A new study has just been published which further elucidates how fluoride may damage the brain. The study, published in the August 2004 issue of the journal Toxicology, is the latest by a team of Chinese and Swedish scientists, members of which have been researching the impact of fluoride on brain for the past 8 years.
The team, headed up by neurotoxicologist Dr. Zhizhong Guan from the Karolinska Institute in Sweden, has probably investigated the impact of fluoride on brain more thoroughly than any other team in the world. Dr. Guan himself has researched the issue since as far back as 1986, although most of his research on the issue has been published since 1997.
The latest study from the Guan team investigates an important finding they first reported in 2002: namely, that rats drinking fluoride in water for 7 months had a decrease in “nicotinic acetylcholine receptors”, or “nAChRs”, in their brains.
The Potential Implications of Reduced nAChRs in the Brain
The potential implications of the Guan team’s finding can be gleaned from a recent review by Dr. Agneta Nordberg, a Swedish neurotoxicologist and expert on nAChRs.
According to Nordberg (who is now working with Dr. Guan on his fluoride/brain research):
“The neuronal nicotinic acetylcholine receptors (nAChRs) in the brain are important for functional processes, including cognitive and memory functions… The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy. The exact role of nAChRs and their full potential as a therapeutic target in these diseases have yet to be clarified.”
In regards to the relationship between decreased nAChRs and alzheimers disease, Nordberg writes:
“A consistent, significant loss of nAChRs has been observed in cortical autopsy brain tissue from [alzheimers] patients relative to age-matched healthy subjects. More recently, we have found that the nAChR deficits in [alzheimers] brains probably represent an early phenomenon in the course of the disease, which can be detected in vivo by positron emission tomography.”
SOURCE: Nordberg A. (2001). Biological Psychiatry 49:200-10.
In 2002, when it was first reported (in the journal Neurotoxicology & Teratology) that fluoride could decrease nAChRs in rat brain, Dr. Guan, Dr. Nordberg and colleagues stated:
“Since nAChRs play major roles in cognitive processes such as learning and memory, the decrease in the number of nAChRs caused by fluoride toxicity may be an important factor in the mechanism of brain dysfunction in the disorder.”
In the new 2004 study, Dr. Guan, Dr. Nordberg, and colleagues, report on how fluoride might be causing the reduction in these nAChRs.
Their tentative conclusion is that the reduction is connected to a fluoride-induced increase in oxidative stress. Supporting this conclusion was the finding that pre-treating the rats with anti-oxidants seemed to prevent the reduction in nAChRs caused by fluoride. The conclusion is also supported by a series of earlier studies from the Guan team which found that oxidative stress plays an important role in fluoride toxicity, not only in the brain, but in the liver and kidney as well.
The dose is the poison
For the skeptical-minded out there, I can imagine the question about dose is coming to the fore: How much fluoride did the rats in these studies receive, and how do these doses compare with what humans receive?
In their studies on fluoride toxicity, Guan and colleagues use 3 groups of rats. 1 group receives no fluoride in their water, 1 group receives 30 ppm fluoride, while 1 group receives 100 ppm fluoride. The duration of the studies is usually 7 months.
Among the 3 groups of rats, Guan has found that – while the damage is consistently greatest in the 100 ppm group – damage also occurs in the 30 ppm group as well. Damage in the 30 ppm group includes increased oxidative stress (as reflected by reduced lipid content) and reductions of some (but not all) nAChRs.
Relevance to humans?
On th