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. 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; (c) 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;" (c) 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); (c) 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 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 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 (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 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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