© Borgis - Postępy Nauk Medycznych 5/2011, s. 453-461
Czy rzeczywiście istnieje epidemia autyzmu?
Is there really an epidemic of autism?
Warsaw School of Social Sciences and Humanities, Psychology Faculty
Head of Psychology Faculty: prof. Jerzy Karyłowski
Zaburzenie autystyczne, zaburzenie Aspergera i całościowe zaburzenie rozwoju – nieokreślone inaczej należą do grupy spektrum zaburzeń autystycznych (autism spectrum disorders, ASD). W ciągu ostatnich 25 lat zaobserwowano znaczny wzrost liczby osób diagnozowanych z ASD, zarówno w USA jaki i w krajach europejskich, w Japonii i w Kanadzie. Wg danych pochodzących z kilkunastu badań epidemiologicznych wykonanych w dwóch minionych dekadach, ASD jest diagnozowane u 60-70 dzieci na każde 10 000. W prasie popularnej i mediach temat większej liczby przypadków ASD jest często określany jako „epidemia autyzmu”, co mogłoby sugerować, że nastąpił wzrost zachorowalności (ncidence) na autyzm a nie wzrost rozpowszechnienia autyzmu (prevalence). Jednakże, publikacje naukowe donoszą, iż za częstsze diagnozowanie ASD w minionych latach są odpowiedzialne inne czynniki niż rzeczywisty wzrost liczby dzieci, które rodzą się z ASD. W artykule omówione zostaną: 1) dane dotyczące rozpowszechnienia autyzmu, całościowego zaburzenia rozwoju – nieokreślonego inaczej i zaburzenia Aspergera, 2) hipoteza o rzeczywistym wzroście zachorowalności, 3) główne nieporozumienia związane z większym rozpowszechnieniem autyzmu.
Autistic disorder, pervasive developmental disorder-not otherwise specified and Asperger syndrome belong to a group of disorders called autism spectrum disorders (ASDs). In the past 25 years, an increase in the prevalence of ASDs has been observed in the USA, Europe, Japan, and Canada. According to data from more than a dozen epidemiological studies conducted in the last two decades, ASD is diagnosed in 60-70 children/10 000. In popular press and the media, this phenomenon is often described as an “autism epidemic”, which may suggest that there has been a real increase in the incidence of autism, not just in the prevalence of the disorder. However, the latest publications clearly indicate that there are other variables (e.g., change in the diagnostic criteria, availability of services, awareness of the disorder) responsible for the rise of ASDs. In this article the following issues will be examined: 1) range of prevalence estimates for autism and related disorders, 2) hypothesis of a secular increase in rates of autism, and 3) major sources of misunderstanding related to the increased number of diagnosed cases of autism.
The answer is straightforward. No. One may not come to this conclusion, however, when he reads popular media, especially articles written in the US press. The possibility that the rate of autism is increasing has sparked and then fueled a debate on the purported epidemic of this disorder and its causes (1). According to Russell, Kelly, and Golding (2) many lay people believe that increased incidence of autism is due to exposure to new environmental, medical and technological hazards, including vaccinations, folate supplements, pluripotent mast cells, and growth of cable television. However, no sound scientific evidence indicates that the increase in the number of diagnosed cases of autism arises from environmental causes that were not present in the world 70 years ago, but came to being during the last decade of the previous century (3). In this article I will: 1) review the range of prevalence estimates for autism and related disorders, 2) examine the hypothesis of a secular increase in rates of autism, and 3) discuss several major sources of misunderstanding related to the increased number of diagnosed cases of autism.
RANGE OF PREVALENCE ESTIMATES FOR AUTISM AND RELATED DISORDERS
Information on the rates of autism comes from epidemiological studies, which started in the mid-1960s in England (4) and have since been conducted in many countries (5). These surveys have focused on a categorical-diagnostic approach to autism that has relied over the years on different sets of criteria. In general, they were concerned with the autistic disorder/childhood autism as characterized by severe impairments in communication and language, social interactions, as well as play (6). In other words, the majority of those studies did not investigate other pervasive developmental disorders (PDD). Some recent epidemiological surveys also included PDDs that fell short of strict diagnostic criteria for autistic disorder (i.e., PDD not otherwise specified – PDD-NOS and Asperger syndrome). Another aspect of the epidemiological research is whether it reports the prevalence or the incidence of a phenomenon. Prevalence refers to the number of individuals in a specified population who have the condition being studied at a specified time. It is the number of cases affected with a given condition divided by the population. It usually is expressed as percentage or the number of cases per 1.000 or 10.000 (7). Incidence refers to the number of individuals in a specified population in whom the condition being studied begins within a specified time period, such as one year. Both indexes are important but the usefulness of each depends on the condition being studied. In the case of autism, knowing the incidence would be vital because incidence rates are a more sensitive indicator than prevalence rates of potential new etiological factors (1). Unfortunately, calculating incidence rates for autism is problematic and thus most epidemiological research reports prevalence. Review of the range of prevalence estimates for autism and other PDDs comes from a series of publications by Fombonne (8-12). In the last article, Fombonne reported the most up-to-date review of published epidemiological surveys of PDDs. He included 53 studies published between 1966 and 2008, 43 of which provided information on the autistic disorder and 19 on all PDDs combined. Surveys were conducted in 17 countries and more than 50% of results were published after the year 2000. Most studies were conducted in urban areas, with school-age samples (median age of 8.0) of a mostly non-immigrant status and median population surveyed of over 63 000 subjects, however the variation in the size of the population surveyed was significant. Most investigations relied on a two-stage approach to identify cases in underlying populations and used batteries of standardized measures, specifically the gold standard diagnostic tools such as the Autism Diagnostic Interview – Revised (ADI-R) or the Autism Diagnostic Observational Schedule (ADOS). The diagnostic criteria used to define caseness varied and reflected historical changes in classification systems. The following criteria were used: Kanner’s, Lotter’s, and Rutter’s for studies done before 1980 and DSM- or ICD-based criteria for studies conducted thereafter.
Autistic disorder (AD). Data on children with autism were available in 43 studies. The earliest one was done by Lotter in 1966 in the UK, Middlesex area. The target population was 78 000 children between ages 8 and 10, 32 subjects with autism were identified with the use of a rating scale, about 15% of them had IQ above 70, gender ratio of males to females was 2.6:1. The estimated prevalence was 4.1/10 000. The latest one was done by Latif and Williams in 2007 also in the UK, Wales region. The target population was slightly over 39 000 children between ages 0 and 17, 50 subjects with autism were identified with the use of Kanner’s criteria, no information was reported on the IQ score, neither on the gender ratio of males to females. The estimated prevalence was 12.7/10 000. For all 43 surveys, prevalence estimates ranged from 0.7/10 000 to 72.6/10 000. Prevalence was negatively correlated with sample size, that is the smaller sample the higher prevalence. The correlation between prevalence and year of publication was significant. All studies published after 1987 reported prevalence higher than 7/10 000. In 18 studies published since 2000, the prevalence varied from 7.2 to 40.5/10 000. The average prevalence for the autistic disorder was 20.6/10 000. The author writes that this value can be used as “the best current estimate” for the prevalence of AD (12), str. 592.
PDD-NOS/Unspecified PDD. Seventeen of the 43 provided separate estimates for the prevalence of the atypical autistic syndromes, which were labeled differently but corresponded to the current diagnostic criteria for PDD-NOS. Fourteen of those 17 studies showed higher prevalence for those disorders than for autism. The ratio of the prevalence for PDD-NOS to the prevalence of autism had a mean value of 1.8, which translates into an average prevalence estimate of 37.1/10 000 for PDD-NOS if we take the value of 20.6/10 000 as the prevalence for autism.
Asperger Syndrome. There are very few epidemiological studies of Asperger Syndrome (AS), most likely due to the fact that this disorder was acknowledged as a separate diagnostic category only in the early 1990s with the revisions of ICD and DSM (ICD-10 and DSM-IV). Only two epidemiological surveys focused exclusively on the prevalence of AS. Unfortunately, due to extremely small number of cases identified (fewer than 5), the resulting prevalence estimates are imprecise. However, from the recent autism surveys we can gather information on the AS prevalence. It is consistently lower than that for autism. It is difficult to establish how much lower, but the ratio of 3 or 4 to 1 appears appropriate. This translates into a prevalence rate for AS of 6/10 000. Fombonne, however, cautions that there are strong limitations of data on AS.
Prevalence for combined PDDs. Based on the calculated estimates for each of the PDDs, the prevalence for all PDDs is approximately 63.7/10 000 (i.e., the sum of estimates for AD, PDD-NOS, and AS). Although these results should be treated as estimations, 19 recent epidemiological studies that have focused on PDD as the case definition obtained similar values (specifically 63.5/10 000). Also, surveys done by the Centers for Disease Control in 2002 and 2006 showed the prevalence for combined PDDs to be at least 60/10 000 (13, 14). Fombonne writes that the estimates of around 60 to 70 per 10 000 for all PDDs represent “the best estimate for the prevalence of PDDs currently available” (12, p. 593).
HYPOTHESIS OF A SECULAR INCREASE IN RATES OF AUTISM
In order to answer the question regarding presence of the epidemic of autism, we must prove that there is a secular increase in rates of autism. Time trends in prevalence and incidence data should be evaluated. Data available from epidemiological research should also be analyzed in the light of such methodological requirements as: constant case definition and constant case ascertainment. Various researchers investigated several factors related to shown increases in the rates of autism (5, 15, 16). First – referral statistics. If we take the number of children referred to special services as a proof for increased incidence of PDDs, we may be mistaken. Increased number of referrals can be confounded by referral patterns, availability of services, public awareness, decreasing age of diagnosis, and changes over time in diagnostic concepts and practices (12). Such confounds can be found in the report from the Department of Developmental Services in California, which is often quoted as evidence for the epidemic of autism (11). Thus, the information provided in the report and showing an increase of several hundred percent in the rates of autism referrals, has to be evaluated critically because the numbers fail to account for changes in the size and composition of the underlying population, no attempt was made to control for changes in diagnostic concepts and definitions, the fact that autistic children are diagnosed nowadays at a much earlier age did not motivate the researchers to get age-specific rates among older children, and finally, changes in the rates of other disorders were not taken into account. Fombonne (12) summarizes that evidence from referral statistics are meager and weak to support the idea of secular increase in rates of autism.
Second – comparisons of cross-sectional epidemiological studies. Many of the epidemiological surveys of autism are characterized by unique design features which makes it difficult to compare their results on the rates of the disorder. Time trends in prevalence and incidence of autism are, thus, very difficult to gauge. If we compare eight surveys conducted at roughly the same time and with similar age groups in the UK and in the USA, four in each country, we will find out large differences in prevalence estimations. As no passage of time was involved, most likely the differences can be attributed to variations in case identification methods (intensive population-based screening techniques vs. administrative methods for case finding). Fombonne writes: “no inference of trends in the incidence of PDDs can be derived from a simple comparison of prevalence estimates over time, since studies conducted at different periods are likely to differ even more with respect to their methodology” (12, p. 595) than studies done at the same time.
Third – repeat surveys in defined geographical areas. Repeated surveys, which use similar methodology and are conducted in the same geographical area at different points in time, can provide useful information on time trends. There were several studies done that strived to achieve this goal, but they also were flawed methodologically. Namely, different age groups were included in the surveys, improved detection among mentally retarded was not controlled for, neither were the changes in the diagnostic concepts and criteria. Thus, prevalence estimates which indeed were increasing should not be taken as proof for an increased incidence in the rate of autism. On the other hand, two surveys (17, 18) which were performed very rigorously did not result in the prevalence rates that were statistically different.
Fourth – successive birth cohorts. If one examined data from well-designed large surveys encompassing a wide age range and found increased prevalence among most recent birth cohorts, this could be interpreted as indicating secular increase in the incidence of a disorder. However, the increased prevalence should be specific only to the disorder of interest. For example, an analysis of special education disability data in Minessota showed a 16-fold increase in the number of children diagnosed with a PDD from 1991-1992 to 2001-2002 (19), but the increase was not specific to autism and also was observed for other disability categories, which may be indicative of better services and methods for diagnosis. Moreover, in the early 1990s PDDs were included in the federal Individual with Disabilities Educational Act (IDEA) funding and reporting mechanisms in the USA.
Fifth – incidence studies. Three studies provided incidence estimates for PDDs. All showed an upward trend in incidence over short periods of time, none of them, however, could determine the impact of other factors (e.g., changes in the diagnostic criteria, improved awareness and service availability) on the upward trend.
To summarize, the available epidemiological studies indeed show an increase in the prevalence of autism, but those estimates cannot be directly attributed to the increase in incidence of the disorder. Rather, other variables may be responsible for such state of affairs. They will be discussed in the next section.
SOURCES OF MISUNDERSTANDING RELATED TO THE INCREASED PREVALENCE OF PDDs
Changes in diagnostic criteria
Autism is a pervasive developmental disorder defined behaviorally and characterized by impairments in three areas: social interactions, reciprocal verbal and nonverbal communication and the range of interests and activities (6). Although recognition of this disorder may have its origins in Jean-Marc Gaspard Itard’s description of the “wild boy of Aveyron” from 1801 (20), the first formal account of autistic individuals was published by Leo Kanner in 1943 (21). It was Kanner and Eisenberg (22) who published a list of diagnostic criteria for “early infantile autism”. They included aloofness and indifference to others as well as resistance to change. These features had to be present in the repertoire of a child by the end of his second year of life. Later, Rutter (23) described a condition that he called “childhood autism” as one characterized by impaired social development, delayed and deviant language development, and insistence on sameness. These symptoms had to be present by 30 months. It was not until when the third edition of the Diagnostic and Statistical Manual of Mental Disorders (24) was published, that there was a major change in the concept of childhood autism. The shift was related to moving autism from a category of psychiatric disorders to a new category of pervasive developmental disorders (PDDs). Within this category, two subcategories were identified: “infantile autism” and “childhood onset pervasive developmental disorder”. There were brief diagnostic criteria provided for each subgroup. In 1987 in the DSM-III-R, broader criteria were provided for what was named “autistic disorder” and “pervasive developmental disorder not otherwise specified (25). The current definition of autism, although consistent with the deficits observed in Kanner’s original group of children, has been refined and broadened. Nowadays, persons with autism are considered to have one of the neurodevelopmental disorders that have such wide range of behavioral consequences and severity that they are collectively referred to as pervasive developmental disorders (PDDs) in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, Text Revised (6). Within the group of five pervasive developmental disorders, a narrower term of autism spectrum disorders (ASDs) is used to refer to: autistic disorder, Asperger’s syndrome and pervasive developmental disorder – not otherwise specified. Thus, until 1980 estimates of prevalence were based on individual clinicians’ or specific researchers’ conceptions, whereas since then they have been based on the diagnostic criteria of ICD and DSM, also reflecting modifications in the subsequent editions of the manuals. Given the nature of the diagnostic criteria for different disorders within ASDs, it is highly probable that the differences in prevalence rates among various studies stem from: 1) using different criteria for autism diagnosis across the years and 2) applying the same criteria differently by different investigators (1).
Increased awareness of autism and development of specialized services
Despite the fact that autism was described by Kanner in 1943, still in the early 1960s there was little general interest in or awareness of the autism. One reason may be that the disorder was thought to be very rare and not malleable to change (20). In the course of the 1960s voluntary associations of parents of autistic children as well as professional-oriented organizations began to operate in the USA and the UK. The goal was to push for educational and treatment services for autistic children and to encourage research on this disorder. Indeed, publicity concerning the children and their needs was ensured and scientific investigations into the nature of autism were undertaken (1). Awareness of the wide spectrum of autistic characteristics, and specifically of the Aspreger syndrome has also grown with the changes in the diagnostic criteria. Despite the fact that the impact of public and professional awareness of autism on prevalence rates is hard to quantify (5), it is also difficult to deny that greater interest in the emotional, social and psychological issues relating to autism did not influence identification of affected children. Moreover, changes in the types of services, the availability of services and the fashion these services are provided for children with autism, may have changed the way the children are labeled and counted. Such “diagnostic switch” was observed in California and in all US states (26), indicating that a relatively high proportion of children previously diagnosed as having mental retardation were now identified as having a PDD diagnosis. Adding autism to the IDEA in early 1990s meant that there were concrete benefits to getting a diagnosis of autism. Thus, although the impact of increased awareness and service changes on prevalence estimates in unknown, it should not be underestimated.
Possible true increase in incidence of autism
Wing and Potter (1) list several potential reasons for a marked rise in prevalence, among them a genuine rise in incidence of ASDs. If there were a true increase in incidence of ASDs it could be attributable to some environmental hazard (27). Many suggestions have been made considering the influence of environmental factors on autism: prenatal exposure to chemical agents such as thalidomide and valproic acid, as well as to infectious agents such as the rubella and influenza viruses, postnatal influences of diets, environmental pollutants, antibiotics, vaccinations, and neurotoxins such as mercury present in preservatives used for some vaccines. None of those, however, has been yet scientifically validated. The purported link between measles-mumps-rubella (MMR) vaccine and ASDs has received much public and political attention (28-30) and will be the focus of the remainder of this section. Information presented below is a summary of an article by Suchowierska and Novak (31).
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1. Wing L, Potter D: The epidemiology of autistic spectrum disorders: Is the prevalence rising? Mental Retardation and Developmental Disabilities Research Reviews 2002; 8: 151-61.
2. Russell G, Kelly S, Golding J: A qualitative analysis of lay beliefs about the aetiology and prevalence of autistic spectrum disorders. Child: care, health and development 2009; 36: 431-36.
3. Gernsbacher MA, Dawson G, Goldsmith HH: Three reasons not to believe in an autism epidemic. Current directions in psychological science 2005; 14: 55-58.
4. Lotter V: Epidemiology of autistic conditions in young children: I. Prevalence. Social Psychiatry 1966; 1: 124-37.
5. Williams K, Mellis C, Peat JK: Incidence and prevalence of autism. Advances in Speech-Language Pathology 2005; 7: 31-40.
6. American Psychiatric Association: Diagnostic and statistical manual of mental disorders – Text Revised. 4th ed. Washington, DC: 2000.
7. Scahill L, Bearss K: The rise in autism and the mercury myth. JCAPN 2009; 22: 51-53.
8. Fombonne E: Epidemiological surveys of autism. In: Volkmar FR, editor. Autism and pervasive developmental disorders. Cambridge: Cambridge University Press; 1998. p. 32-63.
9. Fombonne E: Epidemiologic surveys of autism: a review. Psychol Med 1999; 29: 769-86.
10. Fombonne E: Epidemiological surveys of autism and other pervasive developmental disorders: an update. J Autism Dev Disord 2003; 33: 365-82.
11. Fombonne E: The changing epidemiology of autism. Journal of Applied Research in Intellectual Disabilities 2005; 18: 281-94.
12. Fombonne E: Epidemiology of Pervasive Developmental Disorders. Pediatric Research 2009; 65(6): 591-98.
13. CDC. Prevalence of autism spectrum disorders – Autism and Developmental Disabilities Monitoring Network, 14 sites, United States, 2002. In: Surveillance Summaries, February 9, 2007. MMWR 2007; 56(No. SS-1): 12-28.
14. CDC. Prevalence of autism spectrum disorders – Autism and Developmental Disabilities Monitoring Network, 14 sites, United States, 2006. In: Surveillance Summaries, December 18, 2009. MMWR 2007; 58(No. SS-10): 1-20.
15. Charman T: The prevalence of autism spectrum disorders. Recent evidence and future challenges. European Child & Adolescent Psychiatry 2002; 11: 249-56.
16. Wanzana A, Bresnahan M, Kline J: The autism epidemic: Fact or artifact? J Am Acad Child Adolesc Psychiatry 2007; 46: 721-30.
17. Chakrabarti S, Fombonne E: Pervasive developmental disorders in preschool children. JAMA 2001; 285: 3093-99.
18. Chakrabarti S, Fombonne E: Pervasive developmental disorders in preschool children: confirmation of high prevalence. Am J Psychiatry 2005; 162: 1133-41.
19. Gurney JG, Fritz MS, Ness KK et al.: Analysis of prevalence trends of autism spectrum disorder in Minnesota (comment). Arch Pediatr Adolesc Med 2003; 157: 622-27.
20. Frith U: Autism: Explaining the enigma. Malden, MA: Blackwell Publishing; 2003.
21. Kanner L: Autistic disturbances of affective contact. Nervous child 1943; 2: 217-50.
22. Kanner L, Eisenberg I: Early infantile autism 1943-1955. Am J Orthopsychiatry 1956; 26: 55-65.
23. Rutter M: Diagnosis and definition. [In:] Rutter M, Schopler E, editors. Autism: a reappraisal of concepts and treatment. New York: Plenum Press 1978; p. 1-25.
24. American Psychiatric Association: Diagnostic and statistical manual of mental disorders. 3th ed. Washington, DC: American Psychiatric Association 1980.
25. American Psychiatric Association: Diagnostic and statistical manual of mental disorders – Revised. 3th ed. Washington, DC: American Psychiatric Association 1987.
26. Shattuck PT: The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education. Pediatrics 2006; 117: 1028-37.
27. Rutter M: Incidence of autism spectrum disorders: Changes over time and their meaning. Acta Pediatrica 2005; 94: 2-15.
28. Colgrove J, Bayer R: Could it happen here? Vaccine risk controversies and the specter of derailment. Health Affairs 2005; 24: 729-39.
29. O’Dell L, Brownlow C: Media reports of links between MMR and autism: a discourse analysis. British Journal of Learning Disabilities 2005; 33: 194-99.
30. Speers T, Lewis J: Journalists and jabs: Media coverage of the MMR vaccine. Commun Med 2004; 1 (2): 171-81.
31. Suchowierska M, Novak G: Measles-mumps-rubella vaccine and autistic spectrum disorder: What do doctors need to tell the parents? Postępy Nauk Medycznych 2010; 5: 422-28.
32. Wakefield AJ, Murch SH, Anthony A et al.: Ileal-lymphoidnodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998; 351 (9103): 637-41.
33. Kawashima H, Mori T, Kashiwagi Y et al.: Detection and sequencing of measles virus from peripheral mononuclear cells from patients with inflammatory bowel disease and autism. Digestive Diseases and Sciences 2000; 45 (4): 723-29.
34. Murch SH, Anthony A, Casson DH et al.: Retraction of an interpretation. Lancet 2004; 363: 750.
35. Wilson K, Mills E, Ross C, McGowan J, Jadad A: Association of Autistic Spectrum Disorder and the Measles, Mumps, and Rubella Vaccine. Arch Pediatr Adolesc Med 2003; 157: 428-34.
36. Madsen KM, Hviid A, Vestergaard M et al.: A population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med 2002; 347 (19): 1477-82.
37. Dales L, Hammer SJ, Smith N: Time trends in autism and in MMR immunization coverage in California. JAMA 2001; 285 (9): 1183-85.
38. Fombonne E, Chakrabarti S: No evidence for a new variant of measles-mumps-rubella-induced autism. Pediatrics 2001; 108 (4): E58.
39. Gillberg C, Heijbel H: MMR and autism. Autism 1998; 2: 423-24.
40. Kaye JA, del Mar Melero-Montes M, Jick H: Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: a time trend analysis. British Med J 2001; 322 (7284): 460-63.
41. Taylor B, Miller E, Farrington CP et al.: Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a casual association. Lancet 1999; 353 (9169): 2026-29.
42. Taylor B, Miller E, Lingam R et al.: Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study. British Med J 2002; 324(7334): 393-96.
43. Gillberg G, Steffenburg S, Schaumann H: Is autism more common now than 10 years ago? British Journal of Psychiatry 1991; 158: 403-09.
44. DeWilde S, Carey IM, Richards N et al.: Do children who become autistic consult more often after MMR vaccination? British J General Practice 2001; 51 (464): 226-27.
45. Farrington CP, Miller E, Taylor B: MMR and autism: further evidence against a causal association. Vaccine 2001; 19 (27): 3632-35.
46. Makela A, Nuorti JP, Peltola H: Neurologic disorders after measles-mumps-rubella vaccination. Pediatrics 2002; 110 (5): 957-63.
47. Patja A, Davidkin I, Kurki T et al.: Serious adverse events after measles-mumps-rubella vaccination during a fourteen-year prospective follow-up. Pediatr Infect Dis J 2000; 19 (12): 1127-34.
48. Peltola H, Patja A, Leinikki P et al.: No evidence for measles, mumps, and rubella vaccine-associated inflammatory bowel disease or autism in a 14-year prospective study [letter]. Lancet 1998; 351 (9112): 1327-28.
49. Halsey NA, Hyman SL: Measles-mumps-rubella vaccine and autistic spectrum disorder: report from the New Challenges in Childhood Immunizations Conference convened in Oak Brook; 2000 Jun 12-13, Illinois. Pediatrics 2001; 107 (5): 84.
50. Offit PA, Coffin SE: Communicating science to the public: MMR vaccine and autism. Vaccine 2003; 22: 1-6.
51. Madsen KM, Vestergaard M: MMR vaccination and autism. What is the evidence for causal association? Drug Safety 2004; 27: 831-40.