s 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 the face of it, it would seem that rats drinking 30 ppm fluoride in water are receiving roughly 30 times more fluoride than humans drinking fluoridated water (1 ppm). However, upon closer inspection, this assumption does not hold true.
Why? Because rats are more resistant to fluoride toxicity than humans. The increased resistance of rats to fluoride toxicity seems to stem from the ‘reduced intestinal absorption’ of fluoride found in the rat. In other words, when rats ingest fluoride, less of the ingested fluoride actually makes it into their bloodstream. Because of this, rats are known to have far lower levels of fluoride in their blood than humans when consuming the same level of fluoride in water.
Indeed, while Guan and colleagues do not provide data on the level of fluoride in the rats’ blood, the blood levels normally found in rats drinking ~30 ppm fluoride in water (range = ~76-143 ppb) are actually overlapped and exceeded on a chronic basis by a portion of the human population (particularly those with kidney disease) living in fluoridated, and even unfluoridated, areas.
Moreover, the lower range of the levels normally found in rat’s blood drinking 30 ppm fluoride are also reached by young children (albeit for short duration) after ingesting fluoridated toothpaste and/or fluoride supplements. And, on a less frequent basis, young children’s blood can temporarily be infused with fluoride levels which far surpass (by up to a factor of 10) the levels found in rats drinking 30 ppm. The occasion? Use of high concentration acidulated fluoride gels in the dental chair.
Thus, for reasons that should become even more apparent in future Science-Watch bulletins, any damage found in rats drinking water with just 30 ppm fluoride should be taken very seriously.
A Tale of Two Worlds?
Finally, it is heartening to note that the Guan team has apparently not had any problems securing financial support to continue their research. Their research has consistently received ample funds from branches of the Chinese Government and China