Autism, Brain and EnvironmentBMJ 2006; 333 doi: https://doi.org/10.1136/bmj.333.7560.205-a (Published 20 July 2006) Cite this as: BMJ 2006;333:205
All rapid responses
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
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
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 –
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
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
Competing interests: No competing interests