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Autism & Vaccines: A New Look At An Old Story .2
A Comprehensive Report
This is part 2 of a comprehensive report by the National
Vaccine Information Center on a matter of topical importance to the autism community.
It has been distributed to thousands of health care professionals throughout
the United States, including pediatricians, as well as every member of every
state legislature throughout the country and every member of the US Congress.
Expenses for the production and distribution of the report
has been covered by the NVIC and by the generous contributions from the
attendees of the DAN! conference in San Diego last year.
We are reproducing the report in segments in the FEAT
Daily Newsletter
over the next two weeks.
The document in its entirety can be found at the
NVIC website.
http://www.909shot.com/NVICSpecialReport.htm
Kanner’s young patients came from well-educated middle and
upper class families in Baltimore with mothers and fathers who were doctors,
lawyers and professors. In 1954, Kanner said, “we have not encountered any one
autistic child who came of unintelligent parents.” This concentration of
autistic children in educated and professionally successful families led Kanner
to develop the “refrigerator Mom” theory as the cause of autism, theorizing that
the warm maternal instincts of educated working mothers was absent or diminished.
Embracing the popular psychiatric, Freudian themes echoed by Kanner, for
decades pediatricians were persuaded to blame mothers of autistic children for
being cold and emotionally rejecting, causing the children in turn to coldly
reject contact with other people.
By 1954, Kanner had started to modify his “Blame the
Mother” stance in recognition that the brothers and sisters of autistic
children were often well adjusted, high functioning children and suggested that
the development of autism was also a result of genetic or “constitutional
inadequacies” as well as bad parenting. By 1971, Kanner admitted Mom was not to
blame.
But the damage had already been done. The rejecting parent
theme was taken up by psychoanalyst Bruno Bettleheim in various books and
articles, such as The Empty Fortress (1967). Bettleheim insisted the autistic
child was behaving in abnormal ways in retaliation against a rejecting mother
who had traumatized the child by failing to provide enough love or attention.
But even as Bettleheim’s influence was growing, a
California psychologist and father of an autistic child, Bernard Rimland,
Ph.D., already had taken on the psychiatric establishment which had dominated autism
research and treatment. In his landmark book Infantile Autism: The Syndrome and
Its Implications for a Neural Theory of Behavior published in 1964, Rimland
methodically dismantled the psychoanalytic theory of autism and argued for a
biological, specifically a neurological, basis for autistic behavior. He
documented the similarities between brain injured children and autistic
children, liberating parents from the destructive guilt associated with having
an autistic child and pointing autism research in the direction it should
always have taken: investigation into the biological mechanisms underlying the
brain and immune dysfunction symptoms and their possible causes.
After founding the Autism Society of America (ASA) in 1965
and establishing the Autism Research Institute (ARI) in 1967, Rimland began distributing
a questionnaire to parents of autistic children. Some 33 years later, his
databank includes information on more than 30,000 cases of autism from around
the world. In analyzing the data for age of onset of autism, he discovered that
before the early 1980’s, most of the parents reported their children first
showed signs of abnormal behavior at birth or in the first year of life. But
after the mid-1980’s, there was a reversal of this pattern. The numbers of
parents reporting that their children developed normally in the first year and
a half of life and then, suddenly, became autistic, doubled. Today, said
Rimland, “the onset-at-18 months children outnumber the onset-at-birth children
by 2 to 1.” (http://www.autism.com/ari).
Rimland, like Kanner, noticed early in his research that
autistic children often came from intelligent, well-educated parents who were successful
professionals in their communities. Upper middle class families in America have
always sought out and received quality medical care. Children, whose parents are well educated are the most likely to
take full advantage of the latest developments in medicine. This would have
been especially true in Kanner’s day as two miracle drugs of the 20th
century - antibiotics and new vaccines - elevated trust in and reliance upon pharmaceuticals
to a new plateau.
In the early 1940’s, state-of-the-art pediatric medical
care would have included a smallpox vaccination plus a separate dose of
diphtheria vaccine. In 1944, pertussis vaccine was recommended for all babies.
By 1947, the American Academy of Pediatrics (AAP) recommended routine use of
the new combination DPT vaccine. By 1958, Kanner’s case files contained more
than 100 cases of autism.
In 1969, M.S. and W.C. Goodwin reported a dramatic upsurge
of autism cases in their pediatric psychiatric practice after 1964. By 1964,
the well-cared-for American child was getting simultaneously vaccinated with
DPT as well as polio vaccine at two, four, six and 18 months of age (the inactivated
polio (IPV) was licensed in 1955 and the live virus oral polio (OPV) vaccine
was licensed in 1963). After 1959, more than three million children were
injected with the combination DPT-IPV shot (Quadrigen) before it was pulled off
the market in 1968 for safety and efficacy reasons. By the mid-1960’s, many
state-of-the-art pediatric practices were also giving babies the new live virus
measles vaccine, which had been licensed in 1963 and was routinely used by
1965.
By 1979, a combination live virus measles-mumps-rubella
(MMR) vaccine, which was licensed in 1971, had been added to the routine child
vaccination schedule and given to children at 12 to 15 months of age; federal
grants were being given to states to provide free DPT, polio and MMR vaccines
to children in public health clinics; and the CDC was encouraging states to enforce
mandatory vaccination laws to raise national vaccination rates. By 1979,
rubella vaccine, which had been licensed in 1969 for use in children also began
to be routinely administered to mothers in hospitals after giving birth
(Preblud, 1985; Tingle, 1986).
In 1988, the CDC added haemophilus influenza b (Hib)
vaccine to the child vaccine schedule; in 1991 the CDC recommended the
recombinant hepatitis B vaccine be used by all newborn infants and children; in
1993 the combined DPTH vaccine was licensed; and in 1995, the live varicella
zoster (chicken pox) vaccine was put on the market.
In 1999, the average American child regardless of the
parent’s educational level or ability to pay was being injected with hepatitis
B vaccine at 12 hours of age and 1 month; with DPT or DTaP, Hib, OPV or IPV at two
and four months; with DPT/DTaP, Hib, OPV/IPV and hepatitis B at six months;
with live varicella zoster at 12 to 18 months; with MMR and Hib at 12 to 15
months; with DPT/DTaP, OPV/IPV at 18 months; and with DPT/DTaP, MMR, OPV/IPV
between four and six years for a total of 33 doses of 10 different viral and
bacterial vaccines by the age of five. National vaccination rates for children
under age three have climbed from between 60 to 80 percent in 1967 for DPT,
polio and measles vaccine to 90 percent in 1999 for DPT, polio, MMR, and Hib
vaccines. Vaccine coverage rates with core vaccines for five-year-old children
entering kindergarten have reached 98 percent plus in many states.
Vaccination today is not just a medical intervention
afforded by the rich and taken advantage of by the well educated but an equal
opportunity extended to the rich and poor, the educated and uneducated alike,
and enforced in the U.S. by state mandates. Although cases of autism in the
1940 ‘s and 1950’s were concentrated in the upper and upper middle classes,
today the growing numbers of children affected with autism come from all social
classes.
Inflammation of the brain (encephalitis,
encephalomyelitis, encephalopathy) has been documented for more than 200 years
in the medical literature to be caused by viral and bacterial infections as
well as the vaccines containing altered viruses and bacteria. Smallpox
infection can involve brain inflammation with symptoms ranging from fever,
vomiting, drowsiness, and convulsions which progress over a period of one to
four weeks, sometimes ending in coma and death.
The vaccinia virus used by Edward Jenner in 1796 to
prevent smallpox was found to cause acute disseminated encephalomyelitis (ADEM)
within one to six weeks of smallpox vaccination estimated to occur in 1 in
5,000 persons. Smallpox vaccination has
also been reported to cause a slow, subacute persistent viral infection that
can emerge years after vaccination (Adams et al, 1972) and end in death. (The
myelin sheath that encloses many nerve fibers helps the transmission of neural
impulses and if the myelin sheath is damaged through traumatic injury,
metabolic disorders, toxic insult, viral or bacterial infection or vaccination,
it can cause degeneration or demyelination).
Rabies, a viral disease of the central nervous system
(CNS), can take 10 days to a year for the virus to reach the brain but, once it
does, encephalomyelitis symptoms include excessive motor activity, excitation, agitation,
confusion, combativeness, bizarre aberrations of thought, seizures and other
CNS dysfunction. After Pasteur began to inject patients with rabies vaccine in
the 1880’s, it became obvious that brain inflammation was a side effect.
Encephalitis and polyneuritis has been estimated to occur in as many as 1 in
400 vaccinated individuals, with Hemachudha, Griffin, et al in 1987 presenting
evidence for an immune-mediated mechanism involving antibodies to myelin basic
protein.
Within three weeks of even a mild measles infection, one
in 1,000 cases can develop encephalomyelitis with signs including fever,
headache and drowsiness. Residual brain damage from measles encephalitis ranges
from mental and behavior changes, including subtle changes in performance, to seizure
disorders and mental retardation. Changes in the electroencephalogram (EEG)
have been demonstrated in half of those who have had measles but do not show
other signs of CNS dysfunction.
Measles virus infection has long been known to be
associated with demyelinating disorders. Guillain-Barre syndrome (GBS) has been
reported following measles disease (Lidin-Janson, 1972) and after measles
vaccination (Grose and Spigland, 1976). Optic neuritis and multiple sclerosis
in children has also been reported after measles disease and measles vaccination
(Riikonen, 1989). In 1973, Landrigan and Witte described 45 cases of
encephalitis occurring between 6 and 15 days following measles vaccination.
Subacute sclerosing panencephalitis (SSPE) is a rare
subacute encephalitis complication of measles infection which causes slow demyelination
of the brain over a one to two year period and ends in death. It has also been reported after measles
vaccination (Schneck, 1968). In 1994, the Institute of Medicine concluded that
the live measles virus vaccine can cause death from measles vaccine strain
viral infection.
In 1998, officials of the National Vaccine Injury
Compensation Program, Public Health Service (Pediatrics; March 1998) found that
a causal relationship exists between live measles vaccine and encephalopathy
after analyzing cases of children who received measles vaccine alone or in the combination
MMR shot and, within 15 days of vaccination, suffered neurologic signs that
progressed to death or mental regression, retardation, chronic seizures, motor
and sensory deficits and movement disorders.
An outbreak of aseptic meningitis in Brazil has been
linked to the MMR vaccine (Am J Epidmiol, 2000). A research team found there
was a sharp increase in the number of cases of aseptic meningitis three weeks
after a 1997 mass MMR vaccination campaign in northeastern Brazil. The
researchers “conservatively estimated” that the risk of aseptic meningitis is 1
in about 14,000 MMR vaccine doses. (A type of brain inflammation involving the meninges,
aseptic meningitis can be caused by viruses and bacteria as well as stroke,
lead poisoning, and vaccine reactions (Berkow, 1987). Most people recover from
aseptic meningitis without damage but some are left with muscle weakness or
other motor dysfunction).
Mumps, Rubella and Brain Inflammation
Mumps has been known to cause meningitis and
encephalitis since the
eighteenth century. Russell and Donald, observed in 1958 that
“the clinical resemblance between mumps encephalitis and the encephalitis which
may follow measles, varicella and rubella, and the fact that the histological
appearance of perivascular demyelination are common to them all, suggest that
they arise from the same pathological process. The nature of this process is
unknown, but it may be a non-specific allergic reaction to virus protein
(Miller and Evans, 1953) and similar lesions have been produced experimentally
by the injection of brain material with adjuvants (Lumsden, 1949).”.
There have been many case reports and studies documenting
meningitis within three weeks of mumps vaccination (Brown, 1991), and after MMR
vaccination (Sugiura and Yamada, 1991), primarily with the Urabe vaccine strain
virus. There have also been reports of meningitis after vaccination with the
Jeryl Lynn mumps vaccine strain (Ehrengut and Zastrow, 1989) now used in MMR
vaccine.
Rubella disease is caused by an RNA virus and, although
mild in children, it can be transmitted from mother to fetus in utero and cause
enchephalitis and devastating harm to the unborn child, including mental retardation,
hearing and vision loss, heart and neuromuscular deformity. In the rubella
epidemic that swept the U.S. in 1964, an estimated 20,000 to 30,000 children
whose pregnant mothers were infected with rubella were born severely damaged
and a high rate of classic and “partial” autism was observed in those children
by Chess in 1971. In 1977, Chess reported that the rate of autism in children
born with congenital rubella from the 1964 epidemic was equivalent to a rate of
“412 per 10,000 for the complete syndrome of autism and 329 for the partial
syndrome, giving a combined rate of 741 per 10,000” compared to the rate of
autism in children without congenital rubella syndrome (estimated in 1966 to be
2.1 cases of autism per 10,000 children (Lotter, 1966).
In the 1920’s, when a mini-epidemic of “von Economo’s
encephalitis” swept through Europe and America, doctors found that some of
those who recovered were left with minimal brain damage including changes in
behavior, restlessness, insomnia or disturbed sleep patterns, irritability,
short attention span, emotional disorders and seizures. In 1934, Kahn and Cohen
described a group of children with the inability to sit still or concentrate,
which they attributed to exposure to von Economo’s encephalitis.
Japanese encephalitis can cause permanent CNS changes
including personality and behavior problems featuring emotional lability and irritability,
speech disorders, hemiplegia, mental retardation and seizures. Chicken pox and mumps infections can, in
rare cases, progress to encephalitis and brain inflammation has also been
reported to follow chicken pox and mumps vaccines.
Poliomyelitis is caused by an enterovirus in which one to
two percent of infected individuals develop disease in the central nervous
system, and fewer go on to have residual paralysis or die. Likewise, within one
to six months of receiving the live attenuated polio vaccine, complications can
occur which, according to the Institute of Medicine (IOM) in 1994, can cause Guillain-Barre
syndrome as well as vaccine strain viral infection ending in paralysis and
death. In both cases, the polio virus invades the CNS and destroys neurons.
(Since 1979, the only cases of paralytic polio which have occurred in the US
have been caused by the live oral polio vaccine (OPV) and it is no longer
recommended by the CDC or AAP, having been replaced by the inactivated polio
vaccine (IPV) which cannot cause polio in the person vaccinated or a person who
comes into contact with that person’s body fluids).
But brain inflammation is not only caused by viruses and
viral vaccines. Bacterial infections and bacterial vaccines also can cause
brain inflammation ending in permanent CNS damage.
Encephalitis has always been the most dreaded complication
of pertussis or whooping cough, with endotoxin and pertussis toxin in the B. pertussis bacteria responsible for most of
it. Pertussis toxin is one of the most lethal toxins in nature and can cross
the blood brain barrier when conditions are right. It has long been known that
a severe case of whooping cough accompanied by brain inflammation symptoms such
as fever, lethargy, vomiting and seizures can be fatal or cause permanent brain
damage ranging from seizure disorders and mental retardation to learning,
personality and behavioral disorders (Lurie & Levy, 1942).
Since the 1950’s, scientists conducting experiments have
added pertussis toxin to a solution of nerve tissue and injected it into sensitized
mice to deliberately induce brain inflammation. However pertussis toxin is also
thought to be involved in acquiring immunity to the disease, both after natural
infection and after vaccination (Pittman, 1979).
Vaccine developers continue to have a problem making a
pertussis vaccine that contains pertussis toxin inactivated enough to be safe
but active enough to be immunogenic, which is why the purified DTaP vaccine is associated
with the same CNS complications as the whole cell DPT vaccine, although they
are reported to occur at a much lower rate with DTaP. (The more reactive whole
cell DPT vaccine has not been taken off the market and it is still being used
by some pediatricians, especially in the combination DPTH (DPT plus Hib).
Parents who want the purified DTaP for their children must ask for it by name.)
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