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Age of Autism Science Summary: Death after Quadrivalent Human Papillomavirus (HPV) Vaccination

Science post imagePharmaceutical Regulatory Affairs: Open Access

Research Article            Open Access

Death after Quadrivalent Human Papillomavirus (HPV) Vaccination: (Read the full study  HERE.

Causal or Coincidental?

Lucija Tomljenovic1* and Christopher A Shaw1,2,3

1Department of Ophthalmology and Visual Sciences, University of British Columbia, Canada 2Program in Experimental Medicine, University of British Columbia, Canada 3Program in Neuroscience, University of British Columbia, Canada


Background: The proper understanding of a true risk from vaccines is crucial for avoiding unnecessary adverse reactions (ADRs). However, to this date no solid tests or criteria have been established to determine whether adverse events are causally linked to vaccinations.

Objectives: This research was carried out to determine whether or not some serious autoimmune and neurological ADRs following HPV vaccination are causal or merely coincidental and to validate a biomarker-based immunohistochemical (IHC) protocol for assessing causality in case of vaccination-suspected serious adverse neurological outcomes.

Methods: Post-mortem brain tissue specimens from two young women who suffered from cerebral vasculitis- type symptoms following vaccination with the HPV vaccine Gardasil were analysed by IHC for various immuno- inflammatory markers. Brain sections were also stained for antibodies recognizing HPV-16L1 and HPV-18L1 antigen which are present in Gardasil.

Results: In both cases, the autopsy revealed no anatomical, microbiological nor toxicological findings that might have explained the death of the individuals. In contrast, our IHC analysis showed evidence of an autoimmune vasculitis potentially triggered by the cross-reactive HPV-16L1 antibodies binding to the wall of cerebral blood vessels in all examined brain samples. We also detected the presence of HPV-16L1 particles within the cerebral vasculature with some HPV-16L1 particles adhering to the blood vessel walls. HPV-18L1 antibodies did not bind to cerebral blood vessels nor any other neural tissues. IHC also showed increased T-cell signalling and marked activation of the classical antibody-dependent complement pathway in cerebral vascular tissues from both cases. This pattern of complement activation in the absence of an active brain infection indicates an abnormal triggering of the immune response in which the immune attack is directed towards self-tissue.

Conclusions: Our study suggests that HPV vaccines containing HPV-16L1 antigens pose an inherent risk for triggering potentially fatal autoimmune vasculopathies.

Practice implications: Cerebral vasculitis is a serious disease which typically results in fatal outcomes when undiagnosed and left untreated. The fact that many of the symptoms reported to vaccine safety surveillance databases following HPV vaccination are indicative of cerebral vasculitis, but are unrecognized as such (i.e., intense persistent migraines, syncope, seizures, tremors and tingling, myalgia, locomotor abnormalities, psychotic symptoms and cognitive deficits), is a serious concern in light of the present findings. It thus appears that in some cases vaccination may be the triggering factor of fatal autoimmune/neurological events. Physicians should be aware of this association.

Science Summary: Maternal Vitamin D Levels and the Autism Phenotype Among Offspring.

Science post imageJ Autism Dev Disord. 2012 Oct 16. [Epub ahead of print]

Maternal Vitamin D Levels and the Autism Phenotype Among Offspring.
Whitehouse AJ, Holt BJ, Serralha M, Holt PG, Hart PH, Kusel MM.


Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, 100 Roberts Road, Subiaco, West Perth, WA, 6008, Australia,


We tested whether maternal vitamin D insufficiency during pregnancy is related to the autism phenotype. Serum 25(OH)-vitamin D concentrations of 929 women were measured at 18 weeks' pregnancy. The mothers of the three children with a clinical diagnosis of autism spectrum disorder had 25(OH)-vitamin D concentrations above the population mean. The offspring of 406 women completed the Autism-Spectrum Quotient in early adulthood. Maternal 25(OH)-vitamin D concentrations were unrelated to offspring scores on the majority of scales. However, offspring of mothers with low 25(OH)-vitamin D concentrations (<49 nmol/L) were at increased risk for 'high' scores (≥2SD above mean) on the Attention Switching subscale (odds ratio: 5.46, 95 % confidence interval: 1.29, 23.05). The involvement of maternal vitamin D during pregnancy in autism requires continued investigation.

AofA Science Summary: Are systemizing and autistic traits related to talent and interest in mathematics and engineering?

Science post imageProfessor Simon Baron Cohen's research includes the theory of the extreme male brain: "Research on relatives of people with Asperger syndrome and autism has found that their fathers and grandfathers are twice as likely to be engineers as the general population. Natural science students have more relatives with autism than humanities students. Asperger syndrome is found more often in mathematicians and their siblings than in the general population. Both mothers and fathers of children with Asperger syndrome tend to score high on systemizing. Both mothers and fathers of children with autism or Asperger syndrome often have father who worked in systemizing occupations. Both mothers and fathers of children with autism have a strongly masculine pattern of brain activity when doing systemizing activity.*"  The study below found otherwise.

Item 1 of 1 (Display the citation in PubMed) 1. Br J Psychol. 2012

Nov;103(4):472-96. doi: 10.1111/j.2044-8295.2011.02089.x. Epub 2011 Dec 22.

Are systemizing and autistic traits related to talent and interest in mathematics and engineering? Testing some of the central claims of the empathizing-systemizing theory.


School of Psychology, University of Plymouth, UK Department of Psychology, University of Florence, Italy.


Testing some of the central claims of the empathizing-systemizing theory. Morsanyi K, Primi C, Handley SJ, Chiesi F, Galli S. Source School of Psychology, University of Plymouth, UK Department of Psychology, University of Florence, Italy. Abstract In two experiments, we tested some of the central claims of the empathizing-systemizing (E-S) theory.

Experiment 1 showed that the systemizing quotient (SQ) was unrelated to performance on a mathematics test, although it was correlated with statistics-related attitudes, self-efficacy, and anxiety. In Experiment 2, systemizing skills, and gender differences in these skills, were more strongly related to spatial thinking styles than to SQ. In fact, when we partialled the effect of spatial thinking styles, SQ was no longer related to systemizing skills.

Additionally, there was no relationship between the Autism Spectrum Quotient (AQ) and the SQ, or skills and interest in mathematics and mechanical reasoning. We discuss the implications of our findings for the E-S theory, and for understanding the autistic cognitive profile. ©2011 The British Psychological Society. PMID: 23034108 [PubMed - in process]

*The Oxford Handbook of Evolutionary Psychology, Edited by Robin Dunbar and Louise Barret, Oxford University Press, 2007, Chapter 16 The evolution of empathizing and systemizing: assortative mating of two strong systemizers and the cause of autism, Simon Baron-Cohen.

AofA Science Summary: Reversible blindness in bilateral optic neuritis associated with nasal flu vaccine.

Science post imageBinocul Vis Strabolog Q Simms Romano. 2012;27(3):171-3.

Reversible blindness in bilateral optic neruritis associated with nasal flu vaccine.

Crawford CGrazko MBRaymond WR 4thRivers BAMunson PD.


Various case reports have shown possible associations between optic neuritis and different vaccines. Some of the vaccines include influenza, hepatitis B and anthrax


To present evidence for a causal relationship between optic neuritis and Live Attenuated Influenza Vaccine (LAIV), administered as nasal flu vaccine.


Case Report. In a 13-year-old male with bilateral optic neuritis, detailed clinical history, neuro-ophthalmologic examination, magnetic resonance imaging, stereo-disc photos, visual field testing, ocular coherence tomography, blood tests and cerebral spinal fluid analysis were performed.


Exam findings on presentation: BCVA: 20/CF OD; 20/LP OS. Positive relative afferent pupil defect OD. Unremarkable anterior segment and posterior segment exam. No papillitis or papilledema. Global visual field defect OU based on Humphrey 30-2. MRI: diffuse enlargement of Optic Chiasm with inflammation of distal optic nerves bilateral. Blood cultures and CSF were negative. Patient received 3 divided doses of methyl prednisone with mild improvement of vision upon hospital discharge and marked improvement of vision at 2 month follow up.


In this child, no infectious, vascular, granulomatous, viral or immune-related cause of optic neuritis was identified. This case provides compelling evidence that supports the nasal flu vaccination as a cause of optic neuritis.


Age of Autism Science Summary: Anxiety, Sensory Over-Responsivity, and Gastrointestinal Problems in Children with Autism Spectrum Disorders.

Science post imageJ Abnorm Child Psychol. 2012 Aug 1. [Epub ahead of print]

Anxiety, Sensory Over-Responsivity, and Gastrointestinal Problems in Children with Autism Spectrum Disorders.

Mazurek MO, Vasa RA, Kalb LG, Kanne SM, Rosenberg D, Keefer A, Murray DS, Freedman B, Lowery LA.

Department of Health Psychology and Thompson Center for Autism and Neurodevelopmental Disorders, University of Missouri - Columbia, 205 Portland Street, Columbia, MO, 65211, USA,


Children with autism spectrum disorders (ASD) experience high rates of anxiety, sensory processing problems, and gastrointestinal (GI) problems; however, the associations among these symptoms in children with ASD have not been previously examined. The current study examined bivariate and multivariate relations among anxiety, sensory over-responsivity, and chronic GI problems in a sample of 2,973 children with ASD enrolled in the Autism Treatment Network (ages 2-17 years, 81.6 % male). Twenty-four percent of the sample experienced at least one type of chronic GI problem (constipation, abdominal pain, bloating, diarrhea, and/or nausea lasting three or more months). Children with each type of GI problem had significantly higher rates of both anxiety and sensory over-responsivity. Sensory over-responsivity and anxiety were highly associated, and each provided unique contributions to the prediction of chronic GI problems in logistic regression analyses. The results indicate that anxiety, sensory over-responsivity and GI problems are possibly interrelated phenomenon for children with ASD, and may have common underlying mechanisms.

Free Two Day Event As Talk About Curing Autism Philadelphia Chapter Welcomes Dr. Richard Frye to Speak

Dr. Richard Frye**FREE EVENT** Save the date! TACA 160

Don’t miss this special two-day event where you can hear the latest on Autism research and treatments from one of the top ASD specialists in the country! Come with questions and hear Dr. Frye speak on…

Saint Alban’s Episcopal Church
3625 Chapel Road
Newtown Square, PA 19073Dr. Richard Frye is coming to TACA PA!!

Friday, August 3, 2012, 7:00 - 9:00 PM

• Neurological Abnormalities in ASD

Children with autism have been found to have many neurological abnormalities. These include differences in brain function, structure and connectivity, neurotransmitter and metabolic abnormalities and electrical disturbances in the brain including seizures. This talk will review some of the important aspects of these neurological abnormalities and their treatments.

Saturday, August 4, 2012, 10:00 AM - 12:00 PM

One Talk Covering Two Common Issues

• Mitochondrial Disorders in Autism Mitochondria

There is strong evidence that many children with autism also have a mitochondrial disorder, which means that the mitochondria produce less fuel for the body and for the brain. This talk will discuss the challenges of how to test for mitochondrial disorders, as well as the current treatments available for them.

• Seizures in Autism

A New National Survey on Treatments: Approximately 25% of children and adults with autism have seizures, and another 50% have sub-clinical seizures that are often undetected but may affect their intellectual functioning. This presentation will briefly review seizure issues in autism, and then present the new results of a national survey of over 500 children and adults with seizures, with a comparison of the benefits and possible side effects of many medical, dietary, and nutritional treatments.

Dr. Richard Frye, M.D., Ph.D., who is the Director of Autism Research and Associate Professor of Pediatrics at The University of Arkansas for Medical Sciences, speaks across the country on pediatric neurological disorders. He specializes in pediatric neurology disorders including learning disabilities and dyslexia, autism and developmental delay, speech and language delay, attention deficit, tics and Tourette’s syndrome, sleep disorders, and epileptic encephalopathy. Dr. Frye is board certified in Pediatrics and in Neurology and completed fellowships in behavioral neurology and psychology.
Nationally Renowned Speaker from Autism One, ARI & more!

Lee Silsby logo 09 The treatment category is sponsored by Lee Silsby, the leader in quality compounded medications for autism.

Gene Expression Profiles of Inflamed Bowel Biopsy Tissue in ASD Children Consistent with IBD

BowelGene Expression Profiles of Inflamed Bowel Biopsy Tissue in ASD Children Are Consistent with Inflammatory Bowel Disease

IMFAR Saturday, May 19, 2012
S. J. Walker, J. Fortunato, A. Krigsman

Gene Expression Profiles of Inflamed Bowel Biopsy Tissue in ASD Children Are Consistent with Inflammatory Bowel Disease

Saturday, May 19, 2012

Sheraton Hall (Sheraton Centre Toronto)

9:00 AM

S. J. Walker1, J. Fortunato2 and A. Krigsman3, (1)Wake Forest Institute for Regenerative Medicine, Winston-Salem, NC, (2)Wake Forest University Health Sciences, Winston Salem, NC, (3)Pediatric Gastroenterology Resources of New York, Far Rockaway, NY

Background: Chronic gastrointestinal (GI) symptoms in children with autism spectrum disorders (ASD) are common and not well understood. It is unclear if GI symptoms and intestinal mucosal inflammatory changes seen in children with ASD represent a variant of inflammatory bowel disease (IBD) versus non-specific colitis or “normal” mucosal cellular composition. Some studies have demonstrated histochemical and immunohistochemical features of the bowel mucosa, lamina propria and mucosal basement membrane which may be unique to children with ASD. The recent emergence of gene expression profiling as a valid methodology for distinguishing various forms of IBD potentially adds a further tool in defining the characteristics of ASD-associated intestinal inflammation.

Objectives: The goal of this study was to use a molecular approach to evaluate gene expression profiles in both histologically inflamed and non-inflamed ileocolonic biopsy specimens from ASD children with chronic GI symptoms and to compare them to gene expression profiles in ileocolonic tissue of neurotypical children with Crohn’s disease. Significant overlap of gene expression in these two groups would suggest that ASD-GI represents an IBD variant; differences in the ASD-GI gene expression profile would highlight the nature of its distinction from Crohn’s disease.

Methods: Study tissue consisted of ileocolonic biopsies from two groups: (1) children with an ASD undergoing ileocolonoscopy for active gastrointestinal symptoms and, (2) neurotypical children diagnosed with Crohn’s disease.  All tissue specimens were collected under appropriate IRB approval. For each individual (seven per group; fourteen in total) two biopsies were used: one from the terminal ileum with active inflammatory changes and one from the colon demonstrating normal mucosa (control).  Total RNA was isolated from the individual tissue biopsy specimens and used to query whole genome DNA microarrays. For each of the two groups, ASD-GI and CD, differential gene expression was determined by comparing the inflamed tissue within a group to the control tissues from the same group. Next, differential gene expression was compared between the ASD-GI and CD groups to evaluate similarities and differences.  

Results: In each group there were ~2000 transcripts differentially expressed between inflamed and control tissue. Within the 900 differentially expressed genes shared by both ASD-GI and CD, two highly relevant biological functional groups represented by these transcripts were gastrointestinal disease (including CD [p = 0.001] and IBD [p = 0.001]) and inflammatory response [p = 0.000003]. In the 912 differentially expressed transcripts unique to ASD-GI, the most significant biological functional group represented was gastrointestinal disease (including IBD and CD). In contrast, there were 1200 genes uniquely differentially expressed in CD and the primary biological functions represented by these transcripts were immune response [p = 6.6 x 10-14] and autoimmune disease [p = 4 x 10-7].    

Conclusions: These results demonstrate that ASD-GI presents a gene expression profile significantly overlapping with Crohn’s disease and consistent with the larger category of inflammatory bowel disease.

AofA Science Summary: Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism.

Three eyes fishPLoS One. 2012;7(6):e32917. Epub 2012 Jun 6.

Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism.

Thomas MAKlaper RD.


Department of Biological Sciences, Idaho State University School, Pocatello, Idaho, United States of America.


Idiopathic autism, caused by genetic susceptibility interacting with unknown environmental triggers, has increased dramatically in the past 25 years. Identifying environmental triggers has been difficult due to poorly understood pathophysiology and subjective definitions of autism. The use of antidepressants by pregnant women has been associated with autism. These and other unmetabolized psychoactive pharmaceuticals (UPPs) have also been found in drinking water from surface sources, providing another possible exposure route and raising questions about human health consequences. Here, we examined gene expression patterns of fathead minnows treated with a mixture of three psychoactive pharmaceuticals (fluoxetine, venlafaxine & carbamazepine) in dosages intended to be similar to the highest observed conservative estimates of environmental concentrations. We conducted microarray experiments examining brain tissue of fish exposed to individual pharmaceuticals and a mixture of all three. We used gene-class analysis to test for enrichment of gene sets involved with ten human neurological disorders. Only sets associated with idiopathic autism were unambiguously enriched. We found that UPPs induce autism-like gene expression patterns in fish. Our findings suggest a new potential trigger for idiopathic autism in genetically susceptible individuals involving an overlooked source of environmental contamination.

Age of Autism Science Summary: The Name Game?

Nutty professorYou can call us speechless on this one....  it's just nutty.

Psychopathology. 2012 May 22;45(4):215-219. [Epub ahead of print]

Are Names of Children with Attention Deficit Hyperactivity Disorder More 'Hyperactive'?


Child and Adolescent Division, Psychiatry Department, Geha Mental Health Center, Petah Tiqva, Israel.


Background: The role of the meaning of given names has been noted in psychotherapy as well as in everyday life. This study aimed to investigate the possible association between the nature of given names of children and attention deficit hyperactivity disorder (ADHD) diagnosis. Sampling and Methods: A total of 134 given names of children and adolescent patients diagnosed as having ADHD were compared with those of an age- and gender-matched randomly chosen control group from the general population. The first names of the two cohorts were compared with regard to the following: the literal meaning of their names, whether the name constitutes a verb, the prevalence of each name and their length (number of syllables). Results: The meaning of first names of children and adolescents with ADHD combined type were rated by referees as expressing significantly more activity and containing less syllables than the names of controls. In addition, the prevalence of their names was significantly lower than that of names used in the general population. All findings remained significant following Bonferroni adjustment. Conclusions: Our findings demonstrate an intriguing relationship between children's given names and ADHD diagnosis. Given names may serve as a possible predictor of later diagnosis of ADHD. Clinicians should be more attentive to given names in the context of child psychiatric evaluation and therapy.

Copyright © 2012 S. Karger AG, Basel.

AofA Science Summary: Prenatal Exposure to Organomercury & Association with Developmental Disorders

Science post imagePrenatal exposure to organomercury, thimerosal, persistently impairs the serotonergic and dopaminergic systems in the rat brain: Implications for association with developmental disorders
(See study at Prenatal thimerosal and neurotransmitter imbalances in rats)

Michiru Ida-Eto a,*, Akiko Oyabu a, Takeshi Ohkawara a, Yasura Tashiro a, Naoko Narita b, Masaaki Narita a

a Department of Anatomy II, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan

b Department of Education, Bunkyo University, Koshigaya, Saitama 343-8511, Japan

Received 8 November 2011; received in revised form 2 May 2012; accepted 3 May 2012

* Corresponding author. Address: Department of Anatomy II, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. Tel.: +81 59 232 1111x6326; fax: +81 59 232 8031.

E-mail address: (M. Ida-Eto).

Brain & Development xxx (2012) xxx–xxx

Ida-Eto M et al. Prenatal exposure to organomercury, thimerosal, persistently impairs the serotonergic and dopaminergic systems in the rat brain: Implications for association with developmental disorders. Brain Dev (2012),


Thimerosal, an organomercury compound, has been widely used as a preservative. Therefore, concerns have been raised about its neurotoxicity. We recently demonstrated perturbation of early serotonergic development by prenatal exposure to thimerosal (Ida-Eto et al. (2011) [11]). Here, we investigated whether prenatal thimerosal exposure causes persistent impairment after birth. Analysis on postnatal day 50 showed significant increase in hippocampal serotonin following thimerosal administration on embryonic day 9.

Furthermore, not only serotonin, striatal dopamine was significantly increased. These results indicate that embryonic exposure to thimerosal produces lasting impairment of brain monoaminergic system, and thus every effort should be made to avoid the use of thimerosal.

Keywords: Thimerosal; Serotonin; Dopamine; Embryonic exposure; Developmental disorders; Rat" that closes with (emphasis added):

"These results indicate that embryonic exposure to thimerosal produces lasting impairment of brain monoaminergic system, and thus every effort should be made to avoid the use of thimerosal."



Antipsychotics and Differences in Body Mass Scores in Pediatric Population

Science post imageJ Child Adolesc Psychopharmacol. 2012 Apr;22(2):166-73.

Differences in Body Mass Index z-Scores and Weight Status in a Dutch Pediatric Psychiatric Population With and Without Use of Second-Generation Antipsychotics.

de Hoogd S, Overbeek WA, Heerdink ER, Correll CU, de Graeff ER, Staal WG.


1 Faculty of Pharmaceutical Sciences, University of Utrecht , The Netherlands .


Abstract Objective: Weight gain and metabolic adverse effects of second-generation antipsychotics (SGAs) have become a major concern, particularly in youth. However, the specific contribution of SGAs versus other medications or the underlying illness is unclear. Methods: In a chart review study of psychiatric outpatients aged ≤18 years treated with SGAs and psychiatric controls without lifetime SGA, use body mass index (BMI) z-scores between patients and controls were compared in the entire sample, patients without co-medications, diagnostic subgroups, and age subgroups. In patients with follow-up data, weight z-score change was calculated. Results: Altogether, 592 Caucasian patients aged 4-18 (mean: 10.0) years with a psychiatric diagnosis were included. BMI z-scores in 96 youth treated with SGAs for 9.0±6.1 months were significantly higher than in 496 patients without lifetime SGA use (0.81±1.1 vs. 0.05±1.2; p<0.0001). BMI z-score differences remained significant in all age groups <16 years old. In sub-analyses, results remained the same after eliminating patients on any co-medication (0.82±1.2 vs. 0.23±1.2; p<0.0001) and in patients with (0.75±1.2 vs. 0.17±1.1, p<0.0001) or without autism spectrum disorders (1.1±1.0 vs. -0.02±1.2, p<0.0001). Significantly more SGA-treated youth were obese (27.1% vs. 9.5%, odds ratio [OR]: 3.55, 95% confidence interval [CI]:2.07-6.08) or overweight (21.9% vs. 8.3%, OR: 3.11, 95%CI: 1.75-5.52). In 24 patients (92.3% antipsychotic-naïve) with 6.6 months follow-up, weight z-score increased significantly from -0.17±1.5 to 0.25±1.4 (p<0.0001) with 12.5% transitioning to overweight or obese status.

Conclusion: These data show robust and significant differences in sex- and age-adjusted body weight and weight status in young pediatric Caucasian samples with and without use of SGAs independent of Diagnostic and Statistical Manual of Mental Disorders, 4th edition, Text Revision (DSM-IV-TR) (American Psychiatric Association 2000 ) diagnosis and nonantipsychotic medications. Weight status and metabolic effects of SGAs require careful attention, especially in youth.


PMID: 22506734 [PubMed - in process]


2nd International Symposium on Vaccines

Congress autoi


Held at the 8th Annual Autoimmunity Congress, Granada, Spain

To view abstracts for the symposium click HERE.
Chairperson:  C. Dwoskin, USA
Chairperson:  C. Shaw, Canada

12:30-12:35    Introduction
C. Shaw, Canada
C. Dwoskin, USA

Speaker:  B.A. Golomb, CA, USA


Speaker:  C. Exley, UK

Speaker:  C. Shaw, Canada

Continue reading "2nd International Symposium on Vaccines" »

Dr. Ian Lipkin of Columbia - A Scientist on the Road to Damascus?

Ian LipkinBy Kent Heckenlively, Esq.

There is a most curious interview with Dr. Ian Lipkin in the April 2012 issue of Discover magazine entitled "In the Lab with the World's Greatest Virus Hunter".  I can't help but notice that Dr. Lipkin, director of the Center for Infection and Immunity at Columbia University's Mailman School of Public Health and the scientist who first identified West Nile Virus sounds more like a bio-med autism parent than a CDC spokesman who claims that while we don't know what causes autism, "we're sure it's not vaccines."

Many will no doubt remember it was Lipkin's study which  supposedly  disproved the work of Dr. Andrew Wakefield regarding the persistence of the vaccine strain of the measles in the gut of children with autism.  And it's certainly true that Lipkin has done little to counter that impression. 

However, a closer look at Lipkin's study reveals a more complicated picture.  Lipkin used the same lab as Wakefield and did identify the measles virus from one of the children with autism he studied. The patient selection criteria was significantly different than that used by Wakefield, and as I have written previously, Lipkin has recently used Wakefield's research in the footnotes to his recent article showing that different bacterial colonies are present in the guts of children with autism.  If Wakefield's research was so dishonest, why would Lipkin ever cite him?

Perhaps all this has set the stage for a conversion on the question of autism, similar to that of the apostle Paul, a former Christian hunter who after having a vision of Christ on the Road to Damascus, became one of the founders of the early Church.  For as much as Dr. Lipkin took the wrong road in regards to Dr. Wakefield's work, there has also been evidence of an exceptionally humane side to the man. 

When Dr. Mady Horning released her study showing that the neurotoxic effects of thimerosal in mice were dependent upon a certain genetic profile, the autism community worried that the long knives were out for her.  This could explain why only certain infants were harmed by the thimerosal in vaccines and not others.  Dr. Horning was sheltered by Dr. Ian Lipkin who made her his research partner, probably saving her academic career in the process.

Recently I've come across Lipkin in the controversy over the XMRV retrovirus and its possible link to both ME/chronic fatigue syndrome and autism.  When the situation with Dr. Judy Mikovits and the Whittemore-Peterson Institute fell apart, Dr. Lipkin had the power to determine whether the research would continue.  I am told by sources that Dr. Lipkin was actually threatened with legal action by various entities and he told them to take a hike.  Instead of succumbing to this pressure, he put Drs. Mikovits, Frank Ruscetti of the National Cancer Institute and discoverer of the first human retrovirus, as well as Jose Montoya of Stanford University, and others in charge of determining the possible link between XMRV (or a related human retrovirus) and these diseases.

Lipkin's willingness to remain agnostic on the question of XMRV (or other related human retroviruses) opens up some other possibilities into how a retrovirus could cause conditions like ME/chronic fatigue syndrome and autism.  A virus or other pathogen may cause collateral damage that is not simply due to the infection, but how the body responds to the pathogen. 

From the Discover magazine interview of April 2012:

Have we reached the point where we can link specific infections to specific psychiatric disorders?

No, the connection is much more complex.  When I worked with LCMV, it became clear that any sort of pertubation could damage the nervous system.  Nerves find their way to specific locations through signposts that are part of the immune system.  And if you increase immunological molecules of certain types, a nerve may jog this way as opposed to the way it's supposed to go.  It may not make a difference what the infectious agent is-bacterial, viral, or parasitic.

Continue reading "Dr. Ian Lipkin of Columbia - A Scientist on the Road to Damascus?" »

Age of Autism Science Summary: Conflicts of Interest in Vaccine Safety Research

Science post imageManaging Editor's Note: My apologies - it seems that the free downloads have been used up and so readers can not access the full study.
Click HERE for a pdf. Dr. DeLong invites you to contact her directly at ( for further information.

Abstract: Conflicts of interest (COIs) cloud vaccine safety research. Sponsors of research have competing interests that may impede the objective study of vaccine side effects. Vaccine manufacturers, health officials, and medical journals may have financial and bureaucratic reasons for not wanting to acknowledge the risks of vaccines. Conversely, some advocacy groups may have legislative and financial reasons to sponsor research that finds risks in vaccines. Using the vaccine-autism debate as an illustration, this article details the conflicts of interest each of these groups faces, outlines the current state of vaccine safety research, and suggests remedies to address COIs. Minimizing COIs in vaccine safety research could reduce research bias and restore greater trust in the vaccine program.

Dr. Gayle DeLong is an associate professor in the Economics and Finance Department of Baruch College.  Her research examines regulated industries such as banking and pharmaceuticals.

AofA Science Summary: Autism behaviors may be eased by gluten-free, casein-free diet: Penn State College of Medicine

Science post imageAutism behaviors may be eased by gluten-free, casein-free diet: Penn State College of Medicine

Posted on February 29, 2012 by Stone Hearth News

A gluten-free, casein-free diet may lead to improvements in behavior and physiological symptoms in some children diagnosed with an autism spectrum disorder (ASD), according to researchers at Penn State. The research is the first to use survey data from parents to document the effectiveness of a gluten-free, casein-free diet on children with ASD.

Research has shown that children with ASD commonly have GI [gastrointestinal] symptoms, said Christine Pennesi, medical student at Penn State College of Medicine. Notably, a greater proportion of our study population reported GI and allergy symptoms than what is seen in the general pediatric population. Some experts have suggested that gluten- and casein-derived peptides cause an immune response in children with ASD, and others have proposed that the peptides could trigger GI symptoms and behavioral problems.

The team  which included Laura Cousino Klein, associate professor of biobehavioral health and human development and family studies asked 387 parents or primary caregivers of children with ASD to complete a 90-item online survey about their childrens GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as their children’s degree of adherence to a gluten-free, casein-free diet. The teams results appeared online this month in the journal Nutritional Neuroscience.

Pennesi and Klein and their team found that a gluten-free, casein-free diet was more effective in improving ASD behaviors, physiological symptoms and social behaviors for those children with GI symptoms and with allergy symptoms compared to those without these symptoms. Specifically, parents noted improved GI symptoms in their children as well as increases in their children’s social behaviors, such as language production, eye contact, engagement, attention span, requesting behavior and social responsiveness, when they strictly followed a gluten-free, casein-free diet.

According to Klein, autism may be more than a neurological disease — it may involve the GI tract and the immune system.

There are strong connections between the immune system and the brain, which are mediated through multiple physiological symptoms,” Klein said. “A majority of the pain receptors in the body are located in the gut, so by adhering to a gluten-free, casein-free diet, you’re reducing inflammation and discomfort that may alter brain processing, making the body more receptive to ASD therapies.

The team found that parents who eliminated all gluten and casein from their children’s diets reported that a greater number of their childrens ASD behaviors, physiological symptoms and social behaviors improved after starting the diet compared to children whose parents did not eliminate all gluten and casein. The team also found that parents who implemented the diet for six months or less reported that the diet was less effective in reducing their childs ASD behaviors.

According to the researchers, some of the parents who filled out the surveys had eliminated only gluten or only casein from their children’s diets, but survey results suggested that parents who completely eliminated both gluten and casein from their childs diet reported the most benefit.

While more rigorous research is needed, our findings suggest that a gluten-free, casein-free diet might be beneficial for some children on the autism spectrum, Pennesi said. It is also possible that there are other proteins, such as soy, that are problematic for these children.

The reason Klein and Pennesi examined gluten and casein is because they are two of the most common diet offenders.

“Gluten and casein seem to be the most immunoreactive, Klein said. A childs skin and blood tests for gluten and casein allergies can be negative, but the child still can have a localized immune response in the gut that can lead to behavioral and psychological symptoms. When you add that in with autism you can get an exacerbation of effects.

Kleins advice to parents of children with ASD?

If parents are going to try a gluten-free, casein-free diet with their children, they really need to stick to it in order to receive the possible benefits, she said.

It might give parents an opportunity to talk with their physicians about starting a gluten-free, casein-free diet with their children with ASD.


GI Co-morbidities and Autism. A Microbial Association with Autism.

Science post imageMBio. 2012 Feb 14;3(1). pii: e00019-12. doi: 10.1128/mBio.00019-12. Print 2012.

A microbial association with autism.

Benach JL, Li E, McGovern MM.


Departments of Molecular Genetics and Microbiology, Medicine and Pediatrics, Stony Brook University, Stony Brook, New York, USA.


ABSTRACT Autism is a heterogeneous group of complex developmental disabilities that result from a number of possible etiologies. There are a well-known number of comorbidities associated with autism spectrum disorders (ASD), including, commonly, gastrointestinal (GI) pathology, which can include variable combinations of constipation, diarrhea, abdominal pain, gastroesophageal reflux, and vomiting. An American Academy of Pediatrics consensus panel has recommended that prospective studies be carried out to determine the prevalence of GI disorders in ASD and their pathophysiologic basis. In a recent article, Williams et al. [B. L. Williams, M. Hornig, T. Parekh, and W. I. Lipkin, mBio 3(1):e00261-11, 2012] have provided one such study of autism with GI comorbidities by presenting evidence of Sutterella species in ileal mucosal biopsy specimens from patients diagnosed with ASD but not in control children with GI symptoms, suggesting a specific role for Sutterella in ASD. Sutterella sequences represented ~1 to 7% of the total bacterial sequences, and this is a very large effect size on the ileal mucosal composition of the autism phenotype, rivaling or perhaps exceeding the effect size of the ileal Crohn's disease phenotype. This study opens a new field of investigation to study the etiology or consequences of GI comorbidities in ASD.

Free Article

Autism Diagnosis Age

Big headBy Anne Dachel

The latest discovery about autism is being covered everywhere in the news.  New research from the University of North Carolina, Chapel Hill, has found signs of brain development problems in babies as young as six months using MRI scans. Lead researcher Jason Wolff feels this is very significant because he believes 'there is a potential to intervene, to disrupt autism before it becomes entrenched.'  He described it as 'a whole brain phenomenon.' 

Of course this is only an early study and more needs to be done.  Naturally it doesn't tell us what causes the brains of autistic children to be different and we're cautioned that no one saying that doctors can diagnosis autism in a six month old. 

As far as the cause of autism is concerned, Wolff said it's due to 'a complex interaction between genes and a child's experiences with the world.'   It sounds like 'a child's experiences with the world' could be just about anything and Wolff didn't elaborate.

Reading the coverage this study is getting makes autism sound more like a curiosity than a devastating disorder plaguing a generation of children and one that mainstream medicine can't explain.  You'd never know that this once-rare disorder now strikes one percent of children and almost two percent of boys alone.  There's no sense of urgency in any of the stories on MRI's and autism. 

Sometimes it seems that no one is really interested in finding out anything significant about autism.  Experts are only obligated to come up with some new findings every few months to make it look like someone somewhere is doing something.  That's what's happening with this latest research.   If scientists can find evidence of autism in babies at six months, it would be proof that the parents who claim that their child suddenly regressed into autism following their 18 or 24 month vaccinations are wrong.  It was all just a big coincidence.  The signs of autism were really there much earlier.

Geraldine Dawson, chief science officer at Autism Speaks, was in USA Today trying to capitalize on the findings. 

She'd like to look for the signs of autism in babies in the womb.  Dawson wonders "if brain scans will spot differences in autistic brains even earlier than 6 months, and if the differences could even begin in the womb."

CBS NEWS published the piece, Study: Brain scans detect early signs of autism .  This story began by telling us, "No one is exactly sure what causes autism."  That settled, we hear, "There's also hope that with a better understanding of what causes autism, there may eventually be a more effective treatment or even prevention." 

If you listen to video, CBS News medical correspondent Dr. Jonathan LaPook is heard saying, "I've spoken to a lot of parents of kids who have autism and they are up against it, emotionally, financially.  There's often a sense of guilt.  Was it something I did after the child was born?  This study shows that changes start so early, they may have a sense of relief. "  

In the coverage from MSNBC, Geraldine Dawson was cited saying, "The goal is to be able to reduce the symptoms or even possibly prevent the syndrome from developing." 

ABC News quoted Dr. Nancy Minshew at the University of Pittsburgh who said, 'This adds to the evidence that autism develops on its own, so to speak, and not because parents did something or did not do something to cause autism.'

Continue reading "Autism Diagnosis Age" »

Autistic Children Have Different Guts

Stomach_acheManaging Editor's Note: We'd beg to differ on the autistic children also suffer from gastrointestinal disorders, but so far the connection, if any remains unclear but this is worth noting:

(Ivanhoe Newswire)-- An interesting observation has been made that many autistic children have a different kind of bacteria in their intestinal tract than non-autistic children do.

Brent Williams and colleagues at the Mailman School of Public Health at Columbia University found that bacteria belonging to the group Sutterella are one of the major populations of microorganisms living in the gut of some autistic children. Sutterella was not found in tissue samples from non-autistic children.

It is an enigma what the correlation is between the developmental disorder autism and the existence of Sutterella. Jorge Benach, Chairman of the Department of Microbiology at Stony Brook University and a reviewer of the report is quoted as saying, "Sutterella has been associated with gastrointestinal diseases below the diaphragm, and whether it's a pathogen or not is still not clear. It is not a very well-known bacterium."

Frequently, autistic children also suffer from gastrointestinal disorders, but so far the connection, if any remains unclear. Autism itself is still poorly understood.

"The relationship between different microorganisms and the host and the outcomes for disease and development is an exciting issue," Christine A. Biron, the Brintzenhoff Professor of Medical Science at Brown University and editor of the study was quoted as saying.

Continue reading "Autistic Children Have Different Guts" »

AofA Science Summary: The relationship between the increased frequency of serum antineuronal antibodies and the severity of autism in children

Science post imageEur J Paediatr Neurol. 2012 Jan 5. [Epub ahead of print]

The relationship between the increased frequency of serum antineuronal antibodies and the severity of autism in children.

Mostafa GA, Al-Ayadhi LY.


Autism Research and Treatment Center, AL-Amodi Autism Research Chair, Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia; Department of Pediatrics, Faculty of Medicine, Ain Shams University, Cairo, Egypt.



Autism may involve an autoimmune pathogenesis. Immunotherapy may have a role in autistic children who have brain auto-antibodies.


This study aimed to investigate the frequency of serum antineuronal auto-antibodies, as indicators of the presence of autoimmunity to brain, in a group of autistic children. We are the first to measure the relationship between these antibodies and the degree of the severity of autism.


Serum antineuronal antibodies were measured, by indirect immunofluorescence technique, in 80 autistic children, aged between 6 and 12 years, in comparison to 80 healthy-matched children. The severity of autism was assessed by using the Childhood Autism Rating Scale.


Autistic children had significantly higher percent positivity of serum antineuronal antibodies (62.5%) than healthy controls (5%), P<0.001. The frequency of the positivity of serum antineuronal antibodies was significantly higher in children with severe autism (87.5%) than children with mild to moderate autism (25%), P<0.001. Similarly, the frequency of the positivity of these antibodies was significantly higher in female children with autism (90%) than male autistic children (53.3%), P=0.001.


Serum antineuronal antibodies were found in a subgroup of autistic children and they were significantly correlated to the severity of autism. Thus, autism may be, in part, one of the pediatric autoimmune neuropsychiatric disorders. Further wide-scale studies are warranted to shed light on the etiopathogenic role of antineuronal antibodies in autism. The role of immunotherapy in autistic patients, who are seropositive for antineuronal antibodies, should also be studied.

Copyright © 2011 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.




[PubMed - as supplied by publisher]

AofA Science Summary: Autism spectrum disorders and autisticlike traits: similar etiology in the extreme end and the normal variation.

Science post imageArch Gen Psychiatry. 2012 Jan;69(1):46-52.

Autism spectrum disorders and autisticlike traits: similar etiology in the extreme end and the normal variation.

Lundström SChang ZRåstam MGillberg CLarsson HAnckarsäter HLichtenstein P.


Department of Clinical Sciences, Lund University, Lillhagsparken 3, 422 50 Hisings Backa, Sweden.



Autism spectrum disorders (ASDs) have been suggested to represent the extreme end of a normal distribution of autisticlike traits (ALTs). However, the evidence of this notion is inconclusive.


To study whether there are similar genetic and/or environmental etiologies behind ASDs and ALTs.


A nationwide twin study.


Consenting parents of all Swedish twins aged 9 and 12 years, born between July 1, 1992, and December 31, 2001 (n = 19 208), were interviewed by telephone to screen for child psychiatric conditions, including ASDs.


Two validated cutoffs for ASDs, 2 cutoffs encompassing the normal variation, and 1 continuous measure of ALTs were used with DeFries-Fulker extreme-end analyses and standard twin study methods.


We discerned a strong correlation between the 4 cutoffs and the full variation of ALTs. The correlation was primarily affected by genes. We also found that the heritability for the 4 cutoffs was similar.


We demonstrate an etiological similarity between ASDs and ALTs in the normal variation and, with results from previous studies, our data suggest that ASDs and ALTs are etiologically linked.

AofA Science Summary: Study Shows Educated Mothers More Likely to Forego Birth Dose Hep B Vaccination

Science post imagePediatric Infectious Disease Journal:

January 2012 - Volume 31 - Issue 1 - p 1–4

doi: 10.1097/INF.0b013e3182345995

Original Studies

Maternal Characteristics and Hospital Policies as Risk Factors for Nonreceipt of Hepatitis B Vaccine in the Newborn Nursery

O'Leary, Sean T. MD, MPH*,†,‡; Nelson, Christina MD, MPH; Duran, Julie MPH‡,§

Supplemental Author Material

Background: A birth dose of hepatitis B vaccine (HBV) is a primary focus of the Advisory Committee on Immunization Practices' strategy to eliminate transmission of hepatitis B virus in the United States. We sought to assess the impact of maternal characteristics and hospital policy on the receipt of a birth dose of HBV.

Methods: A retrospective cohort study was performed using data from the 2008 Colorado birth registry. Hospital policy was assessed by state health department personnel. Univariate and multivariate logistic regression analyses were used to examine the association of maternal characteristics and hospital policy with nonreceipt of HBV.

Results: A total of 64,425 infants were identified in the birth cohort, of whom 61.6% received a birth dose of HBV. Higher maternal education and income were associated with nonreceipt of HBV (master's degree vs. eighth grade or less: adjusted odds ratio [OR] = 1.66, 95% confidence interval [CI] = 1.49–1.85; >$75,000 vs. <$15,000: adjusted OR = 1.21, 95% CI = 1.13–1.30). Lack of a hospital policy stipulating a universal birth dose strongly predicted nonreceipt of a birth dose of HBV (policy with no birth dose vs. policy with a birth dose: adjusted OR = 2.21, 95% CI = 2.13–2.30).

Conclusions: Maternal characteristics such as higher education and income are associated with nonreceipt of the HBV during the perinatal period. To effectively reduce risk of perinatal hepatitis B transmission, hospitals should stipulate that all infants are offered HBV and ensure that these policies are implemented and followed.

AofA Science Summary: possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism

Science post imageJ Neuroinflammation. 2011 Dec 21;8(1):180. [Epub ahead of print]

The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism.

Mostafa GAAl-Ayadhi LY.




Neurogenic inflammation is orchestrated by a large number of neuropeptides. Tachykinins (substance P, neurokinin A and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases. Autoimmunity may have a role in the pathogenesis of autism in some patients. We are the first to measure serum neurokinin A levels in autistic children. The relationship between serum levels of neurokinin A and anti-ribosomal P protein antibodies was also studied.


Serum neurokinin A and anti-ribosomal P protein antibodies were measured in 70 autistic children in comparison to 48 healthy-matched children.


Autistic children had significantly higher serum neurokinin A levels than healthy controls (P < 0.001). Children with severe autism had significantly higher serum neurokinin A levels than patients with mild to moderate autism (P < 0.001). Increased serum levels of neurokinin A and anti-ribosomal P protein antibodies were found in 57.1% and 44.3%, respectively of autistic children. There was significant positive correlations between serum levels of neurokinin A and anti-ribosomal P protein antibodies (P = 0.004).


Serum neurokinin A levels were elevated in some autistic children and they were significantly correlated to the severity of autism and to serum levels of anti-ribosomal P protein antibodies. However, this is an initial report that warrants further research to determine the pathogenic role of neurokinin A and its possible link to autoimmunity in autism. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, should also be studied in autism.

AofA Science Summary: Benefits to the Lived Experiences of Female Primary Caregivers of Children with Autism

CrockClin Nurse Spec. 2012 Jan;26(1):48-56.

Seeing the glass half full: benefits to the lived experiences of female primary caregivers of children with autism.

Markoulakis RFletcher PBryden P.


Author Affiliations: PhD student (Ms Markoulakis), Graduate Department of Rehabilitation Science, University of Toronto; Professors (Drs Fletcher and Bryden), Department of Kinesiology and Physical Education, Wilfrid Laurier University, Waterloo, Ontario, Canada.

Abstract PURPOSE:

: Autism spectrum disorders are the most common developmental disorders, affecting 1 in 165 Canadian children. Although the experiences of the caregivers of children with autism have been examined to some extent, a thorough investigation of the benefits of this experience is warranted.


: The lived experiences of 8 married female primary caregivers of children with autism were assessed through a phenomenological study involving background questionnaires and one-on-one, semistructured interviews. All recruited participants completed the study.


: Benefits were found in all areas of questioning, including financial, social, familial, health, and employment implications, in addition to benefits arising from activities and involvements taken on as a result of raising a child with autism. The findings shed light on an unconventional aspect of the effects of raising a child with autism.


: Costs to these women's experiences were not predominant, and benefits arising from the caregiving role lead to positive accounts of their lived experiences. Results have broader implications for the understanding of the primary caregiver situation and the improvement of interactions with individuals with these lived experiences. In this way, clinical nurse specialists may encourage and contribute to support systems that foster a positive experience for caregivers of children with autism spectrum disorder, the children they care for, and their families.

The War on Science – The British Medical Journal & Dr. Wakefield

BMJ GibberishBy Ed Arranga

In January 2011, the British Medical Journal (BMJ) published a blistering 3-part series (here, here, here) and an editorial (here) accusing Dr. Wakefield of committing fraud in his study of bowel disease. 

The tone is harsh, the articles lengthy and involved, the findings absolute, and the judgment final. Dr. Wakefield is a fraud. To top it off, it’s published in the British Medical Journal – one of the UK’s most prestigious journals. There’s only one problem. It’s a manufactured piece of gibberish with no basis in fact.

Dr. Wakefield is being attacked in an attempt to suppress science – specifically his Lancet study (here) that was published in 1998. Wakefield found bowel disease in children with autism spectrum disorder and raised questions about the safety of the MMR (measles, mumps, and rubella) vaccine. The study is valid and scientifically sound.

The British Medical Journal’s campaign to discredit Dr. Wakefield may be the greatest suppression of science episode ever attempted. It is estimated that over 150 million Americans were duped into believing the claims made against him.

The attacks on Dr. Wakefield are a crude reminder that there has always been conflict between those who serve science and those who want to censor it. Science advances at a cost, and the British Medical Journal has shown they are willing to pay any price – to sacrifice science itself – in order to declare victory on the battlefield of autism and vaccines.

Dr. Wakefield is a man of honor, principle, and integrity. He came to the US in 2004, as many scientists do, to continue his research without fear of reprisals. Seven years after leaving the UK – and 13 after his Lancet study – the British Medical Journal pursued Wakefield across the Atlantic in a campaign to silence him once and for all. Science be damned.

The British Medical Journal misjudged Dr. Wakefield’s commitment to science and picked a fight with the wrong guy.

Why Pick a Fight Based on a Lie?

Culture is a tricky thing. Did the British Medical Journal think it would just blow into town and tell a lie so big no one would notice? Did the editors seriously believe the same type of tabloid journalism that is standard practice in the UK would find a welcome home in the US? 

Obviously they did. The allegations, the character assassination, the sensational overblown trumpeting of “Wakefield the fraud,” and the claim of unbiased investigative journalism had, after all, been spoon fed to the British, with nary a hitch. The British public had been duped. Why not the Americans?

To any student of Anglo-American history, this was a risky venture. Americans are fiercely independent – the British not so much. We don’t take kindly to other nations targeting Americans. Europe, on the other hand, is a swirling pot of nations, used to shooting at each other for centuries.

The greatest difference between the US and UK lies in how Americans fight to protect their freedoms. It’s a strange and somewhat dangerous concept to outsiders looking in. But it’s a value that shapes our thoughts and actions from cradle to grave.

We take our freedoms seriously, particularly the freedom of speech. The BMJ’s campaign to silence Wakefield flies in the face of what this country holds most dear.   

The British

Continue reading "The War on Science – The British Medical Journal & Dr. Wakefield" »

Age of Autism Science Summary: Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?

Science post imageJ Inorg Biochem. 2011 Nov;105(11):1489-99. Epub 2011 Aug 23.

Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?


Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, University of British Columbia, 828 W. 10th Ave, Vancouver, BC, Canada V5Z 1L8.


Autism spectrum disorders (ASD) are serious multisystem developmental disorders and an urgent global public health concern. Dysfunctional immunity and impaired brain function are core deficits in ASD. Aluminum (Al), the most commonly used vaccine adjuvant, is a demonstrated neurotoxin and a strong immune stimulator. Hence, adjuvant Al has the potential to induce neuroimmune disorders. When assessing adjuvant toxicity in children, two key points ought to be considered: (i) children should not be viewed as "small adults" as their unique physiology makes them much more vulnerable to toxic insults; and (ii) if exposure to Al from only few vaccines can lead to cognitive impairment and autoimmunity in adults, is it unreasonable to question whether the current pediatric schedules, often containing 18 Al adjuvanted vaccines, are safe for children? By applying Hill's criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r=0.92, p<0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3-4months of age (Pearson r=0.89-0.94, p=0.0018-0.0248). The application of the Hill's criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal. Because children represent a fraction of the population most at risk for complications following exposure to Al, a more rigorous evaluation of Al adjuvant safety seems warranted.

Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.

AofA Science Summary: Inhibition of influenza infection by glutathione.

Science post image Free Radic Biol Med. 2003 Apr 1;34(7):928-36.

Inhibition of influenza infection by glutathione.

Cai JChen YSeth SFurukawa SCompans RWJones DP.


Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.


Infection by RNA virus induces oxidative stress in host cells. Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. In this study, experiments were performed to determine whether the thiol antioxidant glutathione (GSH) blocked influenza viral infection in cultures of Madin-Darby canine kidney cells or human small airway epithelial cells. Protection against production of active virus particles was observed at a low (0.05-0.1) multiplicity of infection (MOI). GSH inhibited expression of viral matrix protein and inhibited virally induced caspase activation and Fas upregulation. In BALB/c mice, inclusion of GSH in the drinking water decreased viral titer in both lung and trachea homogenates 4 d after intranasal inoculation with a mouse-adapted influenza strain A/X-31. Together, the data suggest that the thiol antioxidant GSH has an anti-influenza activity in vitro and in vivo. Oxidative stress or other conditions that deplete GSH in the epithelium of the oral, nasal, and upper airway may, therefore, enhance susceptibility to influenza infection.


AofA Science Summary: Redox regulation of the influenza hemagglutinin maturation process: a new cell-mediated strategy for anti-influenzatherapy.

Science post imageAntioxid Redox Signal. 2011 Aug 1;15(3):593-606. Epub 2011 May 19.

Redox regulation of the influenza hemagglutinin maturation process: a new cell-mediated strategy for anti-influenzatherapy.

Sgarbanti RNencioni LAmatore DColuccio PFraternale ASale PMammola CLCarpino GGaudio EMagnani MCiriolo MRGaraci EPalamara AT.


San Raffaele Pisana Scientific Institute for Research, Hospitalization, and Health Care, Rome, Italy.

Abstract AIM:

The aim of this study was to determine whether GSH-C4, a hydrophobic glutathione derivative, affects in vitro and in vivo influenza virus infection by interfering with redox-sensitive intracellular pathways involved in the maturation of viral hemagglutinin (HA).


GSH-C4 strongly inhibited influenza A virus replication in cultured cells and in lethally infected mice, where it also reduced lung damage and mortality. In cell-culture studies, GSH-C4 arrested viral HA folding; the disulfide-rich glycoprotein remained in the endoplasmic reticulum as a reduced monomer instead of undergoing oligomerization and cell plasma-membrane insertion. HA maturation depends on the host-cell oxidoreductase, protein disulfide isomerase (PDI), whose activity in infected cells is probably facilitated by virus-induced glutathione depletion. By correcting this deficit, GSH-C4 increased levels of reduced PDI and inhibited essential disulfide bond formation in HA. Host-cell glycoprotein expression in uninfected cells was unaffected by glutathione, which thus appears to act exclusively on glutathione-depleted cells.


All currently approved anti-influenza drugs target essential viral structures, and their efficacy is limited by toxicity and by the almost inevitable selection of drug-resistant viral mutants. GSH-C4 inhibits influenza virus replication by modulating redox-sensitive pathways in infected cells, without producing toxicity in uninfected cells or animals. Novel anti-influenza drugs that target intracellular pathways essential for viral replication ("cell-based approach") offer two important potential advantages: they are more difficult for the virus to adapt to and their efficacy should not be dependent on virus type, strain, or antigenic properties.


Redox-sensitive host-cell pathways exploited for viral replication are promising targets for effective anti-influenza strategies.


Autism and PANDAS

AUTISM PANDAS  teresa conrick- graphic adriana gamondes
By Teresa Conrick

My daughter, Megan's recent diagnosis of an autoimmune condition coupled with an abnormal EEG are big, red flags that help illustrate why she is so ill.  Finding that out hardly ends my journey for more answers to help improve her health and her life.  The disturbing behaviors and symptoms of vocal tics, dilated pupils, agitation, enuresis, and OCD are a barometer of brain dysfunction.  Add in estrogen-induced seizures that developed at age seventeen in tandem to her autoimmune diagnosis and that may be another clue.  As a result, I have been exploring more of the issues that connect her to those children who have a P.A.N.D.A.S. (Pediatric Autoimmune Neuropsychiatric Diagnosis Associated with Streptococcal Infections) diagnosis as Megan has had numerous bouts of Strep and other infections that exploded into severe movement and vocal tics over the years.  Her original regression into an autism diagnosis slowly happened after vaccinations along with increasing viral and bacterial infections as a toddler, then an acute rash, fever and loss of language after her MMR vaccine.  We now seem to be in the land of chronic waxing and waning of symptoms and the most sobering part --- we are not alone.

More parents are finding each other and connecting via their child's medical issues.  Autism and P.A.N.D.A.S. may be cousins of a similar origin as there is overlap in symptoms, both behavioral and medical.  A good place to learn more about P.A.N.D.A.S. is this informative site.  A warrior mother in the P.A.N.D.A.S. trenches, Diana Pohlman, developed it in 2009 as she decided to bring parents, research and researchers together to investigate why their children were becoming acutely affected by a monster that Streptococcus bacteria seemed to awaken.  Like so many of us, she saw her son regress into an immune illness that severely affected his mood, behaviors, functioning -- his life.  More and more children each year seem to be developing tics, severe anxiety, obsessive compulsions, involuntary movements and psychiatric issues, not randomly, but due to an infection affecting the brain.  It is usually Streptococcus, an evil little bacteria that these mothers despise, because it is stealing their children.  So Autism parents and P.A.N.D.A.S.parents are beginning to link arms to tackle both cause and cure. As it states on Diana's website above, "Parents Helping Parents," is a key for many families to compare medical issues and treatments.

P.A.N.D.A.S. is a medical diagnosis yet many still do not understand it thus, there is confusion on its causation, how to diagnose it and then appropriate treatments.  We in the trenches of Autism are familiar with these issues as we have been dealing with them for too many years.  Our toddler or child becomes ill, either through an infection or after vaccination and there is a regression in skills. Odd, perseverative and debilitating behaviors creep in.  Life forever changes.  Doctors dismiss the cause and labels are given.  Precious time is lost then more medical symptoms, more labels. A stinging reality -- lack of proper medical treatments cause worsening behaviors.  This continues to happen at an alarming rate.

Some significant research continues to evolve with P.A.N.D.A.S., and the names Cunningham, Swedo and Murphy are becoming instrumental in connecting the hated bacteria to the hosts they have kidnapped.  Another interesting development was the apparent acknowledgement from Dr. Tom Insel that P.A.N.D.A.S. was indeed a real, medical illness. For those who do not know him, Dr. Insel is Director of the National Institute of Mental Health (NIMH), the component of the National Institutes of Health "charged with generating the knowledge needed to understand, treat, and prevent mental disorders", per the website,  including Autism and now also, P.A.N.D.A.S.

Here is a portion of what he reported a year ago:

Continue reading "Autism and PANDAS " »

"Expression of Concern" on Arrest and Incarceration of Dr. Judy Mikovits

150px-Judy_mikovits_croppedThe editors and writers of Age of Autism express their concern over media reports of the arrest and jailing of Dr. Judy Mikovits on Friday, November 18, 2011 in Ventura, California.

According to Science magazine writer Jon Cohen in an article entitled "Controversial CFS Researcher Arrested and Jailed", Dr. Mikovits was arrested on "felony charges that she is a fugitive from justice." 

Dr. Mikovits was the research director at the Whittemore Peterson Institute for Neuro-Immune Diseases in Reno, Nevada until she was fired on September 29, 2011.  Upon being fired she returned to her home in southern California where her husband was staying.  On November 4, the WPI filed suit against Dr. Mikovits, claiming she had kept lab notebooks and other information in her laptop, flash drives, and in her personal e-mail account.  A preliminary injunction on this matter was to be held in Nevada's Second District Judicial Court on November 22, 2011.

Lois Hart, an attorney for Dr. Mikovits denies that her client has any notebooks or other proprietary items.  Age of Autism must note the unusual circumstances which would cause the WPI to arrest Dr. Mikovits when a hearing on the preliminary injunction had already been set.  After her arrest on Friday, November 18, Dr. Mikovits was not allowed to post bail and has spent the weekend in jail.  A hearing for Dr. Mikovits in Ventura, California will take place on Tuesday, November 22 at the Ventura County Government Center, Hall of Justice, Room 13 at 1:30.  She remains in jail at the time of this writing.

The hearing in California will prevent Dr. Mikovits from attending the hearing in Nevada.

Continue reading ""Expression of Concern" on Arrest and Incarceration of Dr. Judy Mikovits" »

AofA Science Summary: Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice

Science post imageDev Neurobiol. 2011 Nov 10. doi: 10.1002/dneu.21000. [Epub ahead of print]

Glutamate carboxypeptidase II and folate deficiencies result in reciprocal protection against cognitive and social deficits in mice: Implications for neurodevelopmental disorders.

Schaevitz LPicker JRana JKolodny NShane BBerger-Sweeney JCoyle J.


Department of Biology, Tufts University, Medford, MA 02155.


Interactions between genetic and environmental risk factors underlie a number of neuropsychiatric disorders, including schizophrenia (SZ) and autism (AD). Due to the complexity and multitude of the genetic and environmental factors attributed to these disorders, recent research strategies focus on elucidating the common molecular pathways through which these multiple risk factors may function. In this study, we examine the combined effects of a haplo-insufficiency of glutamate carboxypeptidase II (GCPII) and dietary folic acid deficiency. In addition to serving as a neuropeptidase, GCPII catalyzes the absorption of folate. GCPII and folate depletion interact within the one-carbon metabolic pathway and/or of modulate the glutamatergic system. Four groups of mice were tested: wildtype, GCPII hypomorphs, and wildtypes and GCPII hypomorphs both fed a folate deficient diet. Due to sex differences in the prevalence of SZ and AD, both male and female mice were assessed on a number of behavioral tasks including locomotor activity, rotorod, social interaction, pre-pulse inhibition, and spatial memory. Wildtype mice of both sexes fed a folic acid deficient diet showed motor coordination impairments and cognitive deficits, while social interactions were decreased only in males. GCPII mutant mice of both sexes also exhibited reduced social propensities. In contrast, all folate-depleted GCPII hypomorphs performed similarly to untreated wildtype mice, suggesting that reduced GCPII expression and folate deficiency are mutually protective. Analyses of folate and neurometabolite levels associated with glutamatergic function suggest several potential mechanisms through which GCPII and folate may be interacting to create this protective effect. © 2011 Wiley Periodicals, Inc. Develop Neurobiol, 2011.

Copyright © 2011 Wiley Periodicals, Inc.

Odds Are It's Wrong: Science News on Statistics and Medical Care

StatsManaging Editor's Note: Thank you to Jean B. for sending me this article from Science News.

For better or for worse, science has long been married to mathematics. Generally it has been for the better. Especially since the days of Galileo and Newton, math has nurtured science. Rigorous mathematical methods have secured science’s fidelity to fact and conferred a timeless reliability to its findings.

During the past century, though, a mutant form of math has deflected science’s heart from the modes of calculation that had long served so faithfully. Science was seduced by statistics, the math rooted in the same principles that guarantee profits for Las Vegas casinos. Supposedly, the proper use of statistics makes relying on scientific results a safe bet. But in practice, widespread misuse of statistical methods makes science more like a crapshoot.

It’s science’s dirtiest secret: The “scientific method” of testing hypotheses by statistical analysis stands on a flimsy foundation. Statistical tests are supposed to guide scientists in judging whether an experimental result reflects some real effect or is merely a random fluke, but the standard methods mix mutually inconsistent philosophies and offer no meaningful basis for making such decisions. Even when performed correctly, statistical tests are widely misunderstood and frequently misinterpreted. As a result, countless conclusions in the scientific literature are erroneous, and tests of medical dangers or treatments are often contradictory and confusing.

Replicating a result helps establish its validity more securely, but the common tactic of combining numerous studies into one analysis, while sound in principle, is seldom conducted properly in practice.

Experts in the math of probability and statistics are well aware of these problems and have for decades expressed concern about them in major journals. Over the years, hundreds of published papers have warned that science’s love affair with statistics has spawned countless illegitimate findings. In fact, if you believe what you read in the scientific literature, you shouldn’t believe what you read in the scientific literature.

“There is increasing concern,” declared epidemiologist John Ioannidis in a highly cited 2005 paper in PLoS Medicine, “that in modern research, false findings may be the majority or even the vast majority of published research claims.”

Ioannidis claimed to prove that more than half of published findings are false, but his analysis came under fire for statistical shortcomings of its own. “It may be true, but he didn’t prove it,” says biostatistician Steven Goodman of the Johns Hopkins University School of Public Health. On the other hand, says Goodman, the basic message stands. “There are more false claims made in the medical literature than anybody appreciates,” he says. “There’s no question about that.”

Nobody contends that all of science is wrong, or that it hasn’t compiled an impressive array of truths about the natural world. Still, any single scientific study alone is quite likely to be incorrect, thanks largely to the fact that the standard statistical system for drawing conclusions is, in essence, illogical. “A lot of scientists don’t understand statistics,” says Goodman. “And they don’t understand statistics because the statistics don’t make sense.”

Continue reading "Odds Are It's Wrong: Science News on Statistics and Medical Care" »

Age of Autism Science Summary: Quantifying and modeling birth order effects in autism.

Science post imagePLoS One. 2011;6(10):e26418. Epub 2011 Oct 19.

Quantifying and modeling birth order effects in autism.

Turner T, Pihur V, Chakravarti A.


Center for Complex Disease Genomics, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.


Autism is a complex genetic disorder with multiple etiologies whose molecular genetic basis is not fully understood. Although a number of rare mutations and dosage abnormalities are specific to autism, these explain no more than 10% of all cases. The high heritability of autism and low recurrence risk suggests multifactorial inheritance from numerous loci but other factors also intervene to modulate risk. In this study, we examine the effect of birth rank on disease risk which is not expected for purely hereditary genetic models.We analyzed the data from three publicly available autism family collections in the USA for potential birth order effects and studied the statistical properties of three tests to show that adequate power to detect these effects exist. We detect statistically significant, yet varying, patterns of birth order effects across these collections. In multiplex families, we identify V-shaped effects where middle births are at high risk; in simplex families, we demonstrate linear effects where risk increases with each additional birth. Moreover, the birth order effect is gender-dependent in the simplex collection. It is currently unknown whether these patterns arise from ascertainment biases or biological factors. Nevertheless, further investigation of parental age-dependent risks yields patterns similar to those observed and could potentially explain part of the increased risk. A search for genes considering these patterns is likely to increase statistical power and uncover novel molecular etiologies.

PMCID: PMC3198479

Free PMC Article

XMRV (HGRV) is Not Dead - The Rituximab Story

Rituximab-rituxan-715856By Kent Heckenlively, Esq.

I think that we have not cared for people with ME (myalgic encephelomyelitis, otherwise known as chronic fatigue syndrome) to a great enough extent.  I think it is correct to say that we have not established proper health care services for these people, and I regret that." - Apology from the Norwegian Directorate of Health on publication of a study showing that the cancer drug rituximab is effective in the treatment of chronic fatigue syndrome/ME.

What was reason for this unprecedented apology from the public health authorities in Norway?

It was the publication of a study which showed that the drug rituximab improved the health of 10 of 15 patients (67%) with chronic fatigue syndrome/ME and that 2 of the 15 patients given the drug staged a complete recovery from their condition.  You can read about the study in Medscape.

Why is this important to the autism community?

It's important because chronic fatigue syndrome/ME and autism share many common clinical indicators, including immune disregulation, increased oxidative stress, heavy metal retention, co-infection by other pathogens, and mitichondrial insufficiency.  What is effective in treating chronic fatigue syndrome/ME may end up having some relevance to treatments for autism.  I have written before about my daughter with autism having tested positive for XMRV.  You can read my previous article for background on XMRV.

The researchers I have spoken with about XMRV and autism have told me their suspicion that the retrovirus likes to enter B cells which have the CD20 receptor.  They also suspect that it isn't the retrovirus itself which is doing the harm, but the toxins or auto-antibodies which are produced in response to the retrovirus.  Rituximab specifically targets those B cells which have the CD20 receptor.  It is a very targeted type of chemotherapy, although it is not without significant risks.

B cells are part of the immune system, but when they go haywire they may cause cancer, or diseases like rheumatoid arthritis.  Rituximab is approved for the treatment of rheumatoid arthritis and many types of lymphoma.

The question of why rituximab's depletion of B cells helps those with chronic fatigue syndrome/ME remains unexplained.  The researchers specifically noted they had searched for XMRV and not found evidence of its presence, but that touches on the greater issue of whether the currently validated test for XMRV is accurate.

Continue reading "XMRV (HGRV) is Not Dead - The Rituximab Story" »

Age of Autism Science Summary lteration of plasma glutamate and glutamine levels in children with high-functioning autism.

Science post imagePLoS One. 2011;6(10):e25340. Epub 2011 Oct 5.

Alteration of plasma glutamate and glutamine levels in children with high-functioning autism.

Shimmura C, Suda S, Tsuchiya KJ, Hashimoto K, Ohno K, Matsuzaki H, Iwata K, Matsumoto K, Wakuda T, Kameno Y, Suzuki K, Tsujii M, Nakamura K, Takei N, Mori N.


Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Japan.



It has recently been hypothesized that hyperglutamatergia in the brain is involved in the pathophysiology of autism. However, there is no conclusive evidence of the validity of this hypothesis. As peripheral glutamate/glutamine levels have been reported to be correlated with those of the central nervous system, the authors examined whether the levels of 25 amino acids, including glutamate and glutamine, in the platelet-poor plasma of drug-naïve, male children with high-functioning autism (HFA) would be altered compared with those of normal controls.


Plasma levels of 25 amino acids in male children (N = 23) with HFA and normally developed healthy male controls (N = 22) were determined using high-performance liquid chromatography. Multiple testing was allowed for in the analyses. Compared with the normal control group, the HFA group had higher levels of plasma glutamate and lower levels of plasma glutamine. No significant group difference was found in the remaining 23 amino acids. The effect size (Cohen's d) for glutamate and glutamine was large: 1.13 and 1.36, respectively. Using discriminant analysis with logistic regression, the two values of plasma glutamate and glutamine were shown to well-differentiate the HFA group from the control group; the rate of correct classification was 91%.


The present study suggests that plasma glutamate and glutamine levels can serve as a diagnostic tool for the early detection of autism, especially normal IQ autism. These findings indicate that glutamatergic abnormalities in the brain may be associated with the pathobiology of autism.

PMCID: PMC3187770

Free Article



[PubMed - in process]

Study on Facial Structure and Autism

Black and white faceManaging Editor's Note: New study looks at facial features and autism. Read more at

The origins of autism may be better understood by kids’ facial features, according to a new study published in the Oct. 14 issue of Molecular Autism.

One out of every 110 children has an autism spectrum disorder (ASD). People with an ASD may experience difficulties with communication, intelligence, behavior or social interaction, according to WebMD.

Children with autism have noticeable differences in facial characteristics than normally developing children, researchers noted.

"There is no clear answer about whether autism is caused by genetics or by environmental influences," study author Dr. Kristina Aldridge, assistant professor of anatomy at the University of Missouri School of Medicine, said in a written statement, CBS News reports."If we can identify when these facial changes occur, we could pinpoint when autism may begin to develop in a child."

Facial features in 64 boys with autism were compared with faces of 41 typically developing boys, all 8-12 years old, with a 3-D camera system. After mapping out 17 points on faces, the researchers discovered considerable differences between the two groups.

According to the study, the autistic children had wider eyes, and a "broader upper face," compared with typically developing children.

Age of Autism Science Source: Research proposes common link between autism, diabetes

Science post imageStudy implicates hyperinsulinemia in increased incidence of autism

HOUSTON -- (Oct. 19, 2011) -- A review of the genetic and biochemical abnormalities associated with autism reveals a possible link between the widely diagnosed neurological disorder and Type 2 diabetes, another medical disorder on the rise in recent decades.

"It appears that both Type 2 diabetes and autism have a common underlying mechanism -- impaired glucose tolerance and hyperinsulinemia," said Rice University biochemist Michael Stern, author of the opinion paper, which appears online in this month's issue of Frontiers in Cellular Endocrinology.

Hyperinsulinemia, often a precursor to insulin resistance, is a condition characterized by excess levels of insulin in the bloodstream. Insulin resistance is often associated with both obesity and Type 2 diabetes.

"It will be very easy for clinicians to test my hypothesis," said Stern, professor of biochemistry and cell biology at Rice. "They could do this by putting autistic children on low-carbohydrate diets that minimize insulin secretion and see if their symptoms improve."

Stern said the new finding also suggests that glucose tolerance in pregnant women may need to be addressed more seriously than it is now.

Stern said he first realized there could be a common link between Type 2 diabetes and autism a few years ago, but he assumed someone else had already thought of the idea.

Stern's lab, which is located at Rice's BioScience Research Collaborative, specializes in investigating the genetic interactions associated with genetic diseases like neurofibromatosis, a disorder in which patients are several times more likely to be afflicted with autism and autism spectrum disorders (ASD) like Asperger's syndrome.

Continue reading "Age of Autism Science Source: Research proposes common link between autism, diabetes" »

Dr. Bradstreet, Nagalase, and the Viral Issue in Autism

JeffBradstreetBy Kent Heckenlively, Esq.

Although my daughter is not a patient of Dr. Jeff Bradstreet I've always had an enormous amount of respect for the good doctor.  I'll usually go on his website once or twice a month to find out what has most recently attracted his interest.  Often it seems we're looking at similar questions; which either means great minds think alike, or we suffer from some of the same delusions. 

I was intrigued by his October 11, 2011 entry, "An Update on Viral Issue in Autism" since it dovetailed with some of my own recent investigations.

In the past months Dr. Bradstreet has become interested in nagalese, which he describes as an enzyme "produced by cancer cells and viruses."  He thinks it unlikely that children with autism have undiagnosed cancers, and thus suspicion falls on a viral etiology.  Dr. Bradstreet writes, "Viruses make the nagalese enzyme as part of their attachment proteins.  It serves to get the virus into the cell and also decreases the body's immune reaction to the virus-thereby increasing the odds of viral survival."

Further on Dr. Bradstreet writes, "It is reasonable and likely that the nature of the immune dysfunction and the frequently observed autoimmune problems in autism are mediated by persistent, unresolved viral infections."  He claims to have tested approximately 400 children with autism for the viral marker, nagalese, and found that nearly 80% have significantly elevated levels.  He hopes to publish soon on this study and believes this information "is one of the most important developments in the clinical treatment of children on the spectrum that I have experienced in the last 15 years."

Continue reading "Dr. Bradstreet, Nagalase, and the Viral Issue in Autism" »

Age of Autism Science Source: Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis?

Science post imageAutism Res. 2011 Aug 31. doi: 10.1002/aur.219. [Epub ahead of print]

Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis?

Hoshiko S, Grether JK, Windham GC, Smith D, Fessel K.


Environmental Health Investigations Branch, California Department of Public Health, Richmond, California.


Thyroid hormones substantially influence central nervous system development during gestation. We hypothesized that perturbations of early thyroid profiles may contribute to the development of autism spectrum disorders (ASD). Thyroid pathways could provide a mechanism by which environmental factors that affect the thyroid system may impact autism occurrence or phenotypic expression. We investigated whether thyroxine (T4) levels at birth are associated with subsequent ASD, using two existing California study groups in multivariate analysis. One study group included children born in the San Francisco Bay Area in 1994, with cases identified through the California Department of Developmental Services (DDS) and/or the Kaiser Permanente Medical Care Program of Northern California (244 cases, 266 controls); the other included children born in California in 1995, with cases identified through DDS (310 cases, 518 controls). Matched controls were selected from birth certificate records. This exploratory analysis suggested that infants with very low T4 (<3rd percentile) may have higher ASD risk, although results reached statistical significance only for the 1995 study group (1995: OR = 2.74 (95% CI 1.30-5.75; 1994: OR = 1.71 (95% CI 0.57-5.19). A variety of alternate analyses were conducted with available data, without further resolution of the difference between the two study groups. The results of our study indicate that further studies are warranted to investigate whether thyroid hormone perturbations play a role in the development of ASD by evaluating additional potential confounders and genotype or phenotype in larger studies. Autism Res 2011,4:xxx-xxx. © 2011 International Society for Autism Research, Wiley Periodicals, Inc.

Copyright © 2011, International Society for Autism Research, Wiley-Liss, Inc.



[PubMed - as supplied by publisher]

Age of Autism Science Summary: Perinatal and neonatal risk factors for autism: a comprehensive meta-analysis.

Science post imageManaging Editor's Note: We'll be posting science abstracts for your information.

Pediatrics. 2011 Aug;128(2):344-55. Epub 2011 Jul 11.

Perinatal and neonatal risk factors for autism: a comprehensive meta-analysis.

Gardener H, Spiegelman D, Buka SL.


Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.



The etiology of autism is unknown, although perinatal and neonatal exposures have been the focus of epidemiologic research for over 40 years.


To provide the first review and meta-analysis of the association between perinatal and neonatal factors and autism risk.


PubMed, Embase, and PsycInfo databases were searched for studies that examined the association between perinatal and neonatal factors and autism through March 2007. Forty studies were eligible for the meta-analysis. For each exposure, a summary effect estimate was calculated using a random-effects model. Heterogeneity in effect estimates across studies was examined, and, if found, a meta-regression was conducted to identify measured methodological factors that could explain between-study variability.


Over 60 perinatal and neonatal factors were examined. Factors associated with autism risk in the meta-analysis were abnormal presentation, umbilical-cord complications, fetal distress, birth injury or trauma, multiple birth, maternal hemorrhage, summer birth, low birth weight, small for gestational age, congenital malformation, low 5-minute Apgar score, feeding difficulties, meconium aspiration, neonatal anemia, ABO or Rh incompatibility, and hyperbilirubinemia. Factors not associated with autism risk included anesthesia, assisted vaginal delivery, postterm birth, high birth weight, and head circumference.


There is insufficient evidence to implicate any 1 perinatal or neonatal factor in autism etiology, although there is some evidence to suggest that exposure to a broad class of conditions reflecting general compromises to perinatal and neonatal health may increase the risk. Methodological variations were likely sources of heterogeneity of risk factor effects across studies.



[PubMed - indexed for MEDLINE]

The Wakefield Rehabilitation?

Lipkin3 By Kent Heckenlively, Esq.

No responsible historian quotes Unabomber Ted Kaczynski for a proper understanding of the Industrial Revolution and the struggles of a technological age.

So why is uber-scientist Dr. W. Ian Lipkin of Columbia University quoting with approval the work of Dr. Andrew Wakefield?  Isn't Wakefield supposed to the author of our common mass delusion that vaccines are linked to autism?

And wasn't it Dr. W. Ian Lipkin who wrote Lack of Association Between Measles Virus Vaccine and Enteropathy: A Case Control Study in September 2008 which was widely seen as the final "nail in the coffin" of the MMR vaccine/autism theory?  (Author's note - Lipkin's study also showed that the lab work of Dr. John O'Leary, relied upon by Dr. Wakefield, was accurate.  And little reported was the fact that the measles virus was detected in the gut tissue of 1 of the 25 children with autism and 1 control.  Perhaps the most serious critcism, and difference from the Wakefield study was that only 5 of the 25 children with autism had received their MMR shot prior to the start of gastrointestinal problems, according to parent reports.  The parents of all Wakefield's patients in the original Lancet study claimed that the development of GI symptoms came after the MMR shot.  That's why he was investigating the shots as a possible cause of the development of GI symptoms AND as a consequence, autism.)

Or to put it a little more clearly, even Dr. W. Ian Lipkin found 20% of the children whose parents claimed that the MMR shot preceeded the development of GI symptoms in their children with autism were positive for the measles virus in their gut.

Continue reading "The Wakefield Rehabilitation?" »

Time to Fix What's Broken at HHS: CAARC Calls for GAO Investigation into Autism Research


Statement from the Working Group of the Combating Autism Act Reauthorization Coalition (CAARC) on the Three Year Extension of the Combating Autism Act; As Autism Epidemic Rages On, CAARC Calls for Government Accountability Office (GAO) Investigation of Autism Spending

On Friday September 30, 2011, President Obama signed the Combating Autism Reauthorization Act of 2011 (CARA 2011) into law. The passage of CARA 2011 maintains valuable momentum, but the developments of the last week are not a time for celebration for the autism community. Five years after Congress first passed the Combating Autism Act of 2006, autism families have yet to see meaningful benefits in terms of prevention, treatment and scientific understanding despite hundreds of millions in spending. Meanwhile, as the autism epidemic rages on, federal bureaucrats evade responsibility, delay critical activities, continue to invest in an obsolete scientific orthodoxy and have even begun promoting the acceptance of autism as a “new normal.”

The lengthy process (CAARC was formed in June 2010) that produced CARA 2011 has led to an outcome that is consistent in many ways with CAARC’s long held and principled positions on autism legislation.

  • Despite the opposition of some advocacy groups to the very notion of “combating autism” the focus of CARA 2011 remains on research into the causes and underlying biology of autism.
  • Unlike the overly broad early proposals, current drafts of bills designed to improve on CARA 2011 and CAA 2006 now separate research from services.
  • Extending CARA 2011 now retains the strategic planning discipline and accountability set in place by CAA 2006.
  • Importantly, CARA 2011 is a three year extension rather than a full five year renewal, recognition of the need to fix what’s broken in the original bill.

The signing of CARA 2011 is an occasion to reinforce the urgent need to combat autism, a relatively new, epidemic disorder that disables children for life, devastates families and is on track to cost America trillions of dollars. In the congressional debates of recent weeks, some Republican senators have called into question the advisability of disease specific legislation. Indeed, as one Senator told us in 2006, “there are thousands of worthy groups in here every day.” He has a good point making single disease bills only rarely a good idea and single disease bills should be the exception rather than the rule.

Continue reading "Time to Fix What's Broken at HHS: CAARC Calls for GAO Investigation into Autism Research" »

Invitation to Participate in Biomedical Autism Treatment Study

JillRibbonHand Managing Editor's Note: Jill has contacted me about this study and we are sharing it with you.


I am a doctoral student under the direction of Professor Linda Reed in the Department of Psychology at Capella University.  I am conducting a research study, titled Autism Spectrum Disorder:  The Relationship Between Biomedical Treatment and Healthy Family Functioning, to determine whether or not biomedical treatment used in children diagnosed with Autism Spectrum Disorder can create a higher rate of healthy family living.  (See IRB here.) I invite you to participate in this study by placing a flyer advertising my study in your office.  You will in no way be endorsing my study or supporting my study.  I am inviting mothers with a child diagnosed with Autism Spectrum Disorder to participate in this study, which will involve answering 8 background questions and 62 questions regarding the FACES IV survey about their family.  FACES IV is an assessment scale that measures family adaptability, cohesion, communication and satisfaction.  These questions are available through the website Autismdeal.comAnswering these questions should take no more than 20 minutes. 

Parent participation in this study is voluntary, they can choose not to participate.  The results of this research study will be published, but the mother and child’s name will not be known in the survey and will not be used for any part of the research.  By agreeing to place a flyer in your school you are not in any way endorsing my study, but simply advertising a link to the study.  If you chose to hang this flyer in your school I will need a permission letter to give to my school showing that I have your permission.

This survey does not provide a direct benefit for you or the participants, but your participation will hopefully result in increased education of whether or not biomedical treatment affects the rate of healthy family functioning. 

If you have any questions concerning this research study or your participation in this study, please call me at 843-377-6837 or email me at or Dr. Linda Reed at 937-550-4269,


Jill Tschikof

If you have any questions about your rights as a research participant or any concerns about the research process, or if you’d like to discuss an unanticipated problem related to the research, please contact the Capella Human Research Protections Office at: 1-888-227-3552, extension 4716.  Your identity, questions, and concerns will be kept confidential. 

How Vaccines Might Cause Autism and Other Diseases

XMRV By Kent Heckenlively, Esq.

When my daughter's test results showed she was positive for the XMRV (xenotropic murine leukemia virus related virus) retrovirus my next step was to find a doctor who could tell me how to treat it.  Since the only other two human retroviruses currently identified are HTLV, found mostly in Asian countries and responsible for causing T-cell leukemia, and HIV, which causes AIDS, I figured I had to find an AIDS doctor.

I called the University of California, San Francisco Pediatric AIDS unit and talked to their media representative.  I figured in our first conversation I'd avoid flying my freak flag and simply tell him my daughter had been diagnosed with this newly identified retrovirus and that she had autism and seizures and I was concerned that the retrovirus might be at least partially responsible for her problems.

"Well, that explains why a vaccination might cause autism," he said, barely missing a breath.  He went onto tell me this question was something he often discussed with his friends.   The idea of an underlying retrovirus was the first time it made sense as to how a vaccination might cause autism.

He explained that if XMRV was similar to HIV then it probably hid out in the cells of the immune system and any stimulation of the immune system was likely to cause XMRV to replicate out of control.  (This had previously been discussed by some of the researchers working on XMRV, but I was still surprised to hear the media representative go right to that point.)  Apparently it is common knowledge among retrovirologists that immunizations can stimulate a retrovirus.  Even the most pro-vaccine physician will admit that vaccinations work by stimulating the immune system.

The media representative was very kind and said he'd try to find a doctor to talk to me.  Predictably, none of them wanted to talk to me, and I can't say I'm unsatisfied with that result.  The currently existing HIV medications don't hold much appeal to me as I worry about some of their side-effects, particularly on the mitochondria.

Continue reading "How Vaccines Might Cause Autism and Other Diseases" »

New IOM Report on Vaccine Adverse Effects Shows Alarming Lack of Good Science SafeMinds Notes: Parents Should Still be Concerned

IOM questions Washington DC.  The Institute of Medicine's Panel on Adverse Effects of Vaccines issued a report today on the evidence and causality of vaccine harms. Despite a glowing press release, the report does little to allay public concerns over adverse effects of vaccines and suggests that we urgently need more science on vaccine adverse effects.

The IOM report took two years to produce, mostly behind closed doors, and was paid for by the Department of Health and Human Services, the government agency which is also a defendant against the vaccine-injured in the government's vaccine court.

Due to a narrow set of objectives defined for the IOM by the government, the report only looked at a small set of published research studies linking just two vaccines to developmental disorders such as autism. Only four epidemiological studies were considered of sufficient quality to evaluate the MMR vaccine in relation to autism and no studies were deemed of sufficient quality for the DtaP vaccine and autism analysis. The committee did not attempt to evaluate six other vaccines for autism causation, the safety of the cumulative vaccine schedule and health outcomes like autism, or the safety of vaccine ingredients like mercury and aluminum in the context of chemical exposures from other sources like air pollution or consumer products.

The report considered 158 potential adverse outcomes from vaccines. Of these, 135 or 85% were found to have inadequate research to accept or reject a causal association. Of the 23 outcomes where the research was deemed adequate, 18 or 78% were found supportive of harm. Vaccines were cleared of safety concerns for just five of the outcomes considered. "These statistics are hardly reassuring to parents who are now asked to give their young children over 32 vaccinations," noted Sallie Bernard, President of SafeMinds.

The report found likely causality of immune dysfunction, seizures and encephalopathy from some vaccines. These conditions are often found in individuals with autism. "It is plausible that a subset of children became autistic because of these adverse events from their vaccines. There are many cases of autism compensated by the vaccine court after having one of these conditions," noted Lyn Redwood, RN, Director of SafeMinds. Details of a recent review are available HERE:    A SafeMinds review (HERE) of the epidemiological studies on MMR and thimerosal and autism is available:

That 85% of even a small subset of health outcomes has inadequate science speaks of the critical need for more research on vaccine safety. SafeMinds calls on Congress and the Administration to institute a rigorous science program on vaccine safety. This program would include the establishment of an independent Vaccine Safety Agency (similar to the National Transportation Safety Board), the launch of a study comparing health outcomes between vaccinated and unvaccinated children, the inclusion of vaccines as an exposure variable in the National Children's Study and mandatory reporting by physicians to the Vaccine Adverse Event Reporting System.

The Coalition for SafeMinds is a 501C-3 organization dedicated to restoring health and protecting future generations by eradicating the devastation of neurological disorders induced by mercury and man-made toxicants.


FDA to Investigate Vaccines for XMRV Retrovirus

Anti-virus By Kent Heckenlively, Esq.

As part of my continuing series of articles which I think should be subtitled, Official Documents which Scare the Living Daylights Out of Me! I offer this July 24, 2011 publication from the Food and Drug Adminstration.

The release is entitled Investigating Viruses in Cells Used to make Vaccines; and Evaluating the Potential Threat Posed by Transmission of Viruses to Humans.  XMRV is prominently featured as a virus about which they are concerned.  Please feel free to read the entire document at

For those of you who may be unfamiliar with the question of XMRV and autism, please allow me to give a brief recap.  The xenotropic murine leukemia virus related virus (XMRV) was discovered in 2006 by scientists working for the University of California at San Francisco and the Cleveland Clinic.  It is a human gamma retrovirus and there are many who say we should be referring to this family as XMRVs or HGRVs. 

The retrovirus was originally found in the tumors of men with an aggressive form of prostate cancer, in 2009 the virus was found in high numbers in people with chronic fatigue syndrome/ME, and there has been some very preliminary findings of its presence in children with autism.  In the interest of full disclosure I must note that my daughter with autism/seizures, my wife who has had a number of mysterious health ailments, and my mother-in-law have all tested positive for the XMRV retrovirus.  I've tested negative, as has my father, who is my only surviving parent.

Chronic fatigue syndrome/ME and autism  share many common clinical features including immune dysregulation, increased expression of pro-inflammatory cytokines and chemokines, mitochondrial abnormalities, and chronic active microbial infections.   In my own investigations I've been surprised how many of the mothers of children with autism say they have either been formally diagnosed with chronic fatigue syndrome/ME, or believe they have subclinical indications of the disorder. 

Onto the FDA release of July 24, 2011.  After first describing the need for new vaccines and that the virus-based vaccines require the use of living cells for a substrate, there's this paragraph. 

In some cases the cell lines that are used might be tumorigenic, that it, they form tumors when injected into rodents.  Some of these tumor-forming cell lines may contain cancer-causing (author's note - autism causing?) viruses that are not actively reproducing.  Such viruses are hard to detect using standard methods.  These latent or "quiet" viruses pose a potential threat, since they might become active under vaccine manufacturing conditions.  Therefore, to ensure the safety of vaccines, our laboratory is investigating ways to activate latent viruses in cell lines and to detect the activated viruses, as well as other unknown viruses, using new technologies.  We are also trying to identify specific biological processes that reflect virus activity.

Translation for the average reader - Hey, the cell lines in which we grow the viruses we want in vaccines, may contain some viruses we don't want!  Including those which may cause cancer!

Continue reading "FDA to Investigate Vaccines for XMRV Retrovirus" »

Part 3: Vaccines and Autism - What Do Epidemiological Studies Really Tell Us?


(Managing Editor's Note: Read Part 1and  Part 2. Also, this report is available in in full .pdf (Vaccines and Autism Epidemiology HERE)

“We have 16 studies already that clearly state that vaccines do not cause autism.”

-- Amy Pisani, Executive Director, Every Child By Two

“16 studies have shown no causal association between vaccines and autism, and these studies carry weight in the scientific industry.”

-- Dr. Nancy Snyderman, NBC Today Show Medical Editor

“The science is largely complete. Ten epidemiological studies have shown MMR vaccine doesn’t cause autism; six have shown thimerosal doesn’t cause autism.”

-- Dr. Paul Offit, “Autism’s False Prophets”



There are 16 epidemiological studies here on MMR vaccines, thimerosal and autism. These studies represent the most often cited papers by scientists, public health officials and members of the media when trying to refute any evidence of an association between vaccinations and autism.

There are serious methodological limitations, design flaws, conflicts of interest or other problems related to each of these 16 studies. These flaws have been pointed out by government officials, other researchers, medical review panels and even the authors of the studies themselves. Taken together, the limitations of these studies make it impossible to conclude that thimerosal and MMR vaccines are not associated with autism.

SafeMinds would like to acknowledge the previous work in this regard gathered by the “Fourteen Studies” project at Generation Rescue:

One additional study on autism and thimerosal was published in September 2010 while this paper was in completed draft form. This study’s methods produced a result that demonstrated that thimerosal exposure was protective against autism. Further analysis of this study is forthcoming but not included here.



There has only been one major scientific review of the main epidemiological studies to examine a potential association between thimerosal containing vaccines (TCVs) and autism spectrum disorders: The Institute of Medicine Immunization Safety Committee Report, issued in May, 2004.[37]

The IOM report focused almost exclusively on large, population-based epidemiological studies based on health records. The committee chose to minimize the importance of several biomedical thimerosal studies conducted in laboratories and animal models. Today, a much larger body of medical literature has been amassed which clearly demonstrates the powerful neurotoxic effects of thimerosal. These are joined by other studies demonstrating the increased risks of simultaneous administration of certain vaccines on the current childhood schedule.


The IOM committee reviewed epidemiological studies examining TCVs and autism, including three controlled observational studies (Hviid et al., 2003; Miller, 2004; Verstraeten et al., 2003) and two uncontrolled observational studies (Madsen et al., 2003; Stehr-Green et al., 2003). The published papers “consistently provided evidence of no association between TCVs and autism, despite the fact that these studies utilized different methods and examined different populations (in Sweden, Denmark, the United States, and the United Kingdom),” the committee wrote.


■ “Based on this body of evidence, the committee concludes that the evidence favors rejection of a causal relationship between thimerosal-containing vaccines and autism.”

■ “In the absence of experimental or human evidence that vaccination (either the MMR vaccine or the preservative thimerosal) affects metabolic, developmental, immune, or other physiological or molecular mechanisms that are causally related to the development of autism, the committee concludes that the hypotheses generated to date are theoretical only.”


■ Because the “vast majority” of ASD cases cannot be accurately sub-classified, “if there is a subset of individuals with autism syndrome triggered by exposure to vaccines, our ability to find it is very limited in the absence of a biological marker.”

■ In fact, the committee admitted, trying to find a cause of autism using population-based epidemiological analyses “requires either a well-defined at-risk population or a large effect in the general population.”

■ But without any known biomarkers, well-defined risk factors, or large effect sizes, “the committee cannot rule out, based on the epidemiological evidence, the possibility that vaccines contribute to autism in some small subset or very unusual circumstances.”

NOTE: Knowledge of biomarkers and risk factors in ASD has increased considerably since the release of the 2004 IOM report.


Mark D. Noble, PhD - Professor of Genetics and of Neurobiology and Anatomy, University of Rochester Medical Center [38]

It is easy to understand why people are not believing the scientific community. It reduces confidence in the scientific enterprise when it turns out that the CDC had information on early versions of the studies of Verstraeten et al. that demonstrated a linkage between thimerosal exposure and autism, that these studies were never published, and that no one has ever explained satisfactorily why different analyses were conducted and why they were changed. But all of these studies have equally debilitating flaws that invalidate any conclusions drawn from them on thimerosal safety. And if it turns out that that there is a subset of children for whom additives in vaccines are a problem, then this is important to know. For then we can focus on how to identify these children in advance. The conclusions I have drawn are that we are not going to solve this problem by ignoring it. So let’s embrace it. Let’s get the data.

Irva Hertz-Picciotto, PhD, MPH, Chief of the Division of Environmental and Occupational Health, University of California, Davis School of Medicine –[39]

Several large studies finding no association are far from robust, as they suffer from numerous biases that seriously limit their definitiveness. These include: noncomparable sources for ascertainment of cases, uncontrolled confounding, unrepresentative sample due to selective exclusions, and an as-yet unexplained pattern whereby children with earliest vaccines are the least likely to have developmental deficits. Thus, the body of evidence at this point is inadequate to draw conclusions… Several investigations have been ecologic studies, widely known to be the weakest possible epidemiologic design. Even restricting discussion to the individual-level designs, published studies conducted in Denmark, the UK, and the US are characterized by serious, even fatal, flaws. To regain the confidence that we in the medical/public health/scientific community need in order to fulfill our mandate to protect health, we cannot avoid facing these tough scientific questions head-on. This means funding solid scientific research into vaccines, thimerosal, and the related issues of susceptibility at the population level.

Richard Deth, PhD, Professor of Pharmacology, Northeastern University – [40]

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Farewell to an Honest Scientist and a Good Friend

Lonsdale Managing Editor's Note: Last week, I spoke at a conference in Cleveland. To my great pleasure, Dr. Derrick Lonsdale of Preventive Medicine Group, who was our first Defeat Autism Now! doctor, was also speaking. Dr. Lonsdale is 87 years old, vigorous, (Hugh Hefner should be so good looking) and still devoted to helping people with autism when mainstream medicine turns its back. He has pioneered the use of Vitamin B1 Thiamine for autism. If you've read All I Can Handle I'm No Mother Teresa, you know that our daugher Mia had a life threatening seizure disorder, written off by the doctors at University Hospitals as, "part of her autism." I willl never forget how I called Dr. Lonsdale in tears, sitting next to Mia's hospital bed, begging for help. When she was released, he brought her into his office for an IV infusion of liquid and nutrition to help get her back to health. He cared. He cares. Dr. Lonsdale is an expert in oxidative stress and its chain of sickness. Please visit his blog called The Spark of Life and tell him a very grateful Kim sent you. Below, Kent describes a doctor who tried to help his own daughter. And who recently died.

Has there been a doctor who has reached out to help you when mainstream medicine had nothing to suggest? Let us know in the comments. KS

By Kent Heckenlively, Esq. Kent doc

Dr. David W. Gregg died on July 6, 2011 at the age of seventy-six.  He was my friend and an honest scientist.

There's a Bible passage from Matthew which reads, "Let the little children come to me, and do not hinder them; for it is to those who are childlike that the Kingdom of the Heavens belongs."

If you knew David you know he faced the world with a child's innocence, curiousity, and sense of fair play.  I have rarely known a better man.

I met David sometime in 2003 when I ran across his web-site.  He was proposing a viral theory for autism and we spent a good deal of time trying to develop treatments for my daughter.  None of them worked.  But on a road filled with so many disappointments, it's also important to take the time to acknowledge the good people you meet on the journey.  Despite the failures, David never lost the optimism that one day an answer would be found.

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Holy Jumpin' Monkey Viruses!

Titi%20monkeys By Kent Heckenlively, Esq.

There's a story a fellow science teacher told me that I've always remembered.  This science teacher headed the Education Center at Lawrence-Livermore Labs and was present when Edward Teller, father of the hydrogen bomb, came to visit the National Ignition Facility, designed to create nuclear fusion, the energy of the Sun.

"What do you think you will learn?" the elderly scientist asked of the director in his thick Hungarian accent.

The chief scientist prattled on about all of the things they expected to discover on the road to nuclear fusion, but Teller was unimpressed.

The famous scientist shook his head and said, "No!  The answer is, you have no idea what you will learn!"

I like the story because it demonstrates a humility in the face of the things we don't understand.  It's not just that we know we don't know.  It's that we might not even know the right questions to ask.

I was reminded of Teller's story when I read an article, dated July 15, 2011 from Science Daily entitled, "First Adenovirus to Jump Between Monkeys and Humans Confirmed."  What?  Adenoviruses can jump from monkeys to humans?  We never knew that!  You can read the article  HERE.

Are you getting my point?

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Late Onset Autism and Anti-NMDA-Receptor Encephalitis: Part 1

Limbic By Teresa Conrick

My daughter, Megan, continues to be severely affected by both the medical and behavioral symptoms of autism. As a result, I continue to read studies and research that correlate with the symptoms that she has.  Some of the factors, if we were to list them like they do in a journal, would be -- seizures, autism, nmda/glutamate dysfunction, cancer signalling, encephalopathy, agitation.  Surprisingly, there was a current, case study just out that had many of these key words:

Late onset autism and anti-NMDA-receptor encephalitis    The Lancet, Vol 378. Issue 9785, Page 98, 2 July 2011

Caroline Creten, MD, Sanne van der Zwaan BSc, Roos J Blankenspoor BSc, Arien Maatkamp, PhD, Prof Jim van Os PhD, Dr Jan NM Schieveld PhD

In December, 2009, a 9-year-old boy was admitted to our hospital with an acute onset of secondary generalised seizures. He had no medical or psychiatric history and functioned very well socially and academically. He presented with speech and swallowing difficulties, which after 10 days developed into a severely agitated catatonic state with opisthotonic posturing, tonic posturing of limbs, insomnia, and dyskinesia. Initially the electroencephalogram showed a normal background pattern with epileptic discharges, and oligoclonal bands were present in cerebrospinal fluid (CSF). Brain MRI and extensive blood tests were normal. The neurological diagnosis was atypical childhood epilepsy with centrotemporal spikes, for which oral corticosteroids and anti-epileptic drugs were prescribed. His catatonia was treated with benzodiazepines. In January, 2010, our patient presented in a robotic state with complete mutism and negativism, and he did not respond to any form of contact. We provisionally diagnosed acute late onset autism with a differential diagnosis of childhood disintegrative disorder or early onset schizophrenia.

Childhood disintegrative disorder, early onset schizophrenia, and late onset autism often share a final common pathway: previous normal development, followed by sudden neuropsychiatric regression of social interaction and communication skills, and a decline in intelligence and daily activities. 1 The disorders are sometimes misrecognised and collectively called as autistic disorder. Although judged to be functional psychiatric diagnoses, the marked deterioration and poor prognosis suggest an organic cause, especially in children with catatonia, a normal development up to at least 5 years of age, or both1,2. In our patient, late onset autism was considered because: it is associated with neurological disorders; 2  it is a known end stage of acquired brain injury; progression of symptoms was fast and severe, unlike in early onset schizophrenia; the absence of positive symptoms made schizophrenia less plausible; the age of onset and rare prevalence made chronic disintegrative disorder unlikely; 1 and accompanying catatonic features were present. 3 After extensive diagnostic assessments, our patient was finally diagnosed with anti-NMDA-receptor encephalitis on the basis of slightly raised anti-NMDA-receptor antibody titres in serum and highly raised titres in CSF. 4 Clinical characteristics of this condition are acute major neuropsychiatric symptoms including anxiety, aggression, agitation, behavioural changes and catatonia, delusional thoughts, progressive speech deterioration, and hallucinations. Neurological symptoms such as dyskinesia, abnormal seizure-like movements, and diffuse and profound autonomic instability have also been reported.4.5 Anti-NMDA-receptor encephalitis can occur in the context of malignant disease; 4 however for our patient extensive oncological investigations were negative. Electroconvulsive therapy was given for the severe catatonic state, and monoclonal antibody treatment (rituximab) was started because of the unsatisfactory response to the initial treatment with benzodiazepines. The acquired autism gradually subsided, he spoke fluently and was able to draw a happy picture (figure). In June, 2011, he only had some mild cognitive dysfunction.

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Part 2: Vaccines and Autism - What Do Epidemiological Studies Really Tell Us?

(Managing Editor's Note: We ran Part 1 earlier this week. this report is available in in full .pdf (Vaccines and Autism Epidemiology HERE)

“We have 16 studies already that clearly state that vaccines do not cause autism.”

-- Amy Pisani, Executive Director, Every Child By Two

“16 studies have shown no causal association between vaccines and autism, and these studies carry weight in the scientific industry.”

-- Dr. Nancy Snyderman, NBC Today Show Medical Editor

“The science is largely complete. Ten epidemiological studies have shown MMR vaccine doesn’t cause autism; six have shown thimerosal doesn’t cause autism.”

-- Dr. Paul Offit, “Autism’s False Prophets”



There are 16 epidemiological studies here on MMR vaccines, thimerosal and autism. These studies represent the most often cited papers by scientists, public health officials and members of the media when trying to refute any evidence of an association between vaccinations and autism.

There are serious methodological limitations, design flaws, conflicts of interest or other problems related to each of these 16 studies. These flaws have been pointed out by government officials, other researchers, medical review panels and even the authors of the studies themselves. Taken together, the limitations of these studies make it impossible to conclude that thimerosal and MMR vaccines are not associated with autism.

SafeMinds would like to acknowledge the previous work in this regard gathered by the “Fourteen Studies” project at Generation Rescue:

One additional study on autism and thimerosal was published in September 2010 while this paper was in completed draft form. This study’s methods produced a result that demonstrated that thimerosal exposure was protective against autism. Further analysis of this study is forthcoming but not included here.



Major Reviews – There have been at least two major reviews of the main studies claiming to examine a potential association between MMR vaccine and autism spectrum disorders. They are the 2005 Cochrane Review and the 2004 Institute of Medicine Immunization Safety Committee Report.

1) The Cochrane Review: “Vaccines for measles, mumps and rubella in children.” October 2005.[1]

According to their sponsors, the Cochrane Reviews report on published (and sometimes unpublished) studies which investigate the effects of interventions for prevention, treatment and rehabilitation in a healthcare setting. Most Cochrane Reviews focus on randomized controlled trials, but other types of evidence may also be taken into account.  The reviews are considered by most experts to provide the gold standard of evidence-based medical science.

In 2005, Cochrane published a review of published studies on the safety and efficacy of MMR vaccine. Their search revealed more than 5,000 papers on the subject, though only 139 of them “possibly satisfied” the reviewers’ inclusion criteria. In the end, they reported on and summarized about 31 studies, only a few of which pertained to autism spectrum disorders (ASD).

Main results - MMR was “likely to be associated” with febrile convulsions within two weeks of vaccination, but “unlikely to be associated” with Crohn's disease, ulcerative colitis, mumps or autism.

General Limitations: the authors concluded that: 

■ There was a moderate-to-high probability of bias in all but one of the cohort studies.

■ The internal validity of some studies was problematic, and the presence of selection, performance, attrition, detection and reporting biases influenced the reviewers’ confidence in these findings. The most common type of bias was selection bias.  

■ There was only limited evidence of MMR’s safety compared to single component vaccines from studies with a low risk of bias. The few studies least likely to be affected by systematic error pointed to a likely association with increased febrile convulsions in the first two weeks post-vaccination.  

■ The cohort studies’ conclusions “that MMR is ‘safe,’ ‘equally safe,’ ‘well-tolerated,’ or has ‘low-reactogenicity,’ need to be interpreted with caution given the potential for confounding.

■ In the cohort studies, the validity of the conclusions was affected by selective reporting in the comparative analysis, with just over half the responses from participants in some cases.

■ There was a lack of clarity in reporting and systematic bias which made it “impossible” to compare the various studies through quantitative synthesis of data.

■ There were general difficulties in ascertaining adequate numbers of unexposed children due to the high uptake of vaccines and the extent of vaccination programs. This is a methodological problem likely to be encountered in all comparative studies of established childhood vaccines.   

■ There was a “lack of adequate description of exposures (vaccine content and schedules)” in all cohort studies.    

■ The failure of any study to provide descriptions of all outcomes was a recurring problem.  

■ Some reports offered inadequate explanations for missing data, accepting as ‘adequate’ explanations such as ‘nonresponse to questionnaire’ and ‘medical records unavailable’.

■ The external validity of the studies was low. Descriptions of the study populations, response rates, vaccine content and exposure - all important indicators of generalizability - “were poorly and inconsistently reported.”  

■ There were inadequate and inconsistent descriptions of reported outcomes, limited observation periods (maximum 42 days) and selective reporting of results. All of these problems contributed to the reviewers’ decision not to attempt pooling data by study design

SUMMARY – Although the reviewers determined that MMR vaccine was “unlikely to be associated” with autism, they concluded that “meaningful inferences from individual studies lacking a non-exposed control group are difficult to make.” They added that there were disappointed by their inability to identify effectiveness studies with population or clinical outcomes.

Many critics question how the authors of Cochrane’s MMR Review could find an “unlikely” association with autism when - in the very same paper - they also concluded that:

(a)   the design and reporting of safety outcomes in MMR vaccine studies, are largely inadequate and

(b)  that critical design and reporting flaws need to be improved and standardized definitions of adverse events adopted.

Sallie Bernard, of SafeMinds, wrote that the Cochrane Review “gives MMR a free pass.” She said the review “Assumes that this version of vaccine is as safe as can be, and so beneficial there is no need to worry about the fact that the safety studies are inadequate. Would this happen for any other drug?  Isn’t it possible, even probable, that the vaccine is effective but still has safety lapses and could be improved?”

In a review presented at the International Meeting for Autism Research (IMFAR) Carol Stott, a UK epidemiologist and Chartered Psychologist, wrote that, given the Cochrane Review’s conclusions, it is important to examine the extent to which the various clinical and population studies have been designed appropriately and with specific reference to the original hypothesis and, thus, to examine the extent to which claims of the hypothesis being refuted or supported are valid.

2) Institute of Medicine, “Immunization Safety Review: Vaccines and Autism.” May, 2004[2]

In February 2004, the IOM’s Immunization Safety Committee held a hearing on the possible association between MMR, thimerosal and autism. The committee reviewed all published and unpublished epidemiological studies on causality as well as potential biologic mechanisms to explain a possible vaccine-autism causal association. Its findings were released in a May, 2004 report. The committee’s conclusions hold wide sway over many scientists, physicians and much of the media to this day.

Main Results: The committee concluded that the body of epidemiological evidence “favor” rejection of a causal relationship between the MMR vaccine and autism,” further stating that studies examining the association between MMR and autism consistently showed evidence of no association between the MMR vaccine and autism.


■ Because the “vast majority” of ASD cases cannot be accurately sub-classified, if there is a subset of individuals with autism syndrome triggered by exposure to vaccines, our ability to find it is very limited in the absence of a biological marker.

■ Although there is no convincing evidence to date that a clearly defined subgroup with susceptibility to MMR-induced autism has been identified, genomics and proteomics could reveal in the future whether or not any genetic susceptibility to vaccine-induced autism exists.

■ A lack of unexposed children is another limitation. The committee noted that they had previously called for studies to enroll children whose families opted against the MMR vaccine, but so far, this type of study has been difficult to do with sufficiently large numbers.

■ The committee also noted that its 2001 report did not exclude the possibility that MMR “could contribute to autism in a small number of children because the epidemiological studies lacked sufficient precision to assess rare occurrences.”

■ They also noted that it was possible that epidemiological studies would not detect a relationship between autism and MMR vaccination in a subset of the population with a genetic predisposition to autism.

The latter two points are covered in the introduction to this document. While the points are well received, it is important to note that ‘epidemiological’ studies lack neither precision nor accuracy simply by virtue of them being ‘epidemiological’. It is entirely possible to design population based studies to maximize the likelihood of identifying small effect sizes; the fact that this hasn’t yet been achieved in the vaccine-autism debate is the fault of the workmen, not the tools. 

SUMMARY: The IOM Committee gave far more emphasis to epidemiological (population based) studies than biological studies, such as clinical studies in children, laboratory studies, and animal model studies. Since the IOM report was released in May, 2004, a large amount of biological data have been generated from several published studies to support an association between vaccines – including MMR - and ASD. A new IOM review that includes these studies is needed.


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