Immunologic risk factors, including maternal infection during pregnancy, autoantibodies to fetal brain proteins, and familial autoimmune disease, have consistently been observed across multiple studies, as have immune abnormalities in individuals with ASD.
VaccinePapers acknowledges the role of Immune Activation during pregnancy, and that Autism occurs without vaccines. In addition to pregnancy immune activation VaccinePapers argues that Autism can occur postnatally citing these cases.
Here are 4 such case reports/case series and a review of the subject:
Case Series, DeLong 1981: This report describes 3 previously-normal children, ages 5(F), 7.5(M) and 11(F) that developed autism due to brain inflammation from an infectious illness. The authors state:
“We report three cases in which striking autistic features developed in previously normal children in the course of an acute encephalopathic illness…”
“These three children each demonstrated a full-blown autistic syndrome in the course of an acute encephalopathic illness…The cases are presented as examples of an acquired and reversible autistic syndrome in childhood, affording some insight into the neurologic substrate of that syndrome.”
“…the behavioral syndrome was acquired at a clearly definable time, in the context of an acute encephalopathic illness…”
Full paper: Acquired reversible autistic syndrome in acute encephalopathic illness in children
Case Report, Marques, 2013: This report describes a previously healthy 32-month old girl that suffered a viral infection of the nervous system. The child experienced “marked developmental regression, autistic features, persistent stereotypes and aphasia” (aphasia=loss of speech).
The authors described this case as “…encephalitis leading to developmental regression with autism spectrum disorder and correlating these 2 distinct entities.” (encephalitis = brain inflammation)
The authors rule out inborn metabolic disorders as a cause (this argument also applies to the other case reports):
“Our patient was previously healthy, with adequate psychomotor development until this infectious episode. Additionally, newborn screening and metabolic tests performed on the admission were negative (normal values for ammonia and lactate) and MRI images do not suggest metabolic disorders. Finally and most importantly, she had a favorable outcome with improvement in all skills and development quotient enhancement. These features do not support an inborn error of metabolism, which are characteristically progressive and lead to severe mental retardation.”
Full Paper: Autism Spectrum Disorder Secondary to Enterovirus Encephalitis
Case Report, Ghaziuddin, 2002: This report describes a previously healthy 11 year old boy that developed illness with fever, seizure and brain inflammation. In the following months, the child developed autism, and never fully recovered. The authors state:
“On the DSM-IV symptom checklist for autistic disorder, he met all the criteria for autism except the onset criterion because he did not have a history of any symptoms before three years of age.”
The authors state that this case “… provides further evidence that autistic symptoms can sometimes emerge after the age of three years following an external event such as an infection.”
Full Paper: Autistic Symptoms Following Herpes Encephalitis
Case Report: Gillberg, 1986: This report describes a previously healthy 14 year old girl that developed illness with fever, seizure and brain inflammation. In the following 70 days, she developed all the symptoms of autism, including echolalia, loss of speech, hand-flapping and other self-stimulating behavior. She never recovered. Gillberg states:
“I will describe the case of a 14-year-old-girl who developed all the classical symptoms of autism over a 70-day period after the onset of convulsions in herpes simplex encephalitis (presumptive diagnosis on the basis of clinical, neurochemical, and neurophysiological tests). Only the age criterion is not met, since she was totally psychiatrically healthy up to her 14th year of life.”
“Severe autistic features-including gaze aversion, abnormal reactions to sound, delayed and immediate echolalia after initial muteness, typical hand-flapping stereotypies, and the acquisition of a set of routines and insistence on sameness that make everyday life totally restricted-developed over a 3-month period after the onset of encephalitis and still remain.”
Full Paper: Onset at age 14 of a typical autistic syndrome: A case report
Custodio et al 2017: This study observed long-lasting (into adulthood) behavioral and immune system changes in mice exposed to immune activation 5 to 7 days after birth. This age in mice roughly corresponds to human infants at term (i.e., at 36-40 weeks gestation). This is when the hepatitis B vaccine is recommended. The exposed mice had long term brain inflammation. The behavioral and immune system changes were sex-dependent: “Male mice presented depressive- like, risk-taking, anxiety-like, and repetitive behaviors with working memory deficits at periadolescence; while at adulthood, only depressive- and anxiety-like behaviors were observed. In contrast, females only presented PPI (pre-pulse inhibition) deficits in both ages studied.” Paper: Neonatal Immune Challenge with Lipopolysaccharide Triggers Long-lasting Sex- and Age-related Behavioral and Immune/Neurotrophic Alterations in Mice
The aluminum contained in vaccines is similar to that found in a liter (about 1 quart or 32 fluid ounces) of infant formula. While infants receive about 4.4 milligrams* of aluminum in the first six months of life from vaccines, they receive more than that in their diet. Breast-fed infants ingest about 7 milligrams, formula-fed infants ingest about 38 milligrams, and infants who are fed soy formula ingest almost 117 milligrams of aluminum during the first six months of life.
This is the response to Dr Offit by VaccinePapers.
The 0.3% factor comes from http://vaccinepapers.org/wp-content/uploads/ganrot-aluminum-health-effects1986.pdf
For the vaccines given in the first 6 months of life, this statement is exactly wrong. The truth is the opposite of what Offit says. In infants, vaccines produce far higher exposure to aluminum than food.
Vaccines in the first 6 months of the CDC vaccine schedule contain about 3,675 mcg aluminum:
Birth (Hep B): 74 mcg/kg (250 mcg for 3.4 kg infant)
2 month: 245 mcg/kg (1225 mcg for 5 kg infant)
4 month: 150 mcg/kg (975 mcg for 6.5 kg infant)
6 month: 153 mcg/kg (1225 mcg for 8 kg infant)
Total for 0-6 months: 3675 mcg aluminum
Compare this to aluminum absorption (for infants) over the first 6 months from milk and formula. The total amount ingested must be multiplied by 0.3% to obtain the amount actually absorbed into the body. Aluminum content numbers come from CHOP, and I have confirmed them in the scientific literature:
breastmilk: 7mg x 0.3% = 21 mcg (0.021 mg)
formula: 38mg x 0.3% = 114 mcg (0.114 mg)
soy formula: 117mg x 0.3% = 351 mcg (0.351mg)
The most credible information has been obtained by determining urinary excretion rates and regarding that as a minimal amount of absorption. Available information from the literature concerning normal excretion of A13+ by the urine is summarized in Table 2. Since contamination gives higher values, the lower values shown in the table are probably more correct. Therefore, normal urinary excretion can be assumed to be 20 to 50R,g/day. If this is also accepted as a measure of the intestinal absorption and the daily intake is supposed to be 20mg, then the normal uptake fraction would be about 0.1 to 0.3%.
Using these updated parameters we found that the body burden of aluminum from vaccines and diet throughout an infant's first year of life is significantly less than the corresponding safe body burden of aluminum modeled using the regulatory MRL. We conclude that episodic exposures to vaccines that contain aluminum adjuvant continue to be extremely low risk to infants and that the benefits of using vaccines containing aluminum adjuvant outweigh any theoretical concerns.
This is the response to Mitkus by VaccinePapers.
VaccinePapers criticizes the 26 mg/kg/day NOAEL (safe dosage)The Mitkus analysis is a reasonable way to estimate the toxicity and retention of ingested water-soluble aluminum (Al3+ ions). But it cannot establish safety of low-solubility, persistent aluminum adjuvant particles. More on this below.
Alawdi et al., 2016
Dosage: 3.4 mg/kg/day Al (from 17mg/kg/day AlCl3)
Dosing duration: 6 weeks
Animal: Adult rats
Full paper: Neuroprotective Effect of Nanodiamond in Alzheimer’s Disease Rat Model: a Pivotal Role for Modulating NF-κB and STAT3 Signaling.
The 3.4 mg/Kg/day dosage is far lower than the 26 mg/Kg/day NOAEL that is the foundation for the Mitkus analysis. The NOAEL used by Mitkus is therefore wrong by a factor of at least 26/3.4 = 7.6.
Alawdi et al performed many behavioral tests and measurements of neurodegeneration and brain inflammation. Alawdi also tested the effects of nanodiamond particles (ND) and memantine (MEM, a drug for alzhiemers disease) on aluminum toxicity. The ND and MEM results are not relevant to the present discussion. However, the MEM results are interesting because they show that aluminum likely produces toxicity via an effect on NMDA receptors (since MEM interacts with NMDA receptors), such as excitotoxicity. The effectiveness of MEM indicates that aluminum causes excitotoxicity. Excitotoxicity occurs in autism.
Alawdi also showed that aluminum caused a 4X increase of IL-6 in the brain. This is an important finding because IL-6 causes autism. The 3.4 mg/Kg/day dosage is relevant to vaccines. The CDC vaccine schedule produces aluminum exposure comparable to or higher than the 3.4 mg/Kg/day dosage.
Borai et al., 2017 (NEW!)
Dosage: 3.4 mg/kg/day Al (from 17mg/kg/day AlCl3)
Dosing duration: 4 weeks
Animal: Adult rats (12-15 weeks)
Full paper: Therapeutic impact of grape leaves polyphenols on certain biochemical and neurological markers in AlCl3-induced Alzheimer’s disease
This is a second study showing adverse effects from 3.4 mg/kg/day ingested aluminum. Adverse effects included decrease in acetylcholine, behavioral changes, increases in inflammatory markers, damage to purkinje cells and cerebellum, and increase in oxidative DNA damage. Note that missing purkinje cells and cerebellum damage are a consistent (essentially universal) findings in human autism.