Hypothyroidism During Pregnancy
Studies have documented that mercury causes hypothyroidism,50. 84, 390, 407 damage of thyroid RNA,458 autoimmune thyroiditis369, 382, 91 and impairment of conversion of thyroid T4 hormone to the active T3 form.369, 382, 390, 407, 50d These studies and clinical experience indicate that mercury and toxic metal exposures appear to be the most common cause of hypothyroidism and the majority treated by metals detoxification recover or significantly improve.503 Thousands of tests at medical labs and many studies have documented that dental amalgam is the largest source of mercury in most adults that have several amalgam fillings, with exposures much above government health guidelines.501 Studies have also documented that for most mothers who have several amalgam fillings, the mothers dental fillings are the largest source of mercury in the fetus and a significant source in infants.502
The estimated prevalence of hypothyroidism from a large federal health survey, NHANES III, was 4.6%, but the incidence was twice as high for women as for men and many with sub clinical hypothyroidism are not aware of their condition.3a Another large study found that 11.7% tested had abnormal thyroid TSH levels with 9.5% being hypothyroid and 2.1% hyperthyroid.3b According to survey tests, 8 to 10 % of untreated women were found to have thyroid imbalances so the actual level of hypothyroidism is higher than commonly recognized.508 Even larger percentages of women had elevated levels of antithyroglobulin(anti-TG) or antithyroid peroxidase antibody(anti-TP). Tests have found approx. 30% of pregnant women to have low free T4 in the first trimeste.509b.
Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain.10a Hypothyroidism of the adults causes most frequently dementia and depression. Nearly all the hyperthyroid patients show minor psychiatric signs, and sometimes psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur.10a These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission, and play an important role in regulating central noradrenergic and GABA function.
Studies indicate that slight thyroid deficiency/imbalance(sub clinical) during the perinatal period can result in delayed neuropsychological development in neonate and child or permanent neuropsychiatric damage in the developing fetus or autism or mental retardation.10, 509, 511 Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result in significantly reduced Iqs509e and causes psychomotor deficits.509f Women with the highest levels of thyroid-stimulating-hormone(TSH) and lowest free levels of thyroxin 17 weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age 8.509a Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children. Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. “Collectively, reports show that 30-60% of women positive for TPO antibodies in pregnancy develop postpartum thyroiditis,” the researchers point out,561, 8 calling it “a strong association.” Without treatment, many of the women with thyroiditis go on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About 7.5% of pregnant women develop thyroiditis after birth.8 Studies have also established a connection between maternal thyroid disease and babies born with heart defects.509h
Infants of women with hypothyroxinemia at 12 weeks’ gestation had significantly lower scores on the Neonatal Behavioral Assessment Scale orientation index compared with subjects.10b Regression analysis showed that first-trimester maternal free thyroid hormone T4 was a significant predictor of orientation scores. This study confirmed that maternal hypothyroxinemia constitutes a serious risk factor for neurodevelopmental difficulties that can be identified in neonates as young as 3 weeks of age.
Mercury (especially mercury vapor from dental amalgam or organic mercury) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, thyroid gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces,14, 19, 85, 99, 273, 274, 407 and likewise rapidly crosses the placenta and accumulates in the fetus including the fetal brain and hormone glands at levels commonly higher than the level in the mother.20, 22-27 Milk from mothers with 7 or more mercury amalgam dental fillings was found to have levels of mercury approximately 10 times that of amalgam free mothers.22b The milk sampled ranged from 0.2 to 57 ug/L. In a population of German women, the concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L.26 A Japanese study found that the average mercury level in samples tested increased 60% between 1980 and 1990.25 The study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway.25 The level of mercury in umbilical cord blood, meconium, and placenta is usually higher than that in mother’s blood.23 25
The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic.392, 394, etc
Alterations of cortical neuronal migration and cerebellar Purkinje cells have been observed in autism. Neuronal migration, via reelin regulation, requires triiodothyronine (T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases.407 Experimental animal models have shown that transient intrauterine deficits of thyroid hormones (as brief as 3 days) result in permanent alterations of cerebral cortical architecture reminiscent of those observed in brains of patients with autism. Early maternal hypothyroxinemia resulting in low T3 in the fetal brain during the period of neuronal cell migration (weeks 8-12 of pregnancy) may produce morphological brain changes leading to autism. Insufficient dietary iodine intake and a number of environmental antithyroid and goitrogenic agents such as mercury, soy, and peanuts can affect maternal thyroid function during pregnancy. The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic.
Mercury can have significant effects on thyroid function even though the main hormone levels remain in the normal range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely affects the activity of selenoenzymes, including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases(5-Di and 5′-DI) in the fetal brain, even though thyroxine(T4) levels are normal(390de). Another mechanism by which mercury exerts such effects is mercurys effects on selenium levels which are required for conversion of T4 to T3.392, 390d Gpx activity is severely inhibited, while 5-DI levels are decreased and 5′-DI increased in the fetal brain, similar to hypothyroidism. Thus normal thyroid tests will not pick up this condition.
Mercury reduces the bloods ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc, selenium and Vit B12;43, 96, 198, 263, 264, 338, 339, 392, 427depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake, autoimmune thyroiditis,& hypothyroidism.50, 91, 212, 222, 369, 382, 392, 394, 407, 35 Minerals such as calcium, zinc, and manganese are also necessary for thyroid health and hormone production, and their absorption is blocked by mercury exposure. Because of the evidence of widespread effects on infants, the American Assoc. of Clinical Endocrinologists advises that all women considering becoming pregnant should get a serum thyrotropin test so that hypothyroidism can be diagnosed and treated early.558, 7b Since mercury and toxic metals are common causes of hypothyroidism, another test that should be considered is a hair element test for mercury or toxic metal exposures and essential mineral imbalances.
3(a) The Third National Health and Nutrition Examination Survey (NHANES III)3(b) Archives of Internal Medicine, Feb 28, 2000, Chester Ridgway, MD, head of the Division of Endocrinology at the University of Colorado Health Sciences Center.6. The study of the prevalence of depressive disorders in primary care patients in Poland], Wiad Lek. 2007;60(3-4):109-13. Drzdz W, Wojnar M, Araszkiewicz A, Nawacka-Pawlaczyk D, Urba?ski R, Cwikli?ska-Jurkowska M, Rybakowski J7 Thyroid malfunction in women; Ginecol Obstet Mex. 2001 May;69:200-5, Zrate A, Basurto L, Hernndez M; & (b) Clinical controversies in screening women for thyroid disorders during pregnancy. Wier FA, Farley CL. J Midwifery Womens Health. 2006 May-Jun;51(3):152-8.8 Postpartum thyroiditis. Best Pract Res Clin Endocrinol Metab. 2004 Jun;18(2):303-16. Stagnaro-Green A; & Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab Clin North Am. 2000 Jun;29(2):417-30, ix. Stagnaro-Green A; & (b) Postpartum depression and thyroid antibody status. Thyroid. 1999, 9(7):699-703,Harris B10(a) Some neurologic and psychiatric complications in endocrine disorders: the thyroid gland, [Article in Hungarian] Aszals Z. Orv Hetil. 2007 Feb 18;148(7):303-10;10(b) Neonatal effects of maternal hypothyroxinemia during early pregnancy. Pediatrics. 2006 Jan;117(1):161-7. Kooistra L, Crawford S, van Baar AL, Brouwers EP, Pop VJ;10(c) Hypothyroidism and pregnancy: impact on mother and child health.] Ann Biol Clin (Paris). 2008 Jan 29;66(1):43-51, [Article in French], Menif O, Omar S, Feki M, Kaabachi N.11(a) Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrine. 2007 Mar;32(1):49-65, Davis JD, Tremont G;11(b) Subclinical hypothyroidism: psychiatric disorders and symptoms. Rev Bras Psiquiatr. 2007 Jun;29(2):157-9, Almeida C, Brasil MA, Costa AJ et al.14(a) Mercury burden of human fetal and infant tissues. Drasch G, Schupp I, Hfl H, Reinke R, Roider G. Eur J Pediatr. 1994 Aug;153(8):607-10;14(b) Dental amalgam and mercury levels in autopsy tissues: food for thought. Guzzi G, Grandi M, Severi G et al. Am J Forensic Med Pathol. 2006 Mar;27(1):42-519(a) Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environ Health. 2007 Oct 11;6:30, Bjrkman L, Lundekvam BF, Vahter M,20(a) Vimy MJ, Takahashi,Y, Lorscheider FL; Maternal Fetal Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine and Medical Physiology , faculty of Medicine, Univ. of Calgary, Calgary Alberta Canada, Amer.J.Physiol.,1990, 258:R939-945;20(b) Hahn LJ, Kloiber R, Leininger RW, Vimy MJ, Lorscheider FL. Distribution of mercury released from amalgam fillings into monkey tissues, FASEB J.,1990, 4:5536;20(c) Mercury from maternal “silver” tooth fillings in sheep and human breast milk. A source of neonatal exposure. Vimy MJ, Hooper DE, King WW, Lorscheider FL. Biol Trace Elem Res. 1997 Feb;56(2):143-5222(a) Oskarsson A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Mercury in breast milk in relation to fish consumption and amalgam. Arch Environ Health, 1996,51(3):234 41;22(b) Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G. Mercury in human colostrum and early breast milk. J Trace Elem Med Biol 1998; 12:23 27;22(c) Paccagnella B, Riolfatti M. Total mercury levels in human milk from Italian mothers. Ann Ig 1989: 1(3-4):661-71;23(a) Yang J, Jiang Z,Wang Y, Qureshi IA, Wu XD. Maternal fetal transfer of metallic mercury via placenta and milk. Ann Clin Lab Sci 1997; 27(2):135 141;23(b) Soong YK, Tseng R, Liu C, Lin PW. J of Formosa Medical Assoc 1991; 90(1): 59 65;23(c) Sundberg J, Ersson B, Lonnerdal B, Oskarsson A. Protein binding of mercury in milk and plasma from mice and man a comparison between methylmercury and inorganic mercury. Toxicology 1999 Oct 1;137(3):169 84.24 Kuhnert PM, Kuhnert BR, Erhard P. Comparison of mercury levels in maternal blood, fetal blood, fetal cord blood, and placental tissues. Am J Obstet Gynecol, 1981, 139(2): 209-13, & Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M, “Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood”, Environ Res 2000 Oct;84(2):186-94; & Kuntz WD, Pitkin RM, Bostrom AW, Hughes MS. Maternal and chord blood mercury background levels; a longitudinal surveillance. Am J Obstet and Gynecol 1982; 143(4): 440 443.25(a) Ramirez GB, Cruz MC, Pagulayan O, Ostrea E, Dalisay C. The Tagum study I: analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants’ hair. Pediatrics 2000 Oct;106(4):774 81;25(b) Ramirez GB, Pagulayan O, Akagi H, Francisco Rivera A, Lee LV, Berroya A, Vince Cruz MC, Casintahan D. Tagum study II: follow-up study at two years of age after prenatal exposure to mercury. Pediatrics. 2003 Mar;111(3):e289-95;25(c) Warfvinge K, Berlin M, Logdberg B. The effect on pregnancy outcome and fetal brain development of prenatal exposure to mercury vapour. Neurotoxicology 1994; 15(4).26 Drexler H, Schaller KH. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Environ Res 1998; 77(2): 124-9.27(a) Mottet NK, Shaw CM, Burbacher, TM, Health Risks from Increases in Methylmercury Exposure, Health Perspect 1985; 63: 133 140;27(b) P.Grandjean et al, MeHg and neurotoxicity in children, Am J Epidemiol, 1999; & Sorensen N, et al; Prenatal mercury exposure raises blood pressure, Epidemiology 1999, 10:370-375; & Grandjean P; Jurgensen35 Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999,43(a) Knapp LT; Klann E. Superoxide induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem 2000 May 22;43(b) B.Rajanna et al, Modulation of protein kinase C by heavy metals, Toxicol Lett, 1995, 81(2-3):197-203.50(a) Sin YM, Teh WF, Wong MK, Reddy PK “Effect of Mercury on Glutathione and Thyroid Hormones” Bulletin of Environmental Contamination and Toxicology 44(4):616-622 (1990);50(b) J.Kawada et al, Effects of inorganic and methyl mercury on thyroidal function, J Pharmacobiodyn, 1980, 3(3):149-59; &(c) Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci 1992, 5(3): 236-40; & (d) Kabuto M “Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress” Arch Toxicol 65(2):164-7 (1991)61(a) E.Lutz et al, Concentrations of mercury in brain and kidney of fetuses and infants, Journal of Trace Elements in Medicine and Biology, 1996,10:61-67; & (b)G.Drasch et al, Mercury Burden of Human Fetal and Infant Tissues, Eur J Pediatr 153:607-610,1994;84(a) J.C.Veltman et al, Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland, Arch Biochem Biophys, 1986, 248(2):467-78;84(b) Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance. J. Orthmol. Med. v6#2 pp67-77 (1991);84(d) Nishida M, Muraoka K, et al, Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells. J Histochem Cytochem. 1989 May;37(5):723-7;85 Weiner JA, Nylander M; The relationship between mercury concentration in human organs and different predictor variables. Sci Total Environ 1993 Sep 30;138(1 3):101 1596 F.Goldberg et al, Effect of Amalgam restorations on whole body potassium and bone mineral content in older men,Gen Dent, 1996, 44(3): 246-8; & (b) K.Schirrmacher,1998, Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells, Calcif Tissue Int 1998 Aug;63(2):134 9.99 M. Nylander et al, Mercury accumulation in tissues from dental staff and controls, Swedish Dental Journal, 13:235-243, 1989; & (b) Nylander M, Mercury in pituitary glands of dentists, Lancet,442, Feb 26, 1986.198 B.R.G.Danielsson et al,Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus, Biol Res Preg Perinatal. 5(3):102-109,1984; & Danielsson et al, Neurotoxicol. Teratol., 18:129-134263 Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders. J Assoc Physicians India. 2002 Mar;50:400-6264 B.R. Danielsson et al, Behavioral effects of prenatal metallic mercury inhalation exposure in rats, Neurotoxicol Teratol, 1993, 15(6): 391-6;& A. Fredriksson et al,Prenatal exposure to metallic mercury vapor and methyl mercury produce interactive behavioral changes in adult rats, Neurotoxicol Teratol, 1996, 18(2): 129-34273 Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). H V Aposhian ; Environ Health Perspect. 1998 August; 106(Suppl 4): 10171025, www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1533322274 L.Friberg et al, Mercury in the brain and CNS in relation to amalgam fillings, Lakartidningen, 83(7):519-521,1986(Swedish Medical Journal), http://home.swipnet.se/misac/research6.html338(a) W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta, Environ Res, 1992, 57(1):96-106;& In vitro exposure to mercury and cadmium alters term human placental membrane fluidity, Pharmacol, 1992, 116(1): 17-23;338(b) J.Urbach et al, Dept. of Obstetrics & Gynecology, Rambam Medical Center, Haifa, Israel, Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption, Reprod Toxicol, 1992,6(1):69-75;& Karp W, Gale TF et al, Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters Environmental Research, 36:351-358; & W.B. Karp et al, Correlation of human placental enzymatic activity with trace metal concentration in placenta, Environ Res. 13:470- 477,1977;338(d) Boot JH. Effects of SH blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct 1995 Jun;20(3):233 8; & Semczuk M, Semczuk Sikora A. New data on toxic metal intoxication (Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit 2001 Mar;7(2):332 340369 Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228. www.melisa.org382(a) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60. www.melisa.org ;382(b) Sterzl I, Hrda P, Prochazkova J, Bartova J, Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45(9):527 31 ;382(c) The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8.www.melisa.org390(a) Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI “Effects of low mercury vapour exposure on the thyroid function in chloralkali workers” J Appl Toxicol 20(6):483-9 (2000) ,390(b) Barregard L, Lindstedt G, Schutz A, Sallsten G “Endocrine function in mercury exposed chloralkali workers” Occup Environ Med 51(8):536-40 (1994) www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid= 7951778&form=6&db=m&Dopt=r ;390(e) Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H. In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain.. Environ Res 1999 Apr;80(3):208-14.392 Selenium and antioxidant defenses as major mediators in the development of chronic heart failure. Heart Fail Rev. 2006 Mar;11(1):13-7. de Lorgeril M, Salen P.394 Amalgam Illness Diagnosis and Treatment, Andrew Hall Cutler, PhD, PE, http://www.noamalgam.com/; & Heavy Metals and Halogens Displace and Block Utilization of Essential Minerals- Iodine and Chelation, International Medical Veritas Association http://www.alkalizeforhealth.net/Liodine2.htm; & The effect of mercuric chloride on thyroid function in the rat., Goldman M, Blackburn P. Toxicol Appl Pharmacol. 1979 Mar 30;48; & THE EFFECT OF CERTAIN METALLIC CATIONS ON THE IODIDE UPTAKE IN THE THYROID GLAND OF MICE. Acta Endocrinol (Copenh). 1964 Aug;46:643-52. ANBAR M, INBAR M.407 Autism: transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007 Nov 15;262(1-2):15-26. Epub 2007 Jul 24.. Romn GC.427 Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Arch Int Physiol Biochem 1990, 98(5):261-7; & Bara M, Guiet-Bara A, Durlach J. Comparison of the effects of taurine and magnesium on electrical characteristics of artificial and natural membranes. V. Study on the human amnion of the antagonism between magnesium, taurine and polluting metals. [ French] Magnesium. 1985;4(5-6):325-32.501 Review: Documentation of common mercury exposure levels from amalgam by medical labs, Government agency studies, peer-reviewed studies. B Windham (Ed), www.flcv.com/damspr1.html & www.flcv.com/amalno1.html502 Effects of prenatal and neonatal mercury exposure on children, B Windham(Ed), over 150 peer-reviewed studies, www.flcv.com/fetaln.html503 Summary of results of treatment of chronic health conditions by amalgam replacement, as reported to the FDA and treatment clinics, www.flcv.com/hgrecovp.html508(a) Bonar DB, McColgan B, Smith DR, Darke C, Guttridge MG, Williams HSmyth PPA, Hypothyroidism and aging: The Rosses Survey. Thyroid 2000, 10(9):821-827;508(b) Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Tntern Med 2000, 160(4):526-34; &508(c) GS Connection 11(12): Prevelence of Thyroid Imbalance, Thyroid in Pregnancy, GSDL, www.gsdl.com509(a) Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE, Mitchell ML, Relation of severity of maternal hypothyroidism to cognitive development of offspring. J Med Screen 2001: 8:18-20;509(b) de Escobar DM, Orbregon MF, del Rey FE, Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? J Clin Endocrin Metab 2000; 3975-3987;509(c) Thyroid Imbalances in Pregnancy Linked to Poor Child Neurodelopment, Great Smokies Diagnostic Lab, www.gsdl.com/news/connections/vol11/conn20010228.html509d J. E. Haddow et al, Babies Born to Mothers with Untreated Hypothyroidism Have Lower I.Q.’s, New England Journal of Medicine, Aug 19, 1999;509(e) Lavado-Autric et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. JCI 111:1073-1082 (2003);509(f) Pop VJ, Vader HL et al, Low maternal free thyroxine during early pregnancy is associated with impaired psychomotor development in infancy, Clin Endocrinol(Oxf), 50:149-55, 1999; & Man EB, Brown JF, Serunian SA. Maternal hypothyroxinemia: psychoneurological deficits of progeny. Ann Clin Lab Sci 1991;21(4):227-39; & Pharoah POD, Connolly KJ et al, Maternal thyroid hormone levels in pregnancy and cognitive and motor performance of the children, Clin Endocrinol(Oxf), 1984, 21:265-70;509(g) Pop VJ, de Vries E, et al, Maternal thyroid peroxidase antibodies during pregnancy: and impaired child development, J Clin Endocrinol Metab., 1995, 80:3561-3566 & Connors MH, Styne DM, Neonatal athyreosis resulting from thyrotropin-binding inhibitory immonoglobulins, Pediatrics, 1986, 78:287-290; &509(h) sami T, Suzuki H, Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid 11: 765-8, 2001; & Kumar R, Chaudhuri BN. Altered maternal thyroid function: fetal and neonatal heart cholesterol and phospholipids, .Indian J Physiol Pharmacol 1993 Jul;37(3):176-82510(a) Morris MS, Bostom AG, Jacques PJ, Selhub J, Rosenberg IH, Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination Survey, Artherosclerosis 2001, 155:195-200;510(b) Shanoudy H. Soliman A, Moe S, Hadian D, Veldhuis F, Iranmanesh A, Russell D, Early manifestations of sick eythyroid syndrome in patients with compensated chronic heart failure, J Card Fail 2001, 7(2):146-52; & (510(c) AE. Hak, HAP. Pols, TJ. Visser, et al., The Rotterdam Study., Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women, Ann Int Med, 2000, vol. 132, pp. 270==278510(d) Thyroid Dysfunction Linked to Elevated Cardiac Risk, GSDL, www.gsdl.com/news/connections/vol12/conn20010411.html.;510(e) Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002 Dec 3;137(11):904-14;510(f) B.G. Nedreboe, O. Nygard, et al, Plasma Total Homocysteine of hypothyroid patients during 12 months of treatment, Haukeland Univ. Hospital, Bergen, Norway, firstname.lastname@example.org (references 7 other studies with similar findings); & (g) Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med 1999; 131:348;511(a) Abramson J, Stagnaro-Green A, Thyroid antibodies and fetal loss, Thyroid 2001, 11(1): 57-63;511(b) Thyroid Antibodies May Spur Pregnancy Loss, GSDL, www.gsdl.con/news/connections/vol12/conn20010411.html511(c) Allan W.(MD), Maternal Hypothyroidism During Pregnancy Linked to Increased Risk for Miscarriage, Journal of Medical Screening, November 22, 2000;511(d) Abstract # 274: Wolfberg, Adam J. and David A. Nagey, “Thyroid Disease During Pregnancy and Subsequent Congenital Anomalies.”St Johns Univ., email@example.com ; & Birth Defect News, Jan 2002, p2;511(e) Emerson, C.H. (1996). Thyroid Disease During and After Pregnancy. In L.E. Braverman & R.D. Utiger (Eds.), The Thyroid, A Fundamental and Clinical Text (pp. 1021-1031;511(f) Man EB, Jones WS, Thyroid function in human pregnancy: retardation in 8-month old infants, Am J Obstet Gynecol, 1969, 104:898-908; & Brent GA, Maternal hyrothyroidism: recognition and management, Thyroid, 1999, 9:661-5.555 Lewis RN; Bowler K. Rat brain (Na+ K+)ATPase: modulation of its ouabain sensitive K+ PNPPase activity by thimerosal. Int J Biochem 1983;15(1):5 7; Bellabarba D, and Tremblay R; Effect of thimerosal on serum binding of thyroid hormones, Can J Physsiol Pharmacol,173, 51:156-159: & Hokkfen B, Kodding R, Hesch RD; Regulation of thyroid hormone metabolism in rat liver fractions, Biochim Biophys Acta 1978, 539:(1): 114-24.558 American Assoc. of Clinical Endocrinologists and American College of Endocrinolog.
AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract., 1995, 1: 54-62.