This section on the brain includes:
Part 1: Fluoride and IQ: the 44 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 human placenta does not prevent the passage of fluoride from a pregnant mother’s bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning.
As highlighted by the excerpts below, three Chinese studies have investigated fluoride’s effect on the fetal brain and each has found evidence of significant neurological damage, including neuronal degeneration and reduced levels of neurotransmitters such as norepinephrine. As noted by Yu (1996), “when norepinephrine levels drop the ability to maintain an appropriate state of activation in the central nervous system is weakened.” Studies of fluoride-treated animals have reported similar effects, including lower levels of norepinephrine. (Kaur 2009; Li 1994).
The Safe Level Is Not Yet Known
The fluoride levels which the pregnant women in these studies were exposed are higher than most women in western countries can expect to ingest. The safety of lower fluoride levels to fetal brain development has not yet been investigated, and remains to be determined. Interestingly, in the 1960s, the FDA banned the use of prenatal fluoride supplements based on its concern about possible untoward effects on the fetus.
It should also be noted that women who drink large quantities of tea will likely have similar blood fluoride levels as the women in these studies. Further, if a pregnant woman receives a fluoride gel treatment from the dentist, her blood fluoride levels can go extremely high for up to 15 hours, exceeding the reported short-term exposure levels that impair glucose metabolism and kidney function in human adults and sperm quality in rams. The potential ramifications of these fluoride spikes on the health of the fetus has not been considered in the literature to date.
Research on fluoride’s effect on Fetal Brain:
A) The Yu/Dong Study
The following two papers provide results from a single investigation of 20 fetuses (10 from a high-fluoride area, and 10 from a low-fluoride area). A third paper from this investigation examined fluoride’s effect on cellular ultrastructure in other tissues and is included at the bottom of this page:
“The mothers of the ten fetuses that formed the subject group for this study all had dental fluorosis, with a corresponding increase in urinary fluoride, indicating that these pregnant women were suffering from chronic fluoride poisoning. The excess fluoride of the mother was passed through the placental barrier into the fetus, and from there through the blood-brain barrier to accumulate in the fetal brain, leading to a significant rise in bone and brain fluoride levels. Our results are consistent with earlier reports. Previous experiments have shown that the brains of fetuses from endemic fluorosis areas as well as fluoride-poisoned rats manifest morphological changes. Following experimental testing of the monoamine neurotransmitters in fetuses from fluorosis endemic areas, the present study found lowered levels of norepinephrine and elevated levels of epinephrine. The presence of norepinephrine in the brain allows the organism to become alert, and guards against the intensification of reflex reactions and other behavior. Norepinephrine also plays a role in the regulation of complex response mechanisms, emotions, cerebrocardiovascular function, etc. When norepinephrine levels drop the ability to maintain an appropriate state of activation in the central nervous system is weakened. The elevated levels of epinephrine could be due to a blockage of the pathway that transforms epinephrine into norepinephrine or possibly due to suppression of the relevant metabolic enzymes, causing the brain levels of epinephrine to increase, and the levels of norepinephrine to decrease.”
SOURCE: Yu Y, et al. (1996). Neurotransmitter and receptor changes in the brains of fetuses from areas of endemic fluorosis. Chinese Journal of Endemiology 15:257-259; re-published in Fluroide 2008, 41(2):134–138.
“The contents of five types of amino-acid neurotransmitters and three types of monoamine neurotransmitters in the brains of fetuses aborted through induced labor in a chronic fluorosis-endemic area were determined. Findings revealed that the content of the excitatory amino acid, aspartic acid, was significantly lower than in the fetuses from the non-endemic area whereas the content of the inhibitory amino acid, taurine, was significantly higher; the content of the major spinal cord-inhibitory glycine was significantly reduced. Among the monoamine neurotransmitters, the content of norepinephrine was significantly reduced; the contents of 5-hydroxytryptamine in the frontal and the occipital lobes were elevated and the content of 5-hydroxytryptamine in the parietal lobe (precentral and postcentral gyri) was reduced.”
SOURCE: Dong Z, et al. (1993). Determination of the contents of amino-acid and monoamine neurotransmitters in fetal brains from a fluorosis-endemic area. Journal of Guiyang Medical College 18(4):241-45.
B) The Du Study
“It is known that fluoride can cross the placenta from the mother’s blood to the developing fetus. However, the theory there is a direct link between fluoride effects and brain cell damage is still controversial due to lack of adequate evidence. In order to determine if there are any adverse effects on the developing human brain, especially starting from formation of the embryo, fetuses from an endemic fluorosis area at the 5th–8th month of gestation were compared with those from a non-endemic area. RESULTS: Normal Purkinje cells from the non-endemic fluorosis area were observed in single or parallel lines and were well organized in the fetal cerebellum. Purkinje cells of fetuses from the endemic fluorosis area were abnormally disorganized and had a thicker granulated layer in the cerebellum. Other dysmorphology, including higher nucleus-cytoplasm ratio of brain cones, hippocampus cones, and Purkinje cone cells, supports the theory that fluoride has an adverse effect on brain development. SEM analysis also found reduced neurons of brain cortex, decreased numerical density, volume density, and surface density in those fetuses from the endemic fluorosis area. In summary, the passage of fluorine through the placenta of mothers with chronic fluorosis and its accumulation within the brain of the fetus impacts the developing central nervous system and stunts neuron development.”
SOURCE: Du L. (1992). The effect of fluorine on the developing human brain. Chinese Journal of Pathology 21(4):218-20; republished in Fluoride 2008, 41(4):327–330.
C) The Han Study
“In recent years, researchers have noted that fluoride poisoning appears to begin in the fetal stage. Our study collected specimens from induced abortions in both fluoride endemic areas and non-affected areas and, by means of histochemical analysis, enzyme-chemical analysis, light microscopy, and electron microcopy, investigated the effects of fluoride on the fetus, providing evidence for early childhood contraction of fluorosis. RESULTS: When the various hard and soft tissues taken from fetuses as part of this study were tested for fluoride, the results showed that the brain and bone tissue of the fluoride endemic area fetuses had higher fluoride content than the controls (P < 0.05). The reason for this disparity is the previous excess fluoride intake of the mother. Fluoride can pass through the blood-brain barrier and accumulate in brain tissue. Thus in our study the brain tissue of the fetuses from the fluoride endemic area showed higher fluoride levels than the control. The mechanisms involved are not yet clear. Besides increased amounts of fluoride, the brain tissue of the endemic subjects also showed nerve cells with swollen mitochondria, expanded granular endoplasmic reticula, grouping of the chromatin, damage to the nuclear envelope, a lower number of synapses, fewer mitochondria, microtubules, and vesicles within the synapses, and damage to the synaptic membrane. These changes indicate that fluoride can retard the growth and division of cells in the cerebral cortex. Fewer mitochondria, microtubules, and vesicles within the synapses could lead to fewer connections between neurons and abnormal synaptic function, influencing the intellectual development after birth. These questions await further research.”
SOURCE: Han H, et al. (1989). Effects of fluorine on the human fetus. Chinese Journal of Control of Endemic Diseases 4(3):136-138, 1989; republished in Fluoride 2008, 41(4):321–326.
The following study involves the same fetal tissue that was examined in the Yu (1996) and Dong (1993) studies. Rather than investigating fluoride’s effect on the brain, however, this study examined fluoride’s effect on the ultrastructure of cells in several tissues in the body, including from the thyroid gland. As can be seen in the following description, the fetuses from the fluoride-exposed women were experiencing a systemic toxic effect.
Objective: Ultrastructural changes of epithelial cells of livers, adrenal glands, and thyroid glands of human fetuses from a fluorosis-endemic area were observed to provide the experimental basis for research into the mechanism of cellular damage caused by fluoride. Methods: 10 human fetuses in a fluorosis-endemic area were collected, whose mothers all had dental fluorosis with urinary fluoride content of (4.37 ± 2.94) mg/L. 10 human fetuses in a non-fluorosis-endemic area were collected, whose mothers had no dental fluorosis with urinary fluoride content of (1.67 ± 0.82) mg/L. The fluoride electrode method was used to test the fluoride content in fetal bones. Tissues of livers, adrenal glands, and thyroid glands of the fetuses were taken for electron microscopic examinations. Results: . . . . Electron microscopic examinations showed: the major changes of cell membranes were microvilli that were shortened, reduced in number or even vanished. Intercellular connections were loose and their structure was disordered. Myelin-like structures were formed in those with severe pathological changes. The major mitochondrial changes were: swollen mitochondria with increased volume, and even vanished and vacuolated cristae. The major pathological changes of endoplasmic reticulum were dilated and vesicular rough endoplasmic reticulum, and partially depleted nucleoproteins on the rough endoplasmic reticulum. The major pathological changes of cell nuclei were damaged and dilated, vesicular dual-layer structures of nuclear membranes. Huge inclusion bodies or particles with relatively high abnormal electron density appeared in some cytoplasm. Conclusions: Fluoride damage to cell structures was multifaceted. Cell membranes, mitochondria, rough endoplasmic reticulum, and nuclear membranes could all be damaged at the time of fluorosis.”
SOURCE: Yu Y. (2000). Effects of fluoride on the ultrastructure of glandular epithelial cells of human fetuses. Chinese Journal of Endemiology 19(2):81-83.