What causes autism? Possible explanations for the sudden rise of autism.

What causes autism?

Currently an increasing amount of parents refuse to have their children vaccinated as an increasing amount of reports come in about how it is said to cause autism. As someone who formerly worked with vaccines, this sounds like an incredibly unlikely link. According to what I've heard one of the reason for the link is research conducted by a scientist who was said to have done fraudulent research. Also it is said autism is generally discovered at around the age a child is being vaccinated so the two things are related by accident and not by causation.

Yet, the rumours are so loud, that we decided to look into the matter and a very lengthy review is shedding light into the darkness, explaining what may cause autism and what not. And lo and behold, there's a link with vaccines after all except things are (as always) more complicated than it seems.
We are making it somewhat easier to read, but it's not possible to truly avoid medical terms.

Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism has increased to is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world.
This review summarizes results that correlate the timing of changes in incidence with environmental changes. Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination.
Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.

Autism is a neuro-developmental disorder characterized by impaired communication and social interaction and repetitive behaviors. Several lines of evidence indicate that genetic, environmental, and immunological factors may play a role in its pathogenesis.
Some investigators expand the nature of autism to that of a multisystem metabolic disease, not just a brain disorder.
The term autistic spectrum disorder (ASD) or pervasive developmental disorders (PDDs) represents a group of disorders which includes five diagnostic subtypes including autism, PDD not otherwise specified (PDD-NOS),  and Asperger’s disorder (currently no longer a subtype but defined as PDD-NOS). It affects abouty 4 times as many boys as girls.

Autism is a lifelong condition for most. Historically, 75% of autistic individuals become either institutionalized as adults or are unable to live independently.
Studies of adults with autism suggest that the cumulative mortality rate is higher among autistic patients than their non-autistic peers.

This complex behavioral disorder encompasses a wide variety of symptoms, defined by deficits in social interaction, communication, and empathy, accompanied by unusual restricted, repetitive behaviors.
Since there are no objective diagnostic tests for autism, a clinical diagnosis is based on behavior, using the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the gold standard.

Using a list of diagnostic criteria, at least six criteria must be exhibited with onset of conditions prior to age three, including at least two relating to social abnormalities and one each regarding impaired communication and range of interests and activities. These criteria are not described in detail, leaving latitude for clinical judgment.
To date, no biological markers have been found to reliably diagnose autism in an individual patient.
However, many biomarkers (hormones, peptides, etc.) have been documented to be significantly different in autistic subjects compared to age- and sex-matched controls.

The onset of autism is usually documented in the first 3 years of life. However, there have been case reports of late-onset autism in individuals who previously had herpes encephalitis. Therefore, autism is not necessarily a developmental disorder.

Incidence and prevalence

It is possible that there are several causes of autism. For decades since first described by Leo Kanner in 1943, autism was believed to occur at a rate of 4–5 per 10,000 children.
Perhaps, the cause of autism at that time might have been primarily genetic.
From surveys done between 1966 and 1998 in 12 countries, the prevalence (number of existing disease cases in a defined group of people during a specific time period) ranged from 0.7–21.1/10,000 (1/14.285 - 1/474)
The most recent official prevalence for the United States is an average of 1/110.

As with prevalence, the incidence (number of new cases of disease in a defined group of people over a specific time) of autism has also increased sharply. The Center for Disease Control and Prevention states that the prevalence of autism is increasing at epidemic rates.   
By comparison, incidence in the United Kingdom is also increasing, with higher rates than in the United States.
Although improved ascertainment accounts for some of the prevalence increases documented, a true increase in the risk for children to develop autism symptoms cannot be ruled out.
It is difficult to compare the figures concerning incidence and prevalence because autism is defined by subjective measures.

Changes in rates of autism incidence

In a study of time trends in prevalence of autism in California between 1995-2007, autism didn't decrease after Thimerosal, a component said to cause autism, was excluded from nearly all childhood vaccines by 2002.
However, Thimerosal is still used in some vaccines, including in those for influenza as is used for all children between 6–23-months old as well as for pregnant moms.

Data from a worldwide composite of studies show that an increase in cumulative incidence began about 1988–1990 about 5 years after the introduction of Thimerosal-containing vaccines for measles, mumps, rubella vaccine (MMR II).
Autism in the United States spiked dramatically between 1983 and 1990 from 4–5/10,000 to 1/500.
Autism spiked in 1988 after a second injection of MMRII was deemed necessary when a first injection wasn't succesful.  The same happened in the UK as well as in Canada, Denmark and Japan.
It is important to note that unlike the former MMR, the rubella component of MMR II was propagated in a human cell line derived from embryonic lung tissue.
The MMR II vaccine is contaminated with human DNA from the cell line. This human DNA could be the cause of the spikes in incidence. An additional increased spike in incidence of autism occurred in 1995 when the chicken pox vaccine was grown in human fetal tissue.

The human DNA from the vaccine can be randomly inserted into the recipient’s genes by homologous recombination, a process that occurs spontaneously only within a species.
Hot spots for DNA insertion are found on the X chromosome in eight autism-associated genes involved in nerve cell synapse formation, central nervous system development, and mitochondrial function. This could provide some explanation of why autism is predominantly a disease of boys. Taken together, these data support the hypothesis that residual human DNA in some vaccines might cause autism.


The incidence and prevalence data indicate the timing of introduction of vaccines and changes in the type and increasing number of vaccines given at one time implicate vaccines as a cause of autism. The current recommended immunization schedule for persons aged 0–6 years in the United States includes six vaccines at 2 months and nine vaccines at 12–15 months.
This is an increase over recommendations 6 years before, with five vaccines at 2 months and 8 at 12–15 months

The immune system is particularly sensitive at 2 months of age. Although specific immune functions are competent in the newborn,  not everything is fully developed yet.
Thus, the immune system of an infant is compromised at 2 months. A challenge by so many vaccines while the immune system is compromised might contribute to an onset of autism.

Vaccine antigens

There are many controversies about vaccines and autism, especially since many parents cite normal development of their children until they receive vaccines at about the age of 18 months.
The vaccine organism itself could be a culprit. For example, one hypothesis of the cause of autism is that the pertussis toxin in the DPT vaccine causes a separation of the G-alpha protein from retinoid receptors in genetically at-risk children.

Another organism of suspect is the live measles virus. When the measles vaccine is given, it depletes the children of their existing supply of Vitamin A, which negatively impacts the retinoid receptors, accounting for the distorted vision in autistic individuals.
This could account for the fact that autistic subjects’ ability to see is not normal, with malfunctioning rods causing distortion of the peripheral vision. When the natural form (cis) of Vitamin A was given to autistic subjects for 2–3 months, followed by urocholine, many autistic children showed immediate improvement in their autistic behaviors, including improved eye contact, ability to socialize, ability to sleep through the night, etcetera.

Vaccine preservative

There is evidence that Thimerosal (which is 49% ethyl mercury) is indeed harmful. Since the 1930s, Thimerosal has been extensively used as an antibacterial agent in vaccines.
Thimerosal has been implicated as a cause of autism. Not only is every major symptom of autism documented in cases of mercury poisoning but also biological abnormalities in autism are very similar to the side effects of mercury poisoning itself: these include psychiatric disturbances (impairments in sociality, stereotypic behaviors, depression, anxiety disorder, and neuroses), increased incidences of allergies and asthma, increases in the presence of IgG auto-antibodies against brain and myelin basic proteins, reductions in natural killer cell function, and increases in immune activation.

Autistic brains show neurotransmitter irregularities that are virtually identical to those arising from mercury exposure like changes in serotonin and dopamine concentrations, elevated epinephrine and norepinephrine levels in the plasma and brain, elevated serum glutamate levels, and an acetylcholine deficiency in the hippocampus.

Due to the extensive parallels between autism and mercury poisoning, the likelihood of a causal relationship is great. More evidence linking autism with mercury poisoning is the timing of inclusion of Thimerosal in vaccines in the 1930s closely preceding the discovery of autism in 1943.

Metal metabolism disorder

Supporting this relationship are reports documenting that heavy metals are increased in the blood and urine of autistic subjects.
Analysis of blood and urine samples of over 500 patients with autism revealed that 85% of them exhibited severely elevated copper:zinc ratios and 99% showed evidence of a metal-metabolism disorder, suggesting defective metallothionein.  

Metallothionein plays an important role in the development and continued function of the immune response, in neuronal development, and in the detoxification of heavy metals.
Many classic symptoms of autism may be explained by a metallothionein defect, including gastrointestinal (GI) tract problems, heightened sensitivity to toxic metals, and abnormal behaviors.

Neurotoxicity of mercury

Mercury is known to be neurotoxic and has effects on the immune system as well. Mast cells are involved in allergic reactions, and also in inflammation, and innate and acquired immunity. Autistic individuals have a 10-fold greater number of hyperactive mast cells in most tissues.
Mercury stimulates vascular endothelial growth factor and interleukin (IL)-6 release from mast cells. These mediators could disrupt the blood–brain barrier and cause brain inflammation.

Sources of mercury in the environment

Cumulative mercury exposure results from mercury as a pollutant in air, soil, dust, water, consumer products, dental amalgam and lighting fixtures, foodstuffs, fish, and seafood.
Concerning air, for every 450kg of mercury (all forms), there was a 61% increase in the rate of autism.
Mercury is found in many foods, including high-fructose corn syrup. The consumption of high-fructose corn syrup could impact the behavior of children with attention deficit hyperactivity disorder (ADHD), which is associated with autism.

Also, the consumption of some artificial food color additives has been shown to lead to zinc deficiency. Dietary zinc is essential for maintaining the metabolic processes required for mercury elimination. Dietary deficiencies of iron, zinc, iodine, selenium, copper, manganese, fluoride, chromium, and molybdenum are associated with mild to significant changes in neuronal function that can lead to poor health and adverse effects on behavior and learning.

Toxicity of Thimerosal

There are dangerous effects of Thimerosal on the immune system, particularly on T-lymphocytes. Mercury induces glutathione depletion, increased oxidative stress, and apoptosis in these cells.
In addition, Thimerosal causes toxic effects on brain cells, inhibits glutamate transport, affects nerve differentiation, induces immunoproliferation and formation of autoantibodies to fibrillin proteins.
Although the timing of the introduction of Thimerosal in vaccines in the 1930s coincides with the discovery and rise in prevalence of autism, a review of 10 epidemiologic studies, concluded that the data do not unequivocally demonstrate a link between Thimerosal-containing vaccines and autism.
This is primarily because the number of diagnosed cases of autism continues to increase despite the fact that most childhood vaccines are free of more than trace levels of Thimerosal since about the year 2000.

In addition, the pharmacokinetics of ethylmercury (the form of mercury in Thimerosal) makes such an association less likely.  With the increasing incidence of autism, the search for a cause of autism continues.

Other reports have also used prevalence data that support an association of the MMR vaccine with an increased prevalence of autism.
Furthermore, an examination of the continuing increase in prevalence in autism in the context of the dates of spikes in increase in prevalence which point to the MMR II vaccine (which did not contain Thimerosal) suggests that something “new” caused the increase in incidence of autism. Changes in vaccine schedule occurred over the years such as changes in the age at which vaccines were given.

These changes could contribute to the increases in incidence of autism. Another change was how some vaccines were propagated. The “new” component could be the human DNA from the preparation of the rubella component of the MMR II vaccine and the chicken pox vaccine.
It is said by experts that autistic conditions can result from encephalopathy following vaccination.


There is indisputable evidence for a genetic component in autism.
With identical twins, if one is autistic, the likelihood that the other twin will have some form of autism is 90%. In great contrast, for fraternal twins, the likelihood that the other twin will have a form of autism is only 2–3%.  
The results fit best with models in which variants of at least 10 genes contribute to the outcome.

The fact that the combination of known genes or genetic diseases associated with autism accounts for only ~1–2% of the cases points to defining autism as a neurodevelopmental syndrome for which there is no single major genetic cause but rather many relatively rare mutations.
Another reason to discount an overall genetic cause is that autism is now considered an epidemic and there is no such thing as a genetic epidemic. To date, there has not been one single gene found to be responsible for autism. Other phenomena may cause mutations in genes or alter gene expression, with the end result being autism.


Clinical features often associated with autism, with 35% displaying co-morbidity with a psychiatric disorder or other medical diagnosis, include depression, bipolar affective disorder, schizophrenia, schizoaffective disorder, Tourette syndrome, Pica, epilepsy, hypothyroidism, Down’s syndrome, and hypertension.
Other disorders associated with autism are several genetic conditions like Fragile X syndrome or tuberous sclerosis, metabolic disorders,  and a variety of other conditions that affect brain development and function.
Autistic patients with a co-existing organic condition or neurological symptoms are not distinct (behaviorally or developmentally) from autistic patients without such features.
Recent data provide the first anatomical evidence of an abnormal amygdala-fusiform system and its behavioral relevance to face-processing deficits in autism.
Some data suggest a link between Type 1 diabetes and autism.
In addition, autoimmunity is very prevalent in autistic subjects and in their parents and close relatives

Age of parents

There are well-documented effects of aging on human genetic traits, especially those that have their effects in early embryonic life.
There are known changes in the rates of chromosome abnormalities at different maternal ages. Rates increase exponentially from about age 30 to 49, with less dramatic change below age of 30.

It appears both parents are 'to blame' for an increased risk for autism when parents are at an advanced age. .
Age-related biological mechanisms through which increasing age of the parents could affect the fetus include, for women, hormonal factors which change the in utero environment, greater risk of infertility and exposure to assisted reproductive technologies, nucleotide repeat instability, and an increase in cumulative toxic exposure. For men, the most likely biologic explanation is increased de novo mutations in sperm occurring more often in older fathers, perhaps affected by cumulative toxic exposure.

Mitochondrial disease and dysfunction

Classical mitochondrial diseases occur in a subset of autism cases and are usually caused by genetic or mitochondrial respiratory pathway abnormalities .
But there is increasing evidence of mitochondrial dysfunction in autistic individuals without the classic features associated with mitochondrial disease. Mitochondrial dysfunction is thought to be caused by environmental toxins and could contribute to the altered energy metabolism in the brains of children with autism.
Some patients with autistic traits clearly have genetic-based primary mitochondrial disease.
The lowered cellular energetics and deficient reserve mitochondrial energy capacity could lead to cognitive impairment and language deficits, both common in autistic individuals. It has been determined that autism can be caused by an underlying predisposition to mitochondrial dysfunction.

These data support theories that autism is a multi-organ metabolic disease caused by the environment or a virus in individuals who are genetically prone to the disorder. Whatever its cause(s), autism affects critical parts of metabolism, with symptoms in the immunological, gastrointestinal, toxicological, and neurological systems. Therefore, other causes of autism must be considered, such as viral, bacterial, and/or environmental.


Immunosuppression induced by pregnancy renders a woman more susceptible to infections
In addition, there are critical windows of time during which the fetus is more vulnerable immunologically
Data reveal that maternal viral infection in the first trimester and bacterial infection in the second trimester are associated with diagnosis of autism in the offspring.

The placenta, the first fetal organ that becomes functional during pregnancy, plays an essential role in fetal development.
Many nutrients such as glucose, amino acids, free fatty acids, cholesterol, and phospholipids are moved from maternal to fetal circulation through the placenta.
The placenta is a major endocrine organ.
The placenta makes progesterone that maintains the pregnancy, relaxing the gravid uterus and inhibiting fetal rejection by suppression of maternal lymphocyte activity.
In addition, placental progestins enter the maternal and fetal circulation, crossing the blood-brain barrier to promote both maternal and fetal neurogenesis. The placenta produces inflammatory and anti-inflammatory cytokines that would influence both the fetus and the mother.
Evidence from animal and human studies suggests transfer of oxytocin from the placenta to the fetus across the immature blood-brain barrier. The oxytocin could shift GABA-signaling from excitatory to inhibitory. Oxytocin concentrations have been linked to social behavior, and oxytocin pathway signaling may be impaired in autism.
It is suggested that autism can be “programmed” by placental signals that fundamentally and permanently change the way the fetus is wired.

Other investigators report that a defective blood-brain barrier is common in autistic patients.
Maternal immune activation due to prenatal viral exposure can lead to an increase in maternal interleukine-6 levels and altered gene expression, which potentially could precipitate autistic behavior and neuropathology in the fetus later in time or after birth.
A dysfunctional chronic pro-inflammatory state has been shown to exist in the brain and cerebral spinal fluid in subsets of autistic patients.

A mother’s immune response to infection includes the formation/release of antibodies and cytokines that could cross the immature blood-brain barrier of the fetus and which, over time, could cause autism.


Infections that appear to be causally related to the development of autistic behavior include encephalitis caused by measles, congenital rubella, herpes simplex virus, mumps, varicella, or cytomegalovirus.
Rubella virus was the first known cause of autism. In addition, measles and mumps viruses can cause encephalitis that can result in autism later in time.  
The viral infections that cause encephalitis that result in autism often occur in utero but is also documented to cause it later in life. Taken together, these data show that some viruses can cause autism.

Intracellular pathogens

The measles virus, cytomegalovirus, human herpesvirus 6, and the bacterium Yersinia enterocolitica have been documented to live inside monocytes in autistic individuals.
Effects of these intracellular pathogens manifest as lowered formation of blood cells, lowered immunity, and altered blood-brain barrier function often accompanied by demyelination.
The viruses may induce an immune response, resulting in neuro-inflammation, auto-immune reactions, and brain injury.
Pathogens are capable of hiding inside cells for long periods and then cause inflammation during replication cycles, resulting in a chronic pattern of inflammatory disease.

Imbalance in neural systems

Based on the fact that seizures are associated with autism and that abnormal evoked potentials have been observed in autistic subjects in response to tasks that require attention, several have proposed that autism might be caused by an imbalance between excitation and inhibition in key neural systems including the cortex.
Three main types of defects have been revealed in autism: the brainstem and cerebellum, the limbic system (amygdala and hippocampus), and the cortex.
Abnormal regulation of brain growth in autism results in early overgrowth followed by abnormally slowed growth .
The strongest evidence implicates the glutamatergic and GABAergic and serotonergic systems, with weaker evidence for catechol-aminergic, peptidergic, and cholinergic systems.
The serotonergic system may be dysregulated in autism; serotonin levels are initially lower than normal but gradually increase to a greater extent than adult levels by 2–15 years of age.


A relatively new theory regarding the etiology of autism suggests it may be a disease of very early fetal development with environmental exposures during pregnancy causing or contributing to autism based on the neurobiology of developmental genes.

Fetal testosterone levels

An extreme-male-brain theory of autism has been proposed, with subsequent evidence presented in various manners,
including psychometric ways, social development and attentional focus, and sexual dimorphism in human behavior.
Autistic traits were documented to be increased following prenatal exposure to abnormally high levels of testosterone caused by congenital adrenal hyperplasia.
Confirming these studies is the work that links autistic traits with fetal testosterone levels measured in amniotic fluid.
Exposure to fetal testosterone was positively correlated with lack of social development and attentional focus.


Medications may also be implicated in autism. One of them is the use of thalidomide by the mother that can cause birth defects, such as malformations. In 1994, it was also discovered to be a contributor to autism causing abnormal ear development and abnormal eye movement or facial expression, but no malformations of the arms or legs.
It is probable that the nerve dysfunctions in people with autism reflect an early brain injury that not only affects the cranial nerves but also has secondary effects on later brain development. Many cases of autism are initiated very early in gestation. Other medications used in early pregnancy are also associated with autism.
Acetaminophen has also been suggested to cause autism.  
Children given acetaminophen after the MMR II vaccine were significantly more likely to become autistic than children given ibuprofen.
During pregnancy, mothers of autistic children commonly suffer more bacterial and viral infections and fevers, which could affect the fetus to predispose the child for autism.
These mothers often take acetaminophen to treat the infections. Acetaminophen overdose depletes the liver’s supplies of sulfate and glutathione, impairing its ability to detoxify and excrete harmful substances.
Therefore, the fetus could be impaired by the mothers consuming acetaminophen. After birth, if acetaminophen were given to the child, and used repeatedly, the drug could cause depletion of sulfate and glutathione, and the child could regress into autism.

Xenobiotic exposure

Porphyrins, derivatives of the heme synthesis pathway and used as measures of xenobiotic exposure, have been documented to be increased in the urine of autistic individuals.
The quantitation of porphyrins allows the identification of environmental exposure that can be correlated with autistic symptoms. Glutathione (GSH) is the most important antioxidant for detoxification and elimination of environmental toxins.
GSH is decreased in the plasma of autistic subjects.
In addition, GSH plays a major role in methylation and is intimately involved in detoxification processes.


Other environmental agents that have been implicated in autism include the phthalates. Phthalates are a class of synthetic chemicals with widespread human exposure because of their use in plastics and other consumer products. Phthalates leach into the environment and expose humans through ingestion, inhalation, and dermal routes. When the concentration of phthalates in the urine of autistic subjects was calculated, there was a significant relationship between the concentration and the degree of autism calculated by teacher-rated ADHD scores.
Polychlorinated biphenyls (PCBs) might also be suspected as causes of autism since prenatal exposures to PCBs have been known to affect cognitive function in infancy through the pre-school years.
In addition, environmental contaminants, including PCBs, herbicides, perchlorates, mercury, and coal derivatives (such as phthalates, ) interfere with thyroid function.

The environmental contaminants alone, or in addition to insufficient dietary iodine intake, can affect maternal thyroid function during pregnancy.
These outcomes can result in low triiodothyronine (T3) levels in the fetal brain during the period of neuronal cell migration (i.e., weeks 8–12 of pregnancy) and may produce morphological brain changes leading to autism.

Organophosphate pesticides

Organophosphate pesticides, at levels common among the United States children, may contribute to ADHD prevalence.
Exposure to the pesticides could be prenatal, direct, or from food, drinking water or residential pesticide use.
Perhaps, additional environmental causes could be responsible for documented unusual brain growth patterns in early life in autism.

There is evidence of a reduced head size at birth and a sudden and excessive increase in head size between 1–2 and 6–14 months, with brain overgrowth in the first year of life in autistic individuals.
Brain volumes in autistic adolescents and adults were normal, perhaps, due to a slight decrease in brain volume for the autistic subjects at the same time that normal individuals are experiencing a slight increase.

There may also be an interaction of genes with the environment. Epidemiology studies have documented the presence of cluster sites of incidence of autism.
Specifically, Brick Township (New Jersey) was documented to have four times more prevalence of autism than that of the entire country. Although no causal agents were known, some suspected agents were three contaminants in the drinking water of Brick Township, e.g., tetrachloroethylene, trichloroethylene, and trihalomethanes.
The trihalomethanes were associated with a two-fold increase in neural tube defects in the same township. This finding supports research suggesting that autism may be caused by a neural tube defect.


Autism has increased to epidemic proportions, affecting four times as many males and females. With a prevalence of 1/110 in the United States, 1/64 in the United Kingdom, and similar ratios in many other countries, a very significant threat to future generations is evident. This review cites documentation of causes of autism, including genetic mutations/deletions, viral infections (i.e., rubella and herpes), and encephalopathy following vaccination.

It is possible that autism results from more than one cause, with different manifestations in different individuals that share common symptoms. Integrating the data presented here, a hypothesis is that autism is the result of genetic defects, with the contributory effect of advancing age of the parents, and/or inflammation of the brain.
The inflammation could be caused by a defective placenta, an immature blood-brain barrier, the immune response of the mother to a viral or bacterial infection, a premature birth, encephalitis in the child after birth, or a toxic environment. Also, intracellular pathogens could induce an immune response, resulting in neuro-inflammation, autoimmune reactions, brain injury, and autism.

Autism has been documented to be caused by genetic defects and/or inflammation of the brain. The inflammation could be caused by a wide variety of environmental toxicants, infections, and co-morbidities in individuals genetically prone to the developmental disorder.

Our Comment

We conclude autism is primarily determined by the genes, but whether or not a child is being affected with autism is a matter of chance, for which the risk has been exponentially increased in the past 50 years due to various factors (older parents and a multitude of toxic substances).
As for vaccines, it is a difficult matter, because the dangers of various diseases is very real and it is only by herd immunity of over 95% of the population being vaccinated that safety can be assured.
Because of the danger of some diseases and the extremely minimal risk of vaccins, we'd want to emphasize how IMPORTANT it is to vaccine your children, if only to protect those that can't be vaccinated due to extreme allergies. If you fear autism, vaccins are among the least dangerous environmental factors.

However, there has also been a virtual explosion in the amount of vaccines as well as the age at which babies are being vaccinated: it should be seriously looked into by the national institutes that compose the vaccinaton programs.

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