Vaxxed: From Cover-Up to Catastrophe

Doctor behind film that links autism to vaccines speaks out featuring Dr. Andrew Wakefield & Polly Tommey

A 2016 American film alleging a cover-up by the Centers for Disease Control and Prevention (CDC) of a purported link between the MMR vaccine and autism.

Official site.

EU should ban brain-harming chlorpyrifos to protect health

Exposure to chlorpyrifos is linked to ADHD and autism. It should not be allowed on the European market

Today, the Health and Environment Alliance (HEAL) together with Générations Futures, Pesticide Action Network Europe and Pesticide Action Network Germany released a factsheet on the health effects of chlorpyrifos.

Chlorpyrifos is one of the most widely used pesticides in Europe and its residues are also commonly found in our food. The current authorisation for chlorpyrifos on the European market will expire on 31 January 2019. We are very concerned about the possibility of an extended authorisation due to its health harming properties. Chlorpyrifos is linked to the disruption of the hormonal system and effects on the developing human brain. Children exposed to chlorpyrifos in the womb or in early life can suffer neurodevelopmental effects later in life, like attention deficit disorders (ADHD) and autism.

This factsheet sets out the case and evidence against the use of chlorpyrifos and explains the health impacts which justify its ban.


Can exposure to insecticide during pregnancy link to autism in children ?

Association of Maternal Insecticide Levels With Autism in Offspring From a National Birth Cohort

New research published in the American Journal of Psychiatry says that exposure to the notorious pesticide dichlorodiphenyltrichloroethane (DDT) during pregnancy could raise the risk of a child developing autism, ScienceAlert reports.

2018 Abstract

Autism is a complex neurodevelopmental disorder with a largely unknown etiology. To date, few studies have investigated prenatal exposure to toxins and risk of autism by using maternal biomarkers of exposure. Persistent organic pollutants are lipophilic halogenated organic compounds and include the insecticide dichlorodiphenyltrichloroethane (DDT), as well as its metabolite p,p′-dichlorodiphenyl dichloroethylene (p,p′-DDE), and polychlorinated biphenyls (PCBs). The objective of this study was to test whether elevated maternal levels of persistent organic pollutants are associated with autism among offspring.

The investigation was derived from the Finnish Prenatal Study of Autism, a national birth cohort study based on a nested case-control design. Cases of autism among children born between 1987 and 2005 were ascertained by national registry linkages. In cases of childhood autism and matched control subjects (778 matched case-control pairs), maternal serum specimens from early pregnancy were assayed for levels of p,p′-DDE and total levels of PCBs.

The odds of autism among offspring were significantly increased with maternal p,p′-DDE levels that were in the highest 75th percentile, with adjustment for maternal age, parity, and history of psychiatric disorders (odds ratio=1.32, 95% CI=1.02, 1.71). The odds of autism with intellectual disability were increased by greater than twofold with maternal p,p′-DDE levels above this threshold (odds ratio=2.21, 95% CI=1.32, 3.69). There was no association between total levels of maternal PCBs and autism.

These findings provide the first biomarker-based evidence that maternal exposure to insecticides is associated with autism among offspring. Although further research is necessary to replicate this finding, this study has implications for the prevention of autism and may provide a better understanding of its pathogenesis.

Widespread risk from brain-harming chlorpyrifos, state scientists find

Current uses of chlorpyrifos put children at risk from unsafe levels of exposure from residues on food, contaminated water, and pesticide drift

Nerve agent chlorpyrifos is a toxic air contaminant that threatens agricultural communities and harms children’s developing brains, PAN North America reports, July 30, 2018.

Sacramento, CA – California took a step closer Monday to curbing the use of a pesticide linked to permanent brain harm, including ADHD, autism and IQ loss. Sixteen months after disgraced former EPA Administrator Scott Pruitt defied his own scientists and refused to ban the neurotoxic organophosphate chlorpyrifos, the California Department of Pesticide Regulation (DPR) has concluded their own study by largely agreeing with the EPA scientists: current uses of chlorpyrifos put children at risk from unsafe levels of exposure from residues on food, contaminated water, and pesticide drift up to half a mile. Now, children’s health advocates are pushing the department to follow the science with sound policy, and become the second state in the nation to ban it. Hawaii’s state legislature passed a statewide ban in May.

DPR’s scientific conclusions were announced at a hearing convened Monday by the state’s Scientific Review Panel (SRP), a body of independent scientists overseeing DPR’s risk assessment of chlorpyrifos. Review of the chemical had been on hold for many years pending the proposed federal ban. The SRP formally accepted the risk assessment Monday, and unanimously agreed to designate chlorpyrifos a Toxic Air Contaminant, joining a list of 46 other chemicals including a number of fumigant pesticides. DPR now has ten working days to initiate the regulatory process formalizing the Toxic Air Contaminant designation.

“We’re glad that the state has finally accepted the overwhelming consensus of federal and independent scientists who’ve studied chlorpyrifos for years and determined that it harms kids’ brains severely and irreversibly,”

said Mark Weller, co-director of the statewide coalition Californians for Pesticide Reform.

It’s what comes next that will determine for how long California’s communities will continue to be put at risk. DPR has the authority to halt exposures immediately by suspending use in California while formal assessment of control options are considered. However, DPR may also follow the timeline under the Toxic Air Contaminant regulations that allow for two years to decide how to mitigate the risk to children’s brain health. And meanwhile, almost a million pounds continues to be used on California’s food crops each year, exposing thousands of children and pregnant women to a chemical that permanently damages the developing brain.

“With everything we now know, it’s unconscionable that this toxic chemical is still being used on food crops in California,”

“The state must immediately suspend all use of chlorpyrifos to protect kids, farmworkers and agricultural communities.”

said Miriam Rotkin-Ellman, senior scientist at the Natural Resources Defense Council (NRDC).

Behavioral effects of prenatal and postnatal PBDE exposures

Exposure to polybrominated diphenyl ethers (PBDEs) and child behavior: Current findings and future directions

2018 Study Highlights

  • Prenatal PBDEs are associated with executive function impairments and inattention.
  • Prenatal and postnatal PBDE exposures increase externalizing problems in children.
  • PBDEs’ association with internalizing, adaptive, and social behaviors is not clear.
  • PBDE exposure adversely affects behavioral development in children.


Polybrominated diphenyl ethers (PBDEs) are recognized neurotoxicants, but the extent to which PBDEs influence various domains of behavior in children is not fully understood.

As such, we reviewed epidemiologic studies published to date to provide an overview of the current state of knowledge on PBDEs’ potential role in behavioral development.

We identified 19 epidemiologic studies reporting on associations of prenatal and childhood concentrations of PBDEs with behaviors assessed in children from 1 to 12 years, including executive function, attention, externalizing and internalizing behaviors, adaptive skills, and social behaviors/Autism Spectrum Disorder (ASD).

While the mechanisms of PBDE neurotoxicity in humans are still not clearly elucidated, findings from this review indicate that PBDE exposure during fetal development is associated with impairments in executive function and poorer attentional control in children. Results from large prospective cohorts demonstrate that prenatal and postnatal PBDE exposure adversely impacts externalizing behavior (e.g., hyperactivity and conduct problems). Additional studies are needed to determine whether PBDEs are associated with internalizing problems, adaptive skills, and social behaviors/ASD in children.

Future studies will help better understand the potential neurotoxic effects of PBDE exposures during adolescence, possible sex-dependent effects, and the impact of exposure to BDE-209 and alternative flame retardants. Future studies should also examine chemical mixtures to capture real-world exposures when examining PBDEs and their impact on various behavioral domains in the context of multiple chemical exposures.

Do EDCs contribute to the rise in ASD ?

Are endocrine disrupting compounds environmental risk factors for autism spectrum disorder?

2018 Study Highlights

  • The increasing prevalence of autism spectrum disorder (ASD) has stimulated research on contributory environmental factors.
  • Human exposures to a broad group of ubiquitously dispersed endocrine disrupting compounds (EDCs) are steadily increasing.
  • Prenatal EDC exposures have been shown to associate with ASD-traits as well as neurobehaviors in both humans and animals.
  • Gene expression profiling of EDC-exposed animals and cultured human cells reveals transcriptomic changes associated with ASD.
  • Transgenerational effects of EDCs on neurobehaviors suggest potential epigenetic contributions to the heritability of ASD.


Recent research on the etiology of autism spectrum disorder (ASD) has shifted in part from a singular focus on genetic causes to the involvement of environmental factors and their gene interactions. This shift in focus is a result of the rapidly increasing prevalence of ASD coupled with the incomplete penetrance of this disorder in monozygotic twins. One such area of environmentally focused research is the association of exposures to endocrine disrupting compounds (EDCs) with elevated risk for ASD. EDCs are exogenous chemicals that can alter endogenous hormone activity and homeostasis, thus potentially disrupting the action of sex and other natural hormones at all stages of human development. Inasmuch as sex hormones play a fundamental role in brain development and sexual differentiation, exposure to EDCs in utero during critical stages of development can have lasting neurological and other physiological influences on the developing fetus and, ultimately, the child as well as adult.

This review will focus on the possible contributions of EDCs to autism risk and pathogenesis by first discussing the influence of endogenous sex hormones on the autistic phenotype, followed by a review of documented human exposures to EDCs and associations with behaviors relevant to ASD. Mechanistic links between EDC exposures and aberrant neurodevelopment and behaviors are then considered, with emphasis on EDC-induced transcriptional profiles derived from animal and cellular studies. Finally, this review will discuss possible mechanisms through which EDC exposure can lead to persistent changes in gene expression and phenotype, which may in turn contribute to transgenerational inheritance of ASD.

Reported rates of autism – across the U.S. – are still increasing

About 1 in 59 children has been identified with autism spectrum disorder (ASD) according to estimates from CDC’s Autism and Developmental Disabilities Monitoring (ADDM) Network

Approximately 1.7% — or 1 in 59 — of 8-year-old kids in 11 diverse communities across the U.S. could be identified as having autism in 2014, according to the CDC report, April 27, 2018. That’s a small but measurable increase over the 2012 estimate of 1.5% — or 1 in 68 kids — and the highest rate ever recorded by the agency’s Autism and Developmental Disabilities Monitoring (ADDM) Network, an extensive tracking system that monitors the prevalence and characteristics of autism spectrum disorder (ASD) among more than 300,000 8-year-old children.


Autism spectrum disorder (ASD).

Period Covered

Description of System
The Autism and Developmental Disabilities Monitoring (ADDM) Network is an active surveillance system that provides estimates of the prevalence of autism spectrum disorder (ASD) among children aged 8 years whose parents or guardians reside within 11 ADDM sites in the United States (Arizona, Arkansas, Colorado, Georgia, Maryland, Minnesota, Missouri, New Jersey, North Carolina, Tennessee, and Wisconsin). ADDM surveillance is conducted in two phases. The first phase involves review and abstraction of comprehensive evaluations that were completed by professional service providers in the community. Staff completing record review and abstraction receive extensive training and supervision and are evaluated according to strict reliability standards to certify effective initial training, identify ongoing training needs, and ensure adherence to the prescribed methodology. Record review and abstraction occurs in a variety of data sources ranging from general pediatric health clinics to specialized programs serving children with developmental disabilities. In addition, most of the ADDM sites also review records for children who have received special education services in public schools. In the second phase of the study, all abstracted information is reviewed systematically by experienced clinicians to determine ASD case status. A child is considered to meet the surveillance case definition for ASD if he or she displays behaviors, as described on one or more comprehensive evaluations completed by community-based professional providers, consistent with the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) diagnostic criteria for autistic disorder; pervasive developmental disorder–not otherwise specified (PDD-NOS, including atypical autism); or Asperger disorder. This report provides updated ASD prevalence estimates for children aged 8 years during the 2014 surveillance year, on the basis of DSM-IV-TR criteria, and describes characteristics of the population of children with ASD. In 2013, the American Psychiatric Association published the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), which made considerable changes to ASD diagnostic criteria. The change in ASD diagnostic criteria might influence ADDM ASD prevalence estimates; therefore, most (85%) of the records used to determine prevalence estimates based on DSM-IV-TR criteria underwent additional review under a newly operationalized surveillance case definition for ASD consistent with the DSM-5 diagnostic criteria. Children meeting this new surveillance case definition could qualify on the basis of one or both of the following criteria, as documented in abstracted comprehensive evaluations: 1) behaviors consistent with the DSM-5 diagnostic features; and/or 2) an ASD diagnosis, whether based on DSM-IV-TR or DSM-5 diagnostic criteria. Stratified comparisons of the number of children meeting either of these two case definitions also are reported.

For 2014, the overall prevalence of ASD among the 11 ADDM sites was 16.8 per 1,000 (one in 59) children aged 8 years. Overall ASD prevalence estimates varied among sites, from 13.1–29.3 per 1,000 children aged 8 years. ASD prevalence estimates also varied by sex and race/ethnicity. Males were four times more likely than females to be identified with ASD. Prevalence estimates were higher for non-Hispanic white (henceforth, white) children compared with non-Hispanic black (henceforth, black) children, and both groups were more likely to be identified with ASD compared with Hispanic children. Among the nine sites with sufficient data on intellectual ability, 31% of children with ASD were classified in the range of intellectual disability (intelligence quotient [IQ] <70), 25% were in the borderline range (IQ 71–85), and 44% had IQ scores in the average to above average range (i.e., IQ >85). The distribution of intellectual ability varied by sex and race/ethnicity. Although mention of developmental concerns by age 36 months was documented for 85% of children with ASD, only 42% had a comprehensive evaluation on record by age 36 months. The median age of earliest known ASD diagnosis was 52 months and did not differ significantly by sex or race/ethnicity. For the targeted comparison of DSM-IV-TR and DSM-5 results, the number and characteristics of children meeting the newly operationalized DSM-5 case definition for ASD were similar to those meeting the DSM-IV-TR case definition, with DSM-IV-TR case counts exceeding DSM-5 counts by less than 5% and approximately 86% overlap between the two case definitions (kappa = 0.85).

Findings from the ADDM Network, on the basis of 2014 data reported from 11 sites, provide updated population-based estimates of the prevalence of ASD among children aged 8 years in multiple communities in the United States. The overall ASD prevalence estimate of 16.8 per 1,000 children aged 8 years in 2014 is higher than previously reported estimates from the ADDM Network. Because the ADDM sites do not provide a representative sample of the entire United States, the combined prevalence estimates presented in this report cannot be generalized to all children aged 8 years in the United States. Consistent with reports from previous ADDM surveillance years, findings from 2014 were marked by variation in ASD prevalence when stratified by geographic area, sex, and level of intellectual ability. Differences in prevalence estimates between black and white children have diminished in most sites, but remained notable for Hispanic children. For 2014, results from application of the DSM-IV-TR and DSM-5 case definitions were similar, overall and when stratified by sex, race/ethnicity, DSM-IV-TR diagnostic subtype, or level of intellectual ability.

Public Health Action
Beginning with surveillance year 2016, the DSM-5 case definition will serve as the basis for ADDM estimates of ASD prevalence in future surveillance reports. Although the DSM-IV-TR case definition will eventually be phased out, it will be applied in a limited geographic area to offer additional data for comparison. Future analyses will examine trends in the continued use of DSM-IV-TR diagnoses, such as autistic disorder, PDD-NOS, and Asperger disorder in health and education records, documentation of symptoms consistent with DSM-5 terminology, and how these trends might influence estimates of ASD prevalence over time. The latest findings from the ADDM Network provide evidence that the prevalence of ASD is higher than previously reported estimates and continues to vary among certain racial/ethnic groups and communities. With prevalence of ASD ranging from 13.1 to 29.3 per 1,000 children aged 8 years in different communities throughout the United States, the need for behavioral, educational, residential, and occupational services remains high, as does the need for increased research on both genetic and nongenetic risk factors for ASD.

Can pregnancy drugs disturb molecular reprogramming of the fetal germline ?

Can pregnancy drugs increase heritable risk for autism and neurodevelopmental disorders ?

2018 Study Abstract

In a seeming paradox, the prevalence of autism spectrum disorder (ASD) has surged, while at the same time research has pointed to the strong heritability of this neurodevelopmental pathology. Here an autism research philanthropist suggests a biological phenomenon of exogenously induced ‘gamete disruption’ that could reconcile these seemingly contradictory observations. Mining information from her own family history and that of her fellow autism parents, while also engaging with the scientific community, she proposes that a subset of the autisms may be rooted in a variety of molecular glitches in parental gametes induced by certain acute exposures during the parents’ own fetal or neonatal development. These exposures include but are not limited to synthetic hormone drugs, tobacco, and general anesthesia. Consistent with this hypothesis, animal models have demonstrated adverse neurobehavioral outcomes in grandoffspring of gestating dams exposed to hormone-disrupting compounds, tobacco components, and general anesthesia. A recent epidemiological study showed a link between grandmaternal smoking and risk for ASD in grandoffspring through the maternal line. Given the urgency of the autism crisis, combined with the biological plausibility of this mostly unexplored paradigm, the writer contends that questions of nongenetic inheritance should be a priority in autism research.

Read the full study (free access) Bugs in the program: can pregnancy drugs and smoking disturb molecular reprogramming of the fetal germline, increasing heritable risk for autism and neurodevelopmental disorders? on Oxford University Press, Environmental Epigenetics, Volume 4, Issue 2, 26 April 2018.

Potential inverse association between maternal multivitamin supplement use and ASD in offspring

Antenatal nutritional supplementation and autism spectrum disorders in the Stockholm youth cohort: population based cohort study

What is already known on this topic

Evidence from observational studies is inconsistent about whether maternal supplementation with multivitamins, iron, or folic acid is protective against autism spectrum disorder (ASD) in offspring
Although the cause of autism spectrum disorder may differ by presence of intellectual disability, few studies have examined relations between nutritional supplements and ASD based on level of cognitive function

What this study adds

This population based study of a large cohort in Stockholm supported a possible inverse association between maternal use of multivitamin supplements in early pregnancy and ASD with intellectual disability in offspring compared with no maternal use of multivitamins, iron, or folic acid

2017 Study Abstract

To determine whether nutritional supplementation during pregnancy is associated with a reduced risk of autism spectrum disorder (ASD) with and without intellectual disability in offspring.

Observational prospective cohort study using multivariable logistic regression, sibling controls, and propensity score matching.

Stockholm County, Sweden.

273 107 mother-child pairs identified through population registers. The study sample was restricted to children who were aged 4 to 15 years by the end of follow-up on 31 December 2011 and were born between 1996 and 2007.

Multivitamin, iron, and folic acid supplement use was reported at the first antenatal visit.

Main outcome measure
Diagnosis of ASD with and without intellectual disability in children determined from register data up to 31 December 2011.

Prevalence of ASD with intellectual disability was 0.26% (158 cases in 61 934) in the maternal multivitamin use group and 0.48% (430 cases in 90 480) in the no nutritional supplementation use group. Maternal multivitamin use with or without additional iron or folic acid, or both was associated with lower odds of ASD with intellectual disability in the child compared with mothers who did not use multivitamins, iron, and folic acid (odds ratio 0.69, 95% confidence interval 0.57 to 0.84). Similar estimates were found in propensity score matched (0.68, 0.54 to 0.86) and sibling control (0.77, 0.52 to 1.15) matched analyses, though the confidence interval for the latter association included 1.0 and was therefore not statistically significant. There was no consistent evidence that either iron or folic acid use were inversely associated with ASD prevalence.

Maternal multivitamin supplementation during pregnancy may be inversely associated with ASD with intellectual disability in offspring. Further scrutiny of maternal nutrition and its role in the cause of autism is recommended.

  • Antenatal nutritional supplementation and autism spectrum disorders in the Stockholm youth cohort: population based cohort study, BMJ 2017;359:j4273, 04 October 2017.
  • Featured image credit @bmj_latest.

Antidepressant use during pregnancy and psychiatric disorders in offspring

Danish nationwide register based cohort study, 2017

What is already known on this topic

  • Several studies have linked selective serotonin reuptake inhibitor use during pregnancy to autism spectrum disorder in offspring, although results have been conflicting
  • The potential explanation for this association is that selective serotonin reuptake inhibitors cross the placental barrier and affect the development of the fetal brain
  • If this holds true, in utero exposure to selective serotonin reuptake inhibitor and other classes of antidepressants may increase risk for various psychiatric disorders besides autism spectrum disorder

What this study adds

  • Antidepressant use during pregnancy was associated with increased risk for various diagnostic groups of psychiatric disorders in offspring
  • The observed associations may be attributable to the severity of underlying maternal psychiatric disorders in combination with in utero antidepressant exposure

Study Abstract

To investigate the association between in utero exposure to antidepressants and risk of psychiatric disorders.

Population based cohort study.

Danish national registers.

905 383 liveborn singletons born during 1998-2012 in Denmark and followed from birth until July 2014, death, emigration, or date of first psychiatric diagnosis, whichever came first. The children were followed for a maximum of 16.5 years and contributed 8.1×106 person years at risk.

Exposures for observational studies
Children were categorised into four groups according to maternal antidepressant use within two years before and during pregnancy: unexposed, antidepressant discontinuation (use before but not during pregnancy), antidepressant continuation (use both before and during pregnancy), and new user (use only during pregnancy).

Main outcome measure
First psychiatric diagnosis in children, defined as first day of inpatient or outpatient treatment for psychiatric disorders. Hazard ratios of psychiatric disorders were estimated using Cox regression models.

Overall, psychiatric disorders were diagnosed in 32 400 children. The adjusted 15 year cumulative incidence of psychiatric disorders was 8.0% (95% confidence interval 7.9% to 8.2%) in the unexposed group, 11.5% (10.3% to 12.9%) in the antidepressant discontinuation group, 13.6% (11.3% to 16.3%) in the continuation group, and 14.5% (10.5% to 19.8%) in the new user group. The antidepressant continuation group had an increased risk of psychiatric disorders (hazard ratio 1.27, 1.17 to 1.38), compared with the discontinuation group.

In utero exposure to antidepressants was associated with increased risk of psychiatric disorders. The association may be attributable to the severity of underlying maternal disorders in combination with antidepressant exposure in utero. The findings suggest that focusing solely on a single psychiatric disorder among offspring in studies of in utero antidepressant exposure may be too restrictive.

  • Antidepressant use during pregnancy and psychiatric disorders in offspring: Danish nationwide register based cohort study, BMJ 2017;358:j3668, 06 September 2017.
  • Characteristics of study population according to maternal antidepressant use before and during pregnancy. Values are numbers (percentages) unless stated otherwise, featured image credit bmj.