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Neurological Impact Of
Fluoride Toxicity
>From Gayle
leaflady@leaflady.org
6-13-1

While the links from fluoride consumption to cancer, osteoporosis, and other physical ailments are long established, recently studies have shown that fluoride impact is much broader and includes neurological and cerebrovascular effects.
 
Fluoride has been banned in Sweden, Norway, Denmark, West Germany (now unified), Italy, Belgium, Austria, France, and The Netherlands.
 
 
Tea (not including the herbal varieties) is a surprising culprit, in addition to fluoridated drinking water supplies and fluoride toothpaste.
 
 
A 52-week study of the factors that enhance or inhibit the bioavailability of aluminum and its effects on the nervous system was published in 1998 in the Journal of Brain Research. According to the report, the equivalent of fluoridated drinking water in terms of elemental fluorine levels had an impact on brain tissue similar to the pathological changes found in humans with Alzheimer's and other forms of dementia.
 
 
The introduction to the report noted, "One of their most remarkable findings was that animals administered the lowest dose of aluminum-fluoride (0.5 ppm) exhibited a greater susceptibility to illness and a higher incidence of mortality than the animals administered the higher levels (5 ppm, 50 ppm) of aluminum [without the fluoride].
 
 
"While the small amount of aluminum-fluoride in the drinking water of rats required for neurotoxic effects is surprising, perhaps even more surprising are the neurological results of the sodium-fluoride at the dose given in the present study (2.1 ppm) [the amount used to achieve 1 ppm of elemental fluorine used in fluoridation].
 
 
"In most reports of chronic fluoride toxicity, the data provided are usually limited to weight loss, dental and skeletal changes, indicators of carcinogenesis, and damage to soft tissues.
 
 
"Fluoride has diverse actions on a variety of cellular and physiological functions, including the inhibition of a variety of enzymes, a corrosive action in acid mediums, hypocalcemia [low blood calcium], hyperkalemia [excess blood potassium], and possibly cerebral impairment."
 
 
The authors summarize, "Chronic administration of aluminum-fluoride and sodium-fluoride in the drinking water of rats resulted in distinct morphological alterations of the brain, including the effects on neurons and cerebrovasculature."
 
 
A previous study by Mullenix, et al. in Neurotoxicology and Teratology, 1995, documents abnormal behavioral responses by animals exposed to fluoride at various stages of gestation, which resulted in permanent hyperactivity if exposed prenatally, or extreme lethargy if exposed after birth, with some animals not able to find their way out of a circular maze to the same food source every day.
 
 
This study of the neurological effects of sodium fluoride, which is commonly touted as a safe and even health-promoting drinking water additive, came on the heels of a recent report in the Journal of the American Medical Association that 2 million people a year become ill, and more than 100,000 die, from medicines judged by the medical community to have been "correctly prescribed and correctly administered."
 
 
The fluoride/aluminum association is of particular importance as it relates to Alzheimer's Disease. Aluminum by itself is not readily absorbed by the body. However, fluoride ions combine with aluminum to form aluminum fluoride, which is absorbed by the body. In the body, the aluminum eventually combines with oxygen to form aluminum oxide or alumina. Protein bound to alumina in afflicted brains forms the plaques and tangles characteristic of Alzheimer's disease.
 
 
In a study by Dr. Robert Isaacson at the State University of New York, aluminum fluoride was added to rats' diet. This, contrary to normal expectations, passed through the brain barrier and gave the rats short-term memory loss, smell sensory loss, unsteady gait, and loss of structures of the neo-cortex and hippocampus, all symptoms of Alzheimer's. A Varner and Jensen study conducted with Isaacson confirmed this in 1998.
 
B-12 AND FOLATE CAN REDUCE ALZHEIMERS RISK<#TABLEtop Elderly people with low blood levels of vitamin B-12 and folic acid (folate) may face an increased risk of developing Alzheimer's disease. Vitamin B-12 plays an important role in maintaining nerve cells, and some research has linked low blood levels of the vitamin to Alzheimer's and mental decline. Few studies have looked at whether there is such a connection between Alzheimer's and folate, a B vitamin key to the production and maintenance of body cells.
 
The May 8, 2001, issue of Neurology reports on a study of 370 individuals aged 75 and older, in which investigators found that those with low levels of either vitamin were twice as susceptible to Alzheimer's over a 3-year period as those with normal levels. The link was even stronger among study participants who performed well on mental tests at the start of the study.
 
 
The reason for the link is unclear, but low blood levels of B-12 and folate can lead to elevations in the amino acid homocysteine, which may in turn damage nerve cells, the authors note. Vitamin B-12 is found in meat, fish, eggs, and milk. Vegetarians are advised to supplement their B-12 intake. Folate occurs naturally in leafy green vegetables, dried beans and peas, and citrus fruits, among others. Many cereals are fortified with folic acid, the synthetic form of folate.
 
 
Alzheimer's is the most common form of dementia, affecting an estimated 4 million Americans. The exact cause remains elusive, but scientists believe genetics and environmental factors conspire to trigger the onset of the disease.
 
 
The May 8, 2001 issue of Neurology Magazine listed the following as warning signs of Alzheimer's Disease: memory loss that affects job skills; language problems; difficulty performing familiar tasks; misplacing objects; changes in mood and behavior; poor judgment; disorientation as to time and place; personality changes; problems with abstract thinking; and loss of initiative.
 
 
Brain imaging is recommended to help rule out other causes of memory loss or dementia. This includes computed tomography (CT) and magnetic resonance imaging (MRI). Genetic testing has not been found particularly useful. [Annual Meeting of the American Academy of Neurology, 2001]
 
 
The elderly are not the only ones that need to worry about B-12. According to one practitioner, the most common cause of B-12 deficiency is a vegetarian diet.
 
 
The drug Prilosec (omeprazole) has been shown to decrease B-12 absorption [Annual of Pharmacotherapy, May 1999]. This is possibly due to its effects on decreasing the production of intrinsic factor, which is needed for proper B-12 absorption. Other medications may have similar adverse effects.
 
 
There is also little question now that B-12 and folic acid are useful to reduce homocysteine and the associated increase in heart disease and birth defects.

                                                



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