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REVIEWS: Michael Fitzpatrick Autism, Brain and Environment BMJ 2006; 333: 205-a [Full text]

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Author reply to Fitzpatrick on Autism, Brain and Environment

Richard Lathe   (1 August 2006)

Author reply to Fitzpatrick on Autism, Brain and Environment 1 August 2006
Richard Lathe, Neuroscience Consultancy Pieta Research, PO Box 27069, Edinburgh EH10 5YW Send response to journal: Re: Author reply to Fitzpatrick on Autism, Brain and Environment	It is an astonishing fact that a medical condition can arouse intense feelings, as evinced by review in these pages1 of my monograph published earlier this year.2 The many misrepresentations and omissions in this emotive commentary demand urgent correction. Briefly, the book under scrutiny2 overviews evidence for (and against) the apparent rise in autism, and concludes that the increase is probably real - pointing to an environmental risk factor so far unknown. The rise is in agreement with the most up-to-date surveys in the UK3 and the USA.4 A central focus of the book is on physiological dysregulation that accompanies and exacerbates autism. It reviews evidence that limbic damage can both cause and reflect physiological problems, with environmental toxins including heavy metals playing a causal role, though concluding that the rise in autism cannot be uniquely attributed to such exposure (but remaining a strong suspect). Just one short chapter refers to possible strategies for therapy and prevention. It is here, and here alone, that the reviewer focuses his critical attentions; the majority of the book is not addressed. The reviewer asserts “there is no coherent scientific rationale for these treatments and little evidence of their efficacy”. This commentary omits to note the considered position taken by the book: “The field is however fraught with uncertainty because very few logical therapeutic approaches have been evaluated in a systematic manner.” The reviewer and the author are therefore substantially in agreement. The commentary draws attention to “an autistic boy … died while receiving chelation therapy”. This is also misleading: it fails to acknowledge that use of the wrong medication was responsible for the tragic death.5;6 The reviewer then states that American Academy of Neurology guidelines7 “explicitly reject” a series of biomedical tests. Also misleading. The recommendations speak not of rejection but of “inadequate supporting evidence”, a different matter. This is an area of debate: some authorities do argue in favour of testing: “The National Center for Environmental Health of the Centers for Disease Control and Prevention recommends that children with developmental delays should be screened for lead poisoning” (quoted in ref. 7). Regarding biomedical intervention, all will agree wholeheartedly that affected children should be spared unproven therapies until such time as efficacy has been demonstrated in controlled trials, and one hopes these will be ongoing. But the reviewer must be reminded that demanding trials (examples: haloperidol, risperidone, ritalin) have been conducted through mainstream medicine, and not by (in the words of the reviewer) “quacks and charlatans”. Valproate continues to be prescribed for epilepsy associated with autism, even though valproic acid is a known cause of autism.8 The reviewer’s exclusive focus on therapeutic options is unfortunate, for this is but a minor aspect. The central thesis offered by the book is of a rational and plausible sequence of events that both produces and exacerbates autism – only addressed by the reviewer in a single word – “speculative”. Peer-review requires that the reviewer must stipulate which arguments he or she feels to be unsound, and explain why they are unsound. This has not been done. Indeed (through the use of sometimes unscholarly and evocative terms) the commentary makes more appeal to emotion than to reason. While I agree with the reviewer that it is a mistake to rush into biomedical remediation without fullest consideration of justification and efficacy, it would be an equally grave error to dismiss, without objective consideration of all the evidence (as laid out in the book), and new research underway (for instance, ref. 9), an environmental and physiological contribution to autism. Richard Lathe DSc 1 Fitzpatrick M. Book review: Autism, Brain and Environment. Brit Med J 2006;333:205. 2 Lathe R. Autism, Brain, and Environment. London and Philadelphia: Jessica Kingsley Publishers, 2006. 3 Baird G, Simonoff E, Pickles A, Chandler S, Loucas T, Meldrum D 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;368:210-5. 4 Centers for Disease Control and Surveillance. Mental health in the United States: parental report of diagnosed autism in children aged 4- 17 years--United States, 2003-2004. Morb Mortal Wkly Rep 2006;55:481-6. 5 Centers for Disease Control and Surveillance. Deaths associated with hypocalcemia from chelation therapy - Texas, Pennsylvania, and Oregon, 2003-2005. Morb Mort Wkly Rep 2006;55:204-7. 6 Srikameswaran A. CDC says 2 deaths caused by chelation drug errors. Pittsburgh Post-Gazette 2006;3 March: http://www.post-gazette.com/pg/06062/664032-114.stm 7 Filipek PA, Accardo PJ, Ashwal S, Baranek GT, Cook EH, Jr., Dawson G et al. Practice parameter: screening and diagnosis of autism: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society. Neurology 2000;55:468-79. 8 Moore SJ, Turnpenny P, Quinn A, Glover S, Lloyd DJ, Montgomery T et al. A clinical study of 57 children with fetal anticonvulsant syndromes. J Med Genet 2000;37:489-97. 9 Hertz-Picciotto I, Croen LA, Hansen R, Jones CR, Van de WJ, Pessah IN. The CHARGE study: an epidemiologic investigation of genetic and environmental factors contributing to autism. Environ Health Perspect 2006;114:1119-25. Competing interests: None declared