Sunday, October 21, 2012

Fluoride, Endocrine Disruption and Implications for Public Health and Environment

I’m sitting on the train to Dublin reading the Sunday newspapers and I see that the front page of The Observer has the following headline, Boys are reaching puberty earlier, reveals US study.

The journalist, Paul Harris writing from New York, reports on what he refers to as a comprehensive new study by the American Academy of Paediatrics (AAP), which demonstrated that American boys are showing signs of puberty six months to two years earlier than previously assumed. Mr Harris notes that the surprise findings builds on previous discoveries reported in the U.S. Journal of Pediatrics  in 2010 that appeared to show girls have also been developing faster. 

Now it appears the AAP study is showing the same trends in boys. While not identifying what may be causing the biological change, the study did mention diet and environmental toxins as possible contributors.  The Observer article notes that all this has led to speculate that weight gain might be a possible factor, as body fat is linked to production of the female hormone oestrogen. Interestingly the study also showed that ethic race also play a role in the early onset of puberty  with black American boys showing signs of puberty earlier than either white or Hispanic counterparts.

So why do I find this interesting?....well it has previously  been clinically documented in human population and ecological studies that exposure to Fluoride may affect the endocrine system, resulting in children living in fluoridated communities  entering puberty earlier than in non fluoridated communicties. It has also been suggested that fluoride toxicity may be a contributory factor in the development of obesity, due to Fluoride being a metabolic inhibitor.   

Luke J et al. of the University of Surrey and the Royal Hospital London published a scientific report in 2001 in the Journal Caries Research on how Fluoride effects the Pineal Gland, and made the following conclusion :
“the human pineal gland contains the highest concentration of fluoride in the body. Fluoride is associated with depressed pineal melatonin synthesis by prepubertal gerbils and an accelerated onset of sexual maturation in the female gerbil. The results strengthen the hypothesis that the pineal has a role in the timing of the onset of puberty.”

This risk was further acknowledged by the U.S. National Academy of Sciences National Research Council in their published findings on Fluoride in 2006 where they acknowledged:
“that recent information on the role of the pineal organ in humans suggests that any agent that affects pineal function could affect human health in a variety of ways, including effects on sexual maturation, calcium metabolism, parathyroid function, postmenopausal osteoporosis, cancer, and psychiatric disease.”

The potential consequences of disturbances to functions of the pineal gland and resultant human health impacts from increased absorption of fluoride through dietary intake from water fluoridation cannot be underestimated. The first step in assessing a health risk by a substance to humans is the identification of its harmful effects on animals. A health risk to humans is assessed using results from human epidemiological studies in conjunction with results from animal studies. As far back as 1956 The Newburgh-Kingston Study (Schlesinger et al., 1956) identified that bone defects, anaemia and earlier female menstruation occur more often in children living in the fluoridated Newburgh than in non-fluoridated Kingston community.

Yet remarkably very little if any research has been undertaken since then to verify or examine these findings further. This is quite astonishing, even more so that the distinguished American Academy of Paediatrics or the Journal of Pediatrics  in reporting on the early onset of puberty would either  not be aware of else deliberately ignored these findings. This is particularly so when in 2001 the  U.S Agency for Toxic Substances and Disease Registry, US Department of Health and Human Services, similarly reported that fluoride negatively affected  endocrine systems.[1]

It is also very significant because the U.S EPA reported[2] in 2010 that with an average Fluoride concentration of 0.9ppm in drinking water, the relative source contribution of fluoridated drinking water to total fluoride exposure can be as high as 70% for infants and for certain adults 60%. They noted that children under seven years of age may be at risk of severe dental fluorosis as a result of this level of exposure. Severe dental fluorosis is a physical visible sign of chronic overexposure to fluoride. The EPA documented that the major source of fluoride to their diets will be fluoridated drinking water, followed by commercial beverages, solid foods and swallowed toothpaste.  Furthermore the EPA noted that in recent decades the total dietary Fluoride intake of the population  is increasing due to a combination of dietary sources.

So why else is the latest study in the NAP journal interesting?.. well because it found that the early onset of puberty was influenced by ethnicity. Yet another fascinating fact about fluoride is that numerous studies have found that African American’s (blacks), followed by Hispanics, appear to be the most sensitive ethic groups to fluoride toxicity.[3] It may well be that DNA and genetic makeup plays an important role in sensitivity or intolerance to fluoride.  This might explain why homogeneous populations are more at risk and poses particular concerns for fluoridated communities  such as the Republic of Ireland, the only EU country with a mandatory policy of fluoridation of drinking water. Which by its geographic remoteness on the edge of Europe, small population, low inward migration and its historical religious and social practices which encouraged members of the same religious community to marry, has ultimately resulted untill very recently in a relatively homogenic population compared to other European or developed countries.

Genetic breeding certainly appears to be the case for certain breeds of horses have been found to be particularly sensitive to fluoride toxicity, as noted in the Journal Fluoride and as documented by Professor Krook, Professor of Pathology, the College of Veterinary Medicine, Department of Biomedical Sciences, Cornell University in 2005. Cornell University found that pure breed quarter horses suffered from chronic fluoride poisoning after ingestion of fluoridated water, which was their principal dietary exposure to Fluoride at levels of 1ppm due to artificial fluoridation. Interestingly, as a result of the Universities extensive studies on these poisoned horses, fluoridation was discontinued in the community from which they were resident.

The ability of Fluoride to stimulate early sexual maturity in freshwater aquatic species was also reported in the peer reviewed scientific Journal Chemosphere (2003)  by environmental eco-toxicologist  Dr. Camargo, of the University of  Madrid.  Camargo reported that Fluoride stimulated female fecundity (stimulating reproductive fertility) in certain aquatic freshwater species.[4],[5],[6]

All of this information was included in the recent report published by Irish Environmental Scientist, Declan Waugh of Enviro Management Services  in his independent report on the Human Health, Environmental Impact and Legal Implications of Water Fluoridation, dated March 2012.

Finally, why is all this important? well for apart from shortening childhood years, early sexual maturation has both physiological and psychological consequences in humans. For girls, it is also associated with an increased risk of certain cancers in later life.[7],[8]  

The implication’s therefore of fluoride exposure for long-term health or the environment cannot be overlooked. It is also important to be aware, that many of the man-made substances that are listed as known endocrine disruptors by the European Commission‘s Community Strategy for Endocrine Disruptors‘ (COM (1999)706), are also fluoridated compounds.

It is inexcusable that public health authorities continue to ignore the adverse health effects of fluoride intoxication of the population. It is criminally neglicent that they still have not conducted any detailed toxicological studies examining the wider toxicological impacts for populations to ingest silicofluoride chemical compounds that are used to fluoridate drinking water especially when they are being medicated without being informed of the risks.

Public health authorities are also failing in their duties not to have commissioned detailed epidemiological health studies or not to have provided appropiate safety standards for the most sensitive subgroups of the population to prevent overexposure to Fluoride in particular babies, diabetics or individuals who are iodine deficient or who suffer from any thyroid disorder. Obviously, its not in their interest, as after all they are the very instigators of this crime in the first place, and the last thing they would wish is to further incriminate themselves.

[1] ATSDR (Agency for Toxic Substances and Disease Registry) (2001) Toxicological profile for fluoride. US Department of Health and Human Services, Atlanta, Georgia.
[2] Fluoride: Exposure  Relative Source Contribution Analysis, Health and Ecological Criteria Division
Office of Water, U.S EPA, December 2010
[3] Russell, 1962; Butler et al., 1985; Williams and Zwemer, 1990; Beltrán-Aguilar et al., 2005; Martinez-Mier and Soto-Rojas, 2010
[4] Camargo, J.A. Fluoride toxicity to aquatic organisms: a review. Chemosphere. 2003 Jan;50(3):251-64.
[5] Connell, A.D., Airey, D.D., 1982. The chronic effects of fluoride on the estuarine amphipods Grandidierella lutosa and G. lignorum. Water Res. 16, 1313–1317
[6][6] McClurg, T.P, 1984. Effects of fluoride, cadmium and mercury on the estuarine prawn Penaeus indicus. Water SA 10, 40–45.
[7] Reproductive History and Breast Cancer Risk, Factsheet, U.S National Cancer Institute, National Institutes of Health, Department of Health and Human Services
[8] Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR, and Berenson GS, Relation of Age at Menarche to Race, Time Period, and Anthropometric Dimensions: The Bogalusa Heart Study, Pediatrics 2002; 110:e43

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