Studies have found that heavy metals such as mercury, cadmium, lead, aluminium,
 nickel, and tin affect chemical synaptic transmission in the brain and the
peripheral and central nervous system. They also have been found
to disrupt brain and cellular calcium levels that
significantly affect many body functions:



A recent study released by the National Academy of Sciences found

that 50% of children born in the U.S. suffer from birth defects,

developmental disorders, or are otherwise chronically unhealthy (82).

  A recent government study in Canada also found significant increases in neurological or allergenic developmental disorders over the last 2 decades (132). Large numbers of peer-reviewed studies have found that the majority of such developmental neurological disorders such as ADD, dyslexia, autism, schizophrenia, other mood disorders, and learning disabilities are primarily caused by prenatal and neonatal exposures to toxic metals or other toxics[A]. Common exposures have been documented for mercury (vaccines, amalgam fillings, and fish), lead (paint, soil, water fixtures), arsenic (treated wood, pesticides, shellfish, other foods), aluminum (processed food, pans), cadmium (shellfish, paint, piping), antimony (Scotch guard), manganese (soy milk, welding, metal works). All of these are documented to be extremely neurotoxic[A]. 

  Studies have found that heavy metals such as mercury, cadmium, lead, aluminum, nickel, and tin affect chemical synaptic transmission in the brain and the peripheral and central nervous system (19,24,37-41,43,56,57,154). They also have been found to disrupt brain and cellular calcium levels that significantly affect many body functions: such as (a) calcium levels in the brain affecting cognitive development and degenerative CNS diseases (5,28,43,74) and (b) calcium-dependent neurotransmitter release which results in depressed levels of serotonin, norepinephrine, and acetylcholine (5,19,28,46,47,83,110,43) – related to  mood and motivation.  Some factors that have been documented in affective disorders, impulsiveness, and violent behavior are low serotonin levels, abnormal glucose tolerance (hypoglycemia), low folate levels, and low chromium levels (126-130,115), which mercury and other toxic metals have also been found to be a cause of (43,81,A).

  Toxic metals have also been found to affect cell membrane permeability and thus cellular transfer and levels of other important minerals and nutrients that have significant neurological and health effects such as magnesium, lithium, zinc, iron, Vitamins B-6 & B12(5,27,43,46,75,83).  Based on thousands of hair tests, at least 20 % of Americans are deficient in magnesium and lithium (5,68,76,83), with zinc deficiencies also common. The resulting deficiency of such essential nutrients caused by toxic metal exposure has been shown to increase toxic metal neurological damage (5,43,74,75,83). Cerebrospinal magnesium was found to be significantly lower in both depression and adjustment disorder and in those who have attempted suicide (166).

  A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids appears to be a major part of the connection to these neurological and immune reactive conditions (81,83,89-91,97,105,43b). For example mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein (89,91,93,43b), and the same protein that is cluster differentiation antigen 26  (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surfact glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors (89). Studies involving a large sample of autistic and schizophrenic patients found that over 90 % of those tested had high levels of the milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein (92,93,83), and similarly for the corresponding enzyme needed to digest wheat gluten (92,94). The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglovulin and IgG and IgM for casein.  Beta-casomorphine-7 is a morphine like compound that results in neural dysfunction (92), Similarly many also had a corresponding form of gluten protein (94). This likewise is related to ADD, mania, and other neurological conditions.

  Due to the large number of vaccinations that are now containing mercury thimerosal, most children have been documented to receive mercury exposure far above the government health guideline for mercury, and the number of causes of autism has increased over 600% in the last decade [81,A,43b]. Other pervasive developmental disorders (PDD) have also increased significantly with well over 20% of children having ADD, dyslexia, or mood disorders [A]. Research on manic patients, on the other hand, has revealed elevated vanadium in the hair‑significantly higher levels than those measured in both a control group and a group of recovered manic patients (84).

  Much of the developmental effects of mercury (and other toxic metals) are due to prenatal and neonatal exposures damage to the developing endocrine (hormonal) system (155). Other agents including mercury are known to accumulate in endocrine system organs such as the pituitary gland, thyroid, and hypothallamous and to alter hormone levels and endocrine system development during crucial periods of development (33,37,43,27,109). Such effects are usually permanent and affect the individual throughout their life. Some of the documented effects of exposure to toxic metals include significant learning and behavioral disabilities, mental retardation, autism, etc. But even some of the relatively subtle effects that have been found to occur such as small decreases in IQ, attention span, and connections to delinquency and violence, if they occur in relatively large numbers over a lifetime can have potentially serious consequences for individuals as well as for society (37,41,42). Prenatal and neonatal toxic metal exposure to mercury, lead, arsenic, cadmium, nickel, and aluminum have been documented in medical publications and medical texts to cause common and widespread neurological and psychological effects including depression, anxiety, obsessive compulsive disorders, social deficits, other mood disorders, schizophrenia, anorexia, cognitive impairments, ADHD, autism, seizures, etc. (152-155,113-115,43,49).  High aluminum levels have been found to be related to encephalopathies and dementia (49,15). Scores for tension, depression, anger, fatigue and confusion in workers exposed to aluminum for more than ten years were significantly more than those in non-exposed controls (49).

  High lead, copper, manganese, or mercury levels have been found to be associated with attention deficit hyperactivity disorder (ADHD), impulsivity, anger, aggression, inability to inhibit inappropriate responding, juvenile delinquency, and criminality (19,20a,21,61,83,122, 133,136,145,151-155,160,43). It has been found that excess levels of copper can cause violent behavior in children (124,115). A study that investigated the effects of zinc and copper on the behavior of schizophrenic patients by comparing blood zinc and copper levels in criminal and noncriminal schizophrenic patients found criminal subjects have significantly lower zinc levels and significantly higher copper levels than non-criminal subjects(165).

  Likewise mercury has been found to be a factor in anger and mood disorders (135,133,153-155,160,A). Occupational mercury exposure has been found to cause depression, anxiety, anger, antisocial behavior, and aggressiveness (160). Manganese toxicity has long been known to be associated with impulsive and violent behavior (37, 61a, 134, 151). The most common significant source of high manganese neonatal exposure is from soy infant formulas, which typically have very high levels of manganese (151,156). Lead has been the subject of extensive research documenting its relation to all of these conditions and juvenile delinquency (19-21,61,151,A). Based on a national sample of children, there is a significant assoc. of lead body burden with aggressive behavior, crime, juvenile delinquency, behavioral problems (62b). After adjustment for covariates and interactions and removal of non-influential covariates, adjudicated delinquents were four times more likely to have bone lead concentrations greater than 25 parts per million (ppm) than controls (21a).

One mechanism by which mercury has been found to be a factor in aggressiveness and violence is its documented inhibition of the brain neurotransmitter acetylcholinesterase (5,19,28,44-47,43,83,110).  Glutathione and N-acetylcysteine (NAC) have been found to have a strongly protective effect on peroxynitrite’s adverse effect on acetylcholine levels (137), as induced by mercury. Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior(127,128,155,115).

  Inhibition of cholinesterase activity in the brain was also found to be associated with toxic metals and pesticides relation to aggressive and violent behavior (110,etc.). Studies have found evidence that abnormal metal and trace elements affected by metal exposure appear to be a factor associated with aggressive or violent behavior (37,60-63, 110,113,115,123,136,21), and that hair trace metal analyses may be a useful tool for identifying those prone to such behavior. Another series of studies found abnormal trace metal concentrations to be associated with violent-prone individuals including elevated serum copper and depressed plasma zinc (115). A group with a history of assaultive and violent-prone behavior had significantly higher median Cu/Zn ratio than for controls. Assaultive, violent-prone individuals usually have abnormal trace-metal concentrations, including elevated serum copper and depressed plasma zinc (115b).

  Similar tests in the California juvenile justice system as well as other studies have found significant relations of trace metal levels and mineral levels to classroom achievement, juvenile delinquency, and criminality (63,120,123,136).

 Three studies in the California prison system found those in prison for violent activity had significantly higher levels of hair manganese than controls (61,37), and studies of an area in Australia with much higher levels of violence as well as autopsies of several mass murderers also found high levels of manganese to be a common factor (37,134b, 115a). Such violent behavior has long been known in those with high manganese exposure. Other studies in the California prison and juvenile justice systems found that those with 5 or more essential mineral imbalances were 90% more likely to be violent 50% more likely to be violent for 2 or more mineral imbalances (120). A study analyzing hair of 28 mass murderers found that all had high metals and abnormal essential mineral levels (115).  Like several other studies they found higher levels of such toxic metals in blacks than in Caucasian populations. Doctors in UK found a woman’s insanity and violent behavior to be related to poisoning from leaking amalgam dental fillings (37), and other studies and clinical results have confirmed the connection of toxic metals to behavioral problems and violence (114c,115,119,120,123,136). A group of violent criminals had significantly higher levels of hair lead and cadmium levels than non-violent controls (62b).

  Studies at the Argonne National Laboratory found that the majority of delinquents and criminals had high metals levels such as cadmium and lead, and to fall into 2 categories. One group with high copper and low zinc, sodium potassium tended to have extreme tempers, while another group with low zinc and copper, but high sodium and potassium tended to be sociopathic (115). But it was found that treatment of delinquent or violent prone individuals for metals related problems including nutritional therapy usually produced significant improvements in mood, violent behavior, and functionality- with complete cure in the majority of cases (115,119,120). In studies at juvenile delinquency centers, nutritional therapy reduced antisocial and violent behavior by over 50%(120,115). Toxic metals detoxification and nutritional treatment have also been found to be effective in recovery from autism, ADD, PDD conditions (81,43,114), and in cases of abnormal glucose tolerance/hypoglycemia (130,115a).

  Manganese can down-regulate serotonin function, reducing sociability and increasing aggressiveness or depression. Excess manganese exposure reduces dopamine levels which can result in violent behavior. Higher levels of manganese exposure are correlated with Parkinson’s Disease and violent behaviorn(151).

  Because lead and other toxic metals are retained in bone and astroglial cells in the brain, uptake during fetal development and early childhood has long-lasting effects on development and behavior (151). Among the toxic effects of lead is a reduction of dopamine function (which disturbs the behavioral inhibition mechanisms in the basal ganglia) and glutamate (which plays an essential role in the long term learning associated with the hippocampus). Research at the individual level showed that the uptake of heavy metals is associated with higher levels of learning disabilities, hyperactivity, substance abuse, violent crime, and other forms of anti-social behavior. In seven different samples of prison inmates, violent offenders had significantly higher levels of lead, cadmium, or manganese in head hair than non-violent offenders or controls. In two prospective studies, high lead levels at age 7 (one measuring lead in blood, the other bone lead) predicted juvenile delinquency and adult crime. A substantial proportion of individuals diagnosed with ADD/ADHD are likely to have dangerously high levels of lead, manganese, or cadmium in bodily tissues. Because alcohol, cocaine and other drugs temporarily restore neurotransmitter functions that are abnormal, substance abuse may often be crude self-medication in response to the effects of toxicity. For example, because lead down-regulates dopamine and cocaine is a non-selective dopamine reuptake inhibitor, lead toxicity could increase the risk of cocaine abuse (151).

  Heavy metals compromise normal brain development and neurotransmitter function, leading to long-term deficits in learning and social behavior (151). At the individual level, earlier studies revealed that hyperactive children and criminal offenders have significantly elevated levels of lead, manganese, or cadmium compared to controls; high blood lead at age seven predicts juvenile delinquency and adult crime. At the environmental level, our research has found that environmental factors associated with toxicity are correlated with higher rates of anti-social behavior. For the period 1977 to 1997, levels of violent crime and teenage homicide were significantly correlated with the probability of prenatal and infant exposure to leaded gasoline years earlier. Across all U.S. counties for both 1985 and 1991, industrial releases of heavy metals were — controlling for over 20 socio-economic and demographic factors — also a risk-factor for higher rates of crime. Excess levels of lead and manganese are correlated with ADHD and violent behavior. Poor diet increases the effects of lead and manganese toxicity. Communities with a higher percentage of children having blood lead over 10 mg/dL are significantly more likely to have higher rates of violent crime and higher rates of educational failure. Studies comparing Toxic Release Inventory (TRI) data to crime rate data for all U.S. counties found a positive correlation between releases of lead and manganese and violent crime rates. A large federal health survey, NHANES III found a significant correlation between mercury exposure from amalgam fillings and mental conditions (6) Specialists at the Pfeiffer Treatment Center in Illinois have found that treatments to reduce levels of lead and other toxins provide lasting improvement without medication (151).

  Surveys of children’s blood lead in Massachusetts, New York, and other states as well as NHANES III and an NIJ study of 24 cities point to another environmental factor: where silicofluorides are used as water treatment agents, risk-ratios for blood lead over 10µμg/dL are from 1.25 to 2.5, with significant interactions between the silicofluorides and other factors associated with lead uptake (152). Communities using silicofluorides also report higher rates of learning disabilities, ADHD, violent crime, and criminals who were using cocaine at the time of arrest.

  The use of fluosilicic acid (H2SiF6) to fluoridate public water supplies significantly increases the amounts of lead in the water (whereas the use of sodium silicofluoride (NaSiF6) or sodium fluoride (NaF) does not. Communities using either fluosilicic acid (H2SiF6) or sodium silicofluoride (NaSiF6) have significantly higher rates of crime than those using sodium fluoride or delivering unfluoridated water. Also where silicofluorides are in use, criminals are more likely to consume alcohol, more likely to have used cocaine at time of arrest – and that communities have significantly higher crime rates. For 105 New York communities, for every age and racial group there was a significant association between siliocfluoride treated community water and elevated blood lead. Data from analysis of national sample of over 4,000 children in NHANES III, show that water fluoridation is associated with a significant increase in children’s blood lead (with especially strong effects among minority children) (152)

  Lithium is an essential mineral that protects brain cells against excess glutamate and calcium, and low levels cause abnormal brain cell balance and neurological disturbances (75). Lithium also is important in Vit-B12 transport and distribution, and studies have found low lithium levels common in learning disabled children, incarcerated violent criminals, and people with heart disease (76). Lithium supplementation has been found to be an effective treatment adjunct in conditions such as bipolar depression, autism, and schizophrenia where mania or extreme hyperactivity are seen (104) Lithium had a significant mood-improving and stabilizing effect on former drug users with psychological conditions (77). In the study a group including violent offenders and family abusers were divided into 2 groups. Half got lithium supplements and half a placebo. The group getting lithium had significantly increased scores for mood, happiness, friendliness, and energy, while the other group did not (77). In a large Texas study, incidence of suicide, homicide, rape, robbery, burglary, theft, and drug use were significantly higher in counties with low lithium levels in drinking water (78). In a placebo controlled study on prisoners with a history of impulsive/aggressive behavior, the group taking lithium supplements had a significant reduction in aggressive behavior and infractions involving violence (79). The authors suggest that for those areas with low lithium levels in water, water systems should add lithium; and those with deficiencies in lithium or displaying aggressive or impulsive behavior would likely benefit from lithium supplements (78,79).


(5) Goyer RA, National Institute of Environmental Health Sciences.  Toxic and essential metal interactions.  Annu Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity. Am J Clin Nutr 1995; 61(Suppl 3): 646S-650S; & Chetty CS, McBride V, Sands S, Rajanna B. 1990. Effects in vitro of mercury on rat brain Mg (__)-ATPase. Arch Int Physiol Biochim 98:261_267; & Freitas AJ, Rocha JB, Wolosker H, Souza DO. 1996. Effects ofHg2_and CH3Hg_on Ca2_fluxes in rat brain microsomes. Brain Res 738:257_264.

(6) NHANES III survey, 35,000 people,

(19) Great Smokies Diagnostic Lab, Developmental Disorders of Toxic Origin: the Persistance of Lead, 2000,; & Emory E, Pattillo R, Archibold E, Bayorh M, Sung F, Neurobehavioral effects of low-level lead exposure in human neonates.  Am J Obstet     Gynecol 1999, 181: S2-11; & Mendelsohn AL, Dreyer BP, et al, Low-level lead exposure and  behavior in early childhood. Pediatrics 1998, 101(3): E10.

(20) Bonithon-Kopp C, Huel G, Moreau T, Wendling R. Prenatal exposure to lead and cadmium and psychomotor development of the child at 6 years. Neurolbehav Toxicol Teratol 1986; 8(3):307-10; &Perino J,  Ernhart CB.  Proc Annu Conv Am Psychol Assoc 1973; 81:719; & Leviton A, Bellinger D,  Allred EN.  Pre- and postnatal low-level lead exposure and children’s disfunction in school.  Environ Res 1993; 60(1): 30-43;   & Brockel BJ, Cory-Slechta DA.  Lead, attention, and impulsive behavior. Pharmacol Biochem Behav 1998; 60

(2) :545-52; & Bellinger D et al, Attentional correlates of dentin levels in adolescents, Arch Environ Health 1994, 49(2):8-105.

(21) Needleman HL, McFarland C, Ness RB, Fienberg SE, Tobin MJ.  Bone lead levels in adjudicated delinquents. A case control study. Neurotoxicol Teratol 2002 Nov-Dec;24

(6) :711-7; &(b) Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB; Bone lead levels and delinquent behavior.  JAMA 1996, 275(5):363-9; & (c) Needleman HL, Schell A, Bellinger D, Leviton A, Allred En.  The long-term effects of exposure to low dose of lead in childhood, N. England Jr Med 1990, 322: 83-88;  & (d)Burns JM, Baghurst PA, Sawyer MG, McMichael Am, Ton SL, Lifetime low-level lead exposure to environmental lead and children’s emotional and behaviorial development at ages 11-13. Am J Epidemiology 1999, 149

(8): 740-49.

(24) Annau Z, Cuomo V.  Mechanisms of neurotoxicity and their relationship to behavioral changes. Toxicology      1988; 49(2-3): 219-25.

(27) Boadi WY, Urbach J, Branes JM, Yannai S.  In vitro exposure to mercury and cadmium alters term human placental membrane fluidity, Pharmacol 1992; 116(1): 17-23; & Rajanna B, Chetty CS, Rajanna S, Hall E, Fail S, Yallapragada PR. 1995. Modulation of protein kinase C by heavy metals.

Toxicol Lett 81:197_203.

(28)  Stewart-Pinkham, S M. The effect of ambient cadmium air pollution on the hair mineral content of children. The Science of the Total Environment 1989; 78: 289-96.

(33)  T. Colburn et al, “Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans”,  Environmental Health Perspectives, Vol 101

(5), Oct 93

(37) H.R. Casdorph, Toxic Metal Syndrome, Avery Publishing Group, 1995  & S.E. Levick, Yale Univ. School of Medicine, New England Journal of Medicine;   July 17, 1980; & Muldoon SB et al, Effects of lead levels on cognitive function of older women, Neuroepidemiology, 1996, 15(2): 62-72; & Neddleman HL et al, The long-term effects of exposure to low doses of lead in childhood.   N Eng J Med, 1990, 322(2):83-8; & Michael Smith, Woman’s poison fillings blamed for attack on mother , The Daily Telegraph, 09‑26‑1998, pp14.

(38) Atchison WD.  Effects of neurotoxicants on synaptic transmission: lessons learned from electrophysiological studies. Neurotoxicol Teratol 1988 Sep-Oct;10(5):393-416.(39) Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995  Feb;18(2):321-36.

(41) Rodier P.M.  Developing brain as a target of toxicity.  Environ Health Perspect 1995; 103(Supp 6): 73-76; & Weiss B, Landrigan PJ. The developing brain and the Environment. Environmental Health Perspectives, Volume 107, Supp 3, June 2000;

(42) Rice, DC, Issues in developmental neurotoxicology: interpretation and implications of the data.  Can J Public Health 1998; 89(Supp1): S31-40; & Rice DC, Barone S, Critical Periods of Vulnerability for the Developing Nervous System: Evidence from human and animal models.  Environ Health Persect 2000, 108(supp 3):511-533; & © A research-orientated framework for risk assessment and prevention of exposure to environmental toxicants; Environ Health Perspectives, 1999, 107(6): 510.

(43) B. Windham, Annotated Bibliography: Health Effects Related to Mercury from Amalgam  Fillings and Documented Clinical Results of Replacement of Amalgam Fillings” 2002. (over 2000 references ) 

(46) Spivey-Fox MR. Nutritional influences on metal toxicity.  Environ Health Perspect 1979; 29: 95-104; & Pfeiffer SI et al, Efficacy of vitamin B6 and magnesium in the treatment of autism.  J Autism Dev Disord 1995, 25(5):481-93; & Srikantaiah MV, Radhakrishnan AN. 1970. Studies on the metabolism of vitamin B6 in the small intestine. 3. Purification and properties of monkey intestinal pyridoxal kinase. Indian J

Biochem 7:151_156.

(47) Hernberg S; & Moore MR.  in Lead Toxicity, R.Singhal & J.Thomas(eds), Urban & Schwarzenberg, Inc. Baltimore, 1980; & Govani S, Memo M.  “Chronic lead treatment differentially affects dopamine synthesis”, Toxicology 1979, 12:343-49;  &  Scheuhammer AM. Cherian MG. Effects of heavy metal cations and sulfhydyl reagents on striatal D2 dopamine receptors. Biochem Pharmacol 1985, 34(19):3405-13..

(49) [Psychological and neurobehavioral effects of aluminum on exposed workers]  Zhonghua Yu Fang Yi Xue Za Zhi. 1998 Sep;32(5):292-4.  Guo G, Ma H, Wang X; &  Bowdler NC, Beasley DS.  Behavioral effects of aluminum ingestion.  Pharmacol Biochem Behav 1979; 10: 505-512; & Trapp GA, Miner GD.  Aluminum levels in brain in Alzheimer’s Disease.  Biol Psychiatry 1978; 13: 709-

(56) Hart RP, et al, Neuropsychological effects of occupational exposure to cadmium.  J Clin Exp Neuropsychol 1989; 11(6):933-43.

(57) Petit TL, et al, Early lead exposure and the hippocampus. Neurotoxicology 1983; 4(1):  74-79.

(60) Hu H. Knowledge of diagnosis and reproductive history among survivors of childhood plumbism. Am J Public Health 1991; 81*8): 1070-2;   &  Lutz PM, et al, Elevated immunoglobulin E (IgE) levels in children with exposure to environmental lead.  Toxicology 1999; 134(1): 63-78.

(61) Gottschalk LA, et al, Abnormalities in hair trace elements as indicators of aberrant behavior.  Compr Psychiatry.

1991; 32(3): 229-37; &(b) Nevin R, How lead exposure relates to temporal changes in IQ, violent crime, and unwed    pregnancy.  Environ Res 2000, 83(1):1-22;   & ©  Stretesky PB; Lynch MJ;  The relationship between lead exposure and homicide. Arch Pediatr Adolesc Med 2001 May;155(5):579‑82

(62) Schauss A.G. Comparative hair mineral analysis in a randomly selected “normal” population and violent criminal offenders. Int J Biosocial Res 1981; 1:21-41, & ; & (b) Pihl RO, Ervin F, Lead and cadmium levels in violent criminals, Psychol Rep 1990, 66(3Pt1): 839-44.

(63) Cromwell P.F. et al, Hair mineral analysis: biochemical imbalances and violent criminal behavior.  Psychol Rep 1989; 64:259-66.

(68) Starobrat-Hermelin B. The effect of deficiency of selected bioelements on hyperactvity in children with certain specified mental disorders. Ann Acad Med Stetin 1998; 44:297-314. [article in Polish]; &  Starobrat- Hermelin B, Kozielec T.  The effects of magnesium physiological supplementation on hyperactivity in  children with ADHD: positive response to magnesium oral loading test. Magnes Res 1997.10(2):149-56.

(74) Smith JB; Dwyer SD; Smith L. Cadmium evokes inositol polyphosphate formation and calcium mobilization. Evidence for a cell surface receptor that cadmium stimulates and zinc antagonizes. J Biol Chem 1989 May 5;264(13):7115‑8.

(75) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., “Lithium treatment  protects neurons in CNS from glutamate induced  excitibility and calcium influx”, Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998; & Rossi AD, Larsson O, Manzo L, et al. 1993. Modifications of Ca2_ signaling by inorganic mercury in PC12 cells. Faseb J 7:1507_1514.

(76) Schrauzer GN, Shrestha KP, Flores‑Arce MF.  Lithium in scalp hair of adults, students, and violent criminals. Effects of supplementation and evidence for interactions of lithium with vitamin B12 and with other trace elements.     Biol Trace Elem Res 1992 Aug;34(2):161‑76.

(77) Schrauzer GN, de Vroey E. Effects of nutritional lithium supplementation on mood. A placebo‑controlled study with former drug users. Biol Trace Elem Res 1994; 40(1):89‑101.

(78) Schrauzer GN, Shrestha KP. Lithium in drinking water and the incidences of crimes, suicides, and arrests related to drug addictions. Biol Trace Elem Res 1990 May;25(2):105‑13

(79) Sheard MH, Marini JL, Bridges CI, Wagner E. The effect of lithium on impulsive aggressive behavior in man. Am J Psychiatry 1976 Dec; 133 (12):1409‑13

(81) Autism: a unique form of mercury poisoning. & Halsey, NA. Limiting Infant Exposure to Thimerosal in vaccines. J. of the Amer. Medical Assoc., 282: 1763-66; & Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; & A. Holmes, http://www.healing‑

(82) National Academy of Sciences, National Research Council, Committee on Developmental Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1, 2000, 313 pages; &  Evaluating Chemical and Other Agent Exposures for  Reproductive and Developmental Toxicity Subcommittee on Reproductive and Developmental Toxicity, Committee on Toxicology, Board on  Environmental Studies and Toxicology, National Research Council National Academy Press, 262 pages,  6 x 9, 2001.

(83) Great Smokies Diagnostic Lab, Depression, ADD & ADHD research web pages (click on: by condition), research studies on causes and treatments, http://; & Dr. G. Klerman, National Istitute of      Health, Factors in the rapid rise of depression, 1997; & ADD case study, ttp://  & Tuthill RW, Hair lead levels related to children’s classroom attention-deficit behavior. Arch Environ Health, 1996, 51(3): 214-20.

(84)  Naylor GJ, Corrigan FM, Smith AH, Connelly P, Ward NI, Further studies of vanadium in depressive psychosis. Br J Psychiatry 1987, 150:656-61; & Naylor GJ, Reversal of vanadate-induced inhibition of Na-K ATPase, J Affect  Disord 1985, 8(1):91-3; & Naylor GJ et al, Tissue vanadium levels in manic-depressive illness,   Psychol Med 1984, 14(4):767-72; & Naylor et al, Elevated vanadium content of hair and mania, Biol Psychiatry 1984, 19(5):759-64; & Simonoff M, Simonoff G, Conri C, Vanadium in depressive states, Acta Pharmacol Toxicol 1986, 59(Supp 7): 463-6.

(89)  Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal  ions and histidine. Neuropharmology 1990; 29(5): 445-52; & Mondal MS, Mitra S.  Inhibition of bovine  xanthine oxidase activity by Hg2+ and other metal ions.  J Inorg Biochem 1996; 62(4): 271-9; & Sastry  KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating  agents: Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol 1978; 20(6): 729-35; & 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”, Environ Res, 1992, 57(1):96-106.

(90) McFadden SA, Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65; & Markovich et al,  “Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1″, Toxicol  Appl Pharmacol, 1999,154(2):181‑7; &  Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions  inhibit reduction of  disulfide bonds. J Biol Chem 1991; 266(19): 12695-702

(91) Puschel G, Mentlein R, Heymann E, ‘Isolation and characterization of dipeptidyl peptidase IV from human placenta’, Eur J Biochem 1982 Aug;126(2):359-65; & Kar NC, Pearson CM.  Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92; & Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8(5): 278-84; & Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev 2000, 5(1):52-63.

(92) (a) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999.; & (b) Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4; & Reichelt KL et al, Biologically active peptide-containing fractions in schizophrenia and childhood  autism. Adv Biochem Psychopharmocol 1981; 28: 627-43;& (c) Lucarelli S, Cardi E, et al, Food allergy and infantile autism. Panminerva Med 1995; 37(3):137-41; & (d) Kurek M, Przybilla B, Hermann K, Ring  JA ,Naturally occurring opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser  in man. Int Arch Allergy immunol 1992; 97(2): 115-20.

(93) Willemsen-Swinkels SH, Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H. Plasma beta-endorphin concentrations in people with learning disability and self-injurious and/or autistic behavior. Br J Psychiary 1996; 168(1): 105-9; & Leboyer M, Launay JM et al.   Difference between plasma N- and C-terminally  directed beta-endorphin immunoreactivity in infantile autism. Am J Psychiatry 1994; 151(12): 1797-1801.

(94) Huebner FR, Lieberman KW, Rubino RP, Wall JS.  Demonstration of high opioid-like activity isolated  peptides from wheat gluten hydrolysates. Peptides 1984; 5(6):1139-47.

(104) Kerbeshian J, Burd L, Fisher W. Lithium carbonate in the treatment of two patients with infantile autism and atypical bipolar symptomology. J Clin Psychopharmacology, 1987, 7(6):401-5.

(109) Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads

Publishing Company Inc; & Hal Huggins, Its All in Your Head, 1993;

(110) Soderstrom S, Fredriksson A, Dencker L, Ebendal T, “The effect of mercury vapor on cholinergic neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995, 85:96-108; Miszta H; Dabrowski Z. Effect of mercury and combined effect of mercury on the activity of acetylcholinesterase of rat lymphocytes during in vitro incubation. Folia Haematol Int Mag Klin Morphol Blutforsch 1989;116(1):151‑5; &  Bear, David; Rosenbaum, Jerrold; Norman, Robert. Aggression in cat and human precipitated by a cholinesterase inhibitor. The journal Psychosomatics, July  1986, vol. 27,  #7, pgs. 535‑536; & Devinsky, Orrin; Kernan, Jennifer: Bear, David. Aggressive Behavior Following Exposure to Cholinesterase Inhibitors. Journal of Neuropsychiatry, vol. 4, #2, Spring 1992, pgs. 189‑199.

(113) (a) Pfeiffer CC, Iliev V. A study of copper excess and zinc deficiency in schizophrenia. in: International Review of Neurobiology, Supplement 1, Academic Press, NY,NY, 1972, p141-164;  & Alexander PE, Van Kammen DP.  Serum magnesium and calcium levels in schizophrenia. Arch Gen Psychiatry 1979;36: 1372-77;&(b) Fatty Acid Profiles of Schizophrenic Phenotypes, D. M. Bibus, R. T. Holman, and W. J. Walsh , 91st AOCS Annual Meeting and Expo, San Diego, California, April 25-28, 2000

& (c) Nutrients and Depression: Food for Your Mood, By: Constantine Bitsas, Executive Director, Health Research Institute and Pfeiffer Treatment Center; ; &Bibliography for Depression,;

(114) (a)Disordered Metal Metabolism in a Large Autism Population, W. J. Walsh, A. Usman, and J. Tarpey,  Presented at the APA Annual Meeting, May, 2001 – New Orleans, ; &

(b) Metal-Metabolism and Human Functioning, W. J. Walsh , Pfeiffer Treatment Center ; &

(c) Zinc Deficiency, Metal Metabolism, and Behavior Disorders, by William J. Walsh; &

(d) Metal-Metabolism and Autism: Defective Functioning of Metallothionein Protein, Amy Holmes, MD;

(115) (a) Biochemical Treatment of Mental Illness and Behavior Disorders, William J. Walsh, Ph.D. Health Research Institute, Minnesota Brain Bio Association November 17, 1997; &(b) Walsh WJ, Isaacson Hr, Hall A, Elevated blood copper to zinc ratios in assaultive young males, Physiol Behav. 1997 Aug;62(2):327-9; & & The Health Research Institute’’s Work with Aggressive Behavior ; & (c) Reduced violent behavior following biochemical therapy, W. J. Walsh, Laura Glab and Mary  Haakenson, Physiology & Behavior, Volume 82, No.5,  15 October 2004, Pages 835-839, ; & (d) Bibliography for Agressive & Violent Behavior,

(119) Coulter HL, Fisher BL. Vaccination, Social Violence, and Criminality, 1990, &

(120) Schoenthaler SJ, “Effect of Nutrition on Crime, Intelligence, Academic Performance, and Brain Function”  paper presented at 15th International Conference on Human Function, Sept 22-24, 2000, Wichita, Kan. 

(121) Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine: Part III–purification and properties of monkey intestinal pyridoxal kinase. Indian J of Biochem 7:151-156 (1970).

(122). Dr Thomas Verstraeten, US Centres for Disease Control and Prevention, Summary Results: Vaccine Safety Datalink Project ‑ a database of 400,000 children, May 2000.

(123) Stretesky P et al, Homicide rates linked to lead levels, Archieves of Pediatrics and Adolescent Med, May 2001

(124)  Lavie R, Iron and Copper overload.  Consumer Health Newsletter, Vol 21, No. 6, June, 1998.

(126) Salzer HM, Relative hypoglycemia as a cause of neuropsychiatric illness, J National Med Assoc, 1996,

58(1): 12-17; & Heninger GR et al, Depressive symptoms, glucose tolerance, and insulin tolerance, J Nervous

     and Mental Dis, 1975; 161(6):421-32; & Winokur A et al, Insulin resistance in patients with major depression,   Am J Psychiatry, 1988, 145(3): 325-30.

(127) Virkkunen M, Huttunen MO; Evidence for abnormal glucose tolerance among violent offenders,

Neuropsychiobilogy, 1982, 8:30-40; & Markku I, Virkkunen L; Aggression, suicidality, and serotonin, J Clinical Psy 1992, 53(10): 46-51;

(128)Linnoila M et al, Low serotonin metabolite differentieates impulsive from nonimpulsive violent (129)behavior, Life Sciences, 1983, 33(26): 2609-2614; & Lopez-Ibor JJ , Serotonin and psychiatric disorders,

Int Clinical Psychopharm, 1992, 7(2): 5-11.

(129) Yaryura-Tobias JA et al, Changes in serum tryptophan and glucose in psychotics and neurotics, Nutrition, No.4557, p1132; Carney MWP, Brit Med J, 1967, 4:512-516.

(130)Urberg M, Zemel MB; Evidence for synergism between chromium and nicotinic acid in the control of glucose

(131) tolrerance in elderly humans, Metabolism, 1987, 36(9): 896-899; & J Family Practice, 1988, 27(6): 603-606;

& Anderson RA et al, Effects of supplemental chromium on patients with reactive hypoglycemia, Metabolism,

1987, 36 (4): 351-355; & Metabolism, 1983, 32 (9): 894-99.

(132) The Health of Canada’s Children—A Canadian Institute of Child Health (CICH), Profile: 3rd Edition, 2000, 325 pages.

(133) Camara Vd et al, Methodology to prevent mercury exposure among adolescents from goldmine areas in   

Mariana, state of Minas Gerais, Brazil, Cad Saude Publica 1996 Apr;12(2):149‑158.

(134) Bowler RM, Roels HA et al, Manganese exposure: Neuropsychological and neurological symptoms and effects in welders.  Neurotoxicology. 2005;& Bowler RM; Mergler D et al; Neuropsychiatric effects of manganese on mood. Neurotoxicology 1999 Apr‑Jun;20(2‑3):367‑78; & (b) Tardiff K. Unusual diagnoses among violent patients.  Psychiatr Clin North Am 1998 Sep;21(3):567‑76; & (c) Lucchini R; Albini E et al, Mechanism of neurobehavioral alteration. Toxicol Lett 2000 Mar 15;112‑113:35‑9; & Lucchini R; Apostoli P et al ; Long‑term exposure to “low levels” of manganese oxides and neurofunctional changes in ferroalloy    workers. Neurotoxicology 1999 Apr‑Jun; 20(2‑3):287‑97  & (d) Mergler D; Baldwin M et al, Manganese neurotoxicity, a continuum of dysfunction: results from a community based study. Neurotoxicology 1999 Apr‑Jun; 20(2‑3):327‑42

(135) R.L.Siblerud et al,”Psychometric evidence that mercury from dental fillings may be a factor in depression,anger,and anxiety”, Psychol Rep,  v74,n1,1994;  & Amer. J. Of Psychotherapy, 1989; 58: 575-87; & B.Windham(Ed.), Depression, Anxiety, and Mood Disorders: the Mercury Connection;

(136) Lead in Air Linked to Increase in Homicides, Arch Pediatr Adolesc Med.

May 2001;155:579-582

(137)   Guermonprez L, Ducrocq C, Gaudry-Talarmain YM.  Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46

(151) Masters, R, Hone, B, and Doshi, A. (1998). “Environmental Pollution, Neurotoxicity, and Criminal Violence,” in J. Rose, ed., Environmental Toxicology: Current Developments (London: Gordon and Breach, 1998), pp. 13-48; & Masters, R. D. and Coplan, M. J., with Hone, B.T., Grelotti, D. J., Gonzalez, D. and Jones, D. “Brain Biochemistry and the Violence Epidemic: Toward a ‘Win-Win’ Strategy for Reducing Crime,” in Stuart Nagel, ed., Super-Optimizing Examples Across Public Policy Problems (NOVA Science Publishers) (2003); & Masters, RD and Coplan, M.J. (1999c). “The Triune Brain, the Environment, and Human Behavior: Hommage to Paul MacLean,” to appear in Russell Gardner, ed. Festschrift in Honor of Paul MacLean. 2003. (First presented at Back Bay Hilton Hotel, Boston, Mass. – July 16, 1999); & Dr. Roger D. Masters and Myron Coplan, Toxins, Brain Chemistry, and Behavior,

(152) Masters, R. and Coplan, M. (1999a) “Water Treatment with Silicofluorides and Lead Toxicity,” International Journal of Environmental Studies, 56: 435-49; & Masters, RD, Coplan, M. J., Hone, B.T., And Dykes, J.E. (2000). “Association of Silicofluoride Treated Water with Elevated Blood Lead,” Neurotoxicology 21: 101-1100; & Coplan, M. J., Masters, R. D., and Hone, B. (1999a) “Silicofluoride Usage, Tooth Decay and Children’s Blood Lead,” Poster presentation to Conference on “Environmental Influences on Children: Brain, Development and Behavior, New York Academy of Medicine, Mt. Sinai Hospital, New York, May 24-25, 1999.

(153) Psychiatric Disturbances and Toxic Metals, Townsend Letter for Doctor’s & Patients April 2002; &Alternative & Complementary Therapies (a magazine for doctors), Aug 2002;

(154) R.A.Goyer,”Toxic effects of metals” in: Caserett and Doull’s Toxicology- The Basic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; &(b) Goodman, Gillman, The Pharmacological Basis of Therapeutics, Mac Millan Publishing Company, N.Y. 1985; &(c) Encyclopedia of Occumpational Health and Safety, International Labour Office, Geneva, Vol 2, 3rd Edition.;&(d) Arena, Drew, Poisoning. Fifth Edition. Toxicology-Symptoms-Treatment, Charles C. Thomas-Publisher, Springfield Il, 1986; & Merritt’s Textbook of Neurology, 9th Ed., Williams and Wilkins, Baltimore, 1995, p668-, & Clinical Management of Poisoning, 3rd Ed.,(p753) Haddad, Shannon, and Winchester, W.B. Saunders and Company, Philadelphia, 1998; & U.S. EPA, Office of Health and Environmental Assessment,  Mercury Health Effects, Update Health Issue Assessment, Final Report, 1984, EOA-600/8-84f.

(155) Developmental effects related to prenatal/neonatal mercury exposure and mercury’s endocrine disruptive effects, B. Windham(Ed.)

(156)  For Immediate Release by Lumen Foods ( Date: June 11, 2001; TITLE: Soy manufacturer warns mothers against feeding newborns their soymilk. CONTACT: Greg Caton Vice President (800) 256-2253

(160) (a) L.Soleo et al, “Effects of low exposure to inorganic mercury on psychological performance”, Br J Ind Med, 1990, 47(2):105-9; & (b)[Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)]  Rev Neurol. 2000 Oct 16-31;31(8):712-6. Tirado V, Garcia MA et al; & (c) Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers. Brain Inj. 2000 Sep;14(9):797-814.  Powell TJ: & (d) Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999;6(4):193-200, Haut MW, Morrow LA et al: & (e) Personality traits in miners with past occupational elemental mercury exposure. Environ Health Perspect. 2006 Feb;114(2):290-6; Kobal Grum D, Kobal AB

& (f) Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers.  Bosn J Basic Med Sci. 2002 Dec;2(1-2):29-34. Pranjic N, Sinanovic O, et al. ; & (g) 
Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers. Bosn J Basic Med Sci. 2002 Dec;2(1-2):29-34. Pranjic N, Sinanovic O, et al.

(165) Blood zinc and copper concentrations in criminal and noncriminal schizophrenic men. Arch Androl. 2003 Sep-Oct;49(5):365-8. Tokdemir M, Polat SA, et al.

(166) Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts.

Biol Psychiatry. 1985 Feb;20(2):163-71. Banki CM, Vojnik M, et al

Original paper→ HERE

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