Density of metallurgy in Ukraine, expressed as monetary output of the industry per capita of total population.
Manganese Madness
When Jonathon Ericson, environmental health scientist, began planning a two-day conference on toxic metals, his thoughts turned to the internal combustion engine. Day One he dedicated to lead of the tetraethyl variety added to silence engine knock. For fifty years, no-knock gasoline containing tetraethyl lead has spewed metallic wastes out of millions of tailpipes, tainting the soil and water—and the lungs and brains of little children.
For Day Two, Ericson planned to focus on MMT, an antiknock ingredient containing manganese. He issued invitations to speakers who could discuss the dangers of manganese to the brains of miners in Europe, Asia, South America and Australia who, after a few years on the job, run an increased risk for Parkinson’s Disease. The manganese particles they inhale through the lungs then move to the brain with devastating effects.
Left with invitations for the final two conference speakers, Ericson turned away from internal combustion engines, tailpipes and toxic exhausts. Instead, he focussed on the dangers of a consumer product that has been on the market for about thirty years—the plastic bottle filled with soybean-based infant formula.
How a bottle of soy formula can be mentioned on the same program with a smoking exhaust pipe and brain damage in manganese miners is what kept the UC Irvine conference audience captivated. The soy story told by speakers Francis Crinella of the UC Irvine faculty and Trinh Tran from the UC Davis Department of Animal Studies unfolded like a Stephen King novel, complete with mindless villains, thickening plot and innocent victims too young to defend themselves.
Ericson’s conference took place in September, 2000 at the University of California at Irvine. His two final speakers, Crinella and Tran, suggested that infants sucking on nipples of plastic bottles containing soy-based formula could absorb toxic amounts of manganese into their rapidly developing brains.
The melodrama—no, the tragedy—of toxic manganese in infant formula begins in 1980 when the Federal Government’s Food and Nutrition Board established safe and acceptable values for manganese in adults, toddlers and infants. Permissible levels for the three age ranges were set at 2.5-3.0 mg/day in adults, 1.0 to 1.5 mg/day in toddlers and 0.5 to 1.0 mg/day in infants. The “safe” level for infants soon translated into soy formula products purchased by millions of mothers.
Despite government assurances, Phillip Collipp, a pediatric physician at Nassau County Medical Center in 1983 tested for the manganese in popular soy brands available locally, including Isomil, ProSoybee and Nursoy. They contained from 0.2 to 1.0 mg of manganese per quart of infant formula. Later that year, Bo Lönnerdal and Carl L. Keen, of the Department of Nutrition of UC Davis, tested baby formula taken from pharmacy shelves in eight countries. The manganese concentrations they found in soy formulas were higher, ranging from 0.4 to 2.2 mg; the mean value of 1.2 mg vastly exceeded the infinitesimal 0.005 mg found in human breast milk.
Nutritional scientists have reported how newborn babies absorb manganese from breast milk. Tiny amounts suckled daily a dozen times by the baby supply an adequate quantity of manganese to catalyze 50 biochemical reactions. The newborn’s digestive system seems superbly attuned to absorb the scanty amounts of manganese it needs from its mother’s milk.
However, soy formula, containing up to 200 times the manganese of breast milk, overloads the little body. The baby’s immature liver cannot handle the load. With each swallow increasing the manganese content in its digestive track, what does the baby do to dispose of the excess? Bo Lönnerdal, a researcher from UC Davis, explained that in newborns, ingested manganese rises to high levels in the blood plasma and red blood cells and then permeates the liver, kidneys and other soft tissues of the body, including the brain. Only later, at the time of weaning, can the infant metabolize such large amounts of manganese.
Francis Crinella calculated that by eight months, an infant fed soy formula daily absorbs approximately 1.1 mg of manganese above metabolic need. “A significant amount, about 8 percent, is deposited in a brain region vulnerable to threat of manganese attack.”
Neurology textbooks identify manganese as a neurotoxic metal. In 1837, an English physician noted that some workers in a manganese mill appeared lethargic and their faces unexpressive. By the turn of the century, the disease of “manganism” had been described in medical journals. The disease struck miners exposed to toxic dust, and appeared to cause emotional lability, irrationality, hallucinations and impulsivity. Chronic exposure produced more severe symptoms, including muscular weakness, difficulty in walking, tremor, immobile facial expression, and speech disturbances—symptoms reminiscent of Parkinson’s Disease. Sufferers of the Parkinson’s-like neurological disease secondary to chronic poisoning accumulate large amounts of manganese in a circumscribed region of the brain.
The primary site of manganese toxicity regardless of the route of exposure—by mouth, inhalation or injection by intravenous tube—in humans, monkeys, rabbits and rats, is a mass of nervous tissue buried deep within the cerebral hemispheres. This is the basal ganglia, part of the extrapyramidal system controlling body movement. The neuronal damage caused by the manganese tends to be more extensive in young, immature animals than in adults.
Six years ago, tragic incidents in two London hospitals alerted the medical community to the vulnerability of sick babies to manganese attack. Suffering liver disease, the babies received nutrient solutions containing small amounts of manganese through intravenous tube feeding. Although the manganese concentration was no greater than that in soy formula, and considered safe by government standards, it caused brain damage after feeding periods lasting a few months to two years. Of 57 babies receiving “safe” amounts of manganese, two fell ill with movement disorders and six suffered damage to their basal ganglia.
John Donaldson, toxicologist and speaker on Day Two at the UC Irvine conference, described how manganese could cause a biochemical lesion in the basal ganglia. He reported how manganese overload can step up the brain’s electric charge, increase its virulence tenfold, and attack vulnerable dopaminergic neurons.
Arvid Carlsson, last year’s Nobel Prize winner in medicine, has shown that damage to these basal ganglia dopamine cells is symptomatic of Parkinson’s Disease. At the conference, Donaldson warned that when “incredible” amounts of manganese are fed to infant mammals, the metal is capable of “running amok” in the basal ganglia dopamine nerve cells. “After chronic early exposure, they can be brain-damaged later in life,” he said.
When Francis M. Crinella, Clinical Professor of Pediatrics at the University of California at Irvine, spoke, he described the effects of manganese overload in adolescents. His research had detected relatively high levels of manganese in the scalp hair of hyperactive children compared to matched controls. This replicated earlier studies by UC Irvine psychiatrist Louis Gottschalk, who detected elevated manganese in scalp hair of youths detained for felony crimes and incarcerated in four Southern California prisons. These findings, wholly unexpected, persuaded Crinella to launch inquiry into the most likely source of manganese in the hair, then to ask whether this had anything to do with hyperactivity in children, a syndrome attributed to a disturbance in the basal ganglia. To Crinella, the low levels of manganese in California soil, air and water meant the primary intake had to be through diet. Since adolescents are able to metabolize at least 97 percent of manganese ingested, exposure had to occur earlier in life, possibly during infancy. This hypothesis was first stated by Collipp in 1983 who had tested hair samples of babies fed soy-based infant formula and found them high in manganese. Crinella speculated that soy infant formula might provide one explanation for the current epidemic of adolescent violence sweeping the nation.
Crinella contacted his colleague Bo Lönnerdal at UC Davis to take a further look at the effects of manganese on the brain, particularly its toxicity to dopamine neurons in the basal ganglia. Lönnerdal and a graduate student Trinh Tran tested for behavioral and brain disorders in rat pups. For 18 days, four groups of rat pups suckled on the mother’s breast and received by micropipette an additional dose of manganese salt dissolved in water. The doses corresponded to the amounts of manganese found in rat breast milk (0.05 mg) and several brands of soy-based infant formula (0.25 mg and 0.50 mg) found on pharmacy shelves today. The control group received just sugar water (0.0 mg). After 18 days of controlled feeding, the rat pups were returned to their cages and left undisturbed until 50 days of age. Then through Day 64 they were given behavior tests for evidence of disability. The animals given high amounts of manganese did less well on maze and shock avoidance than those given lesser amounts.
The audience now turned their attention to the next paper, by Francis Crinella, on levels of basal ganglia dopamine. Crinella’s data were clear-cut, unmistakable and replete with implications. Rats given 0. 05 mg of manganese daily for 18 days, the amount comparable to the manganese in breast milk, did as well as the control group given no manganese. Rats given supplemental manganese in the dose five times higher, or 0.25 mg, suffered a 48 percent decline in levels of basal ganglia dopamine. The rats dosed daily with the highest amount, 0.50 mg, had a staggering 63 percent plunge in dopamine.
When asked the meaning of these dramatic findings, Crinella answered that many labs previously had reported the toxic effects of manganese. The basal ganglia frequently were the target for neurotoxic effects. Dramatic declines in dopamine due to manganese overload had been reported before. He also described the lingering threat of toxic alterations in brain cells weeks after manganese is discontinued.
The value of Crinella’s data and that of Trinh Tran was that they provided a link between a moderate manganese exposure during early infancy, dopamine neurotoxicity and the possibility of cognitive disorders in later life.
“The brain undergoes a tremendous proliferation of neurons, dendrites and synapses during the first months of life. Some neurons will be pruned during childhood for maximum information efficiency,” said Crinella. “The brain is especially vulnerable in early life precisely because such rampant growth is taking place, and at that time intrusions by potentially toxic substances like manganese perturbing the emerging neural organization can exert long-term effects. Manganese ingested during a period of rapid brain growth and deposited in the critical basal ganglia region may affect behavior during puberty when powerful stresses are unleashed on the dopamine neurons and altered behavioral patterns appear.” According to Crinella, these altered behavioral patterns during late childhood and early adolescence may be diagnosed as hyperactivity with attention deficit disorder.
Or perhaps as a “manganese toxicity syndrome.” Crinella’s presentation provoked much discussion. Is the manganese ingested in soy formula at infancy a source for behavioral disorders later on? Bo Lönnerdal and Carl Keen were impressed by the findings but warned against premature generalization. Young rats appear more susceptible than human babies to manganese toxicity. They absorb 80-85 percent of the manganese they ingest, while the figures for human infants at six months old are closer to 35 percent. It is in providing the worst-case scenario of what can happen to human infants fed manganese that the rodent research may prove most instructive.
A dissenting opinion about soy dangers came from John Lasekan, a pediatric nutritionist at Ross Products Division of Abbott Laboratories. His published research claims that manganese is a trace metal absolutely essential for life and that premature and low birth weight infants may be at risk for developing a deficiency in manganese. He claims that the soy-based formulas support normal growth and normal plasma biochemistry, comparable to infants fed human milk during at least two months of life. Mardi Mountford, spokesman for the International Formula Council adds: “There are no reports of manganese toxicity in healthy infants fed soy formula. Parents can be assured that infant soy formulas are safe and nutritious feeding options for their infants.”
Yet some remain unconvinced. “It’s overwhelming,” says Everett “Red” Hodges, founder of the Violence Research Foundation, citing the evidence supporting Crinella’s hypothesis that infants ingesting soy-based infant formula at the levels available in commercial products 15 years ago might be at risk. “Criminals aged sixteen and seventeen years old today, some of whom were born to poor mothers in 1983 and 1984, could have received from the government soy formula with enough manganese to disrupt growing brains, and this may be why these adolescents have difficulty restraining aggressive impulses today.”
Stanley Van Den Noort, a neurology professor and former Dean of the UC Irvine College of Medicine, agrees with Hodges and Crinella. “I think the data presented at the conference are convincing that manganese is a neurotoxin. Newborn infants exposed to high levels of manganese may be predisposed to neurological problems. We should exercise strong caution in the use of soy-based formula around the world.”
Whether or not the manganese in soy formula today, with an average value of 0.16 mg per quart (0.15 mg per liter), poses an acute danger may be secondary to the issue of why more and more mothers in the United States imagine they have given birth to a baby soy bean instead of a human child. “Why else feed so many newborn infants soy ‘milk’?” asks Naomi Baumslag, Clinical Professor of Pediatrics at Georgetown University Medical College and President of the Woman’s International Public Health Network. For years Baumslag has waged a campaign against the medical profession’s cavalier attitude towards soy infant formula. “Only 50 percent of newborns today suckle at the mother’s breast, even once. After six months, the number has fallen to only one mother in five. Often, mothers for the sake of convenience plunk soy bottles into the infant’s mouth. Sales of soy formula have doubled during the past ten years.” Baumslag states, “There is great deal of scientific evidence that soy formula can be damaging to newborns, quite aside from the manganese.” Soy “milk” can be dangerous for what it has and does not have. A spoonful of soy formula lacks many nutritional, immune and developmental factors. The spoonful may be deficient in linoleic and oleic essential fatty acids, DHA-brain growth factor, epidermal growth factor, lactoferrin, casomorphin, and immune factors like IgA, neutrophils, macrophages, T-cells, B-cells and interferon that mother’s milk provides to defend her baby. The spoonful of soy “milk” unfortunately, does contain phytates, protease factors, soy lectins, enormous amounts of phytoproteins, and genistein, a moderately potent estrogen-mimic in humans. She asks, “Why deprive the newborn infants of perfectly good breast milk—nutritionally superior food in every way for the baby—and feed them soy beans?”
The powers in government and corporations have not reacted to these voices raised against the potential dangers of manganese in soy infant formula. The government can hardly be unaware of the simple logic: (1) Excess manganese is toxic. (2) Babies absorb excess manganese. (3) Excess manganese is toxic to babies. Carl L. Keen believes that the original administrative problem was that the government established teenage requirements for manganese, then extrapolated backwards to determine a level they believed to be safe and acceptable for toddlers and newborns. The problem of infant exposure to excessive manganese identified 15 years ago still persists, but what can scientists like Drs. Keen and Crinella do about it?
Sitting at his desk in the Social Ecology building, Jonathon Ericson pondered how he could bring the soy infant formula problem to the public’s attention. Why not, he thought, provide the answer at the end of the two-day conference? Day One would fill the audience’s mind with indisputable evidence that a lead compound of the tetraethyl variety, from inception as a gasoline additive in the 1920s until its removal from fuel in the 1980s, was causing brain damage in children around the world. Day Two would extend the warning to manganese, both in the antiknock compound MMT and as a contaminant in baby formula. What he did was invite two government policy makers, Robert Presley and Phillip Lee, to discuss what society must do today to resolve the soy formula crisis.
Chairing the panel was Senator Robert Presley, California State Secretary of the Adult & Juvenile Corrections Agency, responsible for 170,000 incarcerated felons. Presley thanked Jon Ericson for providing him with the challenge. His solution was to recommend increased funding for studies of brain development. When asked why this was important, he said, “Somewhere in the soy formula story may lie the answer to a lot of crime.” Phillip R. Lee, Former U.S. Undersecretary of Health and Human Services, now Senior Advisor to the Institute for Health Policies, took a moment to applaud independent research. Then he offered his advice: “The MRI scan detected brain damage in the sick babies in London. In the U.S., we might identify sensitive populations of newborns, then launch longitudinal studies combining the scans and behavioral testing to find out what infant feeding has to do with aberrant behaviors occurring during late childhood years.”
Two conclusions emerge from the conference. First, the need to educate the public about the potential dangers posed by the soy formula now fed to 750,000 infants per year. Second, to accelerate studies on the effects of toxic metals on the brain and on human behavior.
How the unfolding melodrama will end, nobody knows. Since the September, 2000 conference, scientists are stepping up their efforts to pinpoint the manganese syndrome. They are investigating the effects on calcium and iron deficiency in pregnant rat dams, known to enhance uptake of manganese in the infant. Second, they are going to look more carefully at the effects of manganese excess in infant primates.
Meanwhile, manganese levels in soy formula remain high. One soy-based product on the shelf today provides up to 0.72 mg manganese daily. And soy products for infants sold in foreign countries can be even higher.
In 1983, Phillip Collipp offered the following advice to the formula industry: “Reduce manganese in infant formula to the levels found in human milk.” So far, the industry has not responded.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2001.
The Toxic Metal connection to ADD, Aggressiveness, Impulsivity, Violence, Delinquency, Criminality, and Mass murderers/Serial killers B. Windham (Ed) -Chemical Engineer
A recent study released by the National Academy of Sciences found that 50% of children born in the
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 xanthineoxidase 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 opioidreceptor 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 violen ce, 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 signif. 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 noninfluential 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
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
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 downregulate 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 behavior(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 downregulates 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
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 silicofluoridesand 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
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
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