 2000
Steven D. Slott, DDS
supposedly found that fluoride accumulated at very high levels in rats’ brains. The researchers used 2 groups of male rats: one experimental group, one control. There were only 6 animals in each group, which is a very small sample size. The control group supposedly received no fluoride, but then there were no data on fluoride levels in the tap water they drank or the rat chow they ate. This is a significant flaw & I’d have thought it should have been picked up by peer review.The experimental rats apparently received 20ppm fluoride by nasogastric tube for 2 months. Actually, it’s not actually clear what dose they received: the abstract says 20ppm NaF, but the methods section says “20ppm concentration of fluoride”. These are 2 different things. Either way the dose is about an order of magnitude higher than you’d find in fluoridated municipal water in New Zealand, in which case the paper didn’t really support the commenter’s assertions.And in addition, both groups of rats lost a great deal of weight during the course of the study. While the average body weight of the animals was 180g (+/-20g), after 2 months the control animals weighed on average 111g, while the experimental group was down to 93g (both +/- 2g). This strongly suggests they were either ill, or not receiving adequate food.
Michael Connett says his mice recieved 5-10PPM at 4weeks old, now that is a good dose to evaluate brain damage, they probably died of fluoride poisoning
And then he bring up our own john Colquhoun and his mate Waldbott , and we all know how credible he was, so if the mud sticks it stands to reason that the 2 of them are suspect
Once again,
Harvard, Columbia, Georgetown, Duke, U. of Michigan, U. of Wisconsin, Vanderbilt, U. of Minnesota, USC, UCLA, Stanford, UC-Berkeley, U. of Washington.
What do all these fine universities have in common? They are all located in fluoridated communities.
The idea that the citizens in each of these communities, including the professors and their families that live there have lower IQ’s than in non-fluoridated communities is ludicrous.
Convince me, Paul, that the similar demographics in 50+ years fluoridated Corvallis, OR are dumber than their counterparts in non-fluoridated Eugene, OR. You showed up in little Philomath, OR, spouting this IQ rubbish, and guess what? The citizens of Philomath voted fluoridation back into their public water supply despite your fearmongering.
Even Paul’s Fluoride Action Network’s world headquarters in Burlington, VT. enjoys the public health benefit of fluoridation.
Lastly, here’s a study, Paul, you can digest:
Appetitive-based learning in rats: Lack of effect of chronic exposure to fluoride
Gary M. Whitford, Jennifer L. Whitford, Stephen H. Hobbs
Neurotox Teratol (2009), doi:10.1016/j.ntt.2009.02.003
Conclusion: Chronic ingestion of fluoride at levels up to 230 times more than that experienced by humans whose main source of fluoride is fluoridated water had no significant effect on appetitive-based learning.
Reddy2011 supposedly found that fluoride accumulated at very high levels in rats’ brains. The researchers used 2 groups of male rats: one experimental group, one control. CITATION for this quote: http://sci.waikato.ac.nz/bioblog/2013/09/fluoridation-it-pays-to-read-carefully.shtml