Central Nervous System Damage from Fluorides

by Phyllis J. Mullenix, Ph.D. September 14, 1998

It was 1982 when fluoride was first brought to my attention as a substance in need of investigation. At that time, I was in the Departments of Psychiatry at Boston’s Children’s Hospital and Neuropathology at the Harvard Medical School. My studies focused on detection procedures for neurotoxicity, and they typically considered a variety of environmental and therapeutic agents, i.e., radiation, lead, amphetamine, phenytoin, nitrous oxide. Dr. John Hein, then Director of Forsyth’s Dental Infirmary for Children in Boston, was interested in neurotoxicity studies and invited me to continue this research at Forsyth and to apply it to substances used in dentistry. Fluoride was prominent on his list.

Five years lapsed before our investigations of fluoride began. The delay was due to time spent on technological improvements, specifically development of a computer pattern recognition system for the objective quantification of behavior in an animal model. In early June of 1986, the Forsyth Dental Center was noted for this achievement in the Wall Street Journal and the Boston Herald, and applications of our research grew. The new technology enabled us to study the clinically recognized neurotoxicity associated with the treatment for childhood leukemia. Simultaneously, we started investigations of fluoride, the “safe and effective” treatment for dental caries.

Initially, the fluoride study sparked little interest, and in fact we were quite anxious to move on to something academically more exciting. Using an animal model developed for the study of dental fluorosis, we expected rats drinking fluoride-treated water would behave the same as matching controls. They did not. The scientific literature led us to believe that rats would easily tolerate 175 ppm fluoride in their drinking water. They did not. Reports in the literature indicated that fluoride would not cross the blood brain barrier. But it did. Prenatal exposure to fluoride was not supposed to permanently alter behavioral outcome. It did. Like walking into quicksand, our confidence that brain function was impervious to fluoride was sinking.

Our 1995 paper in Neurotoxicology and Teratology was the first laboratory study to demonstrate in vivo that central nervous system (CNS) function was vulnerable to fluoride, that the effects on behavior depended on the age at exposure and that fluoride accumulated in brain tissues. The behavioral changes common to weanling and adult exposures were different from those after prenatal exposure. Whereas prenatal exposure dispersed many behaviors as seen in drug-induced hyperactivity, weanling and adult exposures led to behavior- specific changes more related to cognitive deficits. Brain histology was not examined in this study, but we suggested that the effects on behavior were consistent with interrupted hippocampal development (a brain region generally linked with memory).

Establishing a threshold dose for effects on the CNS, in rats or humans, was not the intent of this initial investigation. Yet, one fact relevant to human exposure emerged quite clear. When rats consumed 75-125 ppm and humans 5-10 ppm fluoride in their respective drinking waters, the result was equivalent ranges of plasma fluoride levels. This range is observed with some treatments for osteoporosis, and it is exceeded ten times over, one hour after children receive topical applications of some dental fluoride gels. Thus, humans are being exposed to levels of fluoride we know alters behavior in rats.

We concluded that the rat study flagged potential for motor dysfunction, IQ deficits and/or learning disabilities in humans. Confident as we were, the data were only one piece of the puzzle, the overall picture was still emerging. Soon thereafter we learned of two epidemiological studies (Fluoride, 1995-1996) from China showing IQ deficits in children over-exposed to fluoride via drinking water or soot from burning coal. A recent review (International Clinical Psychopharmacology, 1994) listed case reports of CNS effects in humans excessively exposed to fluoride, information that spans almost 60 years. A common theme appeared in the reported effects: impaired memory and concentration, lethargy, headache, depression and confusion. The same theme was echoed in once classified reports about workers from the Manhatten Project. In all, our rat data seem to fit a consistent picture.

Information linking fluoride and CNS dysfunction continues in 1998.

1) A recent study in Brain Research demonstrated that chronic exposure to fluoride in drinking water of rats compromised neuronal (hippocampal) and cerebrovascular integrity (blood brain barrier) and increased aluminum concentrations in brain tissues.
2) Masters and Coplan have reported (International Journal of Environmental Studies, in press) that silicofluorides in fluoridated drinking water increased levels of lead in children’s blood, a risk factor that predicts higher crime rates, ADD and learning disabilities.
3) Luke at the International Society for Fluoride Research (ISFR) meeting in August reported that fluoride accumulated in the human pineal gland, as much or more so than in bones and teeth, and the pineal gland’s melatonin biosynthesis pathway is affected by fluoride.
4) Also at the ISFR meeting, I reported that the fluorinated steroid (dexamethasone) disrupts behavior in rats to a greater degree than does the nonfluorinated steroid (prednisolone). This finding matched results just completed in a study of children receiving steroids as a part of their treatment for childhood leukemia. Dexamethasone, compared to prednisolone, further reduced IQ, specifically impairing reading comprehension, arithmetic calculation and short-term working memory.

Exposure to fluoride goes well beyond that in our drinking water, toothpastes and mouth rinses. Fluoridation of water dictates that it is in food and processed beverages. Pesticides such as cryolite also increase fluoride content of foods. The trend toward fluorinating pharmaceuticals increases fluoride exposure via medication. Fluoride, in various compounds, plays a heavy role in occupational exposures and for people living in close proximity to industry, i.e., aluminum, steel, brick, glass, petroleum, etc. With exposure so common, we can no longer afford to ignore potential CNS consequences of fluoride.

Phyllis J. Mullenix, Ph.D.

Kucinich Sells Out On Health Care After Ride In Air Force One

Steve Watson
Prisonplanet.com
Wednesday, March 17th, 2010

Democratic Congressman Dennis Kucinich has bowed to intense pressure, culminating in a jaunt onboard Air Force One with President Obama, and decided to to flip his vote on the pending health care bill to help ensure its passage.

The representative from Ohio has repeatedly voiced his opposition to the bill, calling it “a giveaway to the insurance industry”.

“The fact is that one out of every three health care dollars goes for corporate profits, stocks options, executive salaries, advertising, marketing, the cost of paperwork – this bill doesn’t change that.” he said.

Just last week, Kucinich told MSNBC’s Countdown that that even if it meant he had the deciding vote in the House, he would oppose the legislation, effectively signing its death warrant.

As recently as Sunday, Kucinich was still reiterating the same points. In an column for the Cleveland Plain Dealer, he wrote:

“Even with the few modest improvements in the bill, the insurance companies will still have dozens of loopholes to deny care and continue to find ways to leave Americans with the unpayable bill.”

Today, however, Kucinich announced at a Capitol news conference that he will vote yes on the latest version of the bill.

“I have doubts about the bill,” Kucinich said. “This is not the bill I wanted to support… However, after careful discussions with President Obama, Speaker Pelosi, my wife Elizabeth and close friends, I’ve decided to cast a vote in favor of the legislation.”

“I know I have to make a decision, not on the bill as I would like to see it, but as it is,” he added.

“I’ve had four separate meetings with the President,” Kucinich also said this morning. “When the President of the United States wants to have a conversation with you, you take that seriously.”

“We have to be very careful that the potential of President Obama’s presidency not be destroyed by this debate,” the Congressman stated.

“I got an invitation to go on Air Force One – given my previous record in not supporting the administration on many things, I thought that proper attire would include a parachute,” he added.

Watch the video:

On Monday, Kucinich stepped aboard Air Force One in Maryland at 11:13 a.m. and landed 48 minutes later in Cleveland, having discussed the health care bill with Obama.

It is anyone’s guess as to whether the conversation drew upon comments made by Obama last week indicating that he will refuse to campaign for any Democratic congressmen who fails to support health care reform. However, Kucinich cannot have been unaware of the announcement.

Neither can the Ohio Congressman have missed the soft threat Obama directed toward Kucinich at a Rally in his own district Monday.

Kucinich stated that he was not offered any favours by the president, and that Obama made no assurances that he would push for a public option after the bill passes, a provision that Kucinich has long demanded.

In addition to a barrage of pressure from his own party, Kucinich has received harsh criticism from the so called Democratic “Fifth Chief Directorate”, the Daily Kos, Huffington Post, and Democratic Underground.

The day after Kucinich appeared on Countdown, Daily Kos founder Markos Moulitsas appeared on the same show, fiercely criticizing the Ohio representative’s threat to vote against the reform bill, adding that Kucinich should be subject to a primary challenge as a result.

“I’m going to hold people like Dennis Kucinich responsible for the 40,000 Americans that die each year from a lack of health care.” Moulitsas stated, before personally attacking Kucinich with taunts about him using presidential campaigns to score dates.

Investigative journalist Wayne Madsen has some interesting information on Kos and his ilk that sheds some light on their consistent attacks on any liberal figures that do not offer unwavering support for the establishment left and their corporate bedfellows.

Kucinich’s turnaround highlights the fact that, although he is the closest thing the Democrats have, he is no Ron Paul. His own principles, the good of the people, and the Constitution unfortunately come in a poor second place to the special relationship between big government and corporate America.

Sebelius Asks Media to Censor Autism Debate

By Katie Wright, noonehastodietomorrow.com
03-17-2010 01:18

“There are groups out there that insist that vaccines are responsible for a variety of problems, despite all scientific evidence to the contrary. We (the office of Secretary of Health and Human Services) have reached out to media outlets to try to get them not to give the views of these people equal weight in their reporting.”

See Reader’s Digest HERE.

That’s right. Kathleen Sebelius, the Secretary of HHS, has asked newspapers, magazines, television journalists, who knows who else- specifically NOT to listen to parents and scientists in the autism community, not to respect their concerns, not to take seriously the condition of chronically ill children with autism and to disregard a growing body of evidence questioning the safety of our infant and toddlers’ immunization schedule. If I have got anything wrong I would love to hear a tape or see a transcripts of these media “outreaches.”

Pretty frightening stuff. Thank you to Jake Crosby who uncovered this frank and disturbing exchange between Arthur (autism is not so bad and there is no increase anyway) Allen and Ms. Sebelius.

I am taking Ms. Sebelius at her word. Ms. Sebelius has unilaterally said that she knows that every single American parent who saw their child regress post vaccination or experience a severe adverse reaction is wrong and she knows better. Ms. Sebelius has ordered, suggested, beseeched, implored (?) American journalists NOT to “give these people (anyone concerned with vaccine safety) equal weight in their reporting” because she has decided by informal governmental decree that the debate is closed?

Sounds like something that would happen in a communist dictatorship, right? Was there a similar decree when “citizen dissidents” questioned the safety of hormone replacement therapy for women? Was the media instructed to ignore those nuisances who were suspicious of a long denied link between hormone therapy and breast cancer? Did the HHS order a first amendment crackdown of those trouble-making women who had long complained that Fibromalgia was a real disease and not a psychosomatic condition. Menaces everywhere who dared to question medical authorities! They must be silenced! You have got to be kidding.

Sebelius boasts that she holds an H1N1 meeting every single day but cannot find the time to attend one IACC meeting or meet with any autism organizations. Well, not exactly, apparently Ms. Sebelius is personal friends with Ms. Alison Singer, leader a vaccine marketing/ autism org financed in part by Dr. Paul Offit. Newsflash Ms. Seblius: 1 in 100 American children, and rising, have autism and this is a much bigger deal than H1N1. One in four American parents do not think vaccines are safe for their children. At least half of all families affected by autism believe too many vaccines too soon triggered their child’s autism. Hundreds of thousands of parents saw their child regress post multiple vaccinations. Sebelius’ answer to this massive crisis of confidence is media censorship?

Hmmmm…..Censorship has a long and illustrious history- of not working. Thankfully, we live in a democracy with a free press. So I don’t know what is worse, the fact Sebelius asked that journalists censor the autism debate or the fact that they did.
While I have not read more than a few reasoned, balanced or well written pieces of journalism on the subject of autism and vaccines I have read a host of spoon fed press releases masquerading as “news” stories about supposedly important autism research. Journalists from “Time”, “Newsweek”, “The New York Times”, online health resources etc. have reported in depth on such “breakthroughs” as a recent study concluding that “maternal sensitivity” is a good thing for autistic children, or Kennedy Krieger’s incredible finding that autistic kids have bad handwriting (amazing, I know!) or the Children’s Hospital of Boston study which found that cousins from the Middle East who marry are more likely to produce autistic kids. I know, stop the presses, a cure is within sight!

In this embarrassing interview with Arthur Allen Ms. Sebelius asserts all the science is a closed book. At the top of the list of the science of vaccine safety studies are the definitive 2001 and 2003 “Pediatrics” articles. While the media has kept us front row center in the breaking developments regarding ASD kids with bad handwriting, journalists have neglected to report on perhaps one of the most striking recent events concerning the subject of autism research.

An author of one of the most frequently cited “vaccines do not trigger autism” articles is Dr. Poul Thorsen. Well, well, well… this week we learned that Thorsen has allegedly absconded with approximately $2 million of CDC research money and is the target of an international police manhunt. We also learned that the Univ. of Aarhus, Denmark, where Thorsen was employed when conducting the studies (naturally in close cooperation w/ the CDC) has released a letter detailing Thorsen’s recently uncovered crimes. These crimes include but are not limited to: theft, forgery and assorted serious breaches of ethical norms.

Apparently Thorsen was a very, very busy scientist. He was simultaneously and secretly employed at the Univ of Aarhus, Emory University, Drexel University and as a “visiting scientist at the CDC.” Emory and Drexel have, some might say, inappropriately close relationships with the CDC. There appears to be very little room for independent or unbiased science at these research centers. All three are heavily invested in denying any relationships between vaccines and autism. The CDC owns numerous vaccine patents and Emory and Drexel receive tremendous financial support from vaccine companies.

Hmmmm…I know some of you might be thinking “Emory University is in the news a lot lately!” Yes, Emory has been in the news a great deal thanks to the amazing anti- corruption work of Senator Charles Grassley. Ms. Sebelius should dump Arthur Allen and have a conversation with someone who is actually doing something to restore public confidence in our health systems by fighting the fraud and greed inherent at places like Emory. Grassley is conducting an investigation a pervasive pattern of corruption among Emory researchers who fail to disclose significant financial conflicts of interest in the outcomes of the research they conduct. Isn’t it interesting that Thorsen found a second home there?

Thorsen was working hard for everyone’s benefit: his own, his employers, pharmaceutical companies- everyone’s benefit, that is, except the public’s. The health and safety of American kids being administered the world’s most aggressive infant vaccine schedule was last on his list. Thorsen was also employed as a consultant on the official revisions of the all-important DMS V. Thorsen was advising how to count and classify autism cases. It is absolutely frightening that a wanted felon has such an enormous and pervasive influence on the lives of our children.

So I am trying to get this straight Ms. Sebelius. Help me out here. We should take lying thieves with no interest in operating in the public’s interest at their word but the media should ignore parents and legitimate scientists who question the validity of vaccine science research performed by alleged criminals? I’m really confused!

Wouldn’t it be great if Sebelius lifted her fatwa on vaccine research reporting and someone discovered what this creep Thorsen was actually up to at Drexel and Emory? Why was Thorsen a “visiting scientist at the CDC” at the same time? Apparently the CDC has known about this theft (of our money) for some time but has chosen to remain silent. I wonder why? How likely is it that Thorsen was the only scientist involved in what appears to be a massive and long term scheme to manipulate and forge scientific documents? Most importantly, why should the public believe that a thief and a liar with no ethical standards would be honest and scrupulous in his research? I shudder at the thought of Thorsen recounting “the facts” of his studies to students while asserting, as he frequently did, that “absolutely no more vaccine/autism research is warranted.” Now there’s a guarantee you can take to the bank. Oops, maybe a bank Thorsen hasn’t robbed.

Fluoride’s effect on the brain

(www.fluoridation.com) Fluoride’s Neurological Effects: studies show there may be grave implications for Alzheimers, Dementia, Attention Deficit Disorder, reduced IQ in children

Neurotoxicity of fluoride, Fluoride, 1996, 29:2, 57-58 (Editorial by AWB and JC)

The August 1995 issue of this journal contained an abstract (pages 151-152) of an interesting paper by Dr Phyllis Mullenix and her collaborators.1 They recorded behavioral changes in rats after ingestion of fluoride, and found that the severity of the effect on behavior increased directly with plasma fluoride levels and fluoride concentration in specific brain regions. A reading of the full paper is well worthwhile. In their Introduction, after referring to the increase in dental fluorosis in humans after decades of water fluoridation, the authors comment:

“One concern that has not been fully investigated is the link between fluoride and effects an the central nervous system (CNS)…. Many years of ubiquitous fluoride exposure have not resulted in obvious CNS problems such as seizures, lethargy, salivation, tremors, paralysis, or sensory deficits. Still unexplored, however, is the possibility that fluoride exposure is linked with subtle brain dysfunction.”

The carefully designed animal experiment which they report revealed subtle but very real changes in behavior patterns following fluoride ingestion: hyperactivity after prenatal exposure, and cognitive deficits after weanling and adult exposure. Fluoride accumulation in important regions of the rat brain, especially the hippocampus, was found to increase as the drinking water fluoride levels increased. These effects, and the sex differences observed, corresponded to those observed in other studies of hippocampal brain damage.

The authors point out that the plasma fluoride levels recorded in the rats were the same as those sometimes recorded in humans – for example, in children one hour after receiving topical fluoride treatment of their teeth. In their conclusion calling for further rat and human studies they state:

“Experience with other developmental neurotoxicants prompt expectations that changes in behavioral function will be comparable across species, especially humans and rats. Of course behaviors per se do not extrapolate, but a generic behavioral pattern disruption as found in this rat study can be indicative of a potential for motor dysfunction, IQ deficits and/or learning disabilities in humans.”

The authors draw attention to reports from Chinese investigators that high levels of fluoride in drinking water (3-11 ppm) affect the central nervous system directly without first causing the physical deformations of skeletal fluorosis.2-4 Readers of Fluoride will recall the recent (November 1995) research report from China indicating adverse neurological effects on the brain from fluoride exposure.5 This work also suggested that children with dental fluorosis are at greater risk of decreased mental acuity. One can only wonder whether the effects of fluoridated water might extend beyond the appearance of the teeth and include neurotoxicity among children afflicted with dental fluorosis.

Some of our readers may recall also pertinent early clinical findings reported by our founding editor, Dr G L Waldbott, of which Dr Mullenix and her co-workers do not appear to have been aware. These involved a wide range of reversible toxic effects of fluoridated drinking water, including diminished mental acuity and impairment of memory.6-8 In a separate report, Dr Waldbott even gave an account, supported by laboratory data, of a case of tetaniform convulsions induced by drinking fluoridated drinking water.9 For decades proponents of water fluoridation have questioned the validity of these reports without, however, offering objective evidence to refute them. But in the light of the human research in China and now the animal research in the United States, these clinical observations by Dr Waldbott on the neurotoxicity of fluoride in drinking water clearly deserve greater attention and credence. [references not scanned]

Jaqueline Calderon, Machado Blenda, Navarro Marielena, Carrizales Leticia, Ortiz Maria Deogracias, Diaz-Barriga F. Influence of Fluoride Exposure on Reaction Time and Visuospatial Organization in Children, Epidemiology July 2000, Volume 11, Number 4 Supplement S153.

Fluoride exposure is an important public health problem in several Mexican states. In the city of San Luis Potosi, Mexico, above 90% of the children have some degree of dental fluorosis. The main source of exposure to fluoride is tap water. The objective of the study was to evaluate the influence of chronic exposure to fluoride on neuropsychological development in children. Sixty-one children aged 6 to 8 years were included. Fluoride concentration in tap water ranged from 1.2 to 3 mg/L. Fluoride exposure was measured in urine samples by electrothermal ion selective method. Blood lead (PbB) was measured as indicator of lead exposure by atomic absorption spectrophotometry. Height for age index (HAI) was calculated as indicator of past nutritional status. Three tests were used to evaluate the neuropsychological development: (1) Wechsler Intelligence Scale for Children Revisited version for Mexico (WISC-RM), (2) Rey Osterrelth-Complex Figure test and (3) Continuos Performance Test (CPT). Mean value of fluoride in urine was 4.3 mgF/g creatinine (1.6-10.8). Mean PhB value was 6.2 ug/dl (2.0-15.6). After controlling by significant confounders, urinary fluoride correlated positively with reaction time and inversely with the scores in visuospatial organization. IQ scores were not influenced by fluoride exposure. An increase in reaction time could affect the attention process, also the low scores in visuospatial organization could be affecting the reading and writing abilities in these children.

University of North Caroline. Email: Jaqueline.Calderon@sph-unc.edu

Guan ZZ, Wang YN, Xiao KQ, Dai DY, Chen YH, Liu JL, Sindelar P, Dallner G, Influence of chronic fluorosis on membrane lipids in rat brain. Neurotoxicol Teratol 1998 Sep-Oct;20(5):537-42

Brain membrane lipid in rats were analyzed after being fed either 30 or 100 ppm fluoride for 3, 5, and 7 months. The protein content of brain with fluorosis decreased, whereas the DNA content remained stable during the entire period of investigation. After 7 months of fluoride treatment, the total brain phospholipid content decreased by 10% and 20% in the 30 and 100 ppm fluoride groups, respectively. The main species of phospholipid influenced by fluorosis were phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine. The fatty acid and aldehyde compositions of individual phospholipid classes were unchanged. No modifications could be detected in the amounts of cholesterol and dolichol. After 3 months of fluoride treatment, ubiquinone contents in brain were lower; however, at 7 months they were obviously increased in both groups of fluoride treatment. The results demonstrate that the contents of phospholipid and ubiquinone are modified in brains affected by chronic fluorosis and these changes of membrane lipids could be involved in the pathogenesis of this disease.

Department of Pathology, Guiyang Medical College, Guizhou, China. jialiul@public.gy.gz.cn

Jope RS, Modulation of phosphoinositide hydrolysis by NaF and aluminum in rat cortical slices. J Neurochem 1988 Dec;51(6):1731-6

NaF stimulated phosphoinositide hydrolysis in rat cortical slices. The production of [3H]inositol monophosphate was rapid for the first 15 min of incubation with NaF, followed by a plateau. The major product detected was [3H]inositol monophosphate, although significant amounts of [3H]inositol bisphosphate and [3H]inositol trisphosphate were also produced. The stimulation of [3H]inositol monophosphate production by NaF was concentration dependent between 2 and 20 mM NaF. Addition of 10 or 100 microM AlCl3 or aluminum maltol did not alter the effect of NaF, whereas at 500 microM, these aluminum preparations resulted in significant inhibition. Increasing the concentration of K+ from 5 to 20 mM potentiated [3H]inositol monophosphate production induced by carbachol but not by NaF. Incubation with 1 microM phorbol 12-myristate 13-acetate, a phorbol ester, inhibited carbachol-induced, but not NaF-induced, [3H]inositol monophosphate production. These results further support the hypothesis that a guanine nucleotide binding protein that can be activated by NaF is involved in phosphoinositide hydrolysis in brain. The use of NaF provides a means to bypass receptors to study intracellular regulatory sites of phosphoinositide metabolism without disrupting cells.

Department of Pharmacology and Neuropsychiatry Research Program, University of Alabama, Birmingham.

Kay AR, Miles R, Wong RK, Intracellular fluoride alters the kinetic properties of calcium currents facilitating the investigation of synaptic events in hippocampal neurons. J Neurosci 1986 Oct;6(10):2915-20

We have attempted to suppress voltage-dependent conductances in hippocampal neurons by introducing various intracellular agents. Voltage-clamp studies were carried out using acutely dissociated hippocampal neurons from adult guinea pigs. Synaptic events were examined using intracellular recordings in the slice preparation. Sodium conductance was suppressed when the quaternary lidocaine derivative QX 314 was introduced intracellularly. Potassium conductances were blocked by intracellular cesium or Tris. We also found that the anion fluoride could affect calcium conductance by an intracellular action. When anions other than fluoride were used for intracellular recordings, the voltage-dependent calcium current inactivated slowly and showed persistent activation at membrane potentials between -40 and -10 mV. In contrast, when fluoride was present intracellularly, the inactivation kinetics of the calcium current were accelerated and the persistent component of the current was largely suppressed. Intracellular recordings in the hippocampal slice showed that when electrodes contained cesium, QX 314, and fluoride, the spiking and nonlinear responses of the neuronal membrane to depolarization were blocked. In these conditions the time course and voltage-dependence of EPSPs could be examined in detail without complications due to voltage-dependent currents of the postsynaptic cell.

Li Y, Li X, Wei S, Effect of excessive fluoride intake on mental work capacity of children and a preliminary study of its mechanism, Hua Hsi I Ko Ta Hsueh Hsueh Pao,1994 Jun, 25 :2, 188-191 (Translated from Chinese)

We made an investigation in 157 children, aged 12-13, born and grew up in a coal burning pattern endemic fluorosis area and an experiment on excessive fluoride intake in rat. The results showed: (1) Excessive fluoride intake since early childhood would reduce mental work capacity (MWC) and hair zinc content: (2) The effect on zinc metabolism was a mechanism of influence on MWC by excessive fluoride intake; (3) Excessive fluoride intake decreased 5-hydroxy indole acetic acid and increased norepinephrine in rat brain; whether this is also a mechanism of the influence on MWC awaits confirmation.

Li XS, Zhi JL, Gao RO, Effect of Fluoride Exposure on Intelligence in Children, Fluoride, 1995 Nov, 28:4, pp 189-192

The intelligence was measured of 907 children aged 8-13 years living in areas which differed in the amount of fluoride present in the environment. The Intelligence Quotient (IQ) of children living in areas with a medium or severe prevalence of fluorosis was lower than that of children living in areas with only a slight fluorosis or no fluorosis. The development of intelligence appeared to be adversely affected by fluoride in the areas with a medium or severe prevalence of fluorosis but to a minor extent only in areas with only a slight prevalence of fluorosis. A high fluoride intake was associated with a lower intelligence. No correlation was found between age and intelligence in the areas with a medium and severe prevalence of fluorosis. The effect of exposure to a high level of fluoride on intelligence may occur at an early stage of development of the embryo and infant when the differentiation of brain nerve cells is occurring and development is most rapid.

Liu WX, Experimental study of behavior and cerebral morphology of rat pups generated by fluorotic female rat, Chung-hua Ping Li Hsueh Tsa Chih, 1989 Dec, 18:4, 290-292 (Article in Chinese)

In order to study the effects of fluoride on the central nervous system, 33-42-day old rat pups generated by three groups of female Wistar rats, which were given distilled water containing 0, 30 and 60 ppm NaF respectively beforehand as drinking water for 85 days, were used for behavior test and cerebral morphological examination. The results of behavior test showed that the latent period of pain reaction and that of conditioned reflex in the 30 ppm F and 60 ppm F groups were longer than that in the control group (P less than 0.05 or P less than 0.01). morphological examination of the pup brains showed that the nerve cell density of the 60 ppm F group was higher than that of the control group (P less than 0.05). Electronmicroscopically, mild degeneration of organelles of the nerve cells was observed in those brains of the 60 ppm F group.

Mattsson JL, Albee RR, Eisenbrandt DL Chang LW, Subchronic neurotoxicity in rats of the structural fumigant, sulfuryl fluoride, Neurotoxicol-Teratol, 1988 Mar-Apr, 10:2, 127-133

Inhalation exposure of male and female Fischer 344 rats to sulfuryl fluoride [Vikane (Dow Chemical Company) gas fumigant] at 300 ppm for 6 hr/day, 5 days week, for 13 weeks caused diminished wight gain, dental fluorosis, a slight decrease in grooming, decreased flicker fusion threshold, slowing of flash, auditory and somatosensory evoked potentials, mild nasal and pulmonary inflammation, mild kidney effects, and mild vacuolation in the brain. Auditory brainstem responses (ABRs) and brain histology were evaluated two months postexposure in 2 male and 2 female rats. Both the ABRs and brain histology were within normal limits at this time, indicating that these treatment effects were, to at least a great extent, reversible. Exposure to 100 ppm resulted in dental fluorosis and very minor slowing of some evoked responses; all other measures, including brain histology, were normal. No treatment effects were noted at 30 ppm.
Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ, Neurotoxicity of sodium fluoride in rats, Neurotoxicology Teratology, 1995 March,17(2):169-177.

Fluoride (F) is known to affect mineralizing tissues, but effects upon the developing brain have not been previously considered. This study in Sprague-Dawley rats compares behavior, body weight, plasma and brain F levels after sodium fluoride (NaF) exposures during late gestation, at weaning or in adults. For prenatal exposures, dams received injections (SC) of 0.13 mg/kg NaF or saline on gestational days 14-18 or 17-19. Weanlings received drinking water containing 0, 75, 100, or 125 ppm F for 6 or 20 weeks, and 3 month-old adults received water containing 100 ppm F for 6 weeks. Behavior was tested in a computer pattern recognition system that classified acts in a novel environment and quantified act initiations, total times and time structures. Fluoride exposures caused sex- and dose-specific behavioral deficits with a common pattern. Males were most sensitive to prenatal day 17-19 exposure, whereas females were more sensitive to weanling and adult exposures. After fluoride ingestion, the severity of the effect on behavior increased directly with plasma F levels and F concentrations in specific brain regions. Such association is important considering that plasma levels in this rat model (0.059 to 0.640 ppm F) are similar to those reported in humans exposed to high levels of fluoride. [emphasis added]

See also brain2.htm by Dr. P.J. Mullenix

Spittle B, Psychopharmacology of fluoride: a review, Int Clin Psychopharmacol, 9:2, 1994 Summer, 79-82

Although the blood-brain barrier is relatively impermeable to fluoride, it does not pose an absolute barrier and fluoride has the ability to enter the brain. The literature was examined to assess the quality of the evidence for cerebral impairment occurring due to exposure to fluoride from therapeutic or environmental sources. Several surveys of persons chronically exposed to industrial fluoride pollution reported symptoms related to impaired central nervous system functioning with impaired cognition and memory. Examination of individual case reports showed the evidence for aetiological relationships between symptoms and fluoride exposure to be of variable quality. The evidence was seen as being suggestive of a relationship rather than being definitive. The difficulties with concentration and memory described in relation to exposure to fluoride did not occur in isolation but were accompanied by other symptoms of which general malaise and fatigue were central. Possible mechanisms whereby fluoride could affect brain function include influencing calcium currents, altering enzyme configuration by forming strong hydrogen bonds with amide groups, inhibiting cortical adenylyl cyclase activity and increasing phosphoinositide hydrolysis.

[editor's note: this review was published before Mullenix et al., completed their ground-breaking study. The blood-brain barrier is penetrated by fluoride]

Strunecká A, Patoèka J, Pharmacological implications of aluminofluoride complexes, a review of the evidence for pathophysiological effects of aluminium and fluoride on living organism

Varner JA, Jensen KF, Horvath W, Isaacson RL, Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity. Brain Res 1998 Feb 16;784(1-2):284-98

This study describes alterations in the nervous system resulting from chronic administration of the fluoroaluminum complex (AlF3) or equivalent levels of fluoride (F) in the form of sodium-fluoride (NaF). Twenty seven adult male Long-Evans rats were administered one of three treatments for 52 weeks: the control group was administered double distilled deionized drinking water (ddw). The aluminum-treated group received ddw with 0.5 ppm AlF3 and the NaF group received ddw with 2.1 ppm NaF containing the equivalent amount of F as in the AlF3 ddw. Tissue aluminum (Al) levels of brain, liver and kidney were assessed with the Direct Current Plasma (DCP) technique and its distribution assessed with Morin histochemistry. Histological sections of brain were stained with hematoxylin & eosin (H&E), Cresyl violet, Bielschowsky silver stain, or immunohistochemically for beta-amyloid, amyloid A, and IgM. No differences were found between the body weights of rats in the different treatment groups although more rats died in the AlF3 group than in the control group. The Al levels in samples of brain and kidney were higher in both the AlF3 and NaF groups relative to controls. The effects of the two treatments on cerebrovascular and neuronal integrity were qualitatively and quantitatively different. These alterations were greater in animals in the AlF3 group than in the NaF group and greater in the NaF group than in controls. Copyright 1998 Elsevier Science B.V.

Psychology Department, Binghamton University, Binghamton, NY, USA.

Varner JA, Jensen KF, Horvath W, Issacson RL, The Neurotoxicological Evaluation Of The Chronic Administration Of Aluminum-Fluoride and Sodium-Fluoride, Society for Neuroscience Annual Meeting; San Diego, CA, 1995 Nov, abstract.

This study examined the neurotoxic consequences of the chronic ingestion of AlF₃ and the equivalent fluoride concentration given as low doses of NaF in drinking water. Twenty seven male LE rats, 3.5 – 4.5 months of age, were studied. The animals were divided into 3 groups based on the contents of the drinking water: control, NaF, or AlF₃. Water was available ad libium for 52 weeks. Significantly more rats died in the AlF₃ group than the control group during the study. Histological examinations involved the following stains: Cresy Violet, Bielschowsky silver, H&E, Morin Aluminum fluorescence, Beta Amyloid, Amyloid A, and IgM. Overall, neuronal loss was more prominent in the AlF₃ group than the NaF and control groups in the left hemisphere and in the dentate gyrus of both hemispheres. Toxin-induced abnormalities in the AlF₃ group were more apparent in the left hemisphere cortex but changes were found in the right hemisphere hippocampus. Hippocampal argentophillic reactions were common in both treated groups. Beta amyloid reaction product was enhanced in the thalamus in both toxin groups. More IgM antibody reaction product was found in the right hemisphere cortices of rats in both treated groups. Overall brain and kidney Al content was higher in both toxin groups relative to controls. Indications of glomerular disease were found in both treated groups. This reduction and/or abnormal appearance of cells, the presence of beta-amyloid, IgM, and Al indicate that AlF₃ is neurotoxic when chronically administered in the drinking water of rats. The abnormal appearance of cells and the presence of beta-amyloid, IgM, and Al suggest that NaF also induces neurotoxicity, although somewhat different than that found after AlF₃.

Varner JA, Huie C, Horvath W, Jensen KF, Issacson RL, Chronic AlF₃ Administration: II. Selected Histological Observations, Neuroscience Research Communications, 1993, 13:2, 99-104.

[editor's note: this study shows that the bioavailability of Al from drinking water is increased in the presence of fluoride. The Al content in the brain doubled in treated animals. According to an October 28, 1992 Wall Street Journal Article: "Rats fed the highest doses developed irregular mincing steps characteristic of senile animals.... Post mortem examination of the rat brains disclosed 'substantial cell loss in structures associated with dementia -- the neo-cortex and hippocampus'."]

Yang Y, Wang X, Guo X, Effects of high iodine and high fluorine on children’s intelligence and the metabolism of iodine and fluorine, Chung Hua Liu Hsing Ping Hsueh Tsa Chih, 1994 Oct, 15 (5), 296-298 (Translated from Chinese).

An investigation on children’s intelligence and the metabolism of iodine and fluorine in high iodine and fluorine regions was carried out. The results were as follows. In high iodine and high fluorine areas, the thyroid enlargement prevalence rate among inhabitants and that among children were 3.8% and 29.8%, respectively. The dental fluorosis prevalence rate among inhabitants and that among children was 35.48% and 72.9%, respectively. The pupils’ average intelligence quotient (IQ) was 76.67 ± 7.75, slightly lower than the control point, but that of low intelligent pupils was 16.7%. The urinary iodine and urinary fluoride were 816.25 ± 1.80 micrograms/L and 2.08 ± 1.03 mg/L, respectively, markedly higher than the control point. The thyroid iodine-131 (131I) uptake rate was markedly lower than the control point. The values at 3 h and 24 h were 9.36 ± 1.55% and 9.26 ± 4.63%, respectively. The serum TSH was obviously higher than the control point. These results indicate that high iodine and high fluorine exert severe damage to human body.

Zhao LB, Liang GH, Zhang DN, Wu XR, Effect of a high fluoride water supply on children’s intelligence, Fluoride, 1996, 29:4, 190-192

Abstract: In Shanxi Province, China, children living in the endemic fluoride village of Sima (water supply F=4.12 mg/L) located near Xiaoyi City had average IQ (97.69) significantly lower (p <0.02) mg/L; average IQ = 105.21). These differences were not associated with gender, but the IQ scores were directly related to educational level of the parents.
Introduction: It has been reported that fluoride can penetrate the fetal blood-brain barrier and accumulate in cerebral tissue before birth,¹ thereby apparently affecting children’s intelligence.² In the present study, conducted in April 1993, this hypothesis was further investigated by comparing the performance on IQ tests administered to 320 randomly selected children, age 7 to 14, residing in central Shanxi Province, China, in two suburban villages with significantly different fluoride content in drinking water. [...]
Discussion: The results of this study indicated that intake of high-fluoride drinking water from before birth has a significant deleterious influence on children’s IQ in on of two similar villages. No real differences were found for gender. In the high-fluoride village of Sima the number of children with IQ of 69 or below was six times that in the healthier low-fluoride village of Xinghua. There were also fewer children (20) in Sima with superior IQ scores of 120 or higher than the number (27) in Xinghua. Moreover, the fact that the IQ scores increased more slowly with age in Sima than in Xinghua supports the view that exposure to high levels of fluoride in utero exerts a cumulative adverse effect that is not overcome with increasing age in a high-fluoride community.

References
1. He H, Chen ZS, Liu XM, The effects of fluoride on the human embryo, Chinese Journal of Control of Epidemic Diseases, 1989, 4, 136-137.
   
2. Cheng YX, IQ of children in areas of high fluorine content, Chinese Journal of Control of Endemic Diseases, Supplement 1991.

RELATED ARTICLES

• Ding LI, The nervous systemic complications of chronic fluorosis. Chinese Journal of Endemiology, 1983, 2, 97-98.
  
• Hu YH, Direct damage on nervous system by fluorosis. Compilation of First Conference on Neuropsychiatric Diseases in Xinjian, (1982), 86-88.
  
• Shung-Guan CM, et al., The non-skeletal lesions of endemic fluorosis, Chinese Journal of Internal Medicine, 1982, 21, 217-219.
  
• Du L, Wan CW, Cao XM, The influence of chronic fluorosis on the development of the brain of the human embryo, Journal of Fluorosis Research Communications, 1991, 138

Chinese Fluoride of questionable purity being added to US water

Obama may use veto power to obstruct investigation 2001 anthrax mailings

In 2001, certain non-compliant members of congress were targeted by a weaponized form of Anthrax known as the “Ames Strain,” in a very specific powdered and charged form, increasing its effect by becoming airborne and easily inhaled.

Government investigators initially reported this to be the work of extremists, but how could they have access to such a specific type of anthrax that is only supposed to be accessible in secret bioweapons facilities?

Bloomberg reports:

Government “President Barack Obama probably would veto legislation authorizing the next budget for U.S. intelligence agencies if it calls for a new investigation into the 2001 anthrax attacks, an administration official said.”

A proposed probe by the intelligence agencies’ inspector general “would undermine public confidence” in an FBI probe of the attacks “and unfairly cast doubt on its conclusions,” Peter Orszag, director of the Office of Management and Budget, wrote in a letter to leaders of the House and Senate Intelligence committees.

Well duh, we can’t have the government investigating its own false flag attacks now, can we?

Consumers of aspartame (Nutra-Sweet): check out this documentary

Sweet Misery: A Poisoned World

Alan Grayson introduces Public Option Act

Finally, a public option that’s actually an option! Simple, elegant, and efficient. Builds on what we already have instead of throwing the baby out with the bathwater…

Unfortunately “The Young Turks” are a-holes (another topic) but they found the vid, So props for that.