Neurodevelopmental risk from vaccination during pregnancy: autism & schizophrenia

Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
December 31, 2009

An increasing amount of data indicates that when a pregnant woman is vaccinated, cytokines induced by the vaccination increase the likelihood that her embryo or fetus will experience atypical brain development.

For instance, " Maternal immune activation (MIA) can affect fetal brain development and thus behavior of young and adult offspring. Reports have shown that increased Interleukin-6 (IL-6) in the maternal serum plays a key role in altering fetal brain development, and may impair social behaviors in the offspring." (1)

Relevant is the fact that influenza vaccination increases IL-6 (2). Indeed, commenting on the IL-6 finding (1), University of Minnesota neuroscientist S. Hossein Fatemi, M.D., Ph.D., described the autism significance of dysregulation of maternal immunity (3).

Importantly and free online, a detailed but readable elaboration of maternal inflammation and adverse sequelae is presented by M.I.N.D. Institute's Isaac N. Pessah, Ph.D., and colleagues (section V in cite 4). Given findings summarized in that part of the Pessah et al review (4), oft-repeated admonitions to vaccinate pregnant women - and thus recommendations and policies to induce transient elevations of interleukin-6 and other cytokines - may be properly categorized as an insanity of modernity.

When reading section V of Pessah et al (4), a further parallel to vaccinations merits attention. In many experiments maternal inflammation was induced by a non-pathogenic agent that stimulated maternal cytokines in ways akin to pathogen-induced cytokines (4) and vaccination-induced cytokines (2). In other words, effects the cytokines induced in the pregant female may be as important or even more important than the pathogen itself.

A (free online) study published in 2007 states, "The identification of IL-6 as a key intermediary should aid in the molecular dissection of the pathways whereby [maternal immune activation] MIA alters fetal brain development, which can shed new light on the pathophysiological mechanisms that predispose to schizophrenia and autism." (5; see also 6-7)

Needless to say, Hell will have thoroughly frozen over long before high-ranking personnel of the Institute of Medicine, Advisory Committee for Immunization Practices, the FDA, American Academy of Pediatrics, or the American Medical Association move toward vaccine safety by revising vaccination policies in ways consistent with the findings summarized herein (1-7; see also 8).


1. Flavonoids, a prenatal prophylaxis via targeting JAK2/STAT3 signaling to oppose IL-6/MIA associated autism
Parker-Athill E et al.
University of South Florida
J Neuroimmunol. 2009 Dec 10;217(1-2):20-7. Epub 2009 Sep 18.

Maternal immune activation (MIA) can affect fetal brain development and thus behavior of young and adult offspring. Reports have shown that increased Interleukin-6 (IL-6) in the maternal serum plays a key role in altering fetal brain development, and may impair social behaviors in the offspring. Interestingly, these effects could be attenuated by blocking IL-6. The current study investigated the effects of luteolin, a citrus bioflavonoid, and its structural analog, diosmin, on IL-6 induced JAK2/STAT3 (Janus tyrosine kinase-2/signal transducer and activator of transcription-3) phosphorylation and signaling as well as behavioral phenotypes of MIA offspring. Luteolin and diosmin inhibited neuronal JAK2/STAT3 phosphorylation both in vitro and in vivo following IL-6 challenge as well as significantly diminishing behavioral deficits in social interaction. Importantly, our results showed that diosmin (10mg/kgday) was able to block the STAT3 signal pathway; significantly opposing MIA-induced abnormal behavior and neuropathological abnormalities in MIA/adult offspring. Diosmin's molecular inhibition of JAK2/STAT3 pathway may underlie the attenuation of abnormal social interaction in IL-6/MIA adult offspring.

2. Effect of influenza vaccine on markers of inflammation and lipid profile
Tsai MY et al.
University of Minnesota
J Lab Clin Med. 2005 Jun;145(6):323-7.

Despite wide use of the influenza vaccine, relatively little is known about its effect on the measurement of inflammatory markers. Because inflammatory markers such as C-reactive protein (CRP) are increasingly being used in conjunction with lipids for the clinical assessment of cardiovascular disease and in epidemiologic studies, we evaluated the effect of influenza vaccination on markers of inflammation and plasma lipid concentrations. We drew blood from 22 healthy individuals 1 to 6 hours before they were given an influenza vaccination and 1, 3, and 7 days after the vaccination. Plasma CRP, interleukin (IL)-6, monocyte chemotactic protein 1, tumor necrosis factor alpha, IL-2 soluble receptor alpha, and serum amyloid A were measured, and differences in mean concentrations of absolute and normalized values on days 1, 3, and 7 were compared with mean baseline values. There was a significant increase in mean IL-6 (P < .01 absolute values, P < .001 normalized values) on day 1 after receiving the influenza vaccine. The mean increases in normalized high sensitivity CRP values were significant on day 1 (P < .01) and day 3 (P = .05), whereas the mean increase in normalized serum amyloid A was significant only on day 1 (P < .05). No significant changes were seen in mean concentrations of IL-2 soluble receptor alpha, monocyte chemotactic protein-1, or tumor necrosis factor-alpha. Of the lipids, significant decreases in mean concentrations of normalized triglyceride values were seen on days 1 (P < .05), 3 (P < .001), and 7 (P < .05) after vaccination. Our findings show that the influenza vaccination causes transient changes in select markers of inflammation and lipids. Consequently, clinical and epidemiologic interpretation of the biomarkers affected should take into account the possible effects of influenza vaccination.

3. Multiple pathways in prevention of immune-mediated brain disorders: Implications for the prevention of autism
Fatemi SH.
J Neuroimmunol. 2009 Dec 10;217(1-2):8-9. Epub 2009 Oct 14.

4.  V. The Impacts of Maternal Immune Challenge on the Fetal Brain and the Pathological Consequences on Behavior
[a summary of findings by] Benjamin K. Yee, Urs Meyer, and Joram Feldon, Laboratory of Behavioural Neurobiology, ETH Zurich, Switzerland

Immunologic and neurodevelopmental susceptibilities of autism
Pessah IN, Seegal RF, Lein PJ, LaSalle J, Yee BK, Van De Water J, Berman RF.
Neurotoxicology. 2008 May;29(3):532-45.

Symposium 5 focused on research approaches that are aimed at understanding common patterns of immunological and neurological dysfunction contributing to neurodevelopmental disorders such as autism and ADHD. The session focused on genetic, epigenetic, and environmental factors that might act in concert to influence autism risk, severity and co-morbidities, and immunological and neurobiological targets as etiologic contributors. The immune system of children at risk of autism may be therefore especially susceptible to psychological stressors, exposure to chemical triggers, and infectious agents. Identifying early biomarkers of risk provides tangible approaches toward designing studies in animals and humans that yield a better understanding of environmental risk factors, and can help identify rational intervention strategies to mitigate these risks.

5. Maternal immune activation alters fetal brain development through interleukin-6
Smith SE, Li J, Garbett K, Mirnics K, Patterson PH.
California Institute of Technology
J Neurosci. 2007 Oct 3;27(40):10695-702.

Schizophrenia and autism are thought to result from the interaction between a susceptibility genotype and environmental risk factors. The offspring of women who experience infection while pregnant have an increased risk for these disorders. Maternal immune activation (MIA) in pregnant rodents produces offspring with abnormalities in behavior, histology, and gene expression that are reminiscent of schizophrenia and autism, making MIA a useful model of the disorders. However, the mechanism by which MIA causes long-term behavioral deficits in the offspring is unknown. Here we show that the cytokine interleukin-6 (IL-6) is critical for mediating the behavioral and transcriptional changes in the offspring. A single maternal injection of IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) deficits in the adult offspring. Moreover, coadministration of an anti-IL-6 antibody in the poly(I:C) model of MIA prevents the PPI, LI, and exploratory and social deficits caused by poly(I:C) and normalizes the associated changes in gene expression in the brains of adult offspring. Finally, MIA in IL-6 knock-out mice does not result in several of the behavioral changes seen in the offspring of wild-type mice after MIA. The identification of IL-6 as a key intermediary should aid in the molecular dissection of the pathways whereby MIA alters fetal brain development, which can shed new light on the pathophysiological mechanisms that predispose to schizophrenia and autism.

6. The effects of maternal inflammation on neuronal development: possible mechanisms
Jonakait GM.
New Jersey Institute of Technology
Int J Dev Neurosci. 2007 Nov;25(7):415-25. Epub 2007 Sep 14.

That maternal inflammation adversely affects fetal brain development is well established. Less well understood are the mechanisms that account for neurodevelopmental disorders arising from maternal inflammation. This review seeks to begin an examination of possible sites and mechanisms of action whereby inflammatory cytokines - produced by the mother or by the fetal brain - could impact the developing fetus. We focus first on the placenta where cytokines maintain the immunological environment that prevents maternal rejection of the fetus. Following a brief examination of placental transfer of maternal cytokines, the focus turns on embryonic microglia, early and ubiquitous residents of the developing brain. Finally, a more intense examination of interleukin-6 (IL-6) and bone morphogenetic proteins (BMPs) provides examples of glial- or maternal-derived cytokines that are known to have profound effects on developing systems and that could, if dysregulated, have undesirable consequences for brain development.

7. The role of pro-inflammatory factors in mediating the effects on the fetus of prenatal undernutrition: implications for schizophrenia.
Shen Q et al.
Schizophr Res. 2008 Feb;99(1-3):48-55. Epub 2007 Dec 11.

Exposure to prenatal undernutrition or malnutrition increases the risk of schizophrenia, although little is known about the mechanism. Pro-inflammatory factors are critical in brain development, and are believed to play an important role in neurodevelopmental disorders associated with prenatal exposure to infection, including schizophrenia. However it is not known whether pro-inflammatory factors also mediate the effects on the fetus of prenatal malnutrition or undernutrition. In this study, we established a new prenatal undernourished rat model induced by maternal exposure to a diet restricted to 50% of the low (6%) protein diet (RLP50). We observed the disappearance of maternal nest-building behavior in the RLP50 dams, increased levels of TNFA and IL6 in the placentas (P<0.001; P=0.879, respectively) and fetal livers (P<0.001; P<0.05, respectively), and a decrease in the fetal brains (P<0.05; P<0.01, respectively). Our results are similar to previous studies of maternal infection, which implies that a common pathway mediated by pro-inflammatory factors may contribute to the brain development, consequently increasing the risk of schizophrenia and other psychiatric diseases programmed by varied maternal adversities. We also provide a new prenatal undernourished model for researching prenatal problems, which differs from previous malnourished model in terms of the maternal behavior of dams and of observed pro-inflammatory factor levels in fetal tissues.

8. Vaccination-induced cytokines: schizophrenia & developmental disabilities
Teresa Binstock, Sep 07, 2009

Contact Teresa Binstock by email

Back to Index

Search Generation Rescue
Join the Autism Rescue Angels
Donate to cure Autism
GR Autism brochure

Let's go Shopping for Autism Recovery