This section on the brain includes:
Part 1: Fluoride and IQ: the 45 studies
Part 2: Fluoride Damages the Animal Brain
Part 3: Fluoride Affects Learning & Memory in Animals
Part 4: Fluoride’s Neurobehavioral Effects in Humans & Animals
Part 5: Fluoride’s Direct Effects on Brain: Animal Studies
Part 6: Fluoride’s Effect on Fetal Brain
Part 7: NRC (2006): Fluoride’s Neurotoxicity & Neurobehavioral Effects
Part 8: Fluoride & IQ: The 7 “No Effect” Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by research on the human fetal brain as well as a vast body of animal research. The animal research includes 15 laboratory experiments that have found impairments in learning and memory capacity among fluoride-treated animals. The animal research also includes over 40 studies that have investigated fluoride’s impact on various parameters of brain quality. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
As highlighted in the excerpts below, common brain effects from fluoride exposure include:
- reduction in nicotinic receptors,
- reduction in protein content,
- alterations in protein expression
- damage to the hippocampus,
- inhibition of cholinesterase activities
- increase in oxidative stress, and
- neuronal degeneration.
Fluoride’s Effect on Animal Brain:
“Excessive intake of fluoride results in an altered mitochondrial distribution in axon and soma in cortical neurons (i.e., the increase in soma and the decrease in axon), increased expression of Fis1 gene and enhanced mitochondrial fission. The altered mitochondrial distribution may be related to the high expression level of Fis1 and a functional disorder of mitochondria.”
SOURCE: Lou DD, et al. (2012). [Alteration of mitochondrial distribution and gene expression of fission 1 protein in cortical neurons of rats with chronic fluorosis]. [Article in Chinese]. Zhonghua Bing Li Xue Za Zhi. 41(4):243-7.
“The results showed that NaF impairs open-field habituation and increases noradrenaline (NA) and serotonin (5-HT) in the striatum, hippocampus and neocortex. Dopamine (DA) increase was restricted to the striatum. Short-term NaF withdrawal did not reverse these NaF-induced changes, and both NaF treatments led to a mild fluorosis in rat incisors.”
SOURCE: Pereira M, et al. (2011). Memory impairment induced by sodium fluoride is associated with changes in brain monoamine levels. Neurotox Res. 19(1):55-62.
“Presence of eosinophilic Purkinje cells, degenerating neurons, decreased granular cells, and vacuolations were noted in discrete brain regions of the fluoride-treated group. . . . The alterations were more profound in the third generation when compared with the first- and second-generation fluoride-treated group.”
SOURCE: Basha PM, et al. (2011). Fluoride toxicity and status of serum thyroid hormones, brain histopathology, and learning memory in rats: a multigenerational assessment. Biol Trace Elem Res. 144(1-3):1083-94.
“Results showed that the fluidity of brain synaptic membrane decreased gradually with increasing of fluoride concentration, and it was significantly decreased (P < 0.05) in moderate-fluoride group compared with control group, and expression level of PSD-95 was significantly decreased (P < 0.01) in moderate-fluoride group when compared with that of control group. These results indicate that decrease of synaptic membrane fluidity and PSD-95 expression level may be the molecular basis of central nervous system damage caused by fluoride intoxication; PSD-95 in CA3 region of hippocampus is probably a target molecule for fluoride.”
SOURCE: Zhu W, et al. (2011). Effects of fluoride on synaptic membrane fluidity and PSD-95 expression level in rat hippocampus. Biol Trace Elem Res. 139(2):197-203.
“The results indicated that exposure to excessive fluoride resulted in the increase of apoptosis in rat brains and SH-SY5Y cells, in which one of the mechanisms might be activating JNK phosphorylation.”
SOURCE: Liu YJ, et al. (2011). Increased level of apoptosis in rat brains and SH-SY5Y cells exposed to excessive fluoride–a mechanism connected with activating JNK phosphorylation. Toxicol Lett. 204(2-3):183-9.
“The present paper identifies different expressed proteins in the brains of rats under the treatment of high fluoride, low iodine, and both together compared to controls, in order to better understand the changes in functional proteins to gain insight into the mechanisms of high fluoride and low iodine. The proteins that were found to be significantly regulated (up-regulated and down-regulated) included guanine nucleotide-binding proteins (G proteins), synaptotagmin I, lactate dehydrogenase A (LDHA), proteosome, and adenylosuccinate lyase (ASL). Some of these proteins were previously reported to be related to fluorosis and iodine deficiency diseases (IDD). These proteins are involved in the regulation of a number of important cellular functions like cellular signaling, energy metabolism, and protein metabolism.”
SOURCE: Ge Y, et al. (2011). Proteomic analysis of brain proteins of rats exposed to high fluoride and low iodine. Arch. Toxicol. 85:27-33.
“The data indicates significant alterations in the parameters related to haeme synthesis pathway like inhibition of blood delta-aminolevulinic acid dehydratase, delta-aminolevulinic acid synthetase, oxidative stress like depletion of glutathione (GSH) and increase in oxidized glutathione (GSSG) and thiobarbituric acid reactive substances. These changes were accompanied by depletion in GSH:GSSG ratio, whole brain biogenic amine levels and a dose-dependent increase in fluoride concentration. Interestingly and most significantly, these changes were more pronounced at lower concentrations of fluoride compared with higher fluoride dose. Biochemical changes were supported by the histological observations, which also revealed that at high concentrations of fluoride, toxic effects and damages to organs were more pronounced.”
SOURCE: Chouhan S, et al. (2010). Fluoride-induced changes in haem biosynthesis pathway, neurological variables and tissue histopathology of rats. J Appl Toxicol. 30(1):63-73.
“The results showed that in the rat offspring exposed to higher fluoride as compared to controls, the learning and memory ability declined; the cholinesterase activities in the brains were inhibited; the protein levels of alpha3, alpha4 and alpha7 nAChR subunits were decreased which showed certain significant correlations with the declined learning and memory ability; and the mRNA levels of alpha3 and alpha4 nAChRs were decreased, whereas the alpha7 mRNA increased.”
SOURCE: Gui CZ, et al. (2010). Changes of learning and memory ability and brain nicotinic receptors of rat offspring with coal burning fluorosis. Neurotoxicol Teratol. 32(5):536-41.
“The results showed that as compared with controls, the learning and memory capacity in the rats with fluorosis was decreased. The protein expressions of alpha7 and alpha4 nAChR subunits in rat brains with fluorosis were decreased by 35% and 33%, whereas the corresponding receptor subunit mRNAs did not exhibit any changes. The increases of phospho- and total-ERK1/2 as well as phospho-MEK1/2 at the protein levels were found in the brains of rats with fluorosis as compared to controls, and no difference of ERK1/2 mRNA was found. In addition, the activation rate of phospho-ERK1/2 was decreased in the brains affected with fluorosis. The modifications of nAChRs and ERK1/2 pathway might be connected with the molecular mechanisms in the decreased capacity of learning and memory of the rats with fluorosis.”
SOURCE: Liu YJ, et al. (2010). Alterations of nAChRs and ERK1/2 in the brains of rats with chronic fluorosis and their connections with the decreased capacity of learning and memory. Toxicol Lett. 192(3):324-9.
“Following fluoride exposure, oxidative stress increased significantly, estimated by increased lipid peroxidation and a decrease in the activity of the antioxidant enzyme, superoxide dismutase. The neurotransmitter (e.g., dopamine, norepinephrine, and serotonin) content was also altered. However, these aspects were more pronounced in animals given fluoride and aluminum together. Histological evidence showed deprival of neuronal integrity with higher magnitude in concurrent fluoride and aluminum exposure, as compared to fluoride alone. Thus, it can be concluded that aluminum appears to enhance the neurotoxic hazards caused by fluoride.”
SOURCE: Kaur T, et al. (2009). Effect of concurrent chronic exposure of fluoride and aluminum on rat brain. Drug & Chem. Toxicol. 32(3): 215-21.
“Fluoride (F) and lead (Pb) are two common environmental pollutants which are linked to the lowered intelligence, especially for children. Glutamate, a major excitatory neurotransmitter in the central nervous system, plays an important role in the process of learning and memory. However, the impact of F and Pb alone or in combination on glutamate metabolism in brain is little known. The present study was conducted to assess the glutamate level and the activities of glutamate metabolism related enzymes including asparate aminotransferase (AST), alanine aminotransferase (ALT) and glutamic acid decarboxylase (GAD) in the hippocampus, as well as learning abilities of offspring rat pups at postnatal week 6, 8, 10 and 12 exposed to F and/or Pb. . . . Results showed that the learning abilities and hippocampus glutamate levels were significantly decreased by F and Pb individually and the combined interaction of F and Pb. The activities of AST and ALT in treatment groups were significantly inhibited, while the activities of GAD were increased, especially in rats exposed to both F and Pb together. These findings suggested that alteration of hippocampus glutamate by F and/or Pb may in part reduce learning ability in rats.”
SOURCE: Niu R, et al. (2009). Decreased learning ability and low hippocampus glutamate in offspring rats exposed to fluoride and lead. Environ Toxicol Pharmacol. 28(2):254-8.
“Exposure to arsenic and fluoride significantly decreased the levels of brain biogenic amines. However; acetyl cholinesterase (AChE) and monoamine oxidase (MAO) activities showed an increase on fluoride exposure. There was also an increase in reactive oxygen species, thiobarbituric acid reactive species level, glutathione S-transferase and glutathione peroxidase activities and decreased superoxide dismutase activity, GSH:GSSG ratio, glucose 6-phosphate dehydrogenase activity. Combined exposure to these toxicants produced more pronounced effects on AChE, MAO, SOD and catalase activities. Infrared spectra showed less toxicity during combined exposure as the characteristic peaks of cytosine and alpha-helical structure of DNA were observed in normal and arsenic plusfluoride-exposed animals. Vitamin E reduced brain fluoride level and tissue oxidative stress but had no effect on arsenic. Combined exposure to arsenic and fluoride does not necessarily lead to more pronounced toxicity and interestingly exhibit some antagonistic effects. Vitamin E supplementation may be of added value in reverting some of the toxic effects.”
SOURCE: Flora SJ, et al. (2009). Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain. J Neurol Sci. 285(1-2):198-205.
“This study reports the protective effects of selenium on fluoride induced alterations in the activities of pro-oxidative (xanthine oxidase (XOD), lipid peroxidation (LPO) free radical scavenging, [catalase, superoxide dismutase (SOD), glutathione-s-transferase (GST), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione) and metabolic (glucose-6-phosphate dehydrogenase, alanine amino transferase (ALAT), aspartate aminotransferase (AAT), creatine phosphokinase (CPK), acid phosphatase (AP), alkaline phosphatase (ALP)] enzymes along with fluoride and selenium levels in brain of mice. . . . As evident in this study the antioxidative nature of selenium coupled with its reversal effect on metabolic enzymes in brain of mice treated with fluoride suggests its use as antidote agent against fluorosis.”
SOURCE: Reddy KP, et al. (2009). Protective effects of selenium on fluoride induced alterations in certain enzymes in brain of mice. J Environ Biol. 30(5 Suppl):859-64.
“Total protein showed a concentration dependent decrease in brain and muscles but an increase in liver. The results of the study indicate that elevated fluoride in drinking water affects not only mammalian neurotransmitter functions but also antioxidant systems.”
SOURCE: Bhatnagar M, et al. (2006). Biochemical changes in brain and other tissues of young adult female mice from fluoride in their drinking water. Fluoride 39(4):280-84.
“In this study, the percentage of damaged brain cells of grades II and III was up to 12% higher than in the control group, and the ratio of tailing was 24.68%. . . . DNA damage of brain cells exposed to high fluoride, low iodine, and their combined interaction markedly increased, especially in the [High Fluoride + Low Iodine] group.”
SOURCE: Ge Y, et al. (2005). Comet assay of DNA damage in brain cells of adult rats exposed to high fluoride and low iodine. Fluoride 38:209-14.
“In the present study, levels of glutathione and activities of catalase, GSH-PX, and SOD were significantly decreased, whereas lipid peroxide levels were enhanced in the brain of adult rats by treatment with NaF, As2O, or NaF + As2O3, in agreement with earlier reports.”
SOURCE: Chinoy NJ, et al. (2004). Biochemical effects of sodium fluoride and arsenic trioxide toxicity and their reversal in the brain of mice. Fluoride 37: 80-87.
“The histology of the cerebral hemisphere was altered by NaF and/or Arsenic trioxide [As2O3] treatment for 30 days, wherein the effect by As2O3 was greater than by NaF treatment. This result is in agreement with others… The reduced brain acetylcholinesterase (AChE) enzyme activity observed in the present study corroborates data of others in rats exposed for three months to arsenic trioxide and in the brain of NaF-treated mice and rats as compared to controls… The DNA and RNA levels in the cerebral hemisphere were significantly lower in NaF and/or As2O3-treated mice in the present study, which could affect brain function. The ingestion of the antidotes vitimans C and E as well as calcium phosphate, either indivdually or in combination, during the 30-day withdrawal period resulted in significant recovery, probably due to the antioxidant-properties of vitamins C and E and modulation of fluoride-induced toxicity in rats by calcium.”
SOURCE: Shah SD, Chinoy NJ. (2004). Adverse effects of fluoride and/or arsenic on the cerebral hemisphere of mice and recovery by some antidotes. Fluoride 37(3): 162-171.
“Superoxide dismutase (SOD) activity and the malondialdehyde (MDA) content in the brain of the combined high fluoride and low iodine group were significantly higher during and at the end of the 90-day period than in the control group, but the SOD/MDA ratio in this high fluoride and low iodine group was consistently lower than in the control group. These results suggest that [oxidative] stress from high fluoride and low iodine is one of the causes of reduction in learning and memory in offspring rats.”
SOURCE: Wang J, Ge Y, Ning H, Wang S. (2004). Effects of high fluoride and low iodine on biochemical indexes of the brain and learning-memory of offspring rats. Fluoride 37: 201-208.
“Brain protein was decreased by low iodine and even more by the combined interaction of high fluoride and low iodine. The activity of cholinesterase (ChE) in the brain was affected to some extent by high fluoride and low iodine but was especially affected by high fluoride and low iodine together.”
SOURCE: Wang J, et al. (2004). Effects of high fluoride and low iodine on biochemical indexes of the brain and learning-memory of offspring rats. Fluoride 37(4):264–270.
“Recently, we have detected the alterations of nicotinic acetylcholine receptors (nAChRs) in rat brains and PC12 cells affected by fluoride toxicity… [O]xidative stress, including protein oxidation of the receptors and lipid peroxidation in cellular membrane, might be a mechanism of the deficit of the receptors.”
SOURCE: Shan KR, Qi XL, Long YG, Wang YN, Nordberg A, Guan ZZ. (2004). Decreased nicotinic receptors in PC12 cells and rat brains influenced by fluoride toxicity—a mechanism relating to a damage at the level in post-transcription of the receptor genes. Toxicology 200: 169–177.
“Fluorosis had obvious influence on phospholipid and fatty acid composition in brain cells of rats, and its mechanism might be associated with action of lipid peroxidation, and 0.03 mg/L KI (potassium iodine) is the optimal concentration for the antagonistic action with this influence from fluorosis.”
SOURCE: Shen X, Zhang Z, Xu X. (2004). [Influence of combined iodine and fluoride on phospholipid and fatty acid composition in brain cells of rats] Wei Sheng Yan Jiu. 33:158-61.
“These findings suggest that selective decreases in the number of nAChRs may play an important role in the mechanism(s) by which fluoride causes dysfunction of the central nervous system.”
SOURCE: Chen J, Shan KR, Long YG, Wang YN, Nordberg A, Guan ZZ. (2003). Selective decreases of nicotinic acetylcholine receptors in PC12 cells exposed to fluoride. Toxicology 183: 235-42.
“Neuropathological changes occurred with loss of the molecular layer and glial cell layer in the brain tissues of rabbits exposed to the three higher fluoride doses. The Purkinje neurones exhibited chromatolysis and acquired a “ballooned” appearance. Nissl substance showed various degrees of decrease and even complete loss. Fragmented particles were retained in the perinuclear zone. The perikaryon showed vacuolization, and spheroid bodies were present in the neoplasm. These cytoplasmic inclusions appeared as various sized ovoid bodies or elongated eosinophilic masses due to which the nucleus was shifted to the periphery. These neurotoxic changes in the brain suggested that there was a direct action of fluoride upon the nerve tissue which was responsible for central nervous system problems such as tremors, seizures, and paralysis indicating brain dysfunction seen at the two highest doses.”
SOURCE: Shashi A. (2003). Histopathological investigation of fluoride-induced neurotoxicity in rabbits. Fluoride 36: 95-105.
“CONCLUSION: Fluoride may go through the blood-brain barrier and accumulate in rat hippocampus, and inhibit the activity of cholinesterase.”
SOURCE: Zhai JX, et al. (2003). [Studies on fluoride concentration and cholinesterase activity in rat hippocampus]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 21:102-4.
“Light microscopic study of hippocampal sub-regions demonstrated significant number of degenerated nerve cell bodies in the CA3, CA4 and dentate gyrus(Dg) areas of sodium fluoride administered adult female mice. Ultrastructural studies revealed neurodegenerative characteristics like involution of cell membranes, swelling of mitochondria, clumping of chromatin material etc, can be observed in cell bodies of CA3, CA4 and dentate gyrus (Dg).”
SOURCE: Bhatnagar M, et al. (2002). Neurotoxicity of fluoride: neurodegeneration in hippocampus of female mice. Indian Journal of Experimental Biology 40: 546-54.
“The DNA damage in pallium neurons in rats of the fluoride group was much more serious compared with those of the control group…Sodium fluoride could induce DNA damage and apoptosis in rats brain.”
SOURCE: Chen J, Chen X, Yang K, Xia T, Xie H. (2002). [Studies on DNA damage and apoptosis in rat brain induced by fluoride]. Zhonghua Yu Fang Yi Xue Za Zhi 36: 222-224.
“In order to investigate the molecular mechanism(s) underlying brain dysfunction caused by chronic fluorosis, neuronal nicotinic acetylcholine receptors (nAChRs) in the brain of rats receiving either 30 or 100 ppm fluoride in their drinking water for 7 months were analyzed in the present study employing ligand binding and Western blotting… 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.”
SOURCE: Long YG, Wang YN, Chen J, Jiang SF, Nordberg A, Guan ZZ. (2002). Chronic fluoride toxicity decreases the number of nicotinic acetylcholine receptors in rat brain. Neurotoxicology and Teratology 24:751-7.
“These results suggest that fluoride enhances oxidative stress in the brain, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of fluoride toxicity in the brain.”
SOURCE: Shivarajashankara YM , et al. (2002). Brain lipid peroxidation and antioxidant systems of young rats in chronic fluoride intoxication. Fluoride 35: 197-203.
“rats exposed to 100 ppm fluoride showed significant neurodegenerative changes in the hippocampus, amygdala, motor cortex, and cerebellum… These histological changes suggest a toxic effect of high-fluoride intake during the early developing stages of life on the growth, differentiation, and subcellular organization of brain cells in rats.”
SOURCE: Shivarajashankara YM , et al. (2002). Histological changes in the brain of young fluoride-intoxicated rats. Fluoride 35: 12-21.
“The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group (P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively.”
SOURCE: Chen J, Chen X, Yang K. (2000). [Effects of selenium and zinc on the DNA damage caused by fluoride in pallium neural cells of rats]. Wei Sheng Yan Jiu. 29: 216-7.
“This study therefore shows that both brain and muscle are affected by fluoride with inhibition of some enzymes associated with free-radical metabolism, energy production and transfer, membrane transport, and synaptic transmission, but with an enhanced activity of XOD.”
SOURCE: Lakshmi Vani M, Pratap Reddy K. (2000). Effects of fluoride accumulation on some enzymes of brain and gastrocnemius muscle of mice. Fluoride 33: 17-26.
“There is a tendency for neurone apoptosis in chronic fluorosis in rats. It is most evident with changes in pathology. It is not likely that only one form of neurone damage exist in the process of chronic fluorosis. There are recessive changes and apoptosis in the process at the same time.”
SOURCE: Lu XH, et al. (2000). Study of the mechanism of neurone apoptosis in rats from the chronic fluorosis. Chinese Journal of Epidemiology 19: 96-98.
“Over uptake of fluoride for a long term could cause potential increase in the level of oxidative stress in the brain tissue.”
SOURCE: Shao Q, Wang Y, Guan Z. (2000). [Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi 34:330-2.
“It was concluded that aluminium interferes with the metabolism of the neuronal cytoskeleton and that this interference is potentiated by fluoride.”
SOURCE: van der Voet GB, et al. (1999). Fluoride enhances the effect of aluminium chloride on interconnections between aggregates of hippocampal neurons. Archives of Physiology and Biochemistry 107:15-21.
“[T]he thickness of post-synaptic density (PSD) was decreased, and the width of synaptic cleft was remarkably increased. The results suggested that the impairment on the learning capability induced by fluorosis may be closely related with the pathological changes of synaptic structure in the brain of mice.”
SOURCE: Zhang Z, et al. (1999). [Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice] [Article in Chinese]. Wei Sheng Yan Jiu 28:210-2.
“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.”
SOURCE: Guan ZZ, Wang YN, Xiao KQ, Dai DY, Chen YH, Liu JL, Sindelar P, Dallner G. (1998). Influence of chronic fluorosis on membrane lipids in rat brain. Neurotoxicology and Teratology 20: 537-542.
“While the small amount of AlF in the drinking water of rats required for neurotoxic effects is surprising, perhaps even more surprising are the neurotoxic results of NaF at the dose given in the present study [1.0 ppm F]… The results of the present study indicate that more intensive neuropathological evaluations of F effects on brain may prove to be of value… In summary, chronic administration of AlF and NaF in the drinking water of rats resulted in distinct morphological alterations in the brain, including effects on neurons and cerebrovasculature.”
SOURCE: Varner JA, et al. (1998). Chronic administration of aluminum-fluoride and sodium-fluoride to rats in drinking water: Alterations in neuronal and cerebrovascular integrity. Brain Research 784: 284-298.
“These results indicate that fluoride may penetrate the blood brain barrier, interact with AChE located on cell membranes, and interfere with their physiological functions and thus induce the neurotoxicities.”
SOURCE: Zhao XL, Wu JH. (1998). Actions of sodium fluoride on acetylcholinesterase activities in rats. Biomedical and Environmental Sciences 11(1):1-6.
“The metabolism of brain phospholipid might be interfered by fluoride accumulated in brain tissue, which is related with the degeneration of neuron. The changes of brain phospholipid could be involved in the pathogenesis of chronic fluorosis.”
SOURCE: Guan Z, Wang Y, Xiao K. (1997). [Influence of experimental fluorosis on phospholipid content and fatty acid composition in rat brain]. Zhonghua Yi Xue Za Zhi. 77: 592-6.
“Neuronal abnormalities were observed in the NaF treated animals- especially in the deeper cell layers… The NaF treatment also produced distortions of cells and, in some rats, cell losses could be demonstrated in particular brain regions. Both AlF3 and NaF induced vascular inclusions, although of a different character…”
SOURCE: Issacson R, et al. (1997). Toxin-induced blood vessel inclusions caused by the chronic administration of aluminum and sodium fluoride and their implications for dementia. Annals of the New York Academy of Science 825: 152-166.
“Coenzyme Q content of brain tissue in rats fed with fluorine-containing water decreased at early stage of fluorosis, but increased significantly at late stage. It is speculated that changes in content of coenzyme Q could correlate with changes in free radical levels induced by fluorine.”
SOURCE: Wang Y, Guan Z, Xiao K. (1997). [Changes of coenzyme Q content in brain tissues of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi. 31: 330-3.
“Excessive fluoride intake decreased 5-hydroxy indole acetic acid and increased norepinephrine in rat brain.”
SOURCE: Li Y, et al. (1994). [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. 25(2):188-91.
“The results reported here indicate that fluoride has a specific effect on the synthesis of proteins in the brain which may lead to degenerative changes in the form of ballooning degeneration of neurons, various degrees of loss of nisal substance, and changes in the purkinje cells of the cerebellar cortex. Such changes would provide a plausible explanation for some of the diverse neruological complaints in arms and legs such as numbness, muscle spasms and pains, tenaniform convulsions, and spastic paraplegia, encountered in patients with skeletal fluorosis.”
SOURCE: Shashi A, et al. (1994). Effect of long-term administration of fluoride on levels of protein, free amino acids and RNA in rabbit brain. Fluoride 27: 155-159.
“The neurotoxic effect of fluoride on lipid content of brain was assessed in rabbits during experimental fluorosis… Fluoride exerts an inhibitory effect on the free fatty acids in brain of both sexes. The relevance of these results in experimental fluorosis is discussed.”
SOURCE: Shashi A. (1992). Studies on alterations in brain lipid metabolism following experimental fluorosis. Fluoride 25:77-84.