Introduction

Overview: Although autism is often described as a "mystery", understanding of etiologies, individual profiles, and risk factors has increased substantially. Much of this progress is represented in peer-reviewed articles published in clinical and research-oriented medical journals.

Pubmed searches on March 11, 2010, indicated that from 2005 through 2009, the number of studies has virtually doubled. The "tw" limiter selects citations wherein the word autis* occurs in either the title or the abstract. "*" is a wild card.
autis*[tw] AND 2005[dp] - 0918 studies
autis*[tw] AND 2009[dp] - 1725 studies

If a broader search is utilized, the growth trend in Pubmed-indexed studies is similar:
(autis*[tw] OR ASD[tw] OR ASDs[tw] OR PDD[tw] OR PDD*[tw]) AND 2005[dp] - 1189 studies
(autis*[tw] OR ASD[tw] OR ASDs[tw] OR PDD[tw] OR PDD*[tw]) AND 2009[dp] - 2116 studies

The purpose of Advances in Autism Research 2010 is not to present every citation but, instead, is to delineate specific studies and signficant topics relevant to etiologies, clinical profiles, parental concerns, and treatments.

Background: Across decades, Bettelheim's model of "refrigerator mother" was supplanted by a construct wherein autism believed to be necessarily genetic in origin. Subsequently, the well-funded must-be-genetics model has been refined to a guiding theory wherein (a) susceptibility genes and the child's health interact with environmental factors such as pollutants, and (b) the affected child's autism-associated pathologies are not limited to being only "neurological". For example, in January of 2010, "Pediatrics" - the journal of the American Academy of Pediatrics - published two reviews focused upon "evaluation and treatment of common gastrointestinal problems in children" with autism-spectrum disorders (ASDs). (here& here)

One of the most important advances in autism research is the growing realization that a subgroup of children "recover" from autism. In other words, some individual children improve so much - often in response to various biomedical treatments - that the child no longer has traits consistent with an autism diagnosis (eg, here& here). The NIH has launched a study focused upon children who have recovered from accurately diagnosed autism (17).

 

Whole-body process: Many of the peer-reviewed autism studies published recently and during the last several years reflect appreciation (i) that many and perhaps most cases of autism reflect a whole-body process often involving gastrointestinal pathologies and immune dysregulation, and (ii) that many autistic children experience significant improvements as underlying pathologies are identified and treated. Harvard neurologist Martha R. Herbert, M.D., Ph.D., and colleagues are among the first researchers to have presented this new model (eg, 1-3; see also 4-6).

Toxicology & immunology: Other important advances in autism have occurred within toxicology (eg, 7-9) and immunology (eg, 10-12), with many articles clinical in focus (eg, 4-6), including evaluations of the training of autistic children (eg, 13-14).

Gastrointestinal Pathologies: The American Academy of Pediatrics (AAP) allowed publication of two reviews calling attention to gastrointestinal issues in autism and other ASDs (15-16).

Hannah Poling: Hannah Poling was developing as a neurotypical child until soon after she received a batch of vaccines during one vaccination incident. She regressed into traits consistent with DSM-IV autism and was found to have inherited a mitochondria variant shared with her mother, who is not autistic and who is an R.N. and an attorney. The United States Department of Health and Human Services (HHS) conceded that her then newly acquired, autism-related traits had been caused by vaccines. An article in Scientific American focused upon a crucial aspect of Hannah Poling's regression, "Could a group of disorders involving the "power plants of the cell" [mitochondria] explain why some vaccinated children develop autism but the vast majority don't?" (18-19).

Although a goodly number of studies have documented and discussed mitochondria associations with autism, a breakthrough paper by physicians Dan Rossignol and Jeff Bradstreet provided a conceptual framework for understanding why the process of injury underlying Hannah Poling's vaccination-induced regression may be more common than heretofore believed. Although the traditional notion of mitochondria disorder (eg, 20) remains important, mitochondrial dysfunction (21) may be a more common occurrence whereby children are at risk for acquiring vaccination-induced pathologies. Importantly, various pollutants including thimerosal affect mitochondria (22) and thus may be etiologically significant to autism cases related to mitochondrial dysfunction, a measurable phenomenon which has clinical profiles and treatment ramifications (21).

Pollutants: An increasing number of studies report associations between autism and various environmental pollutants.

A. Examples: Findings regarding PBDEs and mercury are presented in autism studies (eg, hereand here) and in studies not focused upon autism (eg, here, here, & here). In other words, autism-pollutants findings occur within a broader context: pollutant-associated pathologies.

B. Detoxification pathways as well as nutrient pathways and nutrient levels are implicated in etiologies, evaluations, and treatments of individuals with a high body-burden of pollutants (eg, here, here, here). The child's gastrointestinal health or lack thereof is often a contributing factor (eg, here&here).

C. Models (interpretive constructs) of pollutant-induced pathologies are important to research methods, findings, and interpretations. Industry prefers and regulatory-agency policies reflect a single-pollutant, low level approach (NOEL; eg, here& here) which can minimize concern for individuals with suboptimal nutritional status, weak alleles in detox pathways, and multiple exposures (eg, here, here, here, & here). Furthermore, focusing upon one pollutant turns attention away from effects of combinations of pollutants, many of which have become intra-body pollutants (eg, here, here, here, & here). These concerns are relevant to autism (eg, here&here).

Indeed, a new European Union study by the EU's Directorate-General for the Environment is titled, "State of the Art Report on Mixture Toxicity". As a scientists' news announcement (here) summarized on March 29, 2010, "The study showed that all the relevant research is unambiguous: the combined "cocktail effect" of environmental chemicals is greater and more toxic than the effect of the chemicals individually." The study itself is available here.

D. Epidemiological complexity: Determining "the cause" of autism remains elusive. The notion "the cause" may be a misleading concept. Aside from specific cases or rare genetic syndromes, searching for "the cause" of autism may be less effective than documenting various co-factors likely to be etiologically significant in specific children and in groups of children.

E. Fetal, embryonic, and infant development are shaped by timings of exposures, by levels of primary exposures and co-exposures, by regional variations in background pollutants, by variation in gastrointestinal pathologies, and by weak alleles of genes which participate in various pathways (eg, digestion, nutrient handling, detoxification, and immune responses including inflammation).

Vaccinations, autism, and other ASDs: Vaccination science published in peer-reviewed journals is remarkably diverse, contrarily so. Although major vaccination/unvaccinated studies remain to be done, studies which avoid that fundamental method continue to be published (eg, here). In contrast, some researchers report adverse effects from vaccinations (eg, here), even as still other researchers write misleading reviews pronouncing vaccination safety, while omitting inculpatory, peer-reviewed evidence regarding adverse effects of thimerosal and the MMR. Examples of mediocre reviews by prominent researchers (here&here) and critiques thereof (eg, here& here) abound.

Noteworthy are observations from Bernadine Healy, M.D., former director of the U.S. NIH, and from Dr Peter Fletcher, former Chief Scientific Officer at the U.K. Department of Health. Healy is reported to have stated that 'public health officials have intentionally avoided researching whether subsets of children are “susceptible” to vaccine side effects - afraid the answer will scare the public' (here), whereas Dr. Fletcher observed that 'he has seen a "steady accumulation of evidence" from scientists worldwide that the measles, mumps and rubella jab is causing brain damage in certain children.' (here) Recent events regarding thimerosal-containing vaccines and MMR vaccinations merit attention.

Two commentaries about the politics of science and vaccinations are offered, The ongoing saga of Wakefield, Murch, and Walker-Smith (here) and the Vaccine Court's thimerosal decisions in 2010 (here).

References:

1. Herbert MR. Autism: A Brain disorder or a disorder that affects the brain? Clinical Neuropsychiatry 2005; 2(6):354-79.

2. Herbert MR, Russo JP, Yang S et al. Autism and environmental genomics. Neurotoxicology 2006; 27(5):671-84.

3. Anderson MP, Hooker BS, Herbert MR. Bridging from Cells to Cognition in Autism Pathophysiology: Biological Pathways to Defective Brain Function and Plasticity. Am J Biochem Biotech 2008; 4(2):167-176.

4. Novel and emerging treatments for autism spectrum disorders: a systematic review
Rossignol DA.
Ann Clin Psychiatry. 2009 Oct-Dec;21(4):213-36.

BACKGROUND: Currently, only one medication (risperidone) is FDA-approved for the treatment of autism spectrum disorders (ASD). Perhaps for this reason, the use of novel, unconventional, and off-label treatments for ASD is common, with up to 74% of children with ASD using these treatments; however, treating physicians are often unaware of this usage. METHODS: A systematic literature search of electronic scientific databases was performed to identify studies of novel and emerging treatments for ASD, including nutritional supplements, diets, medications, and nonbiological treatments. A grade of recommendation ("Grade") was then assigned to each treatment using a validated evidence-based guideline as outlined in this review: A: Supported by at least 2 prospective randomized controlled trials (RCTs) or 1 systematic review. B: Supported by at least 1 prospective RCT or 2 nonrandomized controlled trials. C: Supported by at least 1 nonrandomized controlled trial or 2 case series. D: Troublingly inconsistent or inconclusive studies or studies reporting no improvements. Potential adverse effects for each treatment were also reviewed. RESULTS: Grade A treatments for ASD include melatonin, acetylcholinesterase inhibitors, naltrexone, and music therapy. Grade B treatments include carnitine, tetrahydrobiopterin, vitamin C, alpha-2 adrenergic agonists, hyperbaric oxygen treatment, immunomodulation and anti-inflammatory treatments, oxytocin, and vision therapy. Grade C treatments for ASD include carnosine, multivitamin/mineral complex, piracetam, polyunsaturated fatty acids, vitamin B6/magnesium, elimination diets, chelation, cyproheptadine, famotidine, glutamate antagonists, acupuncture, auditory integration training, massage, and neurofeedback. CONCLUSIONS: The reviewed treatments for ASD are commonly used, and some are supported by prospective RCTs. Promising treatments include melatonin, antioxidants, acetylcholinesterase inhibitors, naltrexone, and music therapy. All of the reviewed treatments are currently considered off-label for ASD (ie, not FDA-approved) and some have adverse effects. Further studies exploring these treatments are needed. Physicians treating children with an ASD should make it standard practice to inquire about each child's possible use of these types of treatments.

5. A review of dietary interventions in autism
Srinivasan P.
Ann Clin Psychiatry. 2009 Oct-Dec;21(4):237-47.

BACKGROUND: Anecdotal reports and parent surveys have shown evidence that dietary interventions have had some success in ameliorating the symptoms of autism. METHODS: In this paper, key findings that prompt a dietary intervention strategy are reviewed and popular intervention diets are described. RESULTS: There is a significant body of literature pertinent to dietary interventions in autism from the perspectives of gastroenterology, immunology, and excitotoxicity. Some articles report benefits to patients on standardized rating scales. CONCLUSIONS: This article presents a survey of the literature related to dietary interventions studied in the context of autism as well as various hypotheses on the rationale for dietary interventions. Patients or caregivers increasingly are attempting such interventions. Further studies are needed to establish the efficacy of these diets, the patients who would best benefit from diets, the mechanism of action, and the role of diets in addition to other treatments

6. Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment
Daniel A. Rossignol, J. Jeffrey Bradstreet
American Journal of Biochemistry and Biotechnology 4 (2): 208-217, 2008
{free online}
http://www.scipub.org/fulltext/ajbb/ajbb42208-217.pdf

Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernable mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions. Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.

7. Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene-environment interactions
D'Amelio M et al.
Mol Psychiatry. 2005 Nov;10(11):1006-16.

Organophosphates (OPs) are routinely used as pesticides in agriculture and as insecticides within the household. Our prior work on Reelin and APOE delineated a gene-environment interactive model of autism pathogenesis, whereby genetically vulnerable individuals prenatally exposed to OPs during critical periods in neurodevelopment could undergo altered neuronal migration, resulting in an autistic syndrome. Since household use of OPs is far greater in the USA than in Italy, this model was predicted to hold validity in North America, but not in Europe. Here, we indirectly test this hypothesis by assessing linkage/association between autism and variants of the paraoxonase gene (PON1) encoding paraoxonase, the enzyme responsible for OP detoxification. Three functional single nucleotide polymorphisms, PON1 C-108T, L55M, and Q192R, were assessed in 177 Italian and 107 Caucasian-American complete trios with primary autistic probands. As predicted, Caucasian-American and not Italian families display a significant association between autism and PON1 variants less active in vitro on the OP diazinon (R192), according to case-control contrasts (Q192R: chi2=6.33, 1 df, P<0.025), transmission/disequilibrium tests (Q192R: TDT chi2=5.26, 1 df, P<0.025), family-based association tests (Q192R and L55M: FBAT Z=2.291 and 2.435 respectively, P<0.025), and haplotype-based association tests (L55/R192: HBAT Z=2.430, P<0.025). These results are consistent with our model and provide further support for the hypothesis that concurrent genetic vulnerability and environmental OP exposure may possibly contribute to autism pathogenesis in a sizable subgroup of North American individuals.

8. Autism spectrum disorders in relation to distribution of hazardous air pollutants in the san francisco bay area
Windham GC, Zhang L, Gunier R, Croen LA, Grether JK.
Environ Health Perspect. 2006 Sep;114(9):1438-44.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570060/?tool=pubmed

OBJECTIVE: To explore possible associations between autism spectrum disorders (ASD) and environmental exposures, we linked the California autism surveillance system to estimated hazardous air pollutant (HAP) concentrations compiled by the U.S. Environmental Protection Agency. METHODS: Subjects included 284 children with ASD and 657 controls, born in 1994 in the San Francisco Bay area. We assigned exposure level by census tract of birth residence for 19 chemicals we identified as potential neurotoxicants, developmental toxicants, and/or endocrine disruptors from the 1996 HAPs database. Because concentrations of many of these were highly correlated, we combined the chemicals into mechanistic and structural groups, calculating summary index scores. We calculated ASD risk in the upper quartiles of these group scores or individual chemical concentrations compared with below the median, adjusting for demographic factors. RESULTS: The adjusted odds ratios (AORs) were elevated by 50% in the top quartile of chlorinated solvents and heavy metals [95% confidence intervals (CIs) , 1.1-2.1], but not for aromatic solvents. Adjusting for these three groups simultaneously led to decreased risks for the solvents and increased risk for metals (AORs for metals: fourth quartile = 1.7 ; 95% CI, 1.0-3.0 ; third quartile = 1.95 ; 95% CI, 1.2-3.1) . The individual compounds that contributed most to these associations included mercury, cadmium, nickel, trichloroethylene, and vinyl chloride. CONCLUSIONS: Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence, requiring confirmation and more refined exposure assessment in future studies.

9. Proximity to point sources of environmental mercury release as a predictor of autism prevalence.
Palmer RF, Blanchard S, Wood R.
Health Place. 2009 Mar;15(1):18-24.
http://images.huffingtonpost.com/2009-01-29-Palmer2008.pdf

The objective of this study was to determine if proximity to sources of mercury pollution in 1998 were related to autism prevalence in 2002. Autism count data from the Texas Educational Agency and environmental mercury release data from the Environmental Protection Agency were used. We found that for every 1000 pounds of industrial release, there was a corresponding 2.6% increase in autism rates (p<.05) and a 3.7% increase associated with power plant emissions(P<.05). Distances to these sources were independent predictors after adjustment for relevant covariates. For every 10 miles from industrial or power plant sources, there was an associated decreased autism Incident Risk of 2.0% and 1.4%, respectively (p<.05). While design limitations preclude interpretation of individual risk, further investigations of environmental risks to child development issues are warranted.

10. Immunologic and neurodevelopmental susceptibilities of autism
Pessah IN et al.
Neurotoxicology. 2008 May;29(3):532-45.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475601/?tool=pubmed

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

11. Prenatal exposures to persistent and non-persistent organic compounds and effects on immune system development
Hertz-Picciotto I et al.
Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):146-54.

Immune system development, particularly in the prenatal period, has far-reaching consequences for health during early childhood, as well as throughout life. Environmental disturbance of the complex balances of Th1 and Th2 response mechanisms can alter that normal development. Dysregulation of this process or an aberrant trajectory or timing of events can result in atopy, asthma, a compromised ability to ward off infection, or other auto-immune disease. A wide range of chemical, physical and biological agents appear to be capable of disrupting immune development. This MiniReview briefly reviews developmental milestones of the immune system in the prenatal period and early life, and then presents examples of environmentally induced alterations in immune markers. The first example involves a birth cohort study linked to an extensive programme of air pollution monitoring; the analysis shows prenatal ambient polycyclic aromatic hydrocarbons (PAH) and fine particle (PM2.5) exposures to be associated with altered lymphocyte immunophenotypic distributions in cord blood and possible changes in cord serum immunoglobulin E levels. The second example is a study of prenatal-polychlorinated biphenyl (PCB) exposures and the foetal development of the thymus, the organ responsible for lymphocyte maturation. Mothers with higher serum concentrations of PCBs gave birth to neonates having smaller indices of thymus size. Finally, this report underscores the tight connection between development of the immune system and that of the central nervous system, and the plausibility that disruption of critical events in immune development may play a role in neurobehavioural disorders.

12. The immune response in autism: a new frontier for autism research
Ashwood et al.
J Leukoc Biol. 2006 Jul;80(1):1-15.
http://www.jleukbio.org/cgi/content/full/80/1/1

Autism spectrum disorders (ASD) are part of a broad spectrum of neurodevelopmental disorders known as pervasive developmental disorders, which occur in childhood. They are characterized by impairments in social interaction, verbal and nonverbal communication and the presence of restricted and repetitive stereotyped behaviors. At the present time, the etiology of ASD is largely unknown, but genetic, environmental, immunological, and neurological factors are thought to play a role in the development of ASD. Recently, increasing research has focused on the connections between the immune system and the nervous system, including its possible role in the development of ASD. These neuroimmune interactions begin early during embryogenesis and pFFersist throughout an individual's lifetime, with successful neurodevelopment contingent upon a normal balanced immune response. Immune aberrations consistent with a dysregulated immune response, which so far, have been reported in autistic children, include abnormal or skewed T helper cell type 1 (T(H)1)/T(H)2 cytokine profiles, decreased lymphocyte numbers, decreased T cell mitogen response, and the imbalance of serum immunoglobulin levels. In addition, autism has been linked with autoimmunity and an association with immune-based genes including human leukocyte antigen (HLA)-DRB1 and complement C4 alleles described. There is potential that such aberrant immune activity during vulnerable and critical periods of neurodevelopment could participate in the generation of neurological dysfunction characteristic of ASD. This review will examine the status of the research linking the immune response with ASD.

13. Behavioural and developmental interventions for autism spectrum disorder: a clinical systematic review
Ospina MB et al.
PLoS One. 2008;3(11):e3755.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003755

BACKGROUND: Much controversy exists regarding the clinical efficacy of behavioural and developmental interventions for improving the core symptoms of autism spectrum disorders (ASD). We conducted a systematic review to summarize the evidence on the effectiveness of behavioural and developmental interventions for ASD. METHODS AND FINDINGS: Comprehensive searches were conducted in 22 electronic databases through May 2007. Further information was obtained through hand searching journals, searching reference lists, databases of theses and dissertations, and contacting experts in the field. Experimental and observational analytic studies were included if they were written in English and reported the efficacy of any behavioural or developmental intervention for individuals with ASD. Two independent reviewers made the final study selection, extracted data, and reached consensus on study quality. Results were summarized descriptively and, where possible, meta-analyses of the study results were conducted. One-hundred-and-one studies at predominantly high risk of bias that reported inconsistent results across various interventions were included in the review. Meta-analyses of three controlled clinical trials showed that Lovaas treatment was superior to special education on measures of adaptive behaviour, communication and interaction, comprehensive language, daily living skills, expressive language, overall intellectual functioning and socialization. High-intensity Lovaas was superior to low-intensity Lovaas on measures of intellectual functioning in two retrospective cohort studies. Pooling the results of two randomized controlled trials favoured developmental approaches based on initiative interaction compared to contingency interaction in the amount of time spent in stereotyped behaviours and distal social behaviour, but the effect sizes were not clinically significant. No statistically significant differences were found for: Lovaas versus special education for non-verbal intellectual functioning; Lovaas versus Developmental Individual-difference relationship-based intervention for communication skills; computer assisted instruction versus no treatment for facial expression recognition; and TEACCH versus standard care for imitation skills and eye-hand integration. CONCLUSIONS: While this review suggests that Lovaas may improve some core symptoms of ASD compared to special education, these findings are based on pooling of a few, methodologically weak studies with few participants and relatively short-term follow-up. As no definitive behavioural or developmental intervention improves all symptoms for all individuals with ASD, it is recommended that clinical management be guided by individual needs and availability of resources.

14. Applied behavior analytic interventions for children with autism: a description and review of treatment research.
Granpeesheh D, Tarbox J, Dixon DR.
Ann Clin Psychiatry. 2009 Jul-Sep;21(3):162-73.

BACKGROUND: Autism is a disorder characterized by pervasive delays in the development of language and socialization, and the presence of stereotyped, repetitive behaviors or nonfunctional interests. Although a multitude of treatments for autism exist, very few have been the subject of scientific research. The only treatment that has been supported by substantial empirical research is treatment based on applied behavior analysis (ABA). METHODS: This article describes components of comprehensive ABA treatment programs, reviews research on effectiveness, and discusses issues related to collaboration between ABA and psychiatry. RESULTS: ABA has been supported by several hundred single case experiments and an increasing number of between-groups studies. Comprehensive ABA treatment programs are comprised of multiple intervention procedures, such as discrete trial instruction and natural environment training, and are founded on basic principles of learning and motivation, such as positive reinforcement, extinction, stimulus control, and generalization. Clinicians in the fields of ABA and psychiatry have similar goals regarding client outcome, and several ABA measurement and analysis procedures produce information that may be useful to psychiatrists. CONCLUSIONS: ABA treatment programs for individuals with autism are supported by a significant amount of scientific evidence and are therefore recommended for use. Patient care would likely benefit from a greater degree of collaboration between practitioners in the fields of ABA and psychiatry.


15. Evaluation, Diagnosis, and Treatment of Gastrointestinal Disorders in Individuals With ASDs: A Consensus Report
Buie T et al.
Pediatrics 2010;125:S1–S18.
http://pediatrics.aappublications.org/cgi/content/full/125/Supplement_1/S1

16. Recommendations for Evaluation and Treatment of Common Gastrointestinal Problems in Children With ASDs
Buie T et al.
Pediatrics 2010;125:S19–S29
http://pediatrics.aappublications.org/cgi/content/full/125/Supplement_1/S19

17. Has your child recovered from autism?
Who is Eligible? Children 8 -17 years of age.
If your child has made significant improvements since being diagnosed with
autism and no longer meets autism criteria, consider participation in research at NIH.
Protocol #: 09-M-0171
http://patientinfo.nimh.nih.gov
http://intramural.nimh.nih.gov/pdn

18. Vaccine Injury Case Offers a Clue to the Causes of Autism
Could a group of disorders involving the "power plants of the cell" explain why some vaccinated children develop autism but the vast majority don't?
By Nikhil Swaminathan
April 22, 2008
http://www.scientificamerican.com/article.cfm?id=vaccine-injury-case-offer

19. Far from Over: Analyzing Hannah Poling vs. HHS
By John Gilmore
Spring 2008
http://www.devdelay.org/newsletter/articles/pdf/403-annalyzing-hannah-poling.pdf

20. Mitochondrial disease in autism spectrum disorder patients: a cohort analysis
Weissman JR et al.
PLoS One. 2008;3(11):e3815. Epub 2008 Nov 26.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003815

21. Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment
Daniel A. Rossignol, J. Jeffrey Bradstreet
American Journal of Biochemistry and Biotechnology 4 (2): 208-217, 2008.
http://www.icdrc.org/documents/Mitoandautism2008.pdf

22. Mitochondria in Autism - Two categories: disorder and dysfunction
Teresa Binstock, April 2008
http://www.autism.com/medical/research/advances/autism-mito.htm