Pletz J, et al. Toxicology. 2016.
A latency period preceding neurotoxicity is a common characteristic in the dose-response relationship induced by organic mercury. Latency periods have typically been observed with genotoxicants in carcinogenesis, with cancer being manifested a long time after the initiating event. These observations indicate that even a very small dose may cause extensive adverse effects later in life, so the toxicity of the genotoxic compound is dose and time-dependent. In children, methylmercury exposure during pregnancy (in utero) has been associated with delays in reaching developmental milestones (e.g., age at first walking) and decreases in intelligence, increasing in severity with increasing exposure. Ethylmercury exposure from thimerosal in some vaccines has been associated, in some studies, with autism and other neurological disorders in children. In this paper, we have examined whether dose-response data from in vitro and in vivo organic mercury toxicity studies fit the Druckrey-Küpfmüller equation c·t(n)=constant (c=exposure concentration, t=latency period), first established for genotoxic carcinogens, and whether or not irreversible effects are enhanced by time of exposure (n≥ 1), or else toxic effects are dose-dependent while time has only minor influence on the adverse outcome (n<1). The mode of action underlying time-dependent toxicity is irreversible binding to critical receptors causing adverse and cumulative effects. The results indicate that the Druckrey-Küpfmüller equation describes well the dose-response characteristics of organic mercury induced neurotoxic effects. This amounts to a paradigm shift in chemical risk assessment of mercurial compounds and highlights that it is vital to perform toxicity testing geared to investigate time-dependent effects.
Copyright © 2016. Published by Elsevier Ireland Ltd.
26945727 [PubMed - as supplied by publisher]
Nathaniel W. Hodgson,
Malav S. Trivedi,
Hamid M. Abdolmaleky,
Kim Quang Do,
Richard C. Deth
Published: January 22, 2016
Many studies indicate a crucial role for the vitamin B12 and folate-dependent enzyme methionine synthase (MS) in brain development and function, but vitamin B12 status in the brain across the lifespan has not been previously investigated. Vitamin B12 (cobalamin, Cbl) exists in multiple forms, including methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl), serving as cofactors for MS and methylmalonylCoA mutase, respectively. We measured levels of five Cbl species in postmortem human frontal cortex of 43 control subjects, from 19 weeks of fetal development through 80 years of age, and 12 autistic and 9 schizophrenic subjects. Total Cbl was significantly lower in older control subjects (> 60 yrs of age), primarily reflecting a >10-fold age-dependent decline in the level of MeCbl. Levels of inactive cyanocobalamin (CNCbl) were remarkably higher in fetal brain samples. In both autistic and schizophrenic subjects MeCbl and AdoCbl levels were more than 3-fold lower than age-matched controls. In autistic subjects lower MeCbl was associated with decreased MS activity and elevated levels of its substrate homocysteine (HCY). Low levels of the antioxidant glutathione (GSH) have been linked to both autism and schizophrenia, and both total Cbl and MeCbl levels were decreased in glutamate-cysteine ligase modulatory subunit knockout (GCLM-KO) mice, which exhibit low GSH levels. Thus our findings reveal a previously unrecognized decrease in brain vitamin B12 status across the lifespan that may reflect an adaptation to increasing antioxidant demand, while accelerated deficits due to GSH deficiency may contribute to neurodevelopmental and neuropsychiatric disorders.
Read more Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia.
By Ginger Taylor
So, yesterday I posted an email I had written to Dr. Tom Insel, head of IACC. You can read it here. I asked if someone could please send me Autism Speaks' Rob Ring's email. And someone kindly obliged. Here's the email I sent to Rob Ring. Both of the emails are a response to the post Katie Wright ran on Thursday regarding the complete and total and seemingly purposeful disregard both Ring and Insel have for meaningful autism research.
|Subject:||Vaccine Autism Research|
|Date:||Fri, 14 Aug 2015 16:36:37 -0400|
This is in the context of broad disapproval and frustration within the autism community over NIH funding priorities. The general level of concern was documented by a 2008 letter signed by eleven major autism organizations (including Autism Speaks, Autism Research Institute, Safeminds, Autism Society of America, Generation Rescue, National Autism Association). The letter stated, "Research on the environment, gene-environment interaction and treatment are underrepresented...." There seems to be great frustration among these groups and others that regardless of acts of Congress, directives or calls for serious investigation into how the environment triggers persons predisposed to autism, there is too much research focused on genetics to the detriment of studies of environmental triggers.
The Inter-Agency Autism Committee (IACC) developed a plan that included serious research spending on investigating autism's environmental causes. Their strategic plan was published. In 2009 there was a program to increase federal spending (the "ARRA" funds related to the need to stimulate the economy out of recession and into recovery) and NIH announced a multitude of new funding opportunities as a result. There was a long "Research Funding Announcement" (RFA) which is a call for scientists to submit proposals to spend available grant money on their research interests.
Persons who get their PhDs in a scientific field learn how to get grants to support their research interests. One thing that is often done is to send an initial, short letter of inquiry, to get some feedback on how to pitch a full application for grant monies. Full applications are big long documents, sometimes 100 pages or more.
Like many researchers employed at a university, I receive emails from my university's grant office calling my attention to new funding opportunities that might be a good match, and I was encouraged to consider the ARRA grant opportunities from NIH. I noted there were a lot of RFA's (the full document was 181 pages!). I searched for calls with the word Autism in the announcement: there were ten. Eight clearly did not match the environmental intent of the strategic plan; they were about developing registries or comparing treatments. One was about gene and environment interactions but mentioned determining specific genetic variations and seemed to require genotyping. Only one mentioned the Interagency Autism Coordinating Committee (IACC) Strategic Plan and measuring biomarkers. This one looked good.
It was the only RFA on the NIH website posted (out of 181 pages of short postings) that mentioned the IACC strategic plan or seemed to be a fit for measures of Autism's environmental triggers or exposures. The NIH document included available grant opportunities for all branches of NIH (including NIEH, NIMH etc). I then looked up the IACC strategic plan and read it carefully. It seemed like a great fit. The RFA I inquired about read:
04-MH-101* Autism: Addressing the challenge. Target research gap areas identified by the Inter-Agency Autism Coordinating Committee (IACC) Strategic Plan for Autism Spectrum Disorder Research, including biomarkers, novel interventions, and new tools for screening, among other topics. Contact: Dr. Ann E. Wagner, 301-443-5944, email@example.com [Note: Ann E Wagner is currently a branch chief at NIMH, the part of NIH directly that houses the IACC]
My plan was to measure toxic levels in the environment, and then directly measure the levels in children with autism and controls (biomarkers of), and correlate levels to symptoms. In this way, I could establish norms for measured biomarkers based on measured environmental exposures among typical children, and then compare those with ASD to the norms. Possibly (this is what I hoped to check), if levels were higher than expected based on similar exposure in autistic children, this would point towards vulnerability to exposure and efforts could be made to limit toxic exposures in vulnerable children. It was a good match to the strategic intent of the IACC plan because I planned to measure biomarkers of exposure, which could lead to a novel intervention. I took the time to look at the IACC strategic plan (since it was directly mentioned in the funding announcement I was interested in pursuing). I located it and read it carefully to see if my aims were congruent. They were. To wit, the IACC website strategic plan on USA's Health and Human Services website (HHS.gov) included these key statements:
Initiate studies on at least five environmental factors identified in the recommendations from the 2007 IOM report.
Identify and standardize at least three measures for identifying markers of environmental exposures.
Determine the effect of at least five environmental factors on risk for subtypes of ASD.
From my read, out of the 181 page NIH document and hundreds of their RFA's, this was quite clearly the only possible match for what I wanted to do, which was to measure environmental exposure both environmentally and via biomarkers, among children with and without autism, and compare to symptom expression which could suggest strategies for intervention. However, I also had a specific methodological question about the possibility of including initial testing of a brand new technology being developed by some physicists to measure toxins. This prompted me to send a short inquiry via email. This is what I wrote.
> -----Original Message-----
> From: Cathy DeSoto [mailto:firstname.lastname@example.org]
> Sent: Thursday, March 19, 2009 5:25 PM
> To: Wagner, Ann (NIH/NIMH) [E]; Rob Hitlan
> Subject: 04-MH-101 Autism: Addressing the challenge
> We are interested in applying for the grant referred to below and will
> be submitting an application in early April. I have read the Interagency
> autism committee strategic plan and believe our aims would be a good match.
> The overall goal will be to investigate environmental risk factors,
> primarily via sources of pollution/toxic emissions from the perspective
> of genetic susceptibility for toxins having neurological effects,
> although we do not intend to measure genotype in anyway. We intend to
> propose direct measures of toxins among those with an ASD and controls
> (blood, hair or both) as well as measures of toxins in the environment
> relating to prevalence patterns, all of which will be elaborated upon in
> the actual proposal, of course.
> My reason for writing is to inquire if it would be appropriate to
> include a relatively small portion of the budget for testing of new
> spectroscopy instrumentation for the purpose of quantifying
> environmental toxins. Because we will already be proposing measures of
> toxins (for example soil samples via a grid layout in pockets of high
> prevalence) and because the new spectroscopy technique would be expected
> to allow easier and more highly accurate measures than is currently
> available (which would be explained in the full proposal), it would be a
> cost effective way to validate the method. Once validates, it is
> possible the new technique would be highly useful in relating toxins to
> health outcomes such as autism.
Conclusions Most vaccine trials are published eventually or the results posted in ClinicalTrials.gov, but delays to publication of several years are common. Actions should focus on the timely dissemination of data from vaccine trials to the public.
BMJ 2014;348:g3058 doi: 10.1136/bmj.g3058 (Published 16 May 2014)
Lamberto Manzoli associate professor 1 2, Maria Elena Flacco resident physician 1 3, Maddalena D’Addario resident physician 4 5, Lorenzo Capasso PhD student 1 Corrado De Vito assistant professor 6, Carolina Marzuillo assistant professor 6, Paolo Villari professor 6, John P A Ioannidis professor 7 8 1Department of Medicine and Aging Sciences, University of Chieti, Via dei Vestini 5 66013 Chieti, Italy; 2CeSI Biotech, Via Colle dell’Ara, Chieti, Italy; 3Local Health Unit of Pescara, Italy; 4Division of Clinical Epidemiology and Biostatistics, Institute of Social and Preventive Medicine, University of Bern, Switzerland; 5Division of International and Environmental Health, Institute of Social and Preventive Medicine, University of Bern, Switzerland; 6Department of Public Health and Infectious Diseases, Sapienza University of Rome, Italy; 7Stanford Prevention Research Center, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA; 8Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA, USA
Objective To evaluate the extent of non-publication or delayed publication of registered randomized trials on vaccines, and to investigate potential determinants of delay to publication.
The Familial Risk of Autism
Sven Sandin, MSc; Paul Lichtenstein, PhD; Ralf Kuja-Halkola, MSc; Henrik Larsson, PhD;
Christina M. Hultman, PhD; Abraham Reichenberg, PhD
IMPORTANCE Autism spectrum disorder (ASD) aggregates in families, but the individual risk
and to what extent this is caused by genetic factors or shared or nonshared environmental
factors remains unresolved.
OBJECTIVE To provide estimates of familial aggregation and heritability of ASD.
DESIGN, SETTING, AND PARTICIPANTS A population-based cohort including 2 049 973
Swedish children born 1982 through 2006.We identified 37 570 twin pairs, 2 642 064 full
sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin
pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
MAIN OUTCOMES AND MEASURES The relative recurrence risk (RRR) measures familial
aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or
cousin who has the diagnosis (exposed) compared with the risk in a participant with no
diagnosed family member (unexposed).We calculated RRR for both ASD and autistic disorder
adjusting for age, birth year, sex, parental psychiatric history, and parental age.We estimated
how much of the probability of developing ASD can be related to genetic (additive and
dominant) and environmental (shared and nonshared) factors.
A Key Role for an Impaired Detoxification Mechanism in the Etiology and Severity of Autism Spectrum Disorders
Behavioral and Brain Functions 2014, 10:14 doi:10.1186/1744-9081-10-14
Altaf Alabdali (email@example.com)
Laila Al-Ayadhi (firstname.lastname@example.org)
Afaf El-Ansary (email@example.com)
Autism Spectrum Disorders (ASD) is a syndrome with a number of etiologies and different
mechanisms that lead to abnormal development. The identification of autism biomarkers in
patients with different degrees of clinical presentation (i.e., mild, moderate and severe) will
give greater insight into the pathogenesis of this disease and will enable effective early
diagnostic strategies and treatments for this disorder.
In this study, the concentration of two toxic heavy metals, lead (Pb) and mercury (Hg), were
measured in red blood cells, while glutathione-s-transferase (GST) and vitamin E, as
enzymatic and non-enzymatic antioxidants, respectively, were measured in the plasma of
subgroups of autistic patients with different Social Responsiveness Scale (SRS) and
Childhood Autism Rating Scale (CARS) scores. The results were compared to age- and
gender-matched healthy controls.
Journal of Child Neurology
Autism and Dietary Therapy
Case Report and Review of the Literature
Martha R. Herbert, PhD, MD1⇑
Julie A. Buckley, MD, FAAP2
1Pediatric Neurology and TRANSCEND Research, Massachusetts General Hospital, Boston, MA, USA
2Pediatric Partners of Ponte Vedra, Ponte Vedra Beach, Florida; Nova Southeastern University, Fort Lauderdale, FL, USA
Martha R. Herbert, PhD, MD, Pediatric Neurology, TRANSCEND Research, Massachusetts General Hospital, Boston, MA 02129, USA. Email: firstname.lastname@example.org
Author Contributions MRH and JAB contributed equally to this work.
We report the history of a child with autism and epilepsy who, after limited response to other interventions following her regression into autism, was placed on a gluten-free, casein-free diet, after which she showed marked improvement in autistic and medical symptoms. Subsequently, following pubertal onset of seizures and after failing to achieve full seizure control pharmacologically she was advanced to a ketogenic diet that was customized to continue the gluten-free, casein-free regimen. On this diet, while still continuing on anticonvulsants, she showed significant improvement in seizure activity. This gluten-free casein-free ketogenic diet used medium-chain triglycerides rather than butter and cream as its primary source of fat. Medium-chain triglycerides are known to be highly ketogenic, and this allowed the use of a lower ratio (1.5:1) leaving more calories available for consumption of vegetables with their associated health benefits. Secondary benefits included resolution of morbid obesity and improvement of cognitive and behavioral features. Over the course of several years following her initial diagnosis, the child’s Childhood Autism Rating Scale score decreased from 49 to 17, representing a change from severe autism to nonautistic, and her intelligence quotient increased 70 points. The initial electroencephalogram after seizure onset showed lengthy 3 Hz spike-wave activity; 14 months after the initiation of the diet the child was essentially seizure free and the electroencephalogram showed only occasional 1-1.5 second spike-wave activity without clinical accompaniments. (see the pdf of the abtract HERE.)
Read the full report at Science Codex.
Children with autism have increased levels of genetic change in regions of the genome prone to DNA rearrangements, so called "hotspots," according to a research discovery to be published in the print edition of the journal Human Molecular Genetics. The research indicates that these genetic changes come in the form of an excess of duplicated DNA segments in hotspot regions and may affect the chances that a child will develop autism -- a behavioral disorder that affects about 1 of every 88 children in the United States, according to the Centers for Disease Control.
Earlier work had identified, in children with autism, a greater frequency of rare DNA deletions or duplications, known as DNA copy number changes. These rare and harmful events are found in approximately 5 to 10 percent of cases, raising the question as to what other genetic changes might contribute to the disorders known as autism spectrum disorders.
The new research shows that children with autism have -- in addition to these rare events -- an excess of duplicated DNA including more common variants not exclusively found in children with autism, but are found at elevated levels compared to typically developing children. The research collaboration includes groups led at Penn State by Scott Selleck; at the University of California Davis/MIND Institute by Isaac Pessah, Irva Hertz-Picciotto, Flora Tassone, and Robin Hansen; and at the University of Washington by Evan Eichler.
In a recently published study in the journal Biological Trace Element Research, Arizona State University researchers report that children with autism had higher levels of several toxic metals in their blood and urine compared to typical children. The study involved 55 children with autism ages five to 16 years old compared to 44 controls of similar age and gender.
The autism group had significantly higher levels of lead in their red blood cells (+41 percent) and significantly higher urinary levels of lead (+74 percent), thallium (+77 percent), tin (+115 percent), and tungsten (+44 percent). Lead, thallium, tin, and tungsten are toxic metals that can impair brain development and function, and also interfere with the normal functioning of other body organs and systems. Read the full study Toxicological Status of Children with Autism vs. Neurotypical Children and the Association with Autism Severity.
Dr. Michael Pichichero is an industry scientist and he endorses a mercury-based compound called Thimerosal as a “safe” and “effective” preservative in vaccines worldwide.
In a recently published report “Perspective – Report to WHO: No New Concerns About Thimerosal” he acknowledges that his “institution has received research grants from GlaxoSmithKline, Sanofi Pasteur, Pfizer, Novartis, and Crucell for new vaccine and product development.” Also he states in his report that “The evidence suggests the 2008 endorsement of the use of thimerosal as a safe and effective preservative in vaccines for children worldwide should remain.”
In addition he alludes to his remote presentation to the United Nations Negotiating Committee Meeting on April 3-4, 2012 which was made for “their consideration and vote” regarding the continuation of mercury in vaccines used worldwide. And it was in that same time frame that the World Health Organization's (WHO's) Strategic Advisory Committee (SAGE) in Geneva recommended that “Thimerosal, a preservative used to prevent contamination in multidose vaccine vials, be exempted from a pending international treaty aimed at reducing global health hazards by limiting exposure to mercury.” (See WHO Weekly Epidemiological Record).
Now it is possible that this industry scientist’s reasoning is based on an unfounded presumption that mercury leaves the brain faster than mercury from fish. He states “[a] total of five studies of blood and hair mercury in children have now been published, and all show that the foundational presumption of similar pharmacokinetics between methylmercury and ethylmercury was incorrect.” But do these studies really indicate what happens in a child’s brain?
To answer that one cannot rely solely on human studies reporting reduced mercury content in blood and hair. It is also important to recognize the fact that an animal study clearly shows that Thimerosal vaccine preservative injections result in inorganic mercury levels in brain tissue in infant monkeys at higher levels and longer time frames than from exposure to mercury in fish.
Thank you to our friends at Autism Science Digest magazine for allowing us to excerpt this article.
Aluminum Toxicity in Mitochondrial Dysfunction and ASD
By Nancy Mullan, MD, and Amy Yasko, PhD, AMD, FAAIM
Currently, there is intense interest and discussion surrounding the high incidence of mitochondrial disease and/or dysfunction in children with autism spectrum disorders (ASDs). This interest is fueled at least in part by the 2008 Hannah Poling decision.1,2 In this landmark case, the federal government’s Vaccine Injury Compensation Program (VICP) agreed to award damages to the Poling family when their daughter Hannah, who had an underlying mitochondrial disorder, developed autism-like symptoms after receiving a series of vaccines in a single day. Because Hannah Poling’s father is a medical doctor who was in the department of neurology at Johns Hopkins Hospital at the time that his daughter’s vaccine injury occurred, her case carried great weight. The Poling case, therefore, served to draw a great deal more attention to mitochondrial disorders within autism than these disorders had previously received.
A carefully executed review and meta-analysis of mitochondrial dysfunction in ASD by Rossignol and Frye discerned that the prevalence of full syndrome mitochondrial disease in children with ASD is significantly higher than it is in children in general.3 Their analysis also revealed that many children with ASD have findings on laboratory tests that indicate some degree of mitochondrial dysfunction, although not full syndrome mitochondrial disease. Together, these findings indicate a high degree of abnormal mitochondrial function in children with ASD, which other research has corroborated.2,4-9
Author's Note: This post originally ran in 2011, after the vaccine lobby's hired gun Brian Deer received his second "Press Award," to explain why his second such award is as meaningless as his first. Later that same year, Deer won another "award" from the UK pharma front group "HealthWatch." Then just a few days ago, another front group in the UK run by pharma-backed "science" writer Simon Singh gave Dr. Andrew Wakefield - whose Lancet paper was vindicted by colleague Prof. John Walker-Smith's successful appeal earlier this year - a mock award for "quackery." In response, we are re-running this piece to remind readers that Brian Deer's "awards" are just as farcical.
By Jake Crosby
The UK’s “Press Awards” are not nicknamed the “Hackademy Awards” for nothing, especially in the case of Brian Deer. He has been given not one, but two such awards. The claim, made by Brian Deer, that the UK Press Awards are like the Pulitzer Prize is laughable and absurd.
The UK’s Society of Editors runs the Press Awards. Sitting on the Editors’ advisory council is Les Hinton, who recently resigned as CEO of Dow Jones in the wake of the Murdoch phone hacking scandal. Also on that committee is Rebekah Brooks, who resigned as senior executive of News International - which publishes The Sunday Times - and was then arrested.
For over a decade, Brian Deer's only award was based on a faulty premise. It was called “Specialist Reporter of the year.” The judges said Deer was “the only journalist in Britain that polices the drug companies.” However, during the year for which he won his award, 1998, Brian Deer wrote an article alleging that patients who suffered neurological injury from the DTP vaccine were not really injured and should therefore not have received legal compensation for their injuries. That is the exact opposite of “policing” the drug companies, but is instead harrassing the victims of defective drug company products. In 2004, Glenn Frankel reported in the Washington Post that one of Brian Deer’s specialties “was tracking down false claims of damage from vaccines.”
Weeks after the bogus premise behind his first award was reported on Age of Autism, Brian Deer was nominated for “News Reporter of the Year” and also for “Specialist Reporter of the year,” the latter of which he won at the ceremony in London’s Savoy Hotel on April 5th, 2011. That award was given to Deer for his smear campaign against Dr. Andrew Wakefield.
The measure of any great or even good journalist must be his independence. Journalism awards are supposed to be based on independent assessments of reporters’ work, otherwise they are meaningless. Furthermore, it seems too perfect that Brian Deer was nominated for a Press Award (that he would later win) mere weeks after Age of Autism revealed he had only won one award.
How surprising can this really be given that the Academy of Judges for this year’s awards ceremony included Richard Caseby, managing editor of The Sunday Times? Caseby became notorious for his exchange with Rosemary Kessick – one of the few parents of the Lancet 12 children that Brian Deer actually interviewed.
Following a 6-hour interrogation of Kessick by Deer in 2003, during which he falsely gave his name as “Brian Lawrence,” she complained to The Sunday Times executive editor John Witherow. The exchange is detailed by Dan Olmsted in his article, An Elaborate Fraud, Part 2: In Which a Murdoch Newspaper’s Deceptive Tactics Infect the British Medical Journal.
Unfortunately, Kessick might as well have been complaining to GlaxoSmithKline, the board of which has retained News International boss, James Murdoch, since 2009. John Witherow recently wrote in a self-congratulatory piece about The Sunday Times’ investigative journalism on July 17th:
There have, of course, been many other investigations, including Brian Deer's outstanding work on exposing the doctor behind the false MMR scare.
This sentence exposes a clear desire to try and shift the arguments off the ground of the Sunday Times and GSK and into a more general arena so showing that what happened to Wakefield was a result of universal investigating and popular will. In fact one of the most staggering things about the Wakefield case was that Deer carried sole responsibility for it prior to lodging it with the GMC; no other investigative journalist in the world uncovered or wrote anything original critical of Wakefield besides Deer.
Instead of Witherow responding to Kessick’s complaint, Richard Caseby wrote back:
Department of Clinical and Applied Psychology, University of Vienna, Vienna, Austria. email@example.com
Hans Asperger originally used the term "autistic psychopathy" to describe his patients on the autism spectrum, leading to a possible confusion with psychopathic disorder and delinquent behaviour. We conducted a penal register search for 177 former patients of Asperger's clinic with a childhood diagnosis of "autistic psychopathy" or features of the disorder in Austria. The mean percentage of registered convictions was similar to that in the general male population of Austria over the studied time period. A qualitative assessment of offence types in Asperger's former patients suggests that the nature of offences does not differ from that in the general population. In this original cohort of Asperger's patients, convictions were no more common than in the general male population.
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.
School of Psychology, University of
Plymouth, UK Department of Psychology,
University of Florence, Italy.
Various case reports have shown possible associations between optic neuritis and different vaccines. Some of the vaccines include influenza, hepatitis B and anthraxPURPOSE:
To present evidence for a causal relationship between optic neuritis and Live Attenuated Influenza Vaccine (LAIV), administered as nasal flu vaccine.METHODS:
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.RESULTS:
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.CONCLUSION:
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.
Anxiety, Sensory Over-Responsivity, and Gastrointestinal Problems in Children with Autism Spectrum Disorders.
Department of Health Psychology and Thompson Center for Autism and Neurodevelopmental Disorders, University of Missouri - Columbia, 205 Portland Street, Columbia, MO, 65211, USA, firstname.lastname@example.org.
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 EVENT** Save the date!
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
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!
The treatment category is sponsored by Lee Silsby, the leader in quality compounded medications for autism.
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)
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.
Psychoactive pharmaceuticals induce fish gene expression profiles associated with human idiopathic autism.
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.
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.
Prenatal 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
E-mail address: email@example.com (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), http://dx.doi.org/10.1016/j.braindev.2012.05.004
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) ). 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."
Differences in Body Mass Index z-Scores and Weight Status in a Dutch Pediatric Psychiatric Population With and Without Use of Second-Generation Antipsychotics.
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 THE DWOSKIN FAMILY FOUNDATION
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
WEDNESDAY, MAY 9, 2012
C. Shaw, Canada
C. Dwoskin, USA
12:35-12:55 VACCINES, OXIDATIVE STRESS, AUTOIMMUNITY, AND CHRONIC MULTISYSTEM HEALTH OUTCOMES
Speaker: B.A. Golomb, CA, USA
12:55-13:15 ALUMINUM ADJUVANTS: RECENT INSIGHTS
Speaker: C. Exley, UK
13:15-13:35 THE NEUROTOXICITY OF ALUMINUM: IMPLICATIONS FOR ALUMINUM ADJUVANTED VACCINES
Speaker: C. Shaw, Canada
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.
Managing 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 (firstname.lastname@example.org) 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.
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 childrens 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 childrens 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, youre 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 childrens 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 childrens 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.
A microbial association with autism.
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.
By 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.'
Managing 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.
The relationship between the increased frequency of serum antineuronal antibodies and the severity of autism in children.
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]
Department of Clinical Sciences, Lund University, Lillhagsparken 3, 422 50 Hisings Backa, Sweden. email@example.com.
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.
January 2012 - Volume 31 - Issue 1 - p 1–4
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.
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.
Seeing the glass half full: benefits to the lived experiences of female primary caregivers of children with autism.
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.
: 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.
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.
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.
Free Radic Biol Med. 2003 Apr 1;34(7):928-36.
Inhibition of influenza infection by glutathione.
Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA. firstname.lastname@example.org
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.