Fluoridation and Heart Disease

Research published in January 2012(1) concluded that there was a direct correlation between the fluoride level in arteries, including coronary arteries, and artherosclerosis, such that the scanning for the fluoride level could be used to diagnose the level of disease.

It found a direct relationship between the fluoride level and the patient’s history of heart disease, and concluded that “[a]n increased fluoride uptake in coronary arteries may be associated with an increased cardiovascular risk.”

This confirms many studies showing a relationship between fluoride and heart disease, as discussed in detail below.
Perhaps most importantly, this unquestionably proves that fluoride does accumulate in soft tissue – something fluoridation promoters deny emphatically, claiming it all goes to the bones or teeth, and never the soft tissues.

Fluoride as a pro-inflammatory factor(2)

Inflammatory reactions underlie the pathogenesis of the atherosclerotic process, and oxygen free radicals formed during these reactions contribute to aggravation of atherosclerotic lesions. Incubation of macrophages in fluoride solutions significantly decreased the amount of synthesized cellular ATP, and increased the formation of reactive oxygen species (ROS) and apoptotic cells in a dose-dependent pattern. Thus fluoride may be considered pro-atherogenic and pro-apoptotic, and long-term exposure to low concentrations of fluoride may lead to harmful changes in cellular metabolism.
This supports the findings of research by Ercan Varol et al, showing fluoride harms heart cells.

Fluoride causes increased levels of heart disease-related death

Ercan Varol et al, Science of the Total Environment, Volume 408, Issue 11, 1 May 2010, Pages 2295-2298
Ercan Varol et al, Biological Trace Element Research, Volume 133, Number 2 / February, 2010

This research shows fluoride affects the aorta (main artery) and heart in ways that lead to increased heart attacks.

This confirms findings from the earliest days of water fluoridation in the USA that deaths from heart attacks sky-rocketed in the fluoridated communities, compared with the non-fluoridated ones. This is shown by official US government data.

The heart beat rate slows, and heart rate abnormalities increase, in direct proportion to increasing fluoride levels. This occurred at the relatively low fluoride levels that cause symptoms mistaken for arthritis, in NZ as elsewhere according to WHO.

Heart disease deaths related to fluoride exposure

Elevated blood-fluoride levels lower available body calcium. Low calcium is directly related to impaired heart function. Extremely low calcium causes cardiac arrest. This is how lethal doses of fluoride (about a tablespoon of silicofluoride) work – by starving the heart of calcium until it stops.

Research published in 2010(3) shows fluoride affects the aorta (main artery) and heart in ways that lead to increased heart attacks. (This refutes claims by fluoridation promoters that fluoride does not accumulate in soft tissue – it does, particularly arteries, ligaments, skeletal muscle, and the brain.) This confirms earlier studies showing high blood-fluoride levels have an effect on body calcium, leading to calcification of the aorta and other arteries.(4,5)

Further research shows that the heart beat rate slows, and heart rate abnormalities increase, in direct proportion to increasing fluoride levels. This occurred at the relatively low fluoride levels that cause symptoms mistaken for arthritis, in NZ as elsewhere according to WHO. Fluoride accumulates over a period of 20 to 40 years to reach the “Class 1” level (that has this effect), shown in the chart below. Arsenic and fluoride (both high in the water supplies under study) were seen to be able to exert toxic effects independently. Fluoride’s effects were evident at water at levels of 0.2 mg/L or more of fluoride:(6,7)

In laboratory studies, cultured myocardial cells of mice were adversely affected by fluoride.(8) Statistically significant increases in the concentrations of sodium and potassium, and decreases in calcium and phosphorus concentrations were observed in rats given fluoride.(9)

While many studies quoted here were conducted in areas with high fluoride levels in drinking water, total fluoride exposure today is at a similar level. Further, since fluoride is a cumulative poison, lower levels of fluoride will have a more subtle long-term effect, thus increasing heart problems – still the number one killer in our society.

This research confirms findings from the earliest days of water fluoridation in the USA that deaths from heart attacks sky-rocketed in the fluoridated communities, compared with the non-fluoridated ones:

Japanese researchers found that children with dental fluorosis have a higher incidence of heart damage than those without fluorosis.(10) Chinese researchers showed an increase in abnormal heart rhythm in patients with dental fluorosis.(11)

NZ studies show twice as many children in fluoridated areas have dental fluorosis than do non-fluoridated children. This epidemic of dental fluorosis in NZ shows that even our children are at risk of heart problems from fluoridation.

References

Li, Yuxin; Berenji, Gholam R.; Shaba, Wisam F.; Tafti, Bashir; Yevdayev, Ella; Dadparvar, Simin “Association of vascular fluoride uptake with vascular calcification and coronary artery disease” Nuclear Medicine Communications: January 2012, Volume 33, Issue 1; p 14–20
Gutowska I, Baranowska-Bosiacha I, Baskiewicz M, Milo B, Siennicka A, Marchiewicz M, Wiszniewska B, Machalinski B, Stachowska E. 2010. Fluoride as a pro-inflammatory factor and inhibitor of ATP bioavailability in differentiated human THP1 monocytic cells. Toxicology Letters 196: 74-79.
Ercan Varol et al, Biological Trace Element Research Feb 2010, Science of The Total Environment May 2010
Song et al “Observations on fluorotic aorta sclerosis by two-dimensional echo cardiography” Endemic diseases Bulletin 5, 1990, (1) 91-93
Liang et al “Investigation and analysis of cardiovascular disease in endemic and non-endemic fluorosis areas” He Bei Province Journal of Endemiology 12, (1984) 44.
Wang et al, “Toxicity From Water Containing Arsenic and Fluoride in Xinjiang” Fluoride Vol. 30 No. 2 81-84 1997
Teitz N., Clinical Chemistry, W B Saunders, Philadelphia. 1976.
Qin CD et al “Effect of fluoride on spontaneous electrical activity of cultured myocardial cells” Chinese Journal of Endemiology 7, 1988, (5) 270-273
R. J. Verma and D. M. Guna Sherlin “Hypocalcaemia in parental and F1 generation rats treated with sodium fluoride“ Food and Chemical Toxicology Volume 40, Issue 4, April 2002, Pages 551-554
The Lancet, Jan. 28, 1961, p. 197, Tokushima J. Exper., Med. 3-50-53, 1956
Wang et al, “Toxicity From Water Containing Arsenic and Fluoride in Xinjiang” Fluoride Vol. 30 No. 2 81-84 1997