[vc_row][vc_column width=”1/2″][vc_column_text]Fluoride damages bone. An early fluoridation trial (Newburgh-Kingston 1945-55) found a significant two-fold increase in cortical bone defects among children in the fluoridated community (Schlesinger 1956). The cortical bone is the outside layer of the bone and is important to protect against fracture. While this result was not considered important at the time with respect to bone fractures, it did prompt questions about a possible link to osteosarcoma (Caffey, 1955; NAS, 1977). In 2001, Alarcon-Herrera and co-workers reported a linear correlation between the severity of dental fluorosis and the frequency of bone fractures in both children and adults in a high fluoride area in Mexico.[/vc_column_text][/vc_column][vc_column width=”1/2″][dt_fancy_image type=”video_in_lightbox” media=”https://www.youtube.com/watch?v=RWyo4WywTD8?start=3&end=61&autoplay=1″ style=”2″ width=”377″ padding=”2″ margin_top=”10″ margin_bottom=”0″ margin_left=”0″ margin_right=”0″ align=”center” animation=”scale” image_alt=”Fluoride: Beneficial or Harmful?” image=”https://elan-organics.co.uk/wp-content/uploads/Fluoride-Beneficial-or-Harmful.png”][/vc_column][/vc_row][vc_row][vc_column width=”1/1″][dt_gap height=”10″][/vc_column][/vc_row][vc_row][vc_column width=”1/1″][vc_column_text]Fluoride may increase hip fractures in the elderly. When high doses of fluoride (average 26 mg per day) were used in trials to treat patients with osteoporosis in an effort to harden their bones and reduce fracture rates, it actually led to a higher number of fractures, particularly hip fractures (Inkovaara 1975; Gerster 1983; Dambacher 1986; O’Duffy 1986; Hedlund 1989; Bayley 1990; Gutteridge 1990. 2002; Orcel 1990; Riggs 1990 and Schnitzler 1990). Hip fracture is a very serious issue for the elderly, often leading to a loss of independence or a shortened life. There have been over a dozen studies published since 1990 that have investigated a possible relationship between hip fractures and long term consumption of artificially fluoridated water or water with high natural levels. The results have been mixed – some have found an association and others have not. Some have even claimed a protective effect. One very important study in China, which examined hip fractures in six Chinese villages, found what appears to be a dose-related increase in hip fracture as the concentration of fluoride rose from 1 ppm to 8 ppm (Li 2001) offering little comfort to those who drink a lot of fluoridated water. Moreover, in the only human epidemiological study to assess bone strength as a function of bone fluoride concentration, researchers from the University of Toronto found that (as with animal studies) the strength of bone declined with increasing fluoride content (Chachra 2010). Finally, a recent study from Iowa (Levy 2009), published data suggesting that low-level fluoride exposure may have a detrimental effect on cortical bone density in girls (an effect that has been repeatedly documented in clinical trials and which has been posited as an important mechanism by which fluoride may increase bone fracture rates).
People with impaired kidney function are particularly vulnerable to bone damage. Because of their inability to effectively excrete fluoride, people with kidney disease are prone to accumulating high levels of fluoride in their bone and blood. As a result of this high fluoride body burden, kidney patients have an elevated risk for developing skeletal fluorosis. In one of the few U.S. studies investigating the matter, crippling skeletal fluorosis was documented among patients with severe kidney disease drinking water with just 1.7 ppm fluoride (Johnson 1979). Since severe skeletal fluorosis in kidney patients has been detected in small case studies, it is likely that larger, systematic studies would detect skeletal fluorosis at even lower fluoride levels.
Fluoride may cause bone cancer (osteosarcoma). A U.S. government-funded animal study found a dose-dependent increase in bone cancer (osteosarcoma) in fluoride-treated, male rats (NTP 1990). Following the results of this study, the National Cancer Institute (NCI) reviewed national cancer data in the U.S. and found a significantly higher rate of osteosarcoma (a bone cancer) in young men in fluoridated versus unfluoridated areas (Hoover et al 1991a). While the NCI concluded (based on an analysis lacking statistical power) that fluoridation was not the cause (Hoover et al 1991b), no explanation was provided to explain the higher rates in the fluoridated areas. A smaller study from New Jersey (Cohn 1992) found osteosarcoma rates to be up to 6 times higher in young men living in fluoridated versus unfluoridated areas. Other epidemiological studies of varying size and quality have failed to find this relationship (a summary of these can be found in Bassin, 2001 and Connett & Neurath, 2005). There are three reasons why a fluoride-osteosarcoma connection is plausible: First, fluoride accumulates to a high level in bone. Second, fluoride stimulates bone growth. And, third, fluoride can interfere with the genetic apparatus of bone cells in several ways; it has been shown to be mutagenic, cause chromosome damage, and interfere with the enzymes involved with DNA repair in both cell and tissue studies (Tsutsui 1984; Caspary 1987; Kishi 1993; Mihashi 1996; Zhang 2009). In addition to cell and tissue studies, a correlation between fluoride exposure and chromosome damage in humans has also been reported (Sheth 1994; Wu 1995; Meng 1997; Joseph 2000).
Fluoride causes arthritic symptoms. Some of the early symptoms of skeletal fluorosis (a fluoride-induced bone and joint disease that impacts millions of people in India, China, and Africa), mimic the symptoms of arthritis (Singh 1963; Franke 1975; Teotia 1976; Carnow 1981; Czerwinski 1988; DHHS 1991). According to a review on fluoridation published in Chemical & Engineering News, “Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed” (Hileman 1988). Few, if any, studies have been done to determine the extent of this misdiagnosis, and whether the high prevalence of arthritis in America (1 in 3 Americans have some form of arthritis – CDC, 2002) and other fluoridated countries is related to growing fluoride exposure, which is highly plausible. Even when individuals in the U.S. suffer advanced forms of skeletal fluorosis (from drinking large amounts of tea), it has taken years of misdiagnoses before doctors finally correctly diagnosed the condition as fluorosis.
Fluoride affects the pineal gland. Studies by Jennifer Luke (2001) show that fluoride accumulates in the human pineal gland to very high levels. In her Ph.D. thesis, Luke has also shown in animal studies that fluoride reduces melatonin production and leads to an earlier onset of puberty (Luke 1997). Consistent with Luke’s findings, one of the earliest fluoridation trials in the U.S. (Schlesinger 1956) reported that on average young girls in the fluoridated community reached menstruation 5 months earlier than girls in the non-fluoridated community. Inexplicably, no fluoridating country has attempted to reproduce either Luke’s or Schlesinger’s findings or examine the issue any further.
Fluoride affects thyroid function. According to the U.S. National Research Council (2006), “several lines of information indicate an effect of fluoride exposure on thyroid function.” In the Ukraine, Bachinskii (1985) found a lowering of thyroid function, among otherwise healthy people, at 2.3 ppm fluoride in water. In the middle of the 20th century, fluoride was prescribed by a number of European doctors to reduce the activity of the thyroid gland for those suffering from hyperthyroidism (overactive thyroid) (Stecher 1960; Waldbott 1978). According to a clinical study by Galletti and Joyet (1958), the thyroid function of hyperthyroid patients was effectively reduced at just 2.3 to 4.5 mg/day of fluoride ion. To put this finding in perspective, the Department of Health and Human Services (DHHS, 1991) has estimated that total fluoride exposure in fluoridated communities ranges from 1.6 to 6.6 mg/day. This is a remarkable fact, particularly considering the rampant and increasing problem of hypothyroidism (underactive thyroid) in the United States and other fluoridated countries. Symptoms of hypothyroidism include depression, fatigue, weight gain, muscle and joint pains, increased cholesterol levels, and heart disease. In 2010, the second most prescribed drug of the year was Synthroid (sodium levothyroxine) which is a hormone replacement drug used to treat an underactive thyroid.
Fluoride may damage the brain. According to the National Research Council (2006), “it is apparent that fluorides have the ability to interfere with the functions of the brain.” In a review of the literature commissioned by the US Environmental Protection Agency (EPA), fluoride has been listed among about 100 chemicals for which there is “substantial evidence of developmental neurotoxicity.” Animal experiments show that fluoride accumulates in the brain and alters mental behavior in a manner consistent with a neurotoxic agent (Mullenix 1995). In total, there have now been over 100 animal experiments showing that fluoride can damage the brain and impact learning and behavior. According to fluoridation proponents, these animal studies can be ignored because high doses were used. However, it is important to note that rats generally require five times more fluoride to reach the same plasma levels in humans (Sawan 2010). Further, one animal experiment found effects at remarkably low doses (Varner 1998). In this study, rats fed for one year with 1 ppm fluoride in their water (the same level used in fluoridation programs), using either sodium fluoride or aluminum fluoride, had morphological changes to their kidneys and brains, an increased uptake of aluminum in the brain, and the formation of beta-amyloid deposits which are associated with Alzheimer’s disease. Other animal studies have found effects on the brain at water fluoride levels as low as 5 ppm (Liu 2010).
Fluoride may lower IQ. There have now been 33 studies from China, Iran, India and Mexico that have reported an association between fluoride exposure and reduced IQ. One of these studies (Lin 1991) indicates that even just moderate levels of fluoride exposure (e.g., 0.9 ppm in the water) can exacerbate the neurological defects of iodine deficiency. Other studies have found IQ reductions at 1.9 ppm (Xiang 2003a,b); 0.3-3.0 ppm (Ding 2011); 1.8-3.9 ppm (Xu 1994); 2.0 ppm (Yao 1996, 1997); 2.1-3.2 ppm (An 1992); 2.38 ppm (Poureslami 2011); 2.45 ppm (Eswar 2011); 2.5 ppm (Seraj 2006); 2.85 ppm (Hong 2001); 2.97 ppm (Wang 2001, Yang 1994); 3.15 ppm (Lu 2000); 4.12 ppm (Zhao 1996). In the Ding study, each 1 ppm increase of fluoride in urine was associated with a loss of 0.59 IQ points. None of these studies indicate an adequate margin of safety to protect all children drinking artificially fluoridated water from this affect. According to the National Research Council (2006), “the consistency of the results [in fluoride/IQ studies] appears significant enough to warrant additional research on the effects of fluoride on intelligence.” The NRC’s conclusion has recently been amplified by a team of Harvard scientists whose fluoride/IQ meta-review concludes that fluoride’s impact on the developing brain should be a “high research priority.” (Choi et al., 2012). Except for one small IQ study from New Zealand (Spittle 1998) no fluoridating country has yet investigated the matter.
Fluoride may cause non-IQ neurotoxic effects. Reduced IQ is not the only neurotoxic effect that may result from fluoride exposure. At least three human studies have reported an association between fluoride exposure and impaired visual-spatial organization (Calderon 2000; Li 2004; Rocha-Amador 2009); while four other studies have found an association between prenatal fluoride exposure and fetal brain damage(Han 1989; Du 1992; Dong 1993; Yu 1996).[/vc_column_text][/vc_column][/vc_row]