by Paul Connett
With public water fluoridation, we are forcing people to drink a possible thyroid-depressing medication that could cause higher levels of both subclinical and clinical hypothyroidism in the general population, with all the attendant problems such as depression, fatigue, weight gain, muscle and joint pain, increased cholesterol levels, and heart disease, as well as cognitive dysfunction and damage to the developing brain. 52 Significantly, in the United States in 1999, the second-most prescribed drug was levothyroxine (Synthroid), a hormone-replacement drug used to treat hypothyroidism.
The interaction between fluoride and thyroid function warrants far more attention from governments promoting fluoridation than it currently receives, which is practically nil. Millions of people worldwide are affected by thyroid dysfunction, and if the condition of only a small fraction of those people is caused or worsened by fluoride, it is a very serious matter indeed. With such uncertainties in the background, continuing to press on with mass medication is inappropriate.
Fluoride and the Pineal Gland
The pineal gland is located between the two hemispheres of the brain. Its most recognized function is production of the extremely important hormone melatonin. Situated outside the blood-brain barrier, the pineal gland has the highest blood flow per unit volume of any tissue except the kidney. It is also a calcifying tissue, laying down crystals of calcium hydroxyapatite, the mineral formed in teeth and bones.
From those known facts, Dr. Jennifer Luke, a dentist in the UK, hypothesized that, like teeth and bones, this little gland would concentrate fluoride. Her theory was confirmed when she had the pineal glands from eleven corpses of elderly people extracted and analyzed. The average level of fluoride found in the crystals in those glands was 9, 000 ppm, one case reaching the extremely high level of 21, 000 ppm. Significantly, 9, 000 ppm approaches the level of fluoride found in the bones of someone suffering from skeletal fluorosis, and 21, 000 ppm is even higher than the bone levels associated with the crippling phase of skeletal fluorosis. This finding was the subject of Luke’s 1997 PhD thesis53 and was published in an article in Caries Research in 2001. 54
The Hormone Melatonin
Melatonin is produced in the pineal gland in a four-step process starting with the natural amino acid tryptophan. Melatonin acts as a biological clock in many timed events in human physiology and development, including jet lag, sleep patterns, and aging. The onset of puberty is another timed event that melatonin is thought to influence. It is at its highest level in young children and decreases as they get older. At a certain point, it is believed that the low level of melatonin triggers the production of sex hormones that leads to puberty.
In her PhD thesis (available at www.FluorideAlert.org), Dr. Jennifer Luke presented evidence that animals (Mongolian gerbils) exposed to high levels of fluoride had lowered melatonin levels and reached puberty earlier than gerbils exposed to lower levels of fluoride. 55
Health agencies in several fluoridating countries have been given copies of Luke’s work, yet none has financed or requested a study to reproduce her findings. By contrast, the 2006 NRC panel acknowledged the potential seriousness of her work:
The single animal study of pineal function indicates that fluoride exposure results in altered melatonin production and altered timing of sexual maturity. . . Whether fluoride affects pineal function in humans remains to be demonstrated. The two studies of menarcheal age in humans show the possibility of earlier menarche in some individuals exposed to fluoride, but no definitive statement can be made. 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. 56
One of those “earlier menarche” studies was the Newburgh-Kingston study published by Schlesinger et al. in 1956 and discussed in chapter 10. 57 The authors of that study found that, on average, girls in fluoridated Newburgh reached menarche five months earlier than girls in unfluoridated Kingston. This finding was ignored at the time and is still ignored by those promoting fluoridation more than fifty years later.
Fluoride and Diabetes
The 2006 NRC review indicated that fluoride may affect diabetics in two ways:
The conclusion from the available studies is that sufficient fluoride exposure appears to bring about increases in blood glucose or impaired glucose tolerance in some individuals and to increase the severity of some types of diabetes. In general, impaired glucose metabolism appears to be associated with serum or plasma fluoride concentrations of about 0. 1 mg/L or greater in both animals and humans. In addition, diabetic individuals will often have higher than normal water intake, and consequently, will have higher than normal fluoride intake for a given concentration of fluoride in drinking water. An estimated 16–20 million people in the U. S. have diabetes mellitus; therefore, any role of fluoride exposure in the development of impaired glucose metabolism or diabetes is potentially significant. 58
Plasma fluoride concentrations of 0. 1 mg/L are easily achieved by people drinking water fluoridated at 1 ppm. With so many people suffering from diabetes today, it is again astonishing how little work has been done to see whether fluoride exposure is worsening their condition. This underlines an important concern: When an entire population is exposed to a toxic substance, simply setting regulatory levels to protect the average person is not enough; those levels must be set to protect the most vulnerable citizens, such as people with diabetes and those susceptible to it.
Summary
The influence of fluoride on the human thyroid gland has a long history, going back to before the days of artificial fluoridation. Until recently, however, fluoridating countries have put virtually no effort into finding out whether drinking fluoridated water might adversely affect the functioning of that gland or other components of the endocrine system. The matter has been ignored or glossed over in officially sponsored reviews. This may well appear negligent, considering the prevalence of thyroid disorders in those countries. There is evidence that consumption of naturally occurring fluoride, even in amounts comparable to the amounts in artificially fluoridated water, can affect human thyroid function, particularly when iodine intake is inadequate. Meanwhile, in vitro experiments confirm that there is cause for concern. Such experiments suggest that fluoride may inhibit the deiodinase enzymes that fine-tune thyroid function; and, in combination with traces of aluminum, fluoride can inappropriately activate intracellular signals on which much hormone function depends, including production and action of thyroid-stimulating hormone. Does fluoridation threaten the thyroid and through it many aspects of human health? We don’t know, but it certainly looks more than possible, and the question should be pursued urgently, not ignored.
The pineal, another endocrine gland, is located between the two hemispheres of the brain and is responsible for the synthesis and secretion of melatonin. Research published in 2001 showed that fluoride accumulates in the human pineal and can reach very high concentrations in old age. Whether this affects pineal function is unknown. However, preliminary animal experiments indicated that fluoride reduced melatonin production and shortened the time to menarche (Luke, 1997). Thirteen years have passed, apparently without any attempt to replicate those potentially important findings.
Fluoride at doses achievable by drinking fluoridated water may impair glucose tolerance in some individuals. In view of the increasing prevalence of diabetes, this is of concern, particularly since diabetics often drink more water than non-diabetics. This requires further research and, meanwhile, underlines the inadequacy of regulatory levels for fluoride that are set merely to protect the majority of people, not the most vulnerable.
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Fluoride and Bone
It has been known for many years that about 50 percent of the daily intake of fluoride is absorbed by and accumulates in the bones. 1 In this chapter,
we review the evidence that this accumulation damages the bones of both children and adults.
Bone Fractures in Children
One of the earliest trials of fluoridation (Newburgh, New York, versus Kingston, New York, 1945–1955) found approximately twice as many cortical bone defects in the fluoridated city, Newburgh, compared with Kingston, the unfluoridated city. 2, 3 The fact that the defects occurred in the cortical part of the bone is significant for the potential for fractures.
The bone is in two parts: the trabecular (or cancellous) and the cortical. The trabecular bone is the inside meshwork that gives the bone its load-bearing ability. (It gets its name from the Latin trabs, which refers to the structures that hold up the roofs of barns and churches built in medieval times. ) Weakness in the trabecular bone can lead to increased rates of compression fractures of the spine in those suffering from osteoporosis.
The cortical bone is the outer sheath of bone, consisting of a layered structure (the lamellae). The cortical bone is critical for protection against breakage when the bone is exposed to a heavy blow or torsional stress.
It is surprising that the finding of a higher frequency of cortical bone defects in fluoridated Newburgh did not prompt a careful investigation of the rates of bone fractures in young children exposed to fluoridated water, either after the Newburgh study or in the fifty-plus years since. This neglect may be explained by McClure’s claims, mentioned previously, that he found no extra bone fractures in boys and army recruits coming from communities with up to 4. 2 ppm of fluoride in the water (see chapter 9).
While very few children’s bone studies have been done in fluoridated countries, an interesting study was done in Mexico in 2001. Dr. M. Teresa Alarcón-Herrera et al. investigated bone fractures in people living in a high-fluoride area (1. 5–5. 5 ppm fluoride in water) and reported that as the severity of dental fluorosis increased, so did the incidence of bone fractures for both children and adults. Although the validity of the scoring methods used for fractures is acknowledged by the authors to be questionable, this is a potentially important finding, because the severity of dental fluorosis can be used as a biomarker of the extent of overexposure to fluoride before the permanent teeth have erupted. Simply put: As fluoride exposure went up, so did the incidence of bone fractures. 4
Spokespersons for governmental agencies promoting fluoridation have contented themselves with criticizing the methodology used in this study; not one of these fluoridated countries has sought to repeat the study since its publication in 2001, even though dental fluorosis affects over 30 percent of children in the United States5, 6 (see chapter 11). This is further evidence of the very poor monitoring of the safety of the fluoridation program, an issue that we summarize in chapter 22.
Fluoride and Arthritis
It has been known since the 1930s that ingesting too much fluoride can cause stiff and painful joints. Some of the early symptoms of skeletal fluorosis— a fluoride-induced bone and joint disease that affects millions of people in India, China, and several other countries with high natural levels of fluoride— mimic the symptoms of arthritis, making it easy to misdiagnose, especially by doctors who are not trained in detecting fluorosis. 7–12
The only stage of skeletal fluorosis recognized by the U. S. EPA in determining the safe drinking water standard for fluoride in 1986 was stage III, the crippling phase. According to a review on fluoridation published in 1988 in Chemical & Engineering News by senior science editor Bette Hileman, “Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed. ”13
Few, if any, studies have been done to determine the extent of misdiagnosis, or whether the high prevalence of arthritis in America (one in five American adults has some form of arthritis14 ) is related to lifelong and ever-growing exposure to fluoride.
According to American Medical News, researchers at the U. S. National Arthritis Data Workgroup compiled data from various large national surveys and found that “some 46. 4 million people, or 21 percent of the population, have physician-diagnosed arthritis. Of this group, 27 million have clinical osteoarthritis, and 1. 3 million have rheumatoid arthritis. ” The number appears to be rising and is predicted to reach 67 million by 2030. 15
The failure to explore the plausible connection between fluoridation and arthritis in any fluoridating country is difficult to understand. It is particularly surprising since the causes of most forms of arthritis (e. g. , osteoarthritis) are unknown but are usually associated with the aging process. For those living in fluoridated communities the aging process will coincide with lifelong accumulation of fluoride in their bones and joints.
In 2006, the NRC report discussed the four stages of skeletal fluorosis:
Excessive intake of fluoride will manifest itself in a musculoskeletal disease with a high morbidity. This pathology has generally been termed skeletal fluorosis. Four stages of this affliction have been defined, including a preclinical stage and three clinical stages that characterize the severity. The preclinical stage and clinical stage I are composed of two grades of increased skeletal density as judged by radiography, neither of which presents with significant clinical symptoms. Clinical stage II is associated with chronic joint pain, arthritic symptoms, calcification of ligaments, and osteosclerosis of cancellous bones. Stage III has been termed “crippling” skeletal fluorosis because mobility is significantly affected as a result of excessive calcifications in joints, ligaments, and vertebral bodies. This stage may also be associated with muscle wasting and neurological deficits due to spinal cord compression. The current MCLG is based on induction of crippling skeletal fluorosis (50 Fed. Reg. 20164 [1985]). Because the symptoms associated with stage II skeletal fluorosis could affect mobility and are precursors to more serious mobility problems, the committee judges that stage II is more appropriately characterized as the first stage at which the condition is adverse to health. Thus, this stage of the affliction should also be considered in evaluating any proposed changes in drinking-water standards for fluoride. 16
The panel recommended more research to fill the gaps in knowledge in this area. They specifically recommended the following:
A systematic study of stage II and stage III skeletal fluorosis should be conducted to clarify the relationship of fluoride ingestion, fluoride concentration in bone, and clinical symptoms. Such a study might be particularly valuable in populations in which predicted bone concentrations are high enough to suggest a risk of stage II skeletal fluorosis (e. g. , areas with water concentrations of fluoride above 2 mg/L).
More research is needed on bone concentrations of fluoride in people with altered renal function, as well as other potentially sensitive populations (e. g. , the elderly, postmenopausal women, people with altered acid-balance), to better understand the risks of musculoskeletal effects in these populations. 17
In a 2003 review Paul Connett and Michael Connett could find only sixteen studies published between 1941 and 1994 in which bone fluoride levels were reported. 18 Worldwide a grand total of 1, 397 bones were measured for fluoride in over fifty years. This, again, despite the fact that since at least the 1960s scientists have known that approximately 50 percent of the fluoride ingested each day accumulates in bones19 —more in the bones of people with poor kidney function.
The problem with this “research gap” on fluoride and arthritis was underscored in 2007 by three studies, one from India and two from the United States.
Gupta et al. 2007
A thirty-five-year-old woman who regularly drank water with 1. 9 ppm fluoride developed a subtle form of fluorosis that doctors initially suspected to be a form of seronegative arthritis. Seronegative arthritis refers to a form of arthritis that mimics the symptoms of rheumatoid arthritis (RA) but lacks the autoantibodies diagnostic of RA. In this case study, the woman “presented with joint pain involving the lower back, both heels, and the knee for the past 3 years. ” In addition to the joint pains, the patient suffered from “gas
trointestinal disturbance, ” prompting the doctors to suspect “the possibility of enteropathic arthritis. ” Enteropathic arthritis is a form of arthritis associated with inflammatory bowel diseases.
The doctors finally began to suspect the role of fluoride after X-rays revealed increased bone density in the pelvic area and calcification of some ligaments. Follow-up tests revealed elevated levels of fluoride in the patient’s drinking water and slightly elevated levels of fluoride in the patient’s blood (0. 05 ppm). 20
Hallanger Johnson et al. 2007
A study published by doctors at the Mayo Clinic suggested that similar cases of fluorosis may be occurring in the United States among habitual tea drinkers (tea leaves often contain high levels of fluoride), especially those with weak kidney function. In this study, the Mayo doctors detailed the cases of four patients who developed bone pains, and in some cases gastrointestinal problems, from drinking large amounts of tea. As with the Indian study, at least one of these patients had previously been misdiagnosed as having arthritis. One woman, who “developed chronic pain and stiffness in her lower back that progressed to include bilateral hip and knee pain, ” had been treated for seven years with various drugs “but with no improvement in symptoms. ”
