One Autism-linked Gene Identified

Original posting at http://www.eurekalert.org/pub_releases/2008-09/econ-tfa082708.php
Public release date: 1-Sep-2008...
Contact: Sonja Maks.mak@update.europe.at43-140-557-340European College of Neuropsychopharmacology
The first autism disease genes
Presented at the 21st Congress of the European College of Neuropsychopharmacology 2008, Barcelona, Spain
This release is available in Spanish.
The autistic disorder was first described, more than sixty years ago, by Dr. Leo Kanner of the Johns Hopkins Hospital (USA), who created the new label ´early infantile autism´. At the same time an Austrian scientist, Dr. Hans Asperger, described a milder form of the disorder that became known as Asperger Syndrome, characterised by higher cognitive abilities and more normal language function. Today, both disorders are classified in the continuum of ´Pervasive Developmental Disorders´ (PDD), more often referred to as Autism Spectrum Disorders (ASD).
The prevalence of (classic) autism in the general population is about 15-20 in 10.000, while all Autism Spectrum Disorders (ASD) affect about 60 in 10.000 children. Males are affected four times more often than females. In approximately 10% of cases, autism is associated with a recognized cause, such as Fragile X Syndrome, Tuberous Sclerosis or diverse chromosomal abnormalities (mean observed rates between 5-10%), but in a vast majority of cases, no known causes are associated with autism (see figure).
All of these neurodevelopmental disorders are characterized by varying deficits in communication skills, social interactions, and restricted, repetitive and stereotyped patterns of interests and activities. Problems that may accompany these disorders are sensory distortion, mental retardation or seizures. Disease onset occurs during the first three years of life. Although early intervention has considerable impact on reducing symptoms and increasing a child´s ability to learn new skills, it is estimated that only 50% of children are diagnosed before the age of 3 years.
Most children with ASD respond well to behavioural management and highly structured, specialized programs in educational settings. Other therapeutic interventions comprise medications to treat behavioural problems such as aggression, self-injury, or severe tantrums.
Warning signs for Autism Spectrum Disorders such as social symptoms, communication deficits and repetitive behaviours should be considered sufficient reason to have a child evaluated by specialized professionals. The earlier the disorder is diagnosed, the sooner the child can be helped through treatment interventions.
Advances in autism research: genetic influences
Research into the causes, diagnosis, and the treatment of ASD has advanced interactively. Imaging studies have shown that many major brain structures are implicated in autism. Other research is focusing on the role of neurotransmitters such as serotonin, dopamine, and epinephrine. The past decade has been marked by an increased interest in the genetic basis of autism, and recent developments point to genetic factors playing a prominent role in the causes for ASD.
The role of gene mutations in autism
Twin and family studies have suggested an underlying genetic vulnerability to ASD. The estimated prevalence of autism in siblings is 5-10%. A higher recurrence risk in families with autistic subjects (45-times greater than the prevalence in the general population) and higher concordance for autism among monozygotic (60-90%) than dizygotic (0-10%) twins argue for a genetic predisposition to idiopathic autism. These data are interpreted as showing that liability to autism is in large part due to oligogenic inheritance in which a combination of multiple – possibly interacting – susceptibility alleles results in autism. A series of multiple independent whole genome scans and chromosomal abnormality studies have pointed out several candidate regions on chromosomes 2q, 7q, 6q, 15q and sex chromosomes. These regions possess candidate genes that have been screened for mutations or association with autism. In a European multicentre project called PARIS (Paris Autism Sib-pair International Study; coordinated by C. Gillberg & M. Leboyer) a large number of multiply affected families were identified, and several mutations of genes encoding proteins implicated in the process of synapse formation (synaptogenesis) have been described.
Autism and synapse formation (synaptogenesis)
In 2003 two new highly conserved members of the human neuroligin family – HNL4, located at Xp22.3 – were characterized (Jamain et al, 2003). A crucial factor in synapse formation, neuroligins are cell adhesion molecules that can trigger the formation of presynaptic structures in non-neuronal cells. The rare mutations of the neuroligins (1%) are associated with autism spectrum conditions. Another step forward in this compelling neurobiological story was the identification of a de novo frame-shift mutation in the X-linked HNL4 gene in two brothers, one with autism and the other with Asperger Syndrome. Since autism and Asperger Syndrome are overly represented in males, mutations in these genes may influence the process of synaptogenesis, and consequently may predispose males to Autism Spectrum Disorders.
In 2007, mutations of another gene encoding SHANK3 were reported (Durand et al, 2007). This gene regulates the structural organization of dendritic spines in neurons and is a binding partner of neuroligins, previously found to be mutated in autism and Asperger Syndrome. Surprisingly, a mutation of a single copy of SHANK3 at chromosome 22q13 is sufficient to induce language impairment, learning disabilities and/or social communication disorders associated with Autism Spectrum Disorders. Frequency of SHANK3 variants is very low even among autism patients and nearly absent in the general population. These results have thus shed light on one synaptic pathway sensitive to gene dosage and associated to Autism Spectrum Disorders.
In a large international study with a sample of 1.168 multiplex families, another exciting discovery led to the detection of sub-microscopic chromosomal abnormalities (Autism Genome Project, 2007): Copy Number Variant analysis (CNV) highlighted the role of a gene encoding neurexin, which is a tightly linked protein to neuroligin, implicated in synapse formation for glutamate neurons. This revealed a hemizygous deletion of coding exon for neurexin gene for a pair of affected siblings. Accumulating evidence thus points out that neurexin/neuroligin/Shank3 (NLGN3/4, SHANK3, NRXN1) genes are related to autism risk, establishing a direct proof of the association of autism with synaptic abnormalities. Neurexin induces glutamate postsynaptic differentiation in contacting dendrites, while neuroligins induce presynaptic differentiation in glutamate axons. The neurexin-neuroligin link thus appears to be fundamental for glutamatergic synapse formation. Furthermore, aberrant glutamate function is often cited as a cause for autism.
By influencing the process of synapse formation for glutamate neurons, gene mutations predispose individuals to Autism Spectrum Disorders.
Autism and circadian rhythms
Another approach in research of the genetics of autism implies the melatonin pathway. Melatonin is produced in the dark by the pineal gland and is a key regulator of circadian and seasonal rhythms. A low melatonin level was reported in individuals with Autism Spectrum Disorders, but the underlying cause of this deficit was unknown. In several individuals with Autism Spectrum Disorders, deletions of the ASMT-gene were found. This gene, located on the pseudo-autosomal region 1 of the sex chromosomes, encodes the last enzyme of melatonin synthesis. Biochemical analyses performed on blood platelets and/or cultured cells revealed a highly significant decrease in AMST activity and melatonin level in individuals with Autism Spectrum Disorders (Melke et al., 2008).
Recent research indicates that a low melatonin level, caused by a primary deficit in gene activity (AMST), is a risk factor for Autism Spectrum Disorders, and highlights the crucial role of melatonin in human cognition and behaviour.
Clinical implications
These findings stress the importance of further research into genetic abnormalities in autism to obtain a better understanding of the underlying disease mechanisms. However, several questions such as correlations between genotypes and phenotypes including cognition and brain imaging studies still remain to be investigated.
Research to unravel autism requires multidisciplinary approaches involving psychiatrists, psychologists, geneticists and brain imaging specialists.
Autistic patients require a broad workout taking into account psychiatric, somatic, cognitive, social and professional issues; furthermore they should be invited to participate in various research projects, ranging from fundamental research to more applied projects on the development of new therapeutic strategies. In view of these requirements the French Ministry of Research has established in 2007 the foundation Fondation FondaMental with the aim to intensify research in this field and to offer high-functioning autistic subjects optimal treatment and care in specialized expert centers.
###
References
Jamain S, Quach H, Betancur C, et al. on behalf of the PARIS study investigators. A de novo frameshift mutation of HNL4, an X-linked neuroligin, is associated with autism. Nature Genetics 2003;34:27-29
Durand C, Betancur C, Boeckers T, et al. Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders. Nature Genetics 2007;39:25-27
The Autism Genome Project. Mapping autism risk loci using genetic linkage and chromosomal rearrangement, Nature Genetics 2007;39:319-328
Melke J, Botros H-G, Chaste P, et al. Abnormal Melatonin Synthesis in Autism Spectrum Disorders. Molecular Psychiatry 2008;13:90-98
Correspondence: Professor Marion Leboyer, M.D., Ph.D. University of Paris 12, Head of Psychiatry Department, Head of Psychiatry Genetic team INSERM, Director Fondation FondaMental E-mail: marion.leboyer@inserm.fr

Need Donations: Treating Civilian Burn Victims in Iraq (non-combat related victims)

I saw this on an emergency medical blog, traced it back, and felt it was important enough that it should be posted and spread:
Military Volunteers Run Burn Clinic in Iraq

Military volunteers run burn clinic in Iraq, providing "tenderness and Tylenol"
Please go check out the link, and watch the two videos.
The two videos are "about the burn clinic for children at CSC Scania in Iraq. It is operated by volunteers from the US Military and using donated medical supplies. SGT Joseph Barzeski of 3rd Squadron, 73rd Cavalry Regiment, 1st Brigade Combat Team, 82nd Airborne Division is the current NCOIC, but the clinic was started by 1st Battalion, 125th Field Artillery, 34th Brigade Combat Team, Minnesota National Guard. It began as a Family Practice clinic for the local Iraqis, but as time went on the medics saw more and more burn victims due to the high number of cooking and heating accidents common in Iraq."
Items needed are:

Medihoney antibacterial cream
Kerlix
Xeroform petroleum dressings
Non-adhesive dressings
Chucks
Tylenol/paracetemol (Infant,Child and Adult)
Motrin/Ibuprofen (Infant,Child and Adult)
IV line sets
Benadryl (Child and Adult)

Additional items needed are:

Flip flops/Sandals
Sneakers
Clothes
Toothbrushes
Toothpaste
Toys
Stuffed Animals
Socks
Crayons and Coloring Books

PLEASE DO NOT SEND CASH OR CHECKS

Mail your donations to:

Jimmy Compton
SOC
CSC Scania
APO AE 09331

For more information, send your email to :
jimmycompton@gmail.com

FDA Recall

FDA News

FOR IMMEDIATE RELEASE May 23, 2008

Media Inquiries: Rita Chappelle, 301-827-6242 Consumer Inquiries: 888-INFO-FDA

FDA Warns Consumers Against Using Mommy's Bliss Nipple Cream
Product can be harmful to nursing infants

The U.S. Food and Drug Administration is warning consumers not to use or purchase Mommy's Bliss Nipple Cream, marketed by MOM Enterprises, Inc., because the product contains potentially harmful ingredients that may cause respiratory distress or vomiting and diarrhea in infants. The product is promoted to nursing mothers to help soothe and heal dry or cracked nipples. Product labeling specifically states that there is no need for mothers to remove the cream prior to nursing. However, the ingredients contained in the product may be harmful to nursing infants.

Potentially harmful ingredients in Mommy's Bliss Nipple Cream are chlorphenesin and phenoxyethanol. Chlorphenesin relaxes skeletal muscle and can depress the central nervous system and cause respiratory depression (slow or shallow breathing) in infants. Phenoxyethanol is a preservative that is primarily used in cosmetics and medications. It also can depress the central nervous system and may cause vomiting and diarrhea, which can lead to dehydration in infants.

Mothers and caregivers should watch for a decrease in an infant's appetite. More serious signs would be difficulty in awakening the child, limpness of extremities or a decrease in an infant's strength of grip and a change in skin color. Please seek immediate medical attention if your child is showing these signs and symptoms.

"The FDA is particularly concerned that nursing infants are being unwittingly exposed by their mothers to this product with dangerous side effects," said Janet Woodcock, M.D., director, FDA's Center for Drug Evaluation and Research. "Additionally, these two ingredients may interact with one another to further compound and increase the risk of respiratory depression in nursing infants."

Though the FDA has not received any reports of injury to infants, the agency is alerting the public because of the potential harm this product can have on a child.

Susceptibility Gene for Asthma Identified

photo from Georgetown University Medical Center website

NEJM link here. That's the very technical article, though. Here is a more public-friendly explanation from Modern Medicine:

Serum levels of YKL-40 correlate with asthma status
Apr 9, 2008
WEDNESDAY, April 9 (HealthDay News) -- Researchers have identified a gene conferring susceptibility to asthma in populations of European descent, according to research published online April 9 in the New England Journal of Medicine.
Carole Ober, Ph.D., of the University of Chicago, and colleagues performed a genome-wide association study to identify genes affecting serum levels of the chitinase-like protein, YKL-40, in 753 Hutterites, a founder population of European descent. The researchers then investigated the association of an implicated single-nucleotide polymorphism (SNP) with asthma in the Hutterites, in two unrelated case-control populations of European descent and in a birth-cohort of children of European descent at high-risk for asthma.
A promoter SNP upstream from the gene encoding YKL-40, the chitinase 3-like 1 (CHI3L1) gene, was associated with serum YKL-40 levels, asthma, bronchial hyperresponsiveness and pulmonary function measures in the Hutterite population. In addition, this SNP predicted the presence of asthma in the two case-control populations and serum YKL-40 levels in the birth cohort.
These findings suggest that "CHI3L1 is a susceptibility gene for asthma, bronchial hyperresponsiveness and reduced lung function, and elevated YKL-40 levels are a biomarker for asthma and decline in lung function," the authors conclude.
Two study authors disclosed receiving consulting fees and grant support from pharmaceutical companies, including MedImmune, a company investigating YKL-40 as a potential therapeutic target in asthma. One co-author is an inventor for a chitinase assay licensed to MedImmune.
AbstractFull TextEditorial

I'm particularly interested in what this could mean for other eosinophil-involved diseases, of course. Further updates, as always, as events warrant.

The joys of insurance nonsense

Our insurance requires us to use a mail-order pharmacy for all drugs other than one-time things like antibiotics. Common sense for other uses is not allowed. We must use the mail-order pharmacy for coverage. They don't take into account that we have some unusual medical situations here which require prescriptions normally only seen in hospital settings, among other oddities.
So today we receive this large box:
It weighed 6 lbs and was sent from Las Vegas, NV.

In it was several layers of styrofoam, 4 ice packs, multiple sheets of bubble wrap:

All to mail this:

One small box of Rx Benadryl. Which doesn't require refridgeration; it's to be kept at room temperature. And it was mailed in March, not mid-summer.

But, they only charged us about $3.00. The ice packs alone are worth more than that. The shipping cost more than that.

Or, they could have let us pick it up at the local pharmacy.

Bear with me--more librarian-type stuff

This is a holding-pen for a bibliography of journal articles disputing the idea that vaccination has any relationship to autism. Just move on by (unless you want the list). As of now (2/8/08) I have just copied and pasted a couple of others' lists; I haven't examined, edited, added to, or verified any of the citations, so do not give me any credit for any of this!
Thanks to Interverbal and Stavros, who have done all the work.

from Stavros:
- Peltola H & Patja A, Leinikki P, Valle M, Davidkin I and Paunio M (1998) No evidence for measles, mumps and rubella vaccine associated inflammatory bowel disease or autism in a 14 year prospective study (Research letters) Lancet 351:1327-8
- Gillberg C & Heijbel H, (1998). MMR and autism [commentary]. Autism, The International Journal of Research and Practice; 2:423-424.
- Taylor B et al (1999) Autism and measles, mumps and rubella vaccine: no epidemiological evidence for a causal association. The Lancet; 353: 2026-29.
- Kaye J et al (2001). Mumps, measles and rubella vaccine and the incidence of autism recorded by general practitioners: A time trend analysis. British Medical Journal 322 :460-3.
- Farrington P et al (2001). MMR and autism: Further evidence against a causal association Vaccine 19:3632-5 Volume 19, Issue 27, 14 June 2001, Pages 3632-3635
- Black C (2002) Relation of childhood gastrointestinal disorders to autism: nested case-control study using data from the UK General Practice Research Database. British Medical Journal 325 :419-21.
- Taylor B et al (2002) Measles, mumps and rubella vaccination and bowel problems or development regression in children with autism: population study. British Medical Journal 324 : 393-396.
- Donald A & Muthu V (2002) No evidence that MMR vaccine is associated with autism or bowel disease. Clinical Evidence, 7:331-40

from Interverbal:
1. Bertrand, J., Mars, A., Boyle, C., Bove, F., Yeargin-Allsop, M., & Decoufle, P. (2001). Prevalence of autism in a United States population: the Brick Township, New Jersey, investigation. Pediatrics, 108, 1155-161.
2. Chakrabarti, S., & Fombonne, E. (2001). Pervasive developmental disorders in preschool children. Journal of the American Medical Association, 285,3093-3099.
3. Chakrabarti, S., Fombonne, E., (2005). Pervasive developmental disorders in preschool children: confirmation of high prevalence. American Journal ofPsychiatry, 162(6), 1133-1141.
4. Fombonne, E. (2002). Prevalence of childhood disintegrative disorder (CDD). Autism 6, 2, 147-155.
5. Fombonne, E. (2003). Epidemiological surveys of autism and other pervasive developmental disorders: an update. Journal of Autism and Developmental Disorders. 33, 365-382.
6. Fombonne, E. (2001). Is there an epidemic of autism? Pediatrics.Vol 107 (2), 411-412.
7. Gernsbacher, M.A., Dawson, M, & Goldsmith, H. H. (2005).Three reasons not to believe in an autism epidemic. Current directions in psychological science, 14 (2), 55-58.
8. Gallo C, Volkmar F. Diagnosis of autism. Trends Evidence-BasedNeuropsychiatry 2003;5(1):23– 8.
9. Honda, H., Shimizu, Y., Imai, M., & Nitto, Y. (2005). Cumulative incidence of childhood autism: a total population study of better accuracy and precision. Developmental Medicine And Child Neurology. 47(1), 10-8.
10. Jick H, Beach KJ, Kaye JA. Incidence of autism over time.Epidemiology. (2006). Epidemiology, 17(1), 120-121.
11. Laidler, J. (2005). US Department of Education data on "autism" are not reliable for tracking autism prevalence. Pediatrics, 116 (1), 120-124.
12. Mandall, D. S., Novak, M. M., Zubritsky, C. D. (2005). Factors associated with age of diagnosis among children with autism spectrum disorders. Pediatrics,Vol 116 (6), 1480-6.
13. Spitzer, R., Siegal, B.(1990). The DSM-III R field trial of pervasive developmental disorders. Journal of American Academy of Child and Adolescent Psychiatry. 29, 855–862.
14. Tidmarsh, L., Volkmar, F, R. (2003)Diagnosis and epidemiology of autism spectrum disorders. Canadian Journal of Psychiatry. 48, 517-525.
15. Yeargin-Allsopp, M., Rice, C., Karapurka, T., Doernberg, N., Boyle, C., Murphy, C. (2003). Prevalence of autism in a US metropolitan area. Journal of the American Medical Association, 289, 49-89.For the MMR:
16. Fombonne E. MMR and autistic enterocolitis: a consistent epidemiological failure to find an association. Mol Psychiatry 2003;8:133–4.
17. Honda Shimizu, Y., Rutter, M. (2005). No effect of MMR withdrawal on the incidence of autism: a total population study. Journal of Child Psychology and Psychiatry, vol 46 (6), 572-579.
18. Horton, R., (2004). A statement by the editors of the Lancet. Lancet, 363, 820-1
19. Kaye, J. A., del Melero-Montes, M., & Jick, H. (2001). Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: A time trend analysis. BritishMedical Journal, 322, 460–463.
20. Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, Thorsen P, andothers. A population-based study of measles, mumps, and rubella vaccinationand autism. New Engl J Med 2002;347:1477–82.
21. Madsen KM. Measles, mumps and rubella vaccination and autism. N Engl J Med2003;348:951–4.
22. Murch, S., Anthony, A., Casson, D., Malik, M., Berelowitz, M., Dhillon, A., Thomson, P., Valentine, A., Davies, S., & Walker-Smith, J. (2004). Retraction of interpretation, 363, 750.
23. Roberts W, Harford M. Immunization and children at risk for autism. PaediatricChild Health 2002;7:623–32.
24. Spitzer W. Measles, mumps, and rubella vaccination and autism. N Engl J Med2003;348:951–4.
25. Stoto MA, Cleary SD, Foster VB . Epidemiologic studies of MMR vaccine andautism. Washington (DC): Institute of Medicine Immunization Safety ReviewCommittee; 2001.
26. Taylor B, Miller E, Farrington CP, et al. Autism and measles, mumps, and rubella vaccine; no epidemiological evidence for a causal association. Lancet, 353, 2026-2029.For Thimerosal:
27. Andrews, N., Miller, E., Grant, A., Stowe, J., Osborne, V., Taylor, B. (2004). Thimerosal exposure in infants and developmental disorders: a retrospective cohort study in the United kingdom does not support a causal association. Pediatrics. 114(3), 584-591.
28.Meadows, M. (2004). IOM report: no link between vaccines and autism. FDA Consumer. 38(5), 38-9.2
9. Nelson K, Bauman M. Thimerosal and autism? Pediatrics 2003. 111, 674–679.
30. Parker, S, K., Schwartz, B., Todd, J., Pickering, L, K. (2004). Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data. Pediatrics. 114(3), 793-804.
31. Singh, V, K., Hanson, J. (2006). Assessment of metallothionein and antibodies to metallothionein in normal and autistic children having exposure to vaccine-derived thimerosal. Pediatric Allergy and Immunology. 17, 291–296.
32. Stehr-Green, P., Tull, P., Stellfeld, M., Mortenson, P., Simpson. (2003). Autism and thimerosal-containing vaccines lack of consistent evidence for an association. American Journal of Preventative Medicine. 25(2), 101-106.
33. Verstraeten T, Davis RL, DeStefano F, et al. Safety of thimerosal-containing vaccines: a two-phased study of computerized health maintenance organization databases. Pediatrics.2003; 112 :1039 –1048
34. Vertraeten, T. (2004). Thimerosal, the Centers for Disease Control and Prevention, and GlaxoSmithKline. Pediatrics. 113(2), 932.


Michael E. Pichichero, Angela Gentile, Norberto Giglio, Veronica Umido, Thomas Clarkson, Elsa Cernichiari, Grazyna Zareba, Carlos Gotelli, Mariano Gotelli, Lihan Yan and John Treanor
Mercury Levels in Newborns and Infants After Receipt of Thimerosal-Containing Vaccines
Pediatrics 2008;121;e208-e214 http://pediatrics.aappublications.org/cgi/reprint/121/2/e208.pdf

University of California - Davis - Health System (2008, February 12). Some Cases Of Autism May Be Traced To The Immune System Of Mothers During Pregnancy. ScienceDaily. Retrieved February 15, 2008, from http://www.sciencedaily.com­ /releases/2008/02/080211172535.htm

From David Gorski at Science-Based Medicine:

Schechter R and JK Grether (2008). Continuing Increases in Autism Reported to California’s Developmental Services System. Arch. Gen. Psychiatry 65: 19-24.
Shattuck P (2006). The Contribution of Diagnostic Substitution to the Growing Administrative Prevalence of Autism in US Special Education. Pediatrics 117:1028-1037.
Hviid A, M Stellfeld, J. Wohlfahrt, and M Melbye (2003). Association between thimerosal-containing vaccines and autism. JAMA 290:1763-1766.
Madsen KM, MB Lauritsen, CB Pedersen, P Thorsen, AM Plesner, PH Andersen, PB Mortensen (2003). Thimerosal and the Occurrence of Autism: Negative Ecological Evidence From Danish Population-Based Data. Pediatrics 112:604-6.
Fombonne E, R Zakarian, A Bennett, L Meng, D. McLean-Heywood (2006). Pervasive Developmental Disorders in Montreal, Quebec, Canada: Prevalence and Links With Immunizations. Pediatrics 118:e139-50.
Thompson WW, C Price, B Goodson, DK Shay, P Benson, VL Hinrichsen, E Lewis, E Eriksen, P Ray, SM Marcy, J Dunn, LA Jackson, TA Lieu, S Black, G Stewart, ES Weintraub, RL Davis, F DeStefano; Vaccine Safety Datalink Team (2007). Early Thimerosal Exposure and Neuropsychological Outcomes at 7 to 10 Years. NEJM 357:1281-1292.
Parker SK, B Schwartz, J Todd, and LKPickering (2004). Thimerosal-containing vaccines and autistic spectrum disorder: a critical review of published original data. Pediatrics 114:793-804.
Fombonne E (2008). Thimerosal disappears but autism remains. Arch. Gen. Psychiatry 65: 15-6.

CDC List of Studies (pdf), with results and findings and citations

article on recall bias specifically related to vaccines:
Murphy, D., Hotopf, M., Wessely, S. (2008). Multiple vaccinations, health, and recall bias within UK armed forces deployed to Iraq: cohort study. BMJ, 337(jun30 1), a220-a220. DOI: 10.1136/bmj.a220
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Info pages and statements:
CDC
IOM Report

AAP especially "Autism Facts for Parents" which states:

The higher number of ASD cases is NOT due to vaccines. At one time it was thought
that thimerosal, a mercury-based preservative in vaccines, could contribute to ASD.
However, studies have shown there is no link. Indeed, thimerosal was removed from
childhood vaccines by 2002, and the cases of ASD have still risen.

A librarian moment

I just have to post for my own thought process on a current professional issue. The peer-reviewed journal Proteomics has an epub advance version of an article which purports to portray "Mitochondria, the missing link between body and soul: Proteomic prospective evidence." Now not only is there question about the level of peer review which went into this, given the poor science portrayed in the abstract, it turns out thanks to some checking by online readers that there is significant plagiarism.

As a medical librarian, I can only hope that the publishers will take a long hard look at this. Was adequate review performed? By whom? Did the authors send a different version to the publisher from what was sent for review? On whose authority? Will the article be retracted? On what grounds? What process failed here, exactly?

Medical literature is only as good as it's proven to be. We cannot make use of material we need to second guess. Librarians depend upon the peer review process to ensure that material we disseminate for clinician and researcher use is up to basic standards of science and publishing. If journals are not doing an adequate job of publishing only science which meets basic standards of practice, we will need to find a new medium of information reporting and management. Up until now the medical journal model has served well; it's up to the publishers of Proteomics to ensure it continues to do so.