Cardiovascular disease remains the leading cause of morbidity and mortality in the world. In the United States alone, over 27 million adults have been diagnosed with heart disease, and nearly 600,000 adults died as a result of cardiovascular disease in 2010. Numerous factors contribute to the development of this disease, including genetics, lifestyle choices, and environmental pollutants.
While it is well known that fluoride accumulates in teeth and bones, fluoride has also been shown to concentrate in the cardiovascular system. This can result in increased blood pressure (hypertension), arterial calcifications, arteriosclerosis, and myocardial damage. Electrocardiogram abnormalities have also been observed in both humans and experimental animals chronically exposed to fluoride. Research has also found that patients with cardiac failure have significantly elevated levels of fluoride in their blood, even more than patients with kidney disease.
Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et al., 2011). A higher incidence of arterial hypertension was also noted among those occupationally exposed to fluoride (Tartatovskaya et al., 1995). Animal studies have also found this association. Bera et al. (2007); Walland (1977). A study, however, of children found that those with dental fluorosis (indicating chronic fluoride overexposure) had lower diastolic blood pressure than those without dental fluorosis (Karademir et al., 2011). Takamori (1962) and Leone et al. (1956) similarly observed hypotension in animals exposed to toxic levels of fluoride. This discrepancy might be attributed to the level of fluoride exposure or to the developmental stage of the subjects. Read more.
The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events.
Increased arterial calcifications have frequently been reported in those with skeletal fluorosis (Tuncel 1984). Fluoride accumulation leads to cellular toxicity, likely causing the accumulation of calcium (Susheela and Kharb, 1990). The aorta has been shown to accumulate more fluoride than possibly any other soft tissue, with 8,400 ppm F reported in one case (Greever et al., 1971). Similarly, studies indicate that animals chronically exposed to fluoride have increased levels of both fluoride and calcium in the aorta (Susheela and Kharb, 1990) and heart (Stookey and Muhler, 1963). Read more.
Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the inner layer of the arteries. Numerous factors can cause or contribute to this damage, including high blood pressure, high cholesterol, diabetes and environmental factors (e.g. smoking).
Several studies have found that those chronically exposed to fluoride are at higher risk of suffering from arteriosclerosis. For example, the elastic properties of the ascending aorta were found to be impaired in patients with mild levels of fluoride toxicity (Varol et al., 2010b). According to Song et al. (1990), “endemic fluorosis might cause aortosclerosis [arteriosclerosis of the aorta], which greatly aggravate the course and range of sclerosis and calcification of the conducting arteries, and which in turn make fluorosis [more severe].” Read more.
An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems with the heart can alter electrical activity, and thus altered ECG readings can indicate underlying problems with heart function. ECGs can help diagnose heart attacks, coronary heart disease, irregular or abnormal heartbeat, heart failure, etc.
Studies have observed higher rates of abnormal ECGs among those with skeletal fluorosis compared to normal controls (Ji et al., 2004; Xu and Xu, 1997). Children with dental fluorosis have also been shown to have altered ECGs, including prolonged Q-T interval (Karademir et al., 2011), which is a biomarker for arrhythmias and a risk factor for sudden death. Similar findings have been reported by Okushi (1954) and Takamori (1956). Still another study found an increased incidence of abnormal systolic time interval (STI) in those living in an endemic fluorosis region (Wang et al., 1983).
Altered ECG readings have also been observed in experimental animals with chronic and subacute exposure to fluoride, including sheep (Dönmez and Çinar, 2003), dogs (Kilicalp et al., 2004), goats (Kant et al., 2010), and rabbits (Kumar et al., 2010; Okushi, 1954b). Read more.
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha and Sujitha, 2011; Cicek et al., 2005; Shashi and thapar, 2001; Pribilla, 1968; Takamori et al., 1956).
Fluoride-induced oxidative stress and inflammatory response have been demonstrated in humans and experimental animals (Barbier et al., 2010), and are likely responsible for this myocardial cell damage (Varol and Varol, 2012). In studies of the cardiovascular system, rats treated chronically with high levels of fluoride have reduced activity of antioxidant enzymes in the heart (Basha and Sujitha, 2011; Cicek et al., 2005), and toxic concentrations of fluoride have been shown to increase gene expression of inflammatory-related molecules in rabbit aorta (Ma et al., 2012). Read more.
Cardiovascular Disease Increases Blood Fluoride Levels
Patients with heart disease have been found to have elevated levels of fluoride in their blood. According to one study, cardiac insufficiency was associated with higher blood fluoride levels than any other disease type in a group of patients at a hospital in a fluoridated area. (Hanhijarvi 1981). Notably, the patients with cardiac insufficiency had higher blood fluoride levels than patients with kidney disease. The authors of the study warned, therefore, that “chronic cardiac failure may, according to the present results, be just as strong a factor as a cause of fluoride accumulation as moderate renal insufficiency.” (Hanhijarvi 1981).
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Basha MP, Sujitha NS. (2011). Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats. Toxicol Int 18(2):99-104.
Barbier O, et al. (2010). Molecular mechanisms of fluoride toxicity. Chemico-Biological Interactions 188:319-33.
Bera I, et al. (2007). Neurofunctional effects of developmental sodium fluoride exposure in rats. Eur Rev Med Pharmacol Sci 11:211-24.
Cicek E, et al. (2005). Effects of chronic ingestion of sodium fluoride on myocardium in a second generation of rats. Human Exper Toxicol 24:79-87.
Dede O, et al. (2011). Chronic fluoride exposure has a role in etiology of coronary artery ectasia: sialic acid/glycosaminoglycan ratio. Biol Trace Elem Res 143:695-701.
Dönmez N, Çinar A. (2003). Effects of chronic fluorosis on electrocardiogram in sheep. Biol Trace Elem Res 92:115-21.
Hanhijärvi H, et al. (1981). Ionic plasma fluoride concentrations related to some diseases in patients from a fluoridated community. Proc Finn Dent Soc. 77(6):324-9.
Ji F, et al. (2004). Study on the cardiovascular damage of skeletal fluorosis patients. Chin J Ctrl Endem Dis 19(6):321-3 (Abstract).
Kant V, et al. (2010). Alterations in electrocardiographic parameters after subacute exposure of fluoride and ameliorative action of aluminum sulphate in goats. Biol Trace Elem Res 134:188-94.
Karademir S, et al. (2011). Effects of fluorosis on QT dispersion, heart rate variability and echocardiographic parameters in children. Anadolu Kardiyol Derg 11:150-5.
Kilicalp D, et al. (2004). Effects of chronic fluorosis on electrocardiogram in dogs. Fluoride 37(2):96-101.
Kumar N, et al. (2010). Effects of sodium fluoride on the electrocardiogram of male rabbits. Fluoride 43(2):124-7.
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Ma Y, et al. (2012). Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta. Arch Toxicol 86:849-56.
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