OBJECTIVES: The reported increasing prevalence of autism spectrum disorder (ASD) and attendant health and family impact make monitoring of ASD prevalence a public health priority.
METHODS: The prevalence of parent-reported diagnosis of ASD among US children aged 3 to 17 years was estimated from the 2007 National Survey of Children's Health (sample size: 78037). A child was considered to have ASD if a parent/guardian reported that a doctor or other health care provider had ever said that the child had ASD and that the child currently had the condition. The point-prevalence for ASD was calculated for those children meeting both criteria. We examined sociodemographic factors associated with current ASD and with a past (but not current) ASD diagnosis. The health care experiences for children in both ASD groups were explored.
RESULTS: The weighted current ASD point-prevalence was 110 per 10,000. We estimate that 673,000 US children have ASD. Odds of having ASD were 4 times as large for boys than girls. Non-Hispanic (NH) black and multiracial children had lower odds of ASD than NH white children. Nearly 40% of those ever diagnosed with ASD did not currently have the condition; NH black children were more likely than NH white children to not have current ASD. Children in both ASD groups were less likely than children without ASD to receive care within a medical home.
CONCLUSIONS: The observed point-prevalence is higher than previous US estimates. More inclusive survey questions, increased population awareness, and improved screening and identification by providers may partly explain this finding.
Dear Editor,
the dramatic increase in autism spectrum disorders (ASD) prevalence recently recorded has been attributed by Kogan et al. [1] mainly to heightened public awareness and public services, widening in diagnostic criteria, changes in referral patterns and improved screening and case identification. While these are plausible reasons, other factors are likely to be involved.
A putative correlation between certain childhood vaccines and ASD has represented one of the greatest controversies over the last few years. The undeniable evidence of parents reporting of ASD onset shortly after a vaccination has been opposed to the lack of compelling scientific evidence. In the US thimerosal/ethylmercury has been removed from most vaccines in 1999. The reported decrease in vaccine-linked ASD cases [2] has been masked by the dramatic rise in ASD prevalence caused by different factors. Indeed, over the period between June 2002 and June 2007 the number of individuals diagnosed with ASD in California had more than doubled, rising from approximately 14,000 in June 2002 to over 34,000 cases in June 2007 (see figure 1 of the California Department of Developmental Services (DDS) report [3]). The data is particularly astounding if compared with epilepsy, cerebral palsy and mental retardation prevalence rates, which did not significantly change over the same period of time (see figure 3 of the DDS report [3]).
In Italy the infant vaccination schedule is relatively “intense” as in the USA, with 13-17 vaccinations administered within the first 18 months of life. However, ASD prevalence in Italy is approximately an order of magnitude smaller than the prevalence recorded in the USA. For example, the point prevalence calculated in the region of Liguria [4] and in the city of Catania (Sicily [5]) cohorts is calculated at about 6-8 cases per 10,000 infants. The data reflects the national prevalence recorded based on the school population (SINPIA [6] and Eurispes [7]). Since in Italy it is mandatory for children to frequent schools until the age of 16 years, the data should provide a reliable estimate of ASD prevalence in the infant and adolescent population, excluding vaccine-origin ASD as a major contributor to the dramatic increase in ASD prevalence recorded in the US. The aetiopathogenetic factor responsible for the dramatic increase in ASD prevalence rate should therefore be searched in a different direction.
Kogan et al. reported also that within the cohort examined “children born in or after 1993 (=< 14 years of age) have higher ASD estimates than those born in the earliest years”. Examining figure 2 of the California DDS report it appears that, while the ASD prevalence rate growth in the California population appears to have originated earlier (‘70s? ‘80s?), the beginning of the exponential growth showed up during the second half of the ‘90s, suggesting that something dramatically different must have occurred in California in the early ‘90s (1993 for example) that did not happen in Italy.
Simon [8] and Morley [9] suggested that the dramatic increase in ASD prevalence recorded in the US (and in other countries like the UK) could be the consequence of the immediate clamping-rescission of the umbilical cord (ICC; within the first 30 seconds-or early cord clamping (ECC) within the first minute) that has often replaced the more physiological delayed cord clamping (DCC; defined to occur at least after 60 seconds, and up to cessation of any pulsation of the umbilical cord -- or at least after 10 minutes). This shift in the management of the third stage of labor has unquestionably occurred over the past few decades in the US and in UK, but not in Italy. In the seventies indications for a rushed clamping of the cord came after concerns were raised about possible negative outcomes subsequent to hypervolemia, hyperviscosity (elevated hematocrit level), polycythemia and jaundice reported after DCC [10]. In the eighties, the determination of pH, PCO2 and PO2 from the umbilical cord replaced the Apgar score evaluation [11-13]. The assessment of these parameters requires a cord clamping as early as within 20-30 seconds [14-15]. It thus appears that ICC from a conventional management in special conditions became a routine practice and then a recommendation [14-15] without rigorous evaluation of possible outcomes. Finally, the “harvesting” of blood cells (early ‘90s), and more recently also stem cells, for medical purposes put a greater pressure for a hurried clamping of the cord. ICC has never been introduced as a recommendation in the “guidelines for labor” issued by the Societa’ Italiana di Ginecologia e Ostetricia (SIGO, [16]) and it is likely employed as an intervention in conditions of special need as also suggested by the Practical Guide of the Department of Reproductive Health and Research of the World Health Organization (page 36, [17]).
The parallel between the adoption of the ICC practice and ASD prevalence rate growth appears astounding even to a naïve eye and the number of adverse consequences caused by a hasty clamping of the cord may well represent a risk factor for ASD. Indeed, in normal term vaginal delivery ICC may prevent approximately 25% of oxygenated placental blood to reach a ‘hypoxic’ newborn (the passage through the partum canal involves arteries compression and transient hypoxia).
This ‘extra’ blood has the following variety of protective functions for the newborn; prevention of hypovolemia and excessive increase in blood viscosity [18], increase vasodilation and perfusion with higher vascular pressure in several organs, reduction of the concentration of the anaerobic metabolites (i.e. reactive oxygen species) produced and accumulated during delivery [19] leading to vasoconstriction [20], facilitation in the lungs functional transition from the fluid-producing fetal to the newborn gas-exchange organ [21, 18].
In addition, the hemolisis of fetal red blood cells provides about 50 mg of iron stores as a ferritin stores [22] critical for a proper myelination process occurring at a very fast pace during early postnatal life [23]. Fetal red blood cells haemolysis provides also bilirubin, which has a beneficial antioxidant effect [24]. Altogether these factors can affect the infant’s metabolic state (i.e. oxygen exchange) during the transition from fetal to newborn life. Male infants that have a higher metabolic demand (which is proportional to body weigh-[25]) may therefore be more sensitive to the adverse effect of the placental blood loss caused by ICC. This would also explain the reported 2.5-4:1 male-to-female ratio in autism prevalence.
Placental blood loss can be more dramatic in preterm babies who contribute a significant fraction of ASD cases [26], and twins that are smaller and lower weigh than single babies for the same gestational age. And it should not be surprising that homozygous twins, sharing the same placenta and competing for the same blood pool, have higher probabilities of having an autistic sibling than heterozygous that have separate blood pools. Finally, twins and pre-terms have usually a higher need for the resuscitoire and their cord is generally clamped faster. In conclusion, it appears that a hasty clamping of the cord induces a state of hypoxia, associated to the lack of essential elements such as iron and bilirubin, with catastrophic effects on newborn with a very high metabolic demand. According to Simon [8] this hypoxic birth has a dramatic impact on developing auditory brain stem nuclei that at birth have a higher metabolic demand [27]. Altered auditory nuclei can affect speech/sound perception resulting in poor language/speech development, the more striking symptom in ASD infants. Indeed, hearing deficits including abnormal auditory brainstem responses (ABRs; [28], reduced discrimination and orientation to speech [29] and increased hearing thresholds [30], have been reported in ASD individuals [31]).
Several animal models of experimental asphyxia at birth support Simon’s view [8]. Monkeys exposed to experimental asphyxia at birth showed increased hearing thresholds and poor orientations to sounds, modality- specific impairments similar to those reported in autistic infants [32- 33]. Reduced sound detection capabilities marked by higher hearing thresholds, degraded tonotopic representations, and reduced temporal precision at both subcortical (i.e. brain stem) and cortical levels have been recently reported in rats exposed to experimental PA [34]. However, more research on the detrimental effects of perinatal asphyxia is required in order to understand the mechanisms underlying the auditory deficits recorded in ASD infants. In conclusion, the possibility that ICC contributes to the large increase in ASD prevalence observed, and since both the Cochrane report [35] and the Royal College of Obstetricians and Gynecologists [36] have recommended to delay the clamping of the cord in order to prevent possible detrimental effects due to ICC, it is highly desirable that ICC could be stopped as soon as possible. It might represent a preventive “therapy” for ASD at zero cost.
REFERENCES
1. Kogan MD, Perrin M, Ghandour RM, Singh GK, Strickland BB, Trevathan E, van Dyck PC et al., Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007. Pediatrics, 2009, 124:1-9.
2. Geier DA, Geier MR, An assessment of downward trends in neurodevelopmental disorders in the United States following removal of Thimerosal from childhood vaccines. Med Sci Monit. 2006.
3. http://www.dds.ca.gov/Autism/docs/AutismReport_2007.pdf
4. http://www.angsaliguria.it/documenti/0- Dati%20autismo%20Liguria.pdf
5. http://www.autismoitalia.org/ARTICOLI_IA.ASP?numero=6&articolo=4
6. http://www.aslcremona.it/html/orma/pdf/LineeGuidaSINPIAautismo.pdf
7. http://www.eurispes.it/index.php/Gli-annunci/10d-rapporto- nazionale-sulla-condizione-dellinfanzia-e-delladolescenza.html
8. Simon EN. Auditory system damage and anoxic birth. Arch Pediatr Adolesc Med. 2007, 161:1106.
9. Morley GM. Autism's Pathogen: The Cord Clamp. [Eletter] Pediatrics, Volume 121, April 2008. http://pediatrics.aappublications.org/cgi/eletters/121/4/758
10. Saigal S, Usher RH. Symptomatic neonatal plethora. Biol Neonate. 1977;32(1-2):62-72.
11. Lievaart M, de Jong PA. Acid-base equilibrium in umbilical cord blood and time of cord clamping. Obstet Gynecol 1984;63:44-47
12. Yeomans ER, Hauth JC, Gilstrap LC III, Strickland DM. Umbilical cord pH, PC+ and bicarbonate following uncomplicated term vaginal deliveries. Am J Obstet Gynecol 1985;151:798-800
13. Thorp JA, Sampson JE, Parisi VM, Creasy RK. Routine umbilical cord blood gas determinations? Am J Obstet Gynecol 1989; 161:600-60.
14. ACOG technical bulletin. Umbilical artery blood acid-base analysis. Number 216--November 1995. (Replaces No. 127, April 1989).
15. American College of Obstetrics and Gynecology Committee on Obstetrics Practice. ACOG Commitee Opinion Number 138, April 1994 (Replaces #91, February 1991): Utility of umbilical cord acid-base assessment.
16. http://www.sigo.it/Documenti/LineeGuida/LineeGuida_TravaglioParto.pdf
17. http://whqlibdoc.who.int/hq/1996/WHO_FRH_MSM_96.24.pdf
18. Mercer JS. Current best evidence: a review of the literature on umbilical cord clamping. J Midwifery Womens Health. 2001 Nov-Dec;46(6):402 -14.
19. Wiberg N, Källén K, Olofsson P. Delayed umbilical cord clamping at birth has effects on arterial and venous blood gases and lactate concentrations. BJOG. 2008 115(6):697-703.
20. Mills TA, Wareing M, Shennan AH, Poston L, Baker PN, Greenwood SL. Acute and chronic modulation of placental chorionic plate artery reactivity by reactive oxygen species. Free Radic Biol Med. 2009 Jul 15;47(2):159-66.
21. JAYKKA S. Capillary erection and the structural appearance of fetal and neonatl lungs. Acta Paediatr. 1958 Sep;47(5):484-500.
22. Venâncio SI, Levy RB, Saldiva SR, Mondini L, Alves MC, Leung SL. Effects of delayed cord clamping on hemoglobin and ferritin levels in infants at three months of age. Cad Saude Publica. 2008; 24 Suppl 2:S323- 31.
23. Lozoff B. Perinatal iron deficiency and the developing brain. Pediatric Res 48:137-139
24. Stocker R, Yamamoto Y, McDonagh AF, Glazer AN, Ames BN. Bilirubin is an antioxidant of possible physiological importance. Science. 1987 Feb 27;235(4792):1043-6.
25. Sugie Y, Sugie H, Fukuda T, Ito M. Neonatal factors in infants with Autistic Disorder and typically developing infants. Autism. 2005 Dec;9(5):487-94.
26. Limperopoulos C, Bassan H, Sullivan NR, Soul JS, Robertson RL Jr, Moore M, Ringer SA, Volpe JJ, du Plessis AJ. Positive screening for autism in ex-preterm infants: prevalence and risk factors. Pediatrics. 2008 Apr;121(4):758-65.
27. Sokoloff L. Relationships among local functional activity, energy metabolism, and blood flow in the central nervous system. Fed Proc. 1981 Jun;40(8):2311-6.
28. Rosenhall U, Nordin V, Brantberg K, Gillberg C. Autism and auditory brain stem responses. Ear Hear. 2003 Jun;24(3):206-14.
29. Teder-Sälejärvi WA, Pierce KL, Courchesne E, Hillyard SA. Auditory spatial localization and attention deficits in autistic adults. Brain Res Cogn Brain Res. 2005 May;23(2-3):221-34.
30. Tharpe AM, Bess FH, Sladen DP, Schissel H, Couch S, Schery T. Auditory characteristics of children with autism. Ear Hear. 2006 Aug;27(4):430-41.
31. Tomchek SD, Dunn W. Sensory processing in children with and without autism: a comparative study using the short sensory profile. Am J Occup Ther. 2007 Mar-Apr;61(2):190-200.
32. Windle WF. Brain damage by asphyxia at birth. Sci Am. 1969 Oct;221(4):76-84.
33. Mirsky AF, Orren MM, Stanton L, Fullerton BC, Harris S, Myers RE. Auditory evoked potentials and auditory behavior following prenatal and perinatal asphyxia in rhesus monkeys. Dev Psychobiol. 1979 Jul;12(4):369- 79.
34. Strata F, deIpolyi AR, Bonham BH, Chang EF, Liu RC, Nakahara H, Merzenich MM. Perinatal anoxia degrades auditory system function in rats. Proc Natl Acad Sci USA. 2005 Dec 27;102(52):19156-61. Epub 2005 Dec 19.
35. McDonald SJ, Middleton P. Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD004074.
36. http://www.rcog.org.uk/files/rcog-corp/uploaded- files/SACPaper14ClampingUmbilicalCord09.pdf
Conflict of Interest:
None declared
Autism was 1 - 2 per 10,000 in the early 1980's when I trained. We have seen the prevalence rise to 1:650 then 1:150 and now 1:91. When we got the mercury out of the vaccines in 2001 there was no change and in fact rates have continued to rise. Alas we moved the Hep B vaccine around that time from teens to newborns. Many Vaccines have a lot of aluminium (eg 330 micrograms in most DTaP's, 250 micrograms in the Hep B and Hep A etc.). The November issue has the article on Aluminium in preterm infants and later bone health. In this article there is mention of the FDA recommended limit of aluminium exposure to <5 micrograms/Kg per day. Clearly our Hep B vaccines in newborns exceed this exposure ten-fold or more. Is it not time we re-consider the routine Hep B vaccine to infants whose mothers are hep B - negative and or/immune and have no risk factors? Most babies in my practice are not sexually active or using IV drugs. The precuationary principle should be sufficient to prevent us from routinely injecting the known neurotoxin aluminium into every baby in this country.
Conflict of Interest:
None declared
It is an interesting notion to question whether this rise in incidence is the result of more accurate diagnosis or more a result of misallocated health policy funding for expensive services.
Usually such studies are utilized to direct policy. For example, the Centers for Disease Control and Prevention estimated New Jersey’s prevalence at 1:94 children in 2007. Later in the year, the state legislature included in its package of bills, one to provide millions of dollars for research and regional treatment centers. Autism spectrum disorders (ASD) along with cerebral palsy, intellectual disability, hearing loss, and vision impairment, are included in the diverse group of developmental disabilities that result in mental and physical impairments that limit independent living.
Fortunately there are Medicaid waivers for children diagnosed with autism and other developmental disabilities requiring high levels of care. Such services include applied behavioral analysis, adult day services and foster care, behavioral support, community transition, family and caregiver training, specialized medical equipment and supplies, respite care, environmental modifications, assistive technology, residential habilitation, day services, personal emergency response system, and therapeutic services (e.g., speech, physical).1
When laws require coverage for therapeutic services for ASD and developmental disabilities, there may be a clouding of the diagnostic picture. Children may be diagnosed with autism spectrum disorders and other developmental disabilities in order to maintain eligibility for necessary behavioral interventions. Per the Autism Society of America, the lifetime cost of caring for a child with autism is $3.5 million to $5 million. With such costs, it should not be a wonder as to why more has to be done for every child’s health care. Childrens’ diagnoses should not be changed in order to obtain services. For support and services, it has to be across the board. Afterall, it is rising water that floats all boats.
1. Medicaid Waivers. Accessed online: http://www.in.gov/fssa/ompp/2549.htm on 10/18/09.
Conflict of Interest:
None declared
To the editor,
Kogan et al. [1] reported prevalence rates of autism spectrum disorders (ASD’s) to be approximately 110 per 10,000 overall (173 per 10,000 for boys) using parent responses to a telephone survey as part of the 2007 National Survey of Children’s Health (NSCH). These findings are quite provocative and underscore observations that ASD’s are diagnosed at a far higher rate than in the past. However, the field should be very cautious in using such findings to estimate the prevalence of ASD because of the form of the survey question and the lack of case confirmation.
The NSCH asked parents whether “a doctor or other health care provider ever told you that [your child] had the condition, even if he/she does not have the condition now…” The question did not ask if the parent was told that the child had a diagnosis or was diagnosed with ASD. Also, what is meant by “health care provider?” Thus, a comment by anyone that the parent sees as a health care provider such as, “Your child may have autism,” even in the context of a recommendation for an evaluation, could be interpreted as “yes” to this question. The vagueness of this question makes it impossible to estimate the accuracy of the results. The estimated point prevalence of children described as having “Mild” ASD in the survey suggests that a large proportion of children identified would at some point have received a diagnosis of PDD-NOS or, more generally, “autism spectrum disorder”. Because DSM-IV offers little specific guidance on appropriate symptomatic thresholds for PDD-NOS, this increases the subjective nature of the diagnosis and results in wide variation in diagnostic practice. There has clearly been a significant surge in awareness of and interest in ASDs in recent years. And for good reason, as these disorders are clearly far more common than was once thought, and thus represent a very significant public health challenge. However, it is precisely because of this high interest, and the highly charged nature of debate about the changing estimates of prevalence, that care must be taken to base estimates of prevalence on rigorous methodology.
The authors, while noting the limitations inherent in their method, nonetheless imply that the impact of these limitations is lessened because 1) their prevalence estimates are similar to previous surveys, 2) the demographic distributions are similar to findings from other CDC surveillance efforts, and 3) a past finding showing good sensitivity of parental report of various diagnoses in special education children. However, the observation that studies with similar methods (and thus similar weaknesses) show comparable results does not lessen the impact of these limitations. Further, other CDC surveillance reports have not yet used direct case confirmation, instead extracting information from medical and educational records. Finally, the observation that parental report is sensitive to diagnosis does not fully address the limitations of this study, which are as likely to result in problems of specificity.
Future research may very well indicate prevalence rates of ASD’s in the range of 1%, although, as with disorders such as schizophrenia [2], estimates will depend on the broadness of case definitions as well as the methods of ascertainment and case confirmation (see Baird et al. [3] for an example of methodological effects on prevalence estimation in autism). The methods reported by Kogan et al. make it impossible to adequately judge the accuracy of their findings. The authors do not provide evidence for the validity of the questions used from the NSCH, and it is therefore not clear that parental responses accurately reflect actual diagnoses. While large-scale direct case confirmation would not have been practical, it may have been feasible to assess the accuracy of surveys by conducting a relatively small-scale validity study to test the correspondence of survey results with formal diagnostic evaluation. The authors do acknowledge that “Data on the validity of parental report of developmental conditions are limited.” This is a critical limitation. It would seem prudent to directly test the accuracy of parental report prior to publication of such a high impact paper. Going forward, firm estimates of the prevalence of ASD’s should await findings from studies with direct case confirmation, and/or those that assess the reliability and validity of more indirect methods of ascertainment.
References:
1. Kogan, M.D., et al., Prevalence of Parent-Reported Diagnosis of Autism Spectrum Disorder Among Children in the US, 2007. Pediatrics, 2009.
2. van Os, J. and S. Kapur, Schizophrenia. Lancet, 2009. 374(9690): p. 635- 45.
3. Baird, G., et al., Prevalence of disorders of the autism spectrum in a population cohort of children in South Thames: the Special Needs and Autism Project (SNAP). Lancet, 2006. 368(9531): p. 210-5.
Conflict of Interest:
None declared
While the rising prevalence of autistic spectrum disorders could be partially explained by "...more inclusive survey questions, increased population awareness, and improved screening and identification by providers...", it is our responsibility as providers and scientists to make sure it may not also be due to rising medical issues that we can alleviate.
Conflict of Interest:
None declared
Dear Authors,
I am curious as to if your survey can pick out those parents who are going to medical doctors and educational professionals in public school to request that their child be diagnosed with the autism label.
This is happening often in the public schools. Since autism is also an educational diagnosis as well as a medical diagnosis, as an evaluator and part of an educational evaluation team I have witnessed many parents asking that their child receive the autism diagnosis because they can then get life-time medical insurance for the condition. I have seen parents study the symptoms of autism and tell their child to act certain ways so that they do look like they have autism. When completing the CARS or GARS or other checklists, they know the right answers to make their child look autistic.
I have also often witnessed medical doctors providing a parent with the autism diagnosis if the parent is insistent. In these cases, it is usually the same medical doctor who easily will give the diagnosis.
It is my hope that the medical field becomes aware that these scenerios are happening, not just in the state I live in but in other states.
Conflict of Interest:
None declared