Autism: a Novel Form of Mercury Poisoning

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[autism-awareness-action] Autism: a Novel Form of Mercury

Poisoning

FEAT DAILY NEWSLETTER Sacramento, California http://www.feat.org

" Healing Autism: No Finer a Cause on the Planet "

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September 20, 2000

Autism: a Novel Form of Mercury Poisoning

[This research paper is a keystone document in the heavy metal theory

of autism. The strong comparison of the symptoms of autism to the symptoms

of mercury poisioning is almost surreal and disturbing in its implication.

The abstract of this study appeared in the June 20, 2000 FEAT Daily

Newsletter.]

S. Bernard, B.A., A. Enayati, M.S.M.E., L. Redwood, M.S.N., H. , B.A.,

T. Binstock

Sallie Bernard, ARC Research, 14 Commerce Drive, Cranford, NJ 07901 USA,

, fax

Summary Autism is a syndrome characterized by impairments in social

relatedness and communication, repetitive behaviors, abnormal movements, and

sensory dysfunction. Recent epidemiological studies suggest that autism may

affect 1 in 150 U. S. children. Exposure to mercury can cause immune,

sensory, neurological, motor, and behavioral dysfunctions similar to traits

defining or associated with autism, and the similarities extend to

neuroanatomy, neurotransmitters, and biochemistry. Thimerosal, a

preservative added to many vaccines, has become a major source of mercury in

children who, within their first two years, may have received a quantity of

mercury that exceeds safety guidelines. A review of medical literature and

U.S. government data suggests that (i) many cases of idiopathic autism are

induced by early mercury exposure from thimerosal; (ii) this type of autism

represents an unrecognized mercurial syndrome; and (iii) genetic and

non-genetic factors establish a predisposition whereby thimerosal's adverse

effects occur only in some children

INTRODUCTION

Autistic Spectrum Disorder (ASD) is a neurodevelopmental syndrome with

onset prior to age 36 months. Diagnostic criteria consist of impairments in

sociality and communication plus repetitive and stereotypic behaviors (1).

Traits strongly associated with autism include movement disorders and

sensory dysfunctions (2). Although autism may be apparent soon after birth,

most autistic children experience at least several months, even a year or

more of normal development -- followed by regression, defined as loss of

function or failure to progress (2,3,4)

The neurotoxicity of mercury (Hg) has long been recognized (5).

Primary data derive from victims of contaminated fish (Japan - Minamata

Disease) or grain (Iraq, Guatemala, Russia); from acrodynia (Pink Disease)

induced by Hg in teething powders; and from individual instances of mercury

poisoning (HgP), many occurring in occupational settings (e.g., Mad Hatter's

Disease). Animal and in vitro studies also provide insights into the

mechanisms of Hg toxicity. More recently, the Food and Drug Administration

(FDA) and the American Academy of Pediatrics (AAP) have determined that the

typical amount of Hg injected into infants and toddlers via childhood

immunizations has exceeded government safety guidelines on an individual (6)

and cumulative vaccine basis (7). The mercury in vaccines derives from

thimerosal (TMS), a preservative which is 49.6% ethylmercury (eHg) (7)

Past cases of HgP have presented with much inter-individual variation,

depending on the dose, type of mercury, method of administration, duration

of exposure, and individual sensitivity. Thus, while commonalities exist

across the various instances of HgP, each set of variables has given rise to

a different disease manifestation (8,9,10,11). It is hypothesized that the

regressive form of autism represents another form of mercury poisoning,

based on a thorough correspondence between autistic and HgP traits and

physiological abnormalities, as well as on the known exposure to mercury

through vaccines. Furthermore, other phenomena are consistent with a causal

Hg-ASD relationship. These include (a) symptom onset shortly after

immunization; ( ASD prevalence increases corresponding to vaccination

increases; © similar sex ratios of affected individuals; (d) a high

heritability rate for autism paralleling a genetic predisposition to Hg

sensitivity at low doses; and (e) parental reports of autistic children with

elevated Hg

TRAIT COMPARISON

ASD manifests a constellation of symptoms with much inter-individual

variation (3,4). A comparison of traits defining, nearly universal to, or

commonly found in autism with those known to arise from mercury poisoning is

given in Table I. The characteristics defining or strongly associated with

autism are also more fully described

Autism has been conceived primarily as a psychiatric condition; and

two of its three diagnostic criteria are based upon the observable traits of

(a) impairments in sociality, most commonly social withdrawal or aloofness,

and ( a variety of perseverative or stereotypic behaviors and the need for

sameness, which strongly resemble obsessive-compulsive tendencies.

Differential diagnosis may include childhood schizophrenia, depression,

obsessive-compulsive disorder (OCD), anxiety disorder, and other neuroses.

Related behaviors commonly found in ASD individuals are irrational fears,

poor eye contact, aggressive behaviors, temper tantrums, irritability, and

inexplicable changes in mood (1,2,12-17). Mercury poisoning, when

undetected, is often initially diagnosed as a psychiatric disorder (18).

Commonly occurring symptoms include (a) " extreme shyness, " indifference to

others, active avoidance of others, or " a desire to be alone " ; (

depression, " lack of interest " and " mental confusion; " © irritability,

aggression, and tantrums in children and adults; (d) anxiety and

fearfulness; and (e) emotional lability. Neuroses, including schizoid and

obsessive-compulsive traits, problems in inhibition of perseveration, and

stereotyped behaviors, have been reported in a number of cases; and lack of

eye contact was observed in one 12 year old girl with mercury vapor

poisoning (18-35)

The third diagnostic criterion for ASD is impairment in communication

(1). Historically, about half of those with classic autism failed to develop

meaningful speech (2), and articulation difficulties are common (3). Higher

functioning individuals may have language fluency but still show semantic

and pragmatic errors (3,36). In many cases of ASD, verbal IQ is lower than

performance IQ (3). Similarly, mercury-exposed children and adults show a

marked difficulty with speech (9,19,37). In milder cases scores on language

tests may be lower than those of unexposed controls (31,38). Iraqi children

who were postnatally poisoned developed articulation problems, from slow,

slurred word production to an inability to generate meaningful speech; while

Iraqi babies exposed prenatally either failed to develop language or

presented with severe language deficits in childhood (23,24,39). Workers

with Mad Hatter's disease had word retrieval and articulation difficulties

(21)

Nearly all cases of ASD and HgP involve disorders of physical movement

(2,30,40). Clumsiness or lack of coordination has been described in many

higher functioning ASD individuals (41). Infants and toddlers later

diagnosed with autism may fail to crawl properly or may fall over while

sitting or standing; and the movement disturbances typically occur on the

right side of the body (42). Problems with intentional movement and

imitation are common in ASD, as are a variety of unusual stereotypic

behaviors such as toe walking, rocking, abnormal postures, choreiform

movements, spinning; and hand flapping (2,3,43,44). Noteworthy because of

similarities to autism are reports in Hg literature of (a) children in Iraq

and Japan who were unable to stand, sit, or crawl (34,39); ( Minamata

disease patients whose movement disturbances were localized to one side of

the body, and a girl exposed to Hg vapor who tended to fall to the right

(18,34); © flapping motions in an infant poisoned from contaminated pork

(37) and in a man injected with thimerosal (27); (d) choreiform movements in

mercury vapor intoxication (19); (e) toe walking in a moderately poisoned

Minamata child (34); (f) poor coordination and clumsiness among victims of

acrodynia (45); (g) rocking among infants with acrodynia (11); and (h)

unusual postures observed in both acrodynia and mercury vapor poisoning

(11,31). The presence of flapping motions in both diseases is of interest

because it is such an unusual behavior that it has been recommended as a

diagnostic marker for autism (46)

Virtually all ASD subjects show a variety of sensory abnormalities

(2). Auditory deficits are present in a minority of individuals and can

range from mild to profound hearing loss (2,47). Over- or under-reaction to

sound is nearly universal (2,48), and deficits in language comprehension are

often present (3). Pain sensitivity or insensitivity is common, as is a

general aversion to touch; abnormal sensation in the extremities and mouth

may also be present and has been detected even in toddlers under 12 months

old (2,49). There may be a variety of visual disturbances, including

sensitivity to light (2,50,51,52). As in autism, sensory issues are reported

in virtually all instances of Hg toxicity (40). HgP can lead to mild to

profound hearing loss (40); speech discrimination is especially impaired

(9,34,). Iraqi babies exposed prenatally showed exaggerated reaction to

noise (23), while in acrodynia, patients reported noise sensitivity (45).

Abnormal sensation in the extremities and mouth is the most common sensory

disturbance (25,28). Acrodynia sufferers and prenatally exposed Iraqi babies

exhibited excessive pain when bumping limbs and an aversion to touch

(23,24,45,53). A range of visual problems has been reported, including

photophobia (18,23,34)

COMPARISON OF BIOLOGICAL ABNORMALITIES

The biological abnormalities commonly found in autism are listed in

Table II, along with the corresponding pathologies arising from mercury

exposure. Especially noteworthy similarities are described

Autism is a neurodevelopmental disorder which has been characterized

as " a disorder of neuronal organization, that is, the development of the

dentritic tree, synaptogenesis, and the development of the complex

connectivity within and between brain regions " (54). Depressed expression of

neural cell adhesion molecules (NCAMs), which are critical during brain

development for proper synaptic structuring, has been found in one study of

autism (55). Organic mercury, which readily crosses the blood-brain barrier,

preferentially targets nerve cells and nerve fibers (56); primates

accumulate the highest Hg-levels in the brain relative to other organs (40).

Furthermore, although most cells respond to mercurial injury by modulating

levels of glutathione (GSH), metallothionein, hemoxygenase, and other stress

proteins, neurons tend to be " markedly deficient in these responses " and

thus are less able to remove Hg and more prone to Hg-induced injury (56). In

the developing brain, mercury interferes with neuronal migration, depresses

cell division, disrupts microtubule function, and reduces NCAMs (28, 57-59)

While damage has been observed in a number of brain areas in autism,

many nuclei and functions are spared (36). HgP's damage is similarly

selective (40). Numerous studies link autism with neuronal atypicalities

within the amygdala, hippocampi, basal ganglia, the Purkinje and granule

cells of the cerebellum, brainstem, basal ganglia, and cerebral cortex

(36,60-69). Each of these areas can be affected by HgP (10,34,40,70-73).

Migration of Hg, including eHg, into the amygdala is particularly

noteworthy, because in primates this brain region has neurons specific for

eye contact (74) and it is implicated in autism and in social behaviors

(65,66,75)

Autistic brains show neurotransmitter irregularities which are

virtually identical to those arising from Hg exposure: both high or low

serotonin and dopamine, depending on the subjects studied; elevated

epinephrine and norepinephrine in plasma and brain; elevated glutamate; and

acetylcholine deficiency in hippocampus (2,21,76-83)

Gillberg and (2) estimate that 35-45% of autistics eventually

develop epilepsy. A recent MEG study reported epileptiform activity in 82%

of 50 regressive autistic children; in another study, half the autistic

children expressed abnormal EEG activity during sleep (84). Autistic EEG

abnormalities tend to be non-specific and have a variety of patterns (85).

Unusual epileptiform activity has been found in a number of mercury

poisoning cases (18,27,34,86-88). Early mHg exposure enhances tendencies

toward epileptiform activity with a reduced level of seizure-discharge

amplitude (89), a finding consistent with the subtlety of seizures in many

autism spectrum children (84,85). The fact that Hg increases extracellular

glutamate would also contribute to epileptiform activity (90)

Some autistic children show a low capacity to oxidize sulfur compounds

and low levels of sulfate (91,92). These findings may be linked with HgP

because (a) Hg preferentially binds to sulfhydryl molecules (-SH) such as

cysteine and GSH, thereby impairing various cellular functions (40), and (

mercury can irreversibly block the sulfate transporter NaSi cotransporter

NaSi-1, present in kidneys and intestines, thus reducing sulfate absorption

(93). Besides low sulfate, many autistics have low GSH levels, abnormal

GSH-peroxidase activity within erythrocytes, and decreased hepatic ability

to detoxify xenobiotics (91,94,95). GSH participates in cellular

detoxification of heavy metals (96); hepatic GSH is a primary substrate for

organic-Hg clearance from the human (40); and intraneuronal GSH participates

in various protective responses against Hg in the CNS (56). By

preferentially binding with GSH, preventing absorption of sulfate, or

inhibiting the enzymes of glutathione metabolism (97), Hg might diminish GSH

bioavailability. Low GSH can also derive from chronic infection (98,99),

which would be more likely in the presence of immune impairments arising

from mercury (100). Furthermore, mercury disrupts purine and pyrimidine

metabolism (97,10). Altered purine or pyrimidine metabolism can induce

autistic features and classical autism (2,101,102), suggesting another

mechanism by which Hg can contribute to autistic traits

Autistics are more likely to have allergies, asthma, selective IgA

deficiency (sIgAd), enhanced expression of HLA-DR antigen, and an absence of

interleukin-2 receptors, as well as familial autoimmunity and a variety of

autoimmune phenomena. These include elevated serum IgG and ANA titers, IgM

and IgG brain antibodies, and myelin basic protein (MBP) antibodies

(103-110). Similarly, atypical responses to Hg have been ascribed to

allergic or autoimmune reactions (8), and genetic predisposition to such

reactions may explain why Hg sensitivity varies so widely by individual

(88,111). Children who developed acrodynia were more likely to have asthma

and other allergies (11); IgG brain autoantibodies, MBP, and ANA have been

found in HgP subjects (18,111,112); and mice genetically prone to develop

autoimmune diseases " are highly susceptible to mercury-induced

immunopathological alterations " even at the lowest doses (113).

Additionally, many autistics have reduced natural killer cell (NK) function,

as well as immune-cell subsets shifted in a Th2 direction and increased

urine neopterin levels, indicating immune system activiation (103,114-116).

Depending upon genetic predisposition, Hg can induce immune activation, an

expansion of Th2 subsets, and decreased NK activity (117-120)

POPULATION CHARACTERISTICS

In most affected children, autistic symptoms emerge gradually,

although there are cases of sudden onset (3). The earliest abnormalities

have been detected in 4 month olds and consist of subtle movement

disturbances; subtle motor-sensory disturbances have been observed in 9

month olds (49). More overt speech and hearing difficulties become

noticeable to parents and pediatricians between 12 and 18 months (2). TMS

vaccines have been given in repeated intervals starting from infancy and

continuing until 12 to 18 months. While HgP symptoms, may arise suddenly in

especially sensitive individuals (11), usually there is a preclinical

" silent stage " in which subtle neurological changes are occuring (121) and

then a gradual emergence of symptoms. The first symptoms are typically

sensory- and motor-related, which are followed by speech and hearing

deficits, and finally the full array of HgP characteristics (40). Thus, both

the timing and nature of symptom emergence in ASD are fully consistent with

a vaccinal Hg etiology. This parallel is reinforced by parental reports of

excessive amounts of mercury in urine or hair from younger autistic

children, as well as some improvement in symptoms with standard chelation

therapy (122)

The discovery and rise in prevalence of ASD mirrors the introduction

and spread of TMS in vaccines. Autism was first described in 1943 among

children born in the 1930s (123). Thimerosal was first introduced into

vaccines in the 1930s (7). In studies conducted prior to 1970, autism

prevalence was estimated, at 1 in 2000; in studies from 1970 to 1990 it

averaged 1 in 1000 (124). This was a period of increased vaccination rates

of the TMS-containing DPT vaccines among children in the developed world. In

the early 1990s, the prevalence of autism was found to be 1 in 500 (125),

and in 2000 the CDC found 1 in 150 children affected in one community, which

was consistent with reports from other areas in the country (126). In the

late 1980s and early 1990s, two new TMS vaccines, the HIB and Hepatitis B,

were added to the recommended schedule (7)

Nearly all US children are immunized, yet only a small proportion

develop autism. A pertinent characteristic of mercury is the great

variability in its effects by individual, so that at the same exposure

level, some will be affected severely while others will be asymptomatic

(9,11,28). An example is acrodynia, which arose in the early 20th Century

from mercury in teething powders and afflicted only 1 in 500-1000 children

given the same low dose (28). Studies in mice as well as humans indicate

that susceptibility to Hg effects arises from genetic status, in some cases

including a propensity to autoimmune disorders (113,34,40). ASD exhibits a

strong genetic component, with high concordance in monozygotic twins and a

higher than expected incidence among siblings (4); autism is also more

prevalent in families with autoimmune disorders (106)

Additionally, autism is more prevalent among boys than girls, with the

ratio estimated at 4:1 (2). Mercury studies in mice and humans consistently

report greater effects on males than females, except for kidney damage (57).

At high doses, both sexes are affected equally; at low doses only males are

affected (38,40,127)

DISCUSSION

We have shown that every major characteristic of autism has been

exhibited in at least several cases of documented mercury poisoning.

Recently, the FDA and AAP have revealed that the amount of mercury given to

infants from vaccinations has exceeded safety levels. The timing of mercury

administration via vaccines coincides with the onset of autistic symptoms.

Parental reports of autistic children with measurable mercury levels in hair

and urine indicate a history of mercury exposure. Thus the standard primary

criteria for a diagnosis of mercury poisoning - observable symptoms, known

exposure at the time of symptom onset, and detectable levels in biologic

samples (11,31) - have been met in autism. As such, mercury toxicity may be

a significant etiological factor in at least some cases of regressive

autism. Further, each known form of HgP in the past has resulted in a unique

variation of mercurialism - e.g., Minamata disease, acrodynia, Mad Hatter's

disease - none of which has been autism, suggesting that the Hg source which

may be involved in ASD has not yet been characterized; given that most

infants receive eHg via vaccines, and given that the effect on infants of

eHg in vaccines has never been studied (129), vaccinal thimerosal should be

considered a probable source. It is also possible that vaccinal eHg may be

additive to a prenatal mercury load derived from maternal amalgams, immune

globulin injections, or fish consumption, and environmental sources

CONCLUSION

The history of acrodynia illustrates that a severe disorder,

afflicting a small but significant percentage of children, can arise from a

seemingly benign application of low doses of mercury. This review

establishes the likelihood that Hg may likewise be etiologically significant

in ASD, with the Hg derived from thimerosal in vaccines rather than teething

powders. Due to the extensive parallels between autism and HgP, the

likelihood of a causal relationship is great. Given this possibility, TMS

should be removed from all childhood vaccines, and the mechanisms of Hg

toxicity in autism should be thoroughly investigated. With perhaps 1 in 150

children now diagnosed with ASD, development of HgP-related treatments, such

as chelation, would prove beneficial for this large and seemingly growing

population.

For references, go to http://www.autism.com/ari/mercury.html .

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