Although the central remit of this excellent Conference was to explore the role of bowel disorder and of nutritional intervention in the symptoms and behaviours of children diagnosed as AS (Autistic Spectrum) or ADS (Attention Deficit Spectrum) the topics covered were very wide ranging, beginning with current psychological understanding of The Autistic Spectrum, and Autistic Spectrum Disorder and concluding with the latest educational perceptions and approaches.

Dr John Richer, Consultant Clinical Psychologist in Paediatrics at the John Radcliffe Hospital in Oxford, had recently constructed a questionnaire that identifies 16 types, or possible combinations, of behaviour preference.
The aim was to see whether autistic children exhibited marked Sensing and Thinking preferences analogous to poor Central Coherence or Theory of Mind Deficit, identified as critical features of autism. In fact there was little correspondence, except in the area of Introversion. This translates as low frustration tolerance (particularly of ‘'stop' stimuli), low fear threshold, and avoidance tendencies.

Dr Richer's main conclusion was that differences in behaviour between ASD and other children are primarily ones of degree – and that the individuality of a child should never be obscured by crude grouping, or labels.

The danger of the label was a theme also addressed by Dr Michael Tettenborn, a Consultant Paediatrician with a special interest in allergies and intolerances. His concern was to identify children likely to benefit from dietary interventions. Most likely to benefit are those with late onset or Regressive Pattern autism, features of which include high incidence of allergic disorders in child and family; frequent incidence of bowel symptoms; history of frequent use of antibiotics in the first year of life. ‘'Soft' symptoms include excessive thirst, excessive sweating, incidence of Otitis Media, and disturbed sleep.
Dr Tettenborn's principal area of research was into anti-fungal therapy –- a low sugar/low yeast diet combined with extremely finely titrated doses of Nystatin. Much work still needs to be done, but this had proved a promising intervention in a significant number of cases (interestingly, Tettenborn did, however, feel there was little evidence of Candida presenting a particular problem). Main points of advice: follow the principle of sequential intervention and treat all promises of universal treatment with extreme suspicion.

Though a Professor Psychiatry at the University of Oxford, Anthony Bailey's interests span the neurobiological basis of autism, and his concern was with recent twin and family studies of autism.

While non-identical twins exhibited a risk factor of developing autism of 5% (that of normal siblings), 60% of identical twins developed autistic traits, strongly suggestive of a genetic element. Research in the area is still peppered with red herrings: though there is some overlap in identified susceptibility regions of the genome, claims to have identified particular susceptibility genes still await replication.

The search for these genes remains vital, however, if only to aid identification of environmental factors, which need not be toxic in normal circumstances but will prove a trigger in conjunction with genetic susceptibility. Very little can be predicted at present; what constantly emerges is a picture of a highly complex and alarmingly common condition (defined as incidence >1 per thousand individuals; current estimate set at 6/1000).

Professor Glenn Gibson heads up the Microbiology Department of the Institute of Food Research in Reading, and is a founder member of the International Scientific Association for Probiotics & Prebiotics.

Foods Matter readers will be familiar with the role of breast-feeding, weaning, and early antibiotic use in determining gut flora balance. The tools are still lacking to determine causes of the apparent gut flora imbalance that leads to the diarrhoea/constipation/abdominal discomfort patterns evidenced by a large number of autistic children although Professor Gibson posits early infection leading to an overgrowth of certain strains of yeast and bacteria. However his analysis of faecal samples from affected individuals has shown nine strains of Clostridia bacteria not found in control samples, a number of which produce potent neurotoxins. (Again, there was little evidence of Candida playing a particular role).

Work on probiotics as intervention has begun, but so far only L.plantarum has exhibited any inhibitory effect, and there is uncertainty over which Colstridium species it affects. But Professor Gibson reminded those tempted to despair that probiotics don't do any harm.

Dr Simon Murch, Consultant in Paediatric Gastroenterology at The Royal Free Hospital is, of course, a former colleague of Dr Andrew Wakefield, who notoriously linked their joint research into the role that the MMR vaccine may play in the intestinal inflammation and lymphoid hyperplasia in at least a subgroup of autistic children. At the conference, Murch gave little hint of the contents of his letter to be published the next day in The Lancet in which he denied that there was any evidence to link the vaccine and onset of autism – a letter instantly repudiated by Wakefield. He did suggest gently that while vaccine links had not been replicated, connections with intestinal disease continued to be.

Within a highly technical presentation indicating certain advances, the central vision was of autism as a body-wide disturbance of cellular control mechanisms, with cognitive abnormalities as the tip of an iceberg of a complex, multi-system disorder. No facile unitary hypothesis could be formed –- indeed a lot more had come to light that ‘'we had never considered'.

Dr John Mclaren Howard announced his presentation with ‘'now to the witchcraft!' In fact, the co-founder of the Biolab Medical Unit (www.biolab.co.uk) has developed highly pragmatic, unique tests for investigating, inter alia, trace element function, gastric function and biotin status. Recent lab investigations on 61 autistic children had uncovered intriguing differences of pattern between three clinical groups: what Howard called ‘'frank' autism; Asperger's type autism and ADHD type autism.

For instance, while all exhibited a high degree of Vitamin B deficiency, the frank autists were particularly deficient in B3 and biotin; Asperger's in B1 and ADHD in B6 and biotin. Frank autists tended to be chromium deficient, Asperger's manganese and intra-cellular magnesium deficient and ADHD manganese deficient with a high incidence of toxic metal DNA adducts.

Nutrient supplementation programmes had variable effects – the most obvious progress was generally made by those with the greatest number of test abnormalities. In some cases improvement in behaviour and cognitive function had been dramatic (and very moving to recount); yet one case showed no response to any intervention whatsoever.

The November 2003 issue of Foods Matter carried a long extract from a paper examining the role of fatty acids in ADHD (and autism) published by Dr Alex Richardson, Senior Research Fellow in Neuroscience at Mansfield College.

Much of this material was reprised at the conference presentation; but it was particularly interesting to note, hard on the heels of Dr Howard's account, that a lack of co-factors (e.g., B3, B6, Magnesium, Manganese, Zinc) as well as hormone activity induced by stress (the ‘'Introversion' type identified by Dr Richer) create conversion blockages disrupting the synthesis of HUFA from EFA. Thus dietary EFA is not in itself a magic cure, and it is difficult to predict individual response.

Dr Richardson sympathised with those speakers who had placed an emphasis on the variability of autistic expression and the need to move forward in establishing phenotypes, meaningful subgroups.

Dr Rita Jordan runs the autism study programmes for the University of Birmingham and is a teacher of considerable experience and insight.

While demonstrating a firm grasp of the complex biological factors giving rise to autistic expression, Dr Jordan's presentation was principally a critique of current teaching methods (often ‘'horrifically confusing') and of general societal attitudes, which see the label first, the individual second (if at all).

'We train autistics to interpret our behaviour, yet refuse to set aside our intuitive understanding of others when interpreting theirs. ‘Once we can show empathy, we begin to have a chance of helping those with autism to develop it.'

The general conclusion of the Conference? No immediate cause for huge optimism, but a collective sense of progress.

Further information from:

The Allergy Research Foundation, PO Box 18 Aylesbury HP22 4XJ Tel/fax: 01296 655818

Click here for more general articles on autism

First Published in 2003

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