Autism: a Novel Form of Mercury Poisoning

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[sSRI-Research] Autism: a Novel Form of Mercury Poisoning

 

 

Autism: a Novel Form of Mercury Poisoning

 

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

B.A., T. Binstock

 

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

USA, 908.276.6300, fax 908.276.1301

 

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;

 

(b) 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

 

b) 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 " ;(b) 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);

 

(b) 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:

 

a.. both high or low serotonin and dopamine, depending on the subjects

studied;

b.. elevated epinephrine and norepinephrine in plasma and brain;

elevated glutamate; and

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

Gillberg and Coleman (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 Hg 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 (b) 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:

 

a.. allergies

b.. asthma

c.. selective IgA deficiency (sIgAd)

d.. enhanced _expression of HLA-DR antigen

e.. and an absence of interleukin-2 receptors

f.. as well as familial autoimmunity

g.. and a variety of autoimmune phenomena

a.. These include elevated serum IgG

b.. and ANA titers,

c.. IgM and

d.. IgG brain antibodies,

e.. 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 thimerosol 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 Click Here

 

Originally published in the FEAT (http://www.feat.org) online newsletter.

 

-------------------------

 

Dr. Mercola's Comment:

 

This is an excellent review of the mercury-autism link and is well

referenced. It has been increasingly obvious that mercury should be

screened for in autism which is why I have started to aggressively

screen and treat this problem in the autistic children that I care for.

 

This week I post my pediatric mercury detoxification program which is

a modification of the program that I have used for adults for many

years. I will start chelating my first patients in about one month as

many are in the process of preparing for the chelation process with

some homeopathic preparations.

 

Table I:

 

Summary Comparison of Traits of Autism & Mercury Poisoning

 

(ASD references in bold; HgP references in italics)

 

Psychiatric Disturbances

 

Social deficits, shyness, social withdrawal (1,2,130,131; 21,31,45,53,132

Repetitive, perseverative, stereotypic behaviors; obsessive-compulsive

tendencies (1,2,43,48,133; 20,33-35,132)

Depression/depressive traits, mood swings, flat affect; impaired face

recognition (14,15,17,103, 134,135; 19,21,24,26,31)

Anxiety; schizoid tendencies; irrational fears (2,15,16; 21,27,29,31)

Irritability, aggression, temper tantrums (12,13,43; 18,21,22,25)

Lacks eye contact; impaired visual fixation (HgP)/ problems in joint

attention (ASD) (3,36,136,137; 18,19,34)

Speech and Language Deficits

Loss of speech, delayed language, failure to develop speech

(1-3,138,139; 11,23,24,27,30,37)

Dysarthria; articulation problems (3; 21,25,27,39)

Speech comprehension deficits (3,4,140; 9,25,34,38)

Verbalizing and word retrieval problems (HgP); echolalia, word use and

pragmatic errors (ASD) (1,3,36; 21,27,70)

Sensory Abnormalities

Abnormal sensation in mouth and extremities (2,49; 25,28,34,39)

Sound sensitivity; mild to profound hearing loss (2,47,48; 19,23-25,39,40)

Abnormal touch sensations; touch aversion (2,49; 23,24,45,53)

Over-sensitivity to light; blurred vision (2,50,51; 18,23,31,34,45)

Motor Disorders

Flapping, myoclonal jerks, choreiform movements, circling, rocking,

toe walking, unusual postures (2,3,43,44; 11,19,27,30,31,34,39)

Deficits in eye-hand coordination; limb apraxia; intention tremors

(HgP)/problems with intentional movement or imitation (ASD)

(2,3,36,181; 25,29,32,38,70,87)

Abnormal gait and posture, clumsiness and incoordination; difficulties

sitting, lying, crawling, and walking; problem on one side of body

(4,41,42,123; 18,25,31,34,39,45)

Cognitive Impairments

Poor concentration, attention, response inhibition (HgP)/shifting

attention (ASD) (4,36,153; 21,25,31,38,141)

Uneven performance on IQ subtests; verbal IQ higher than performance

IQ (3,4,36; 31,38)

Poor short term, verbal, and auditory memory (36,140;

21,29,31,35,38,87,141)

Borderline intelligence, mental retardation - some cases reversible

(2,3,151,152; 19,25,31,39,70)

Poor visual and perceptual motor skills; impairment in simple reaction

time (HgP)/ lower performance on timed tests (ASD) (4,140,181;

21,29,142) Agitation, unprovoked crying, grimacing, staring spells

3,154; 11,23,37,88) Sleep difficulties (2,156,157; 11,22,31)

Deficits in understanding abstract ideas & symbolism; degeneration of

higher mental powers (HgP)/sequencing, planning & organizing (ASD);

difficulty carrying out complex commands (3,4,36,153; 9,18,37,57,142)

Unusual Behaviors

Self injurious behavior, e.g. head banging (3,154; 11,18,53) ADHD

traits (2,36,155; 35,70)

ADHD traits (2,36,155; 35,70) )

Agitation, unprovoked crying, grimacing, staring spells 3,154; 11,23,37,88

Sleep difficulties (2,156,157; 11,22,31)

Physical Disturbances

Hyper- or hypotonia; abnormal reflexes; decreased muscle strength,

especially upper body; incontinence; problems chewing, swallowing

(3,42,145,181; 19,27,31,32,39)

Rashes, dermatitis, eczema, itching (107,146; 22,26,143)

Diarrhea; abdominal pain/discomfort, constipation, ?colitis?

(107,147-149; 18,23,26,27,31,32)

Anorexia; nausea (HgP)/vomiting (ASD); poor appetite (HgP)/restricted

diet (ASD) (2,123; 18,22)

Lesions of ileum and colon; increased gut permeability (147,150; 57,144)

Table II:

 

Summary Comparison of Biological Abnormalities in Mercury Exposure &

Autism

 

Mercury Exposure Autism

Biochemistry

Binds -SH groups; blocks sulfate transporter in intestines, kidneys

(40,93) ) Low sulfate levels (91,92)

Reduces glutathione availability; inhibits enzymes of glutathione

metabolism; glutathione needed in neurons, cells, and liver to

detoxify heavy metals; reduces glutathione peroxidase and reductase

(97,100,161,162) Low levels of glutathione; decreased ability of liver

to detoxify xenobiotics; abnormal glutathione peroxidase activity in

erythrocytes (91,94,95)

Disrupts purine and pyrimidine metabolism (10,97,158,159) Purine and

pyrimidine metabolism errors lead to autistic features (2,101,102)

Disrupts mitochondrial activities, especially in brain (160,163,164)

Mitochondrial dysfunction, especially in brain (76,172

Immune System

Sensitive individuals more likely to have allergies, asthma,

autoimmune-like symptoms, especially rheumatoid-like ones

(8,11,18,24,28,31,111,113) ) More likely to have allergies and asthma;

familial presence of autoimmune diseases, especially rheumatoid

arthritis; IgA deficiencies (103,106-109,115)

Can produce an immune response in CNS; causes brain/MBP autoantibodies

(18,111,165 On-going immune response in CNS; brain/MBP autoantibodies

present (104,105,109,110)

Causes overproduction of Th2 subset; kills/inhibits lymphocytes,

T-cells, and monocytes; decreases NK T-cell activity; induces or

suppresses IFNg & IL-2 (100,112,117-120,166) Skewed immune-cell subset

in the Th2 direction; decreased responses to T-cell mitogens; reduced

NK T-cell function; increased IFNg & IL-12 (103,108,114-116,173,174)

CNS Structure

Selectively targets brain areas unable to detoxify or reduce

Hg-induced oxidative stress (40,56,161) Specific areas of brain

pathology; many functions spared (36)

Accummulates in amygdala, hippocampus, basal ganglia, cerebral cortex;

damages Purkinje and granule cells in cerebellum; brain stem defects

in some cases (10,34,40,70-73) Pathology in amygdala, hippocampus,

basal ganglia, cerebral cortex; damage to Purkinje and granule cells

in cerebellum; brain stem defects in some cases (36,60-69)

Causes abnormal neuronal cytoarchitecture; disrupts neuronal

migration, microtubules, and cell division; reduces NCAMs

(10,28,57-59,161) Neuronal disorganization; increased neuronal cell

replication, increased glial cells; depressed _expression of NCAMs

(4,54,55)

Progressive microcephaly (24) Progressive microcephaly and

macrocephaly (175)

Prevents presynaptic serotonin release and inhibits serotonin

transport; causes calcium disruptions (78,79,163,167,168) Decreased

serotonin synthesis in children; abnormal calcium metabolism

(76,77,103,179)

Alters dopamine systems; peroxidine deficiency in rats resembles

mercurialism in humans (8,80) Either high or low dopamine levels;

positive response to peroxidine, which lowers dopamine levels (2,177,178)

Elevates epinephrine and norepinephrine levels by blocking enzyme that

degrades epinephrine (81,160) Elevated norepinephrine and epinephrine (2)

Elevates glutamate (21,171) Elevated glutamate and aspartate (82,176)

Leads to cortical acetylcholine deficiency; increases muscarinic

receptor density in hippocampus and cerebellum (57,170) Cortical

acetylcholine deficiency; reduced muscarinic receptor binding in

hippocampus (83)

Causes demyelinating neuropathy (22,169) Demyelination in brain (105)

Neurophysiology

Causes abnormal EEGs, epileptiform activity, variable patterns, e.g.,

subtle, low amplitude seizure activities (27,31,34,86-89) Abnormal

EEGs, epileptiform activity, variable patterns, including subtle, low

amplitude seizure activities (2,4,84,85)

Causes abnormal vestibular nystagmus responses; loss of sense of

position in space (9,19,34,70) Abnormal vestibular nystagmus

responses; loss of sense of position in space (27,180)

Results in autonomic disturbance: excessive sweating, poor

circulation, elevated heart rate (11,18,31,45) Autonomic disturbance:

unusual sweating, poor circulation, elevated heart rate (17,180)

 

 

http://www.mercola.com/2000/oct/1/autism_mercury.htm

 

 

[Guest guest]

After reading this very informative article on ASD, which is also known as

Asperger's syndrome, one wonders just how many souls diagnosed by " The Experts "

as Schizophrenic are in fact high functioning autistic.

 

Ray.

 

 

[Guest guest]

My son, now 23 yrs old, has Asperger's Syndrome but it took me 11 long years

to get him correctly diagnosed! He was initially diagnosed as having ADD

and put on the " appropriate " drugs which of course made him worse because he

did not have ADD. At birth he was a perfectly normal bright eyed baby,

alert and happy. Then the lights went out after receiving his pre-school

vaccinations and immediately the light in his eyes went out and his facial

expressions gone! I knew there was something wrong with him almost

immediately but could not get any Dr to admit that something was " wrong " .

 

huggs

Lyndall

 

-

" vergil " <vergil7

<alternative_Medicine_Forum >

Thursday, July 06, 2006 5:32 AM

Re: Autism: a Novel Form of Mercury

Poisoning

 

 

After reading this very informative article on ASD, which is also known as

Asperger's syndrome, one wonders just how many souls diagnosed by " The

Experts " as Schizophrenic are in fact high functioning autistic.

 

Ray.

 

 

 

 

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[Guest guest]

Sorry to hear about your Son Lyndall, Asperger's are very special people and

correct diet can do wonders !

Caffeine is a no, no and wheat can be a problem but fish oil's are an absolute

must.

Obviously there are different degree's of Asperger's but Isaac Newton and

Einstein were likely candidates as in their attention to detail and methodical

way of working i.e. in a world of their own !

 

Kind regards - Ray.