Past news posts


Postby pfpcnews » Tue Jan 17, 2017 7:54 pm


Feb.18, 2000
©2000 PFPC



In her 1995 paper (1) Dr. Mullenix and co-workers reported that brain function was vulnerable to fluoride and that the effects on behavior depended on the age at exposure. Rats exposed as adults displayed behavior-specific changes typical of cognitive deficits, whereas rats exposed prenatally had dispersed behaviors typical of hyperactivity.

Dr. Mullenix' study on rats compared 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***.... Fluoride exposures caused sex- and dose-specific behavioural 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."
Unfortunately Dr. Mullenix did not have a chance to examine HOW this occurred and brain histology was not examined. (histology = study of cells and tissue on the microscopic level). Dr. Mullenix apparently was not aware that identical neurological defects - correlating EXACTLY with her findings and timeline - had been reported numerous times elsewhere relating to iodine deficiency in the mother. Perhaps she would have made similar findings had her funding not been cut off...

We now know that fluoride intake causes correlating iodine deficiency in a direct dose-responsive relationship. We have extensive data on mice, rats, sheep, cattle, etc., but most importantly - HUMANS. The more fluoride in the system, the less iodine. HOW this happens one can argue over, for several different important mechanisms can be identified. That it DOES happen is very clear - beyond any doubt, not just sometimes, not maybe - and is all that shall be of importance for now.

NOTE 1: When a mother is iodine deficient, it obviously results in the same condition in the infant, for the fetus is not able to create its own thyroid hormones until weeks 12-14 in gestation, and is therefore WHOLLY dependent on the parental supply.

NOTE 2: At critical periods in fetal development and in early childhood biochemical hypothyroidism, due to "iodine deficiency", results in a wide range of devastating and irreversible effects now known as iodine-deficiency disorders (IDD). These diverse effects affect neonates, children, and adults. Iodine deficiency is by far the most common preventable cause of mental deficits in the world. The evidence has emerged from a variety of disciplines including epidemiology, endocrinology, and neurology, who showed again that it is MATERNAL THYROID STATUS which influences early brain development and, consequently, cognitive and motor function in humans and rats. The time period indentified by Evans in his study on rats was between **16 and 19** days in the gestation period (Gestation in rats = 23 days). It is during this period that parts of the central nervous system (CNS), namely the cerebral neocortex, the cochlea, and the basal ganglia are most affected by iodine deficiency, as numerous clinical studies have shown (3).

Further confirmation of the effect of maternal iodine deficiency on fetal brain development, as well as the importance of placental transfer, can be obtained from many studies in animals as well as humans (4-8).

Among iodine-replete but hypothyroid women, there is an increased frequency of stillbirths as well as of cretinism and less severe neurologic defects of motor and cognitive performance in live-born infants. These effects were also correlated with the maternal serum concentration of T4, but not T3, further indicating the importance of maternal T4 to the fetus(9).

Cao et al. had reported in 1994 (testing the timing of vulnerability of the brain to iodine deficiency in endemic cretinism) that iodine treatment improves the neurologic outcome slightly when done during the first trimester. Treatment in the third trimester did not improve neurologic status(9)

Evans wrote in his study (2) that the prenatal disturbances may have wide-ranging consequences since they occur when neurotransmitters have putative neurotropic roles in brain development. Furthermore, the chronic disturbances in enzyme activity which were observed during postnatal life may affect neurotransmission, thereby contributing to the behavioural dysfunction which was seen in female adult hypothyroid rats.

Gender differences as related to thyroid disorders can also be observed in all age groups, differing according to race.

When comparing the data of Mullenix with data on iodine deficiency it is only too obvious that thyroid function and iodine deficiency are involved [low Free T3].

Subclincial hypothyroidism is increasingly being recognized as a cause of developmental disease - a rather frightening situation. (=> Subclinical hypothyroidism -> various symptoms reported, correlating with the symptoms reported in Moolenburgh's double-blind study on subjects ingesting fluoridated water at 1ppm)

In August 1999 the New England Journal of Medicine (NEJM) published results of a study done by Dr. James Haddow and co-workers of the Foundation for Blood Research (11) This largest study of its kind to address the relationship between pregnant mothers with hypothyroidism and developmental problems in children also showed that low IQ in the newborn were related to thyroid hormone deficiency in the mother. What was particularly disturbing about Haddow's findings was the fact that even a slight iodine deficiency in the mother was enough to cause this loss of IQ. Only 14 of the 62 women with hypothyroidism in this study had the condition detected and treated before their pregnancies, and on average the remaining women did not receive proper diagnosis until five years (!) after their pregnancies.

Haddow further reported that pregnant women with underactive thyroids are four times more likely to have children with low IQs. The study found that 19 percent of the children born to mothers with thyroid deficiency had IQ scores of 85 or lower, compared with only 5 percent of those born to mothers without such problems. The children who score in this range may face lifelong developmental challenges. In a accompanying press release Haddow said, "It's the kind of cutoff that tells you you're going to have more troubles in school and more troubles in life in general."

In 1992 Gilberg and others from the Child Neuropsychiatry Centre in Sweden described five children (three boys and two girls) with autism or autistic-like conditions. Three of them had congenital hypothyroidism and two had mothers who had probably been hypothyroid in pregnancy(12).

A study published last year in the Journal of Child Neurology again found hypothyroidism as being among the most common medical risk factors in autism (13).

Many more studies have shown that attention deficit and/or hyperactivity disorders in children are linked to changes in the levels of thyroid hormone in the blood, and that also irritability and aggressive behaviour are linked to thyroid hormone levels and hypothyroidism (14-19).

In 1997 Aronson and Dodman wrote, "the hypothyroid human patient has been reported to show a wider range of behavioral symptoms. Particularly in the early stages of the disease reduced cognitive function and concentration together with impaired short-term memory may be confused with attention deficit-hyperactivity disorder, and in one study 66% of patients diagnosed with ADBD were found to be hypothyroid. Supplementing their thyroid levels was largely curative. Visual and auditory hallucinations may result from altered perception and have been misdiagnosed as schizophrenia or psychosis. Other behavioral symptoms have included fear - ranging from mild anxiety to frank paranoia, mood swings and aggression." Thyroid hormone disorders may induce almost any psychiatric symptom or syndrome, including rage(20). Littleton and fluorinated psychiatric drugs come to mind...(Prozac and Luvox contain fluorides)

Behaviour disorders have been associated with thyroid function for over 100 years, ever since the Clinical Society of London issued a report underlining the importance of normal thyroid function on development of the brain in 1888.


Since Mullenix et al. two more studies have been widely cited as evidence that fluorides inhibit IQ. These two epidemiology studies from China showed IQ deficits in children over-exposed to fluoride either via drinking water (Zhao et al, 1996) or soot from burning coal (Li et al, 1994) (21,22).

Incidentally, both studies were done in areas with both severe iodine deficiency AND severe endemic fluorosis! (23,24)

Xinjiang is actually the worst IDD area in China, with 43% of all children between 8 and 10 years old suffering from goiter.

In Zhao's study, we find the same. Shanxi Province is also a region of severe iodine deficiency with 24% percent of the children between 8 and 10 suffering from goiter.

In 1991 Lin Fa-Fu et al. clearly showed the fluoride-iodine relationship. Investigating low iodine areas for evidence of sub-clinical cretinism he compared data from a "high" F- area (0.88ppm!) to a "low" F- area (0.34ppm), under a UNICEF Aid Project involving schoolchildren between 7 and 14 years old (25).

In the "Low" area the goiter prevalence was 82% and dental fluorosis of 16.00%. In the "High" area the goiter prevalence was 91% and dental fluorosis 20.80%.

Both iodine deficient areas (A and B) differed from the control Area C by having lower IQ's, higher hearing threshold, increased 131I uptake (acknowledged cause of thyroid cancer!), and higher TSH.

"High" area A (high fluoride, low iodine) differed from area B (normal fluoride, low iodine) by having lower mean IQ, higher TSH, yet higher 131I uptake, and higher urinary iodine.

In the "high" area 29% showed detectable bone retardation, compared with 13% in the "low" area and 6% in the control.

Lin Fa-Fu also showed the increase of reverse T3 (rT3) according to fluoride intake. Production of rT3 results in a decrease of aerobic glycolysis and a decrease of most valuable T3 (also see PFPC#3). rT3 is formed from T4 by 3-deiodination in peripheral tissue. T4 3-deiodination is involved in the placenta. We all know that fluorides easily cross the placenta.

The rT3 value was 21ng/dl in the control, 32 ng/dl in "low" area B and 58 ng/dl in "high" area A, clearly showing the dose-responsive increase in rT3.

There are hundreds upon hundreds of studies documenting the direct antagonistic relationship between fluoride and iodine [Table 1, Table 2].

Roholm's 1935 figures as a definite reference set to evaluate fluoride "safety" are completely irrelevant in this context, as are any studies checking ONLY for fluoride levels in the system.

All authority regarding the "safety" of fluorides are to be placed into the hands of the FDA, not the EPA, for fluorides are a most effective anti-thyroid drug, with a proven pharmacological track record. Considering its effect on (absolutely essential!) iodine levels and the threat of sub-clinical thyroid disease there simply is NO SAFE LEVEL for fluoride, nor should there ever be anything like a Daily Recommended Intake (DRI) even suggested!!!

The World Health Organization estimated in 1990 that 20 million people had some degree of brain damage due to iodine deficiency experienced in fetal life.


In her letter to Dr. Kash (26), Dr. Mullenix writes that "it has been well documented that tooth enamel defects occur more often in brain damaged and low IQ groups of children, and in fact, obvious enamel defects may be used as markers of not so obvious neurological problems. Since fluoride causes tooth enamel defects in the developing child, fluoride belongs in the behavioral spotlight."

This of course is very important and we agree wholeheartedly. Again, this is directly due to thyroid dysfunction. Enamel effects are simply NOT possible without a thyroid gland. This has been show by Avededo et al (27,28, 29) as well as by DeEds and Wilson (30) decades ago as it relates to fluorosis. The delayed eruption effect commonly described in the literature on fluoridated areas is identical to the one described in hypothyroidism, MORE so in boys than in girls. Dental fluorosis is also more prevalent in boys than girls. The later the tooth erupts, the more severe the degree of fluorosis.

Identical enamel defects (enamel hypoplasia AND diffuse opacities) are reported in thyroid disorders and associated diseases. In primary teeth they are extremely closely associated with low birth weight/preterm delivery, which in turn are closely related to placental T4 transfer:

Paul et al (31), in a study investigating the relationship between thyroid function and neonatal outcome, reported T4 values strongly correlated with gestational age. Overall, 289 (85%) of 342 infants had transient hypothyroxenimia (hypothyroidism). After controlling for potential confounding variables, T4 value remained associated with an increased odds of mortality.

An Australian longitudinal study investigating the sequelae of enamel defects in 25 very low birth weight children found that, at all examinations, VLBW children had significantly higher prevalence of enamel hypoplasia than did the NBW children. At the last recall examination, 96% of VLBW group had at least one tooth with enamel defect, with a mean of 7.6 +/- 4.9 affected teeth per VLBW child, and only 1.0 +/- 1.3 affected teeth per control child (P < 0.001). The defect identified to be most significantly associated with dental caries was a variant showing both **enamel hypoplasia AND opacity**(32).

Sounds like "dental fluorosis"...

"Dental Fluorosis" is the first visible sign that thyroid dysfunction has occurred, and it should therefore be used as marker for minimal brain dysfunction.

Where this can be easiest seen is in the black population, for black women have more thyroid disorders in child bearing years than whites or hispanics. Long et al.(33) found that in San Diego 14% of black teenagers presented for prenatal care had goiter, while only 2% of pregnant whites and 4% of pregnant Mexican-American teenagers had this condition. Blacks also suffer more from developmental defects and have higher preterm delivery/low birth weignt babies, and neo-natal death rates. If our claim is true they should also have a higher incidence of "dental fluorosis". This is indeed so, again with the same relationship:

White and Spanish-surname children have about the same prevalence of mottling while Blacks have a higher prevalence, odds ratio (OR) = 2.3, 95% confidence interval = 1.4 to 3.7. (34) (compare to Paul above...)

Parents of Fluoride Poisoned Children
Vancouver, BC, Canada

1) Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ -"Neurotoxicity of sodium fluoride in rats" Neurotoxicology Teratology 17(2):169-177 (1995)

2) Evans IM, Sinha AK, Pickard MR, Edwards PR, Leonard AJ, Elkins RP - "Maternal hypothyroxinemia disrupts neurotransmitter metabolic enzymes in developing brain." J Endocrinol 161(2):273-9 (1999)

3) DeLong GR - "Observations on the neurology of endemic cretinism" In: DeLong GR, Robbins J, Condliffe PG, eds. Iodine and the brain. New York: Plenum Press 231-8 (1989)

4) Stanbury JB, ed. - "The damaged brain of iodine deficiency: cognitive, behavioral, neuromotor, and educative aspects" Elmsford, N.Y.: Cognizant Communication (1994)

5) Hetzel BS, Mano MT -"A review of experimental studies of iodine
deficiency during fetal development" J Nutr 119:145-51(1989)

6) Vulsma T, Gons MH, de Vijlder JJM -"Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis." NEJM 321:13-6 (1989)

7) Morreale de Escobar G, Ruiz de Ona C, Obregon MJ, Escobar del Rey F -"Models of fetal iodine deficiency." In: DeLong GR, Robbins J, Condliffe PG, eds. 'Iodine and the brain' New York: Plenum Press, 1989:187-201(1989)

8) Pop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJ, Vulsma T, Wiersinga WM, Drexhage HA, Vader HL - "Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy." Clin Endocrinol (Oxf50(2):149-55 (1999)

"After correction for confounding variables, a fT4 concentration below the 10th percentile at 12 weeks' gestation was a significant risk factor for impaired psychomotor development (RR): 5.8, 95% CI: 1.3-12.6)."

9) Hetzel BS -"Iodine Deficiency and Fetal Brain Damage" NEJM 331(26) 1770

10) Cao XY, Jiang XM, Dou ZH, et al. - "Timing of vulnerability of the brain to iodine deficiency in endemic cretinism" N Engl J Med 331:1739-44 (1994)

11) Haddow JE, Palomaki GE, Allan WC, et al. -"Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child." N Engl J Med 341:549-55 (1999)

12) Gillberg IC, Gillberg C, Kopp S - "Hypothyroidism and autism spectrum disorders."J Child Psychol Psychiatry 33(3):531-42 (1992)

13) Comi AM, Zimmerman AW, Frye VH, Law PA, Peeden JN - "Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism." J Child Neurol 14(6):388-94 (1999)

14) Whybrow, P.C.-"Behavioral and psychiatric manifestations of hypothyroidism" In Braverman LE, Utiger RD (eds) Werner and Ingbar's "The thyroid: a fundamental and clinical text" (7th edition). Philadelphia, Lippincott-Raven,866-870(1996)

15) Denicoff K.D, Joffe RT, Lakschmanan, MC, Robbins J; Rubinow DR - "Neuropsychiatric manifestations of altered thyroid state" Am J Psychiatry 147:94-99 (1990)

16) Herman, J.P, Cullina, W.E. "Neurocircuitry of stress: central control of the hypothalamo- pituitary-adrenocortical axis" TINS 20:78-84 (1997)

17) Dluhy, R.J.- "The adrenal cortex in hypothyroidism" In: Braverman, L.E; Utiger, R.D (eds) Werner and Ingbar's "The thyroid, a fundamental and clinical text" (7th edition). Philadelphia. Lippincott-Raven, 841-844 (1996)

18) Hauser, P; Zametkin, A.J; Martinez, P- "Attention deficit-hyperactivity disorder in people with generalized resistance to thyroid hormone" NEJM 328:997-1001(1993)

19) Cameron, D.L. Crocker, A.D. "The hypothyroid rat as a model of increased sensitivity to dopamine receptor agonists" Pharm Biachem & Behav 37:627-632 (1990)

20) Aronson LP, Dodman NH - "Thyroid Dysfunction as a Cause of Aggression in Dogs and Cats" Presented at the 43. Jahrestagung der Deutschen Veterinarmedizinischen Gesellschaft Fachgruppe Kleintierkrankheiten 29-31 August 1997 in HCC Hannover, Germany

21) 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 25(2):188-91 (1994)

"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."

22) Zhao LB, Liang GH, Zhang DN, Wu XR -"Effect of a high fluoride water supply on children's intelligence" Fluoride 29:190-192 (1996)

23) Wang LF, Huang JZ - "Outline of control practice of endemic fluorosis in China" Soc Sci Med 41(8):1191-5 (1995)

http://www.people.Virginia.EDU/~jtd/icc ... dd_035.htm

25) Lin Fa-Fu, Aihaiti, Zhao Hong-Xin, Lin Jin, Jiang Ji-Yong, Maimaiti, and Aiken - "The Relationship of a Low-Iodine and High-Fluoride Environment to Subclinical Cretinism in Xinjiang" IDD Newsletter, Volume 7 Number 3 August 1991
http://www.people.Virginia.EDU/~jtd/icc ... idd891.htm

26) LETTER BY DR. MULLENIX to Dr. Irwin Kash, School Health Advisory Committee, June 17, 1999

27) Acevedo AC, Chardin H, Septier D, Staub JF, Goldberg M -"Effects of thyro-parathyroidectomy and parathyroidectomy upon dentinogenesis: Part II: Electron microscopy." Connect Tissue Res 32(1-4):269-74 (1995)

28) Acevedo AC, Chardin H, Staub JF, Septier D, Goldberg M - "Morphological study of amelogenesis in the rat lower incisor after thyro-parathyroidectomy, parathyroidectomy and thyroidectomy." Cell Tissue Res 283(1):151-7 (1996)

29) Chardin H, Acevedo AC, Risnes S - "Scanning electron microscopy and energy-dispersive X-ray analysis of defects in mature rat incisor enamel after thyroparathyroidectomy." Arch Oral Biol 43(4):317-27 (1998)

30) Wilson RH, DeEds F - "The Synergistic Action Of Thyroid On Fluorine Toxicity" Endocrinology 26:851 (1940)

31) Paul DA, Leef KH, Stefano JL, Bartoshesky L - "Low serum thyroxine on initial newborn screening is associated with intraventricular hemorrhage and death in very low birth weight infants." Pediatrics 101(5):903-7 (1998)

32) Lai PY, Seow WK, Tudehope DI, Rogers Y - "Enamel hypoplasia and dental caries in very-low birthweight children: a case-controlled, longitudinal study." Pediatr Dent 19(1):42-9 (1997)

33) Long TJ, Felice ME, Hollingsworth R - "Goitre in pregnant teenagers" Am J Obstet Gynecol 152:670-674 (1985)

34) Butler WJ, Segreto V, Collins E - "Prevalence of dental mottling in school-aged lifetime residents of 16 Texas communities."Am J Public Health 75(12):1408-12 (1985)

35) Boyle CA, Decoufle P, Holmgreen P - "Contribution of developmental disabilities to childhood mortality in the United States: a multiple-cause-of-death analysis" Paediatr Perinat Epidemiol 8(4):411-22 (1994)
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