AGE OF AUTISM

Autistic Children Have Different Guts

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.

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

Eur 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.

Source

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.

Abstract

BACKGROUND:

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

AIM:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

 

PMID:

22226851

[PubMed - as supplied by publisher]

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

Arch 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 S, Chang Z, Råstam M, Gillberg C, Larsson H, Anckarsäter H, Lichtenstein P.

Source

Department of Clinical Sciences, Lund University, Lillhagsparken 3, 422 50 Hisings Backa, Sweden. sebastian.lundstrom@neuro.gu.se.

Abstract

CONTEXT:

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.

OBJECTIVE:

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

DESIGN:

A nationwide twin study.

PARTICIPANTS:

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.

MAIN OUTCOME MEASURES:

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.

RESULTS:

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.

CONCLUSION:

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

Pediatric 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

J 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 GA, Al-Ayadhi LY.

Abstract

ABSTRACT:

BACKGROUND:

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.

METHODS:

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

RESULTS:

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).

CONCLUSIONS:

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

Clin 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 R, Fletcher P, Bryden P.

Source

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.

METHODS:

: 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.

RESULTS:

: 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.

CONCLUSIONS:

: 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

By 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

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

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

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

Tomljenovic L, Shaw CA.

Source

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

Abstract

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.

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

Inhibition of influenza infection by glutathione.

Cai J, Chen Y, Seth S, Furukawa S, Compans RW, Jones DP.

Source

Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA. jcai@learnlink.emory.edu

Abstract

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.

Antioxid 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 R, Nencioni L, Amatore D, Coluccio P, Fraternale A, Sale P, Mammola CL, Carpino G, Gaudio E, Magnani M, Ciriolo MR, Garaci E, Palamara AT.

Source

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).

RESULTS:

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.

INNOVATION:

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.

CONCLUSION:

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