Vaccinazioni per l’infanzia ed
Metalli tossici dei
vaccini = Autismo
vedi: PDF - dott.
raccolta di dati medico-scientifici sui gravi danni dei Vaccini
Vaccini ed Autismo = Bibliografie che comprovano il
Altra Bibliografia,157 studi scientifici, che confermano il
nesso Vaccini= Autismo !
Sentenza 2012 - Trib. Rimini su
Commento NdR: sulla sentenza di Rimini: vaccini =
fatto il Giudice del Tribunale di Rimini (Italia) a
sentenziare in quel modo, perche' egli non si e'
lasciato influenzare dalle FALSITA' del
Ministero della "salute" (che e'
stato da noi
informato sui Danni dei vaccini dal 1996 e
se ne sta zitto.....assieme a
tutti gli altri "enti"....) fino agli ordini
dei medici......tutti al servizio di
Big Pharma !
- vedi lo studio del dott.:
In CINA dopo le campagne vaccinali esplode
l'Autismo ! - Maggio 2016
VERISSIMO, ma non solo l'autismo....ma una
innumerevole sequela di altre
e non solo dai Vaccini:
USA, Giugno 2013 - AUTISMO = 1 bambino
autistico su 26, non come era nel 2010, 1
su 80 ....
molta importanza hanno anche i cibi assunti non
adatti al gruppo sanguigno del soggetto.
I Tribunali anche USA, confermano tranquillamente che il
MMR causa l'autismo. Austin (USA) - 27 Luglio 2013
Dopo decenni di appassionato dibattito, per i genitori che
probabilmente hanno perso i ripetuti ricorsi richiesti dalle
aziende farmaceutiche e governi, che i vaccini infatti causano
Per i genitori interessati alla ricerca della verità, vale la
pena ricordare che le stesse persone che possiedono le aziende
farmaceutiche di tutto il mondo possono anche possedere agenzie
di stampa americane.
La Ricerca di informazioni prive di propaganda è stata fino ad
ora molto difficile.
Ma Whiteout Press non è qui per sostenere o contrastare i
vaccini. Siamo qui per portare i lettori la notizia che è il
tema e’ in black-out, cover-up e censurato dalle autorita’Sanitarie
conferma che i Vaccini possono produrre l'
La prova della FRODE del
per le cause dei
- CONFESSIONE di un alto dirigente
CDC, davanti al Congresso US
Gli esperti di
CDC, hanno spesso
Conflitti di interesse - 1
CDC e Conflitti
di interesse - 2
CDC e Conflitti
di interesse - 3
anche per i vaccini +
anche per la FDA
Davvero inquietante !
Questo medico il Dott.
Andrew Moulden è MORTO (probabilmente
assassinato) in modo inspiegabile nel
novembre 2013 al età di 49, subito dopo
aver pubblicato Le SUE RICERCHE che
DIMOSTRANO il DANNO CAUSATO dai VACCINI,
RICONOSCIBILI SOLO da un SEMPLICE ESAME
Parlamentari pagati dalle Lobbies ? -
Roma Ott. 2013
L'intervista a un assistente di un Senatore
che svelerebbe i traffici illeciti tra
CONFESSA la FRODE e le FALSIFICAZIONI sugli
studi della correlazione VACCINO=AUTISMO
QUI, tutti gli studi, ricerche, interviste, citate nel
documentario sull'autismo dai Vaccini Vaxxed
MECHANISMS, SOURCES & EPIDEMIOLOGY OF EXPOSURE
injections are a known source of mercury (Plotkin and Orenstein, 1999),
and the typical amount of mercury given to infants and toddlers in this
manner exceeds government safety limits, according to Neal Halsey of the
American Academy of Pediatrics (1999) and William Egan of the Biologics
Division of the FDA (1999).
vaccines given to children 2 years and under are stored in a solution
containing thimerosal, which is 49.6% mercury by weight. Once inside
humans, thimerosal (sodium ethylmercurrithio–salicylate) is metabolized
to ethylmercury and thiosalicylate (Gosselin et al, 1984). The vaccines
mixed with this solution are DTaP, HIB, and Hepatitis B (Egan, 1999).
Thimerosal is not an integral component of vaccines, but is a
preservative added to prevent bacterial contamination.
Many vaccine products are available without the thimerosal
preservative; however, these alternatives have not been widely used (Egan,
1999). In addition, thimerosal is used during the manufacturing process
for a number of vaccines, from which trace amounts are still present in
the final injected product (FDA, personal communication; Smith-Kline press
release on Hepatitis B, March 31, 2000).
at least 1977 clinicians have recognized thimerosal as being potentially
dangerous, especially in situations of long term exposure (Haeney et al,
1979; Rohyans et al, 1984; Fagan et al, 1977; Matheson et al, 1980). For nearly twenty years the US government has also singled
out thimerosal as a potential toxin (FDA, 1982).
In response to the Food and Drug Administration (FDA) Modernization
Act of 1997, which called for the FDA to review and assess the risk of all
mercury containing food and drugs (MMWR, 1999, July 9), the FDA
issued a final rule in 1998 stating that over-the-counter drug products
containing thimerosal and other mercury forms “are not generally
recognized as safe and effective” (FDA, 1998).
In December 1998 and April 1999, the FDA requested US vaccine
manufacturers to provide more information about the thimerosal content in
vaccines (MMWR, 1999, July 9); and in July 1999, the CDC asked
manufacturers to start removing thimerosal from vaccines and rescheduled
the Hepatitus B vaccine so it is given at 9 months of age instead of at
birth (CDC, July 1999). In
November 1999, the CDC repeated its recommendation that vaccine
manufacturers move to thimerosal-free products (CDC, November 1999).
based on the CDC’s own recommended childhood immunization schedule (and
excluding any trace amounts), the amount of mercury a typically vaccinated
two year old child born in the 1990s would receive is 237.5 micrograms;
and a typical six month old might receive 187.5 micrograms (Egan, 1999).
These amounts equate to 3.53 x 1017 molecules and
2.79 x 1017 molecules of mercury respectively
(353,000,000,000,000,000 and 279,000,000,000,000,000 molecules). Since
thimerosal is injected during vaccinations, the mercury is given
intermittently in large, or ‘bolus’, doses:
at birth and at 2, 4, 6, and approximately 15 months (Egan, 1999).
The amount of mercury injected at birth is 12.5 micrograms,
followed by 62.5 micrograms at 2 months, 50 micrograms at 4 months,
another 62.5 micrograms during the infant’s 6-month immunizations, and a
final 50 micrograms at about 15 months (Halsey, 1999).
is recognized as a time of rapid neurological development, to the best of
our belief and knowledge, there are no published studies on the effect of
injected ethylmercury in intermittent bolus doses in infants from birth to
six months or to 2 years (Hepatitis Control Report, 1999; Pediatrics,
1999; EPA, 1997, p.6-56). In
contrast, four government agencies have set safety thresholds for daily
mercury exposure based on ingested fish or whale meat containing
methylmercury. Two of these guidelines are based on adult values and two are
for pregnant women/fetuses (Egan, 1999).
Applying these guidelines to a bolus dose scenario (see Halsey,
1999 for bolus vs. daily dose discussion), the sum of Hg-doses given at 6
months of age or younger, correlated to infant weights, exceed all of the
Hg-total guidelines for all infants.
The 2 month dose is especially high relative to the typical infant
body weight. Halsey (1999)
has calculated the 2 month dose to be over 30 times the recommended daily
maximum exposure, with babies of the smallest weight category receiving
almost three months worth of daily exposures on a single day.
observation is all the more important because even at doses which were not
previously thought to be associated with adverse affects, mercury has
resulted in some damage to humans (Grandjean et al, 1998).
Given that ethylmercury is equally neurotoxic as methylmercury
(Magos et al, 1985), and that injected mercury is more harmful than
ingested mercury (EPA, 1997,p.3-55; Diner and Brenner, 1998), the amount
of injected ethylmercury given to young children is cause for concern.
The potential for Hg-induced harm is compounded by the special
vulnerability of infants (Gosselin et al, 1984). Mercury, which primarily affects the central nervous system,
is most toxic to the developing brain (Davis et al, 1994; Grandjean et al,
1999; Yeates and Mortensen, 1994), and neonates exposed to methyl
(organic) mercury have been shown to accumulate significantly more Hg in
the brain relative to other tissues than do adults ( EPA, 1997, p.4-1).
Mercury may also be more likely to enter the infant brain
because the blood-brain barrier has not fully closed (Wild & Benzel,
1994). In addition, infants
under 6 months are unable to excrete mercury, most likely due to their
inability to produce bile, the main excretion route for organic mercury
(Koos and Longo, 1976; Clarkson, 1993).
Bakir et al (1973) have shown that those with the longest half-time
of clearance are most likely to experience adverse sequelae, while Aschner
and Aschner (1990) have demonstrated that the longer that organic mercury
remains in neurons, the more it is converted to its inorganic
irreversibly-bound form, which has greater neurotoxicity.
all children in the United States are immunized, yet only a small
proportion of children develop autism.
The NIH (Bristol et al, 1996) estimates the current prevalence of
autism to be 1 in 500.
pertinent characteristicof mercury is the great variability in its effects
by individual. At the same exposure level of mercury, some will be affected
severely, while others will be asymptomatic or only mildly impaired (Dale,
1972; Warkany and Hubbard, 1953; Clarkson, 1997). Aten-fold difference in sensitivity to the same exposure
level has been reported (Koos and Longo, 1976; Davis et al, 1994; Pierce
et al, 1972; Amin-Zaki, 1979).
example of variability in children is the mercury-induced disease called
acrodynia. In the earlier
half of this century, from one in 500 to one in 1000 children exposed to
the same chronic, low-dose of mercury in teething powders developed this
disorder (Matheson et al, 1980; Clarkson, 1997), and the likelihood of
developing the disease“appears to be dominated more by individual
susceptibility and possibly age rather than the dose of the mercury”
(Clarkson, 1992). Given the
documented inter-individual variability of responses to Hg, and the young
age at which exposure occurs, the doses of mercury given concurrently with
vaccines are such that only a certain percentage of children will develop
overt symptoms, even as other children might have trait irregularities
sufficiently mild as to remain unrecognized as having been induced by
is more prevalent among boys than girls, with the ratio generally
recognized as approximately 4:1 (Gillberg & Coleman, 1992, p.90).
Mercury studies have consistently shown a greater effect on males
than females, except in instances of kidney damage (EPA, 1997).
At the highest doses, both sexes are affected equally, but at lower
doses only males are affected. This
is true of mice as well as humans (Sager et al, 1984; Rossi et al, 1997;
Clarkson, 1992; Grandjean et al, 1998; McKeown-Eyssen et al, 1983; see
also review in EPA, 1997, p.6-50).
Exposure Levels & Autism Prevalence
not coincidentally, autism’s initial description and subsequent
epidemiological increase mirror the introduction and use of thimerosal as
a vaccine preservative. In
the late 1930s, Leo Kanner, an experienced child psychologist and
the“discoverer” of autism, first began to notice the type of child he
would later label “autistic.” In
his initial paper, published in 1943, he remarked that this type of child
had never been described previously:“Since 1938, there have come to our
attention a number of children whose condition differs so markedly and
uniquely from anything reported so far, that each case merits…a detailed
consideration of its fascinating peculiarities.”
All these patients were born in the 1930s.
Thimerosal was introduced as a component of vaccine solutions in
the 1930s (Egan, 1999).
Not only does
the effect of mercury vary by individual, as noted above, it also varies
in a dose-dependent manner, so that the higher the exposure level, the
more individuals that are affected. At
higher dose levels, the most sensitive individuals will be more severely
impaired, and the less sensitive individuals will be only moderately
impaired, and the majority of individuals may still show no overt symptoms
(Nielson and Hultman, 1999).
vaccination rate, and hence the rate of mercury exposure via thimerosal,
has steadily increased since the 1930s.
In 1999 it was the highest ever, at close to 90% or above,
depending on the vaccine (CDC, 1999, press release). The rate of autism
has increased dramatically since its discovery by Kanner:
prior to 1970, studies showed an average prevalence of 1 in 2000;
for studies after 1970, the average rate had doubled to1 in 1000 (Gillberg
and Wing, 1999). In 1996, the NIH estimated occurrence to be 1 in 500
(Bristol et al, 1996).
large increase in prevalence, yet to be confirmed by stricter
epidemiological analysis, appears to be occurring since the mid-1990s, as
evidenced by several state departments of education statistics reflecting
substantial rises in enrolment of ASD children (California, Florida,
Maryland, Illinois, summarized by Yazbak, 1999). These increases have
paralleled the increased mercury intake induced by mandatory
innoculations: in 1991, two
vaccines, HIB and Hepatitis B, both of which generally include thimerosal
as a preservative, were added to the recommended vaccine schedule (Egan,
is one of the most heritable of developmental and psychiatric disorders
(Bailey et al, 1996).
is 90% concordance in monozygotic twins and a 3-5% risk of autism in
siblings of affected probands (Rogers et al, 1999), a rate 50 to 100 times
higher than would be expected in the general population (Smalley &
Collins, 1996; Rutter, 1996). From
2 to 10 genes are believed to be involved (Bailey et al, 1996).
differences in susceptibility to mercury are said to arise from genetic
factors and these too may be multiple in nature (Pierce et al, 1972;
Amin-Zaki, 1979). They
include innate differences in (i) the ability to detoxify heavy metals,
(ii) the ability to maintain balanced gut microflora, which can impair
detoxification processes, and (iii) immune over-reactivity to
mercury(Nielson and Hultman, 1999; Hultman and Nielson, 199; Johansson et
al, 1998; Clarkson, 1992; EPA, review 1997, p.3-26). Many autistic
children are described as having (i) difficulties with detoxification of
heavy metals (Edelson & Cantor, 1998), possiblydue to low glutathione
levels (O’Reilly and Waring, 1993), (ii) intestinal microflora
imbalances that can impede excretion (Shattock, 1997), and (iii)
autoimmune dysfunction (Zimmerman et al, 1993).
These characteristics might be reflective of the underlying
“susceptibility genes” that predispose to mercury-induced sequelae and
hence to autism.
As noted above,
autism family studies show an exceptionally high concordance rate of 90%
for identical twins. Most
environmental factors, such as a postnatal viral infection, tend not to be
present at exactly the same time or at the same level or rate for each
twin. This would cause a
difference in phenotype expression, and thus postnatal environmental
influences in general reduce the concordance rate for identical twins.
However, given the extremely high vaccination rate and the high
likelihood of vaccination of one twin at the same time and with the same
vaccines as the other twin, mercury-induced autism via vaccination
injection, even though it is an environmental factor, would still lead to
the high concordance rate seen in twins.
among identical twin pairs, the 90% concordance rate is for the milder
phenotype: if one twin has
pure classic autism, there is (i) a 60% chance that the other twin will
have pure classic autism; (ii) a 30% chance that the other twin will
exhibit some type of impairment falling on the autism spectrum, but with
less severe symptoms; and (iii) a 10% chance the other twin will be
unimpaired. The difference in symptom severity among the 40% of
monozygotic pairs who do not exhibit classic autism may arise from either
(i) a different vaccination history within pairs, or (ii) the tendency of
thimerosal to “clump” or be unevenly distributed in solution, so that
one twin might receive more or less mercury than the other.
One study found a 62% difference in the mercury concentration of
ampoules drawn from the same container of immunoglabulin batches
containing thimerosal (Roberts and Roberts, 1979).
f. Course of
Autism emerges during the same time period as infant and toddler
thimerosal injections during vaccinations.
As noted above, the recommended childhood vaccination schedule from
1991 to 1999 has called for injections of thimerosal starting at birth and
continuing at 2, 4, 6, and approximately 15 months (Halsey, 1999); a
similar schedule occurred prior to this time but for DTP alone.
In the great majority of cases, the
more noticeable symptoms of autism emerge between 6 and 20 months
old – and mostly between 12 and 18 months (Gillberg & Coleman,
1992). Teitelbaum et al
(1998), who have claimed the ability to detect subtle abnormalities at the
youngest age so far, have observed these abnormalities at 4 months old at
the earliest, the exception being a“Moebius mouth” seen at birth in a
small number of subjects.
mercury poisoning do not usually appear immediately upon exposure,
although in especially sensitive individuals or in cases of excessive
exposure they can (Warkany and Hubbard, 1953; Amin-Zaki, 1978).
Rather, there is generally a preclinical“silent stage,” seen in
both animals and humans, during which subtle neurological changes are
occurring (Mattsson et al, 1981). The
delayed reaction between exposure and overt signs can last from weeks to
months to years (Adams et al, 1983; Clarkson, 1992; Fagala & Wigg,
1992; Davis et al, 1994; Kark et al, 1971).
Consequently, mercury given in vaccines before age 6 months would
not in most individuals lead to an observable or recognizable disorder,
except for subtle signs, prior to age 6-12 months, and for some
individuals, symptoms induced by early vaccinal Hg might not emerge until
the infant had become a toddler (Joselow et al, 1972).
A few autism
researchers have suggested a prenatal onset for autism (Rodier et al,
1997; Bauman & Kemper, 1994), which would preclude a vaccinal-mercury
etiology. Others, however,
have evidence that suggest post-natal timings (Bailey, 1998; Courchesne,
1999; Bristol Power, NICHD, Dateline Interview, 1999).
consensus at this point is that the timing cannot be determined (Bailey et
al, 1996; Bristol et al, 1996); and, further, that there is “little
evidence” that prenatal or perinatal events “predict to later
autism” (Bristol et al, 1996), even though clustering of adverse effects
(suboptimality factors) are associated with autism (Prechtel, 1968; Bryson
et al, 1988; Finegan and Quarrington, 1979). There is also a general agreement that, in the great majority
of cases, autistic signs emerge among infants and toddlers who had looked
“normal”, developed normally, met major milestones, and had
unremarkable pediatric evaluations (Gillberg & Coleman, 1992; Filipek
et al, 1999; Bailey et al, 1996), so that autism presents as an obvious
deterioration or regression, either before age two or before age three
(Baranek, 1999; Bristol Power, NICHD, Dateline Interview, 1999; LeWine,
It is worthwhile
to note that early and intensive educational and behavioral intervention
can produce dramatic gains in function, and the gains made by these
children “may be somewhat unique among the more severe developmental
disabilities” (Rogers, 1996). This
phenomenon further suggests that autism arises from an environmental
overlay rather than being purely an organic disease. Additionally, at
least one study has reported that “re-education and physical
treatment” can improve outcomes in mercurialism (Amin-zaki, 1978).
The manner in which symptoms emerge in many cases of autism is consistent
with a multiple low-dose vaccinal exposure model of mercury poisoning.
From a parent's and pediatrician's perspective, such an individual
is a“normal” looking child who regresses or fails to develop after
thimerosal administration. Clinically relevant symptoms generally emerge gradually over
many months, although there have been scattered parental reports of sudden
onset (Filipek, et al, 1999). The
initial signs, occurring shortly after the first injections, are subtle,
suggesting disease emergence, and consist of abnormalities in motor
behavior and in sensory systems, particularly touch sensitivity, vision,
and numbness in the mouth (excessive mouthing of objects) (Teitelbaum et
al, 1998; Baranek, 1999). These signs persist and are followed by parental
reports of speech and hearing abnormalities appearing before the child’s
second birthday (Prizant, 1996; Gillberg & Coleman, 1992), that is,
within several months of when additional and final injections are given.
Finally, in year two, there is a full blossoming of ASD traits and
a continuing regression or lack of development, so that the most severe
expression of symptoms occurs at approximately 3-5 years of age.
symptoms then begin to ameliorate (Church & Coplan, 1995; Wing &
Attwood, 1987; Paul, 1987).
exceptions are the subset of those with regression during adolescence or
early adulthood, which may involve onset of seizures and associated
neurodegeneration (Howlin, 2000; Paul, 1987; Tuunanen et al, 1996, 1997,
As in autism,
onset of Hg toxicity symptoms is gradual in some cases, sudden in others
(Amin-Zaki et al, 1979 & 1978; Joselow et al, 1972; Warkany and
Hubbard, 1953). In the case
of organic poisoning, the first signs to emerge are abnormal sensation and
motor disturbances; as exposure levels increase, these signs are followed
by speech and articulation problems and then hearing deficits (Clarkson,
1992), just like autism.
the mercury source is removed symptoms tend to ameliorate (though not
necessarily disappear) except in instances of severe poisoning, which may
lead to a progressive course or death (Amin-Zaki et al, 1978).
As in autism, epilepsy in Hg exposure also predicts a poorer
outcome (Brenner & Snyder, 1980).
The long term outcomes of ASD and mercury poisoning show the same wide
variation. Autism is viewed as a lifelong condition for most;
historically, three-fourths of autistic individuals become either
institutionalized as adults or are unable to live independently (Paul,
There are, however, many instances of partial to full
recovery, in which autistic traits persist in a much milder form or, in
some individuals, disappear altogether once adulthood is reached (Rogers,
1996; Church & Coplan, 1994; Szatmari et al, 1989; Rimland 1994; Wing
& Attwood, 1987).
mercury entering the bloodstream tends to accumulate in tissues and
organs, primarily the brain (Koos and Long, 1976; Lorscheider et al,
1995). Once inside tissues, and particularly the brain, mercury will
linger for years, as shown on X rays of a poisoned man 22 years after
exposure (Gosselin et al, 1984), as well as autopsies of humans with known
mercury exposure (Pedersen etal, 1999; Joselow et al, 1972) and primate
studies (Vahter et al, 1994). The
continued presence of mercury in organs and the CNS in particualr would
explain why autistic symptoms might persist, why researchers such as
Zimmerman or Singh would detect an on-going immune reaction, why epilepsy
might not emerge until adolescence, or why sulfate transporters in the
intestine or kidney might continue to be blocked.
despite the continued presence of Hg in tissue, the degree of recovery
from mercurialism varies greatly. Even
in severe cases, there are reports of full or partial recovery (e.g.,
Adams et al, 1983; Vroom & Greer, 1972; Amin-Zaki et al, 1978).
In less severe cases, especially those in which exposure occurs
early in life, the more severe symptoms may ameliorate over time, but
milder impairments remain, especially neurological ones (Feldman, 1982;
Yeates & Mortensen, 1994; Amin-Zaki, 1974 & 1978; Mathiesin et al,
1999; Vroom and Greer, 1972; EPA 1997, pp.3-10, 3-14, and 3-75).
The widevariation in outcome is believed to be due, again, to
individual sensitivity to mercury, in this case, the ability of some
victims to develop “immunity” or a “tolerance” to Hg even when the
metal is still present in tissue (Warkany & Hubbard, 1953).
Autism & Ingested Organic Mercury
Autism Progression & Thimerosal Administration
signs – move-ment
signs - sensory
signs -hearing & speech
array of symptoms
of symptom severity
full or partial recovery
& Dose-Response Relationship for Effects of Ingested Methylmercury
sign – sensory
sign – movement
sign – speech/
sign – hearing
array of symp-toms
ameliora-tion (or death)
Interaction with Vaccines
noted above, for most ASD children symptom onset is gradual, but for a
significant minority it is sudden. Additionally, many parents believe
there is a connection between their child’s autism and his or her
immunizations. The Cure
Autism Now Foundation, for example, reports that half the parents who
call its hotline mention such a connection (Portia Iversen, CAN
president, personal communication).
The association extends not only to the mercury-containing
vaccines – DTP/DTaP, HIB, and Hepatitis B – but also to those
without thimerosal, particularly the MMR (Bernard Rimland, president,
Autism Research Institute, personal communication).
Parents may describe a variety of post-vaccine scenarios:
a fever followed by a short recovery period and then a more
gradual symptom onset; onset of symptoms immediately and suddenly after
inoculation with or without fever; or even a mildly impaired child whose
condition worsened after vaccination (CAN Parent Advisory Board Internet
list; St. John’s Autism Internet list).
While it is
possible that any temporal association between vaccination and emergence
of autism is due to chance, Warkany and Hubbard, who successfully proved
the connection between acrodynia and mercury poisoning to the medical
community 50 years ago,offer alternate explanations.
In their 1953 article in Pediatrics, they made the
They noted that high fever accompanied by a rash after mercury
administration can be signs of a “typical, acute, mercurial
reaction,” and “acrodyniamay follow, immediately or after short
intervals, acute idiosyncratic reactions to mercury.” This reaction
was independent of hypersensitivity to mercury, as detected from skin
tests, as they reported that only 10% of acrodynia victims responded
positively to Hg on patch tests.
Thus in ASD, the
fevers and deteriorations seen by parents immediately after a
thimerosal-containing vaccine injection may be a systemic reaction (and
not a hypersensitivity response) to the mercury content, and this
reaction may subsequently progress to the emergence of autism, just as
topical mercury administration produced fever and then acrodynia over 50
and Hubbard provided some tentative observations that the administration
of a vaccine, irrespective of whether or not it contains thimerosal, can
set off a reaction to any mercuric compound that may also be given to a
child, which in the case of acrodynia, would be topical mercury in
powders or rinses. This
inter-reactivity might explain the pronounced effects from the MMR among
subsequently-diagnosed autistic children:
patient] underwent a fourteen day course of antirabies injections six
weeks before outbreak of acrodynia. Ten days after completion of the
therapy she was treated with ammoniated mercury ointment and
subsequently acrodynia developed...[In another case] antirabies
treatment preceded the disease by three months. In several children
various immunization procedures preceded the onset of acrodynia in
addition to [topical] mercurial exposure. This could be purely
coincidental or the vaccination material may play a role as an accessory
factor. It is noteworthy that many vaccines andsera contain small
amounts of mercury as preservatives which are injected together with the
These small amounts of mercurial compounds could act
as sensitizing substances. In several instances vaccination against
smallpox preceded the development of acrodynic symptoms, and some
patients were exposed to bismuth, arsenic, lead, and antimony in
addition to mercury.
Such observations deserve attention.”
these two researchers observed that some individuals would react to
mercury and then, upon re-exposure, not show any effects, i.e., they had
acquired an unexplained tolerance to it. In other cases, Hg sensitivity
would be maintained. Rarely, though, would reactivity occur with the
first dose: “more often the patient tolerates several” before the
organism can harbor appreciable amounts of mercury while remaining in
perfect health, and then, for unknown reasons, these innocuous stores of
mercury become toxic. It seems in such cases as if the barriers which
held the mercury in check break down without provocation, or as if the
mercury had been converted from a nontoxic to a toxic form...”
ASD, this delayed sensitivity would explain why some might develop
autism later, not after the first few vaccines, andit would also explain
in part why the more vaccines that are given, the more likely it is that
a given individual will develop a reaction since there are more
“sensitizing” opportunities. Importantly, in susceptible individuals, the reactions
described by Warkany and Hubbard are likely to occur if mercury's
presence occurred via injected thimerosal.
Autismo dai VACCINI
Autismo - La prova dei
Danni dei Vaccini
Bibliografia su Autismo dai vaccini +
Danni dei vaccini +
2 + Amish
senza autismo perche' NON vaccinano +
1.000 studi sui Danni dei Vaccini
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