AUTISM AND NUTRITIONAL INTERVENTION
These notes were stimulated by an earlier request for information about the possible benefits of dietary interventions (such as the use of supplements containing fatty acids) among children with behavioural problems of a hyperactive and impulsive type *, but this present summary focuses upon findings relating to individuals with autism and ASD.
(* Please see “ Attention Deficit Disorder : Research Update 29 ” January 2004)
The converging view is that there may be positive benefits for many children from carefully supervised dietary elements (supplements and exclusions) within a programme of intervention; but that there is currently reliance upon anecdotal or small scale studies hence the need for caution in generalising available evidence and in establishing expectations.
The Influence of Fatty Acids in Autism (and other conditions)
The work relating to the apparent significance of nutrition and nutritional deficiencies in a range of disorders (such as autism, dyslexia and ADHD) completed by Richardson (2001) begins with a reference to the way in which different diagnostic processes and core defining features underline the differentiability of such conditions and of the involvement of given professionals.
However, one school of thought holds that there may be common features among seemingly different conditions, and it is Richardson’s view that there is insufficient attention given to the possible impact of nutrition and that this issue does not feature in “standard” evaluation and management practices.
She goes on to cite the “obvious and fundamental” importance of a balanced diet and adequate intake of essential nutrients for the most effective operation of the central nervous system, and refers to the growing evidence for the particular significance of deficiencies or imbalances in some highly saturated fatty acids (HUFA) within the omega-3 or omega-6 series in the aetiology of dyslexia, dyspraxia, ADHD, and autism. The further implication is for the probable benefits in managing these forms of learning and behavioural disorders, or reducing the severity of symptoms, from the use of dietary supplements containing the relevant HUFA.
(The present writer – MJC – would refer at this point to earlier research, such as that of a few years ago linking vitamin supplementation with IQ performance, which has highlighted possible benefits from dietary treatment, but which has also demonstrated that this is no universal panacea and, importantly, that dietary supplements of vitamins or minerals, etc. will only be significant among those cases where there is a deficiency. To provide this treatment for children who already have a balanced nutritional intake will not be relevant, and there may even be some potential harm from too great a concentration of particular substances.
Filling a nutritional deficit will ensure more effective physiological and cognitive functioning, and greater utilisation of a child’s capacities, but this is hardly the same as increasing those basic capacities.
However, one would acknowledge the possibly enhanced significance of such treatment among very young children for whom some learning or behavioural difficulties may be averted if nutritional deficiencies are detected and compensated during early and crucial stages of [neural] growth and development.)
Richardson argues that the overlap between the conditions listed is high so that “pure” cases are the exception rather than the norm, but notes that these diagnostic categories are largely descriptive of certain permutations of symptoms and that milder forms of the symptoms are quite common among the child population at large.
However, she emphasises how they are all complex developmental syndromes with a biological basis and a genetic predisposition; and reference is made to the recently coined term “phospholipid spectrum disorders” (Peet et al 1999) to describe a range of conditions which may be inter-related and involve some underlying deficit in fatty acid or phospholipid metabolism.
The argument continues that conditions like autism may involve the impact of a number of genes, as yet not clearly specified, but possibly linked within chromosomal regions that operate upon enzyme facilitation of fatty acid and phospholipid metabolism. Meanwhile, only environmental factors are thought likely to be behind the apparent increase in the incidence of conditions like ADHD and, particularly, autism, with exposure to environmental toxins as one likely factor, and changes in children’s nutritional intake as another.
Fatty acid and phospholipid metabolism are perceived as being at the “interface” of gene-environment interactions, and certain features associated with ADHD, autism, etc., (eg the imbalance in the male-female ratio, increased incidence of auto-immune disorders, or motor/visual/language anomalies) do appear potentially explicable by deficient fatty acid metabolism.
The omega-3 and omega-6 highly unsaturated fatty acids (HUFA) are known to be very important for normal brain structure and functioning, and two of the essential HUFA are linoleic acid and alpha-linolenic acid which can only be provided by diet. The more complex HUFA into which these two substances are converted are major components of neuronal membranes, with a significant relevance to brain growth and to synapse and photoreceptor operation respectively.
Further, adequate amounts of HUFA are required for the fluidity of neuronal membranes and neurotransmission.
However, the process of converting basic linoleic acid into the more complex HUFA is inefficient, and other dietary factors can further impair the process such as a high intake of saturated fatty acids as found in most processed foods or an inadequate intake of some minerals or vitamins such as magnesium or vitamin B3, B6, or C.
There is evidence (eg Stevens et al 1995) that signs of HUFA deficiencies, such as dry skin, frequent thirst, and some behavioural abnormalities, are higher in children with problems like ADHD or dyslexia compared to controls; and recent findings (eg Bell 2001) have shown an even higher level of these signs of deficiency in individuals with autistic spectrum disorders.
Richardson then refers to much anecdotal evidence for the benefits of dietary supplementation with fatty acids for many individuals; however, it is recognised that there is a lack of systematic investigation involving randomised, controlled trials, complicated by the heterogeneous nature of the populations which appear to share behavioural or metabolic symptoms. In other words, hard evidence for the effectiveness of HUFA as a treatment for autism or other developmental conditions remains very limited, and carefully controlled trials which can deal with the complications of comorbidity and heterogeneity are required.
The current advice has it that HUFA supplementation should not be seen as a positive treatment for all children or young people with these developmental conditions because of the variability among cases and the multi-factorial nature of the conditions. However, a high intake of HUFA is associated with a range of benefits so that it is deemed reasonable to try nutritional approaches, alongside other strategies, under the guidance of a suitably qualified professional.
Omega-3 HUFA is said to be the probably more relevant supplement given its limited presence in typical diets, and its natural source being limited to seafood. There is also evolving evidence that the omega-3 fatty acid EPA is associated with improvements in attention, perception, memory, and mood.
Accordingly, a high-EPA fish oil is recommended in 500mg doses for individuals with dyslexia and dyspraxia, and for those with the milder forms of ADHD or autistic spectrum disorder.
Needs and reactions will differ among individuals hence the need for consistent monitoring and variation of dosages, as well as assessment of other elements of nutritional management such as the adequacy of mineral intake, or the avoidance of high levels of dairy products, and the ideal context is that of a properly balanced normal diet.
In a separate and brief presentation from Bell (2002), describing his experiences as a researcher and as a father of an autistic child, there is a further expression of the perceived significance of a deficiency in fatty acids among children with autism. He further recommends the use of fish oils rich in EPA and GLA and of vitamin E as dietary supplements.
He refers to the reports of parents using such supplements with their autistic children of reduced aggressiveness and hyperactivity, and improved sleep patterns. Some reports have included improvements in speech and spans of attention and concentration.
(Again, one might be cautious and note that the evidence is anecdotal and non-systematic, and that there is no reference to a change in the underlying autistic state albeit with reduced severity or number of symptoms. On the other hand, one might argue that what matters is that those most directly involved in the care of the child, and most affected by maladaptive symptoms, do see improvements from this relatively unintrusive dietary approach.)
A largely similar theme is pursued by Taylor (undated) who cites common estimates of between 5 and 10% of the child population as experiencing behavioural difficulties, with frequent additional problems with language, social skill development, and coordination. He refers to the high comorbidity of conditions like dyslexia, dyspraxia, ADHD, and autism, and to the legitimacy of assuming some common external influence.
One very significant external factor is nutrition, and one might further assume that the chemical composition of what is eaten will impact for the better or worse upon behaviours. Taylor reviews earlier findings (such as Lucas et al 1989) which highlighted the importance of maternal diet and its impact upon feeding problems in new-born infants; and which found that a polyunsaturated fatty acid (DHA) detectable in breast milk was a key factor in promoting development in the child, both during the pre-natal and neo-natal periods.
This DHA appears to have a particular role with regard to increasing the efficiency of receptor cells and retinal performance, as well as enhancing memory, attention, language, and motor skills. The corollary is that a lack of DHA would be associated with various types or levels of developmental difficulties.
Accordingly, the advice is to include dietary supplements rich in this fatty acid within any intervention “package” addressing developmental disorders; and Taylor quotes evidence to show that atypical early development is very commonly associated with marked feeding problems starting from the earliest days. It is further reported that many of the children and young people given DHA supplements were described by their parents as showing rapid improvements in coordination and information-processing abilities.
(Taylor introduces a note of caution in highlighting how the introduction of polyunsaturated fatty acids among individuals where there is some [familial] evidence for enhanced electrical activity of an epileptic type may be linked with an increase in the incidence of seizures.)
Other Dietary Exclusion or Supplement Treatments
The question of the therapeutic value of diet and dietary supplements in autism is explored by Converse (2002) whose initial review of studies indicates how a diagnosis of ASD is now regarded as distinct and differentiable from other forms of pervasive developmental disorder (such as Rett’s Syndrome).
However, while recognising the genetic features of ASD, she cites recent debate
(eg Risch et al 1999) over the possibility that it is a systemic condition, amenable to intervention, and precipitated by some genetic predisposition in interaction with an environmental trigger.
This debate was stimulated by the apparently sharp increase in incidence rates over the last 10 or 15 years which would be difficult to explain in purely genetic terms, the observation of a frequent association between ASD and gastrointestinal or auto-immune problems, and the claims of significant improvements (even “recovery”) as a result of early and intensive intervention.
(Converse acknowledges the difficulty in clarifying whether there has been a steep rise in ASD rates or whether it is a matter of widened diagnostic criteria including the concept of an autistic spectrum. Her own view is that the criteria theory hardly accounts for the continuing rise in diagnoses following initial increases when the different criteria were being implemented, but she suggests that one might simply note the marked and unarguable rise in referrals to specialist services of children with ASD and the substantial rise in costs of resources for this population.)
In any event, there has been a drive among parents to explore all treatment options, including diet, perhaps stimulated by (single case) studies of the benefits of gluten and casein free diets for children with autism.
One such study (Lewis 1998) highlighted improvements following the adoption of a restricted diet with the implication that maldigestion of gluten and casein and the subsequent formation of opiate-like substances like casomorphin may be responsible for the language delay, idiosyncratic behaviour, and digestive problems commonly observed in autism ….. and the survey completed by Shattock and Savery (1997) found that nearly 900 of 1100 autistic children tested had unusually high gluten and casein based opiates in their urine.
Converse then cites a number of anecdotal and single case studies which claim success in terms of symptom reduction and improved functioning from the use of restricted diets; and she reports her own short experience of testing 15 ASD children of whom 10 were found to have excess casomorphin or gliadomorphin and who responded positively to strict dietary avoidance of casein and gluten according to parental reports and qualitative clinical impressions at follow up. A further sample of 25 ASD children, not given any urinanalysis, all showed a positive response to the restricted diet.
Converse recognises that there is no hard and systematic evidence for the benefits of this approach, and also that objections to such an intervention may be based upon the anxiety lest children with autism are even more inhibited from easy interaction with other children such as at meal-times.
Nevertheless, she argues that dietary approaches are relatively easy to organise and whether or not there are benefits equally easy to determine … on condition that sufficient time is allowed for the trial use of the restricted diet, and vitamin or mineral supplements given as necessary.
There is also the possibility that the initial reaction among children so-treated is for a lapse into worse behaviour or poorer levels of functioning, such that patience is required to pursue the intervention for a meaningful period, especially if a difficult withdrawal period is indeed an indicator of longer term benefits such as heightened alertness and awareness, enhanced language use, and increased acceptance of other foods.
With regard to immune responses, Converse cites the lack of convergence of views in this field, but refers to evidence from a number of different studies (eg Lucarelli et al 1995) that intestinal permeability and inflammation are more frequent in children with ASD than controls, and both conditions may increase the chance of the absorption of only partially digested peptides which can evoke antibody responses.
Physical symptoms accompanying this food intolerance include pallor, bloating, low weight, oral hypersensitivity, eczema, poor sleep, and irritability.
The foods thought most likely to give rise to theses problems include eggs, dairy foods, soy, and gluten, but a range of foods may be implicated.
Again, the advice from Converse is that exclusion diets may be effective, but there is no point in dabbling. Rather, a full exclusion diet must be pursued for a long enough trial and under professional guidance and monitoring (including ensuring that the diet is adequate and supplemented if necessary with mineral or vitamins).
Finally, Converse refers to anecdotal reports of success with certain supplements per se, such as ascorbic acid, or fish oils (including cod liver oil), in improving social and language performance such as heightened eye contact, reducing perseverative actions, and increasing compliance.
While acknowledging the significance of such reports from parents who are most directly involved with the children, Converse stresses the need for specialist assessment of the possible causes for poor digestion or reflux, or other symptoms, before agreeing to a trial of dietary supplements.
Her conclusion notes that there has been a long presumption that the gastrointestinal symptoms reportedly common among children with autism are the reaction to anxiety or other psychological states, but she notes the gradually evolving school of thought which suggests that any causal connection may be the other way about with gastrointestinal problems insidiously operating to create the symptoms of ASD. However, while there appears therapeutic value in some nutritional interventions, it is necessary to organise systematic trials to determine which children are likely to respond most positively to this kind of intervention.
Shattock and Savery (1997) had previously discussed the view that excess peptides
(the breakdown products of dairy proteins) may have an inhibitory impact upon neurotransmission within the central nervous system.
Normally, proteins are digested by enzymes and converted to peptides which, in turn, are converted into smaller amino acid components which can be absorbed through blood capillaries in the gut. Larger peptides are usually unable to cross the gut membrane barrier but, when they do, the impact upon neurotransmission may be observable in behavioural symptoms.
The possible implication is that individuals with autism may be particularly prone to this peptide effect, and the authors hypothesize that the excess peptides in the gut may reflect defective enzyme activity or a lack of an adequate supply of enzymes. Alternatively, in these individuals, the barrier between the gut and CNS may be more permeable, due to some genetic effect or to the residual effects of a viral illness or infection, or imbalance between healthy and harmful bacteria …. with possible benefits arising from the use of a probiotic dietary supplement to redress this imbalance.
This kind of hypothesis receives some support from the findings of Shaw et al (1995) that children with autism do show signs of abnormal gut flora, especially an elevated level of yeast; and from those of Isolaurie et al (2000) who highlighted how intestinal inflammation can disrupt the gut barrier and increase permeability to antigens and peptides and how some probiotics may improve gut mucosal strength by limiting allergic inflammation.
However, it is still appropriate to express caution in that autism is a complex set of disabling disorders whose permutation of causal routes and symptom expression will vary widely across individuals. Accordingly, it is inappropriate to generalise findings from single case studies or from small scale research to all or many children with autism, although dietary intervention would appear a reasonable intervention to explore over a given trial period, especially given the relatively common belief in the beneficial effects of removing food components containing gluten or casein.
Finally, one notes the findings of a piece of local action research completed by Firman (2000) who explored the benefits of a modified diet on a sample of 12 children with autism, 6 of whom were at a pre-school stage and all showing serious social problems, 3 in primary school (and all showing social and communication problems), and 3 in specialist schools or units and showing a range of behavioural, social, and language needs.
The author refers to her direct or indirect experience with regard to positive effects on behaviour in the case of children with autism when treated for the maldigestion of certain foods, notably dairy products and gluten, and when given supplements including vitamins and minerals. It was the regularity of parental reports of improvement which stimulated her interest in this area.
Firman’s study involved differentiating children into those with a high level of stomach acid from those with a low level, with the hypothesis that an inappropriate level of acid may lead to the maldigestion of some proteins.
Eventually, the sample was subdivided into an ADHD group treated with fish oils and evening primrose oil; a high acid group treated with calcium carbonate, with the intake of fruit avoided on an empty stomach and intake of fruit juices reduced, and eventually shifted to vitamin B supplements; and a low acid group treated with an iron or multivitamin supplement.
It was noted that only 1 child failed to make positive gains, while 2 were described as making good progress and 9 as making very good progress. Progress was judged in terms of parental and teacher reports of more settled behaviour, social development, and language functioning.
However, there was reference to the erratic path in that after some weeks of steady progress, the children would show a sudden deterioration, apparently linked to infections, before resuming the positive progress … with the risk that some parents would seek to discontinue the dietary trial at this point especially if the improvements that had occurred were relatively subtle.
The general advice to emerge from this study is a confirmation of the legitimacy of exploring dietary elements of a treatment package, albeit under professional supervision and applied consistently over an agreed time scale. It was acknowledged by Firman that the study was very small and involved no blind, placebo controlled conditions; but the observations from the parents and teachers directly involved with the children indicated useful effects from this kind of dietary intervention, with the implication for support for their continuation as well as for instigating larger scale and systematic studies by which to gain greater and more valid sets of data.
* * * * * *
Bell G. 2001 Fatty acid deficiency and phospholipase A2 in autistic spectrum disorders. Research workshop on fatty acids in neurodevelopmental disorders : St. Anne’s College, Oxford. September 2001
Bell G. 2002 Essential fatty acids as treatment for autistic behaviours. Research workshop at Stirling University : March 2002.
Converse J. 2002 Diet, supplements, and autism spectrum. email@example.com
Firman N. 2000 My experiences of using diet and supplements with ASD children. In Autism : Perspectives on Progress. (pp 183-192) Autism Research Unit, University of Sunderland.
Isolaurie E., Arvola T., Sutas Y., Moilanen E., and Salminen S. 2000 Probiotics in the management of atopic eczema. Clinical and Experimental Allergy 30 1604-1610
Lewis L. 1998 Special Diets for Special Kids. Arlington, Texas : Future Horizons
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Shattock P. and Savery D. 1997 Autism as a Metabolic Disorder. Autism Research Unit, Unversity of Sunderland.
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Shaw W., Kassen E., and Chaves E. 1995 Increased excretion of analogs of krebs cycle metabolites and arabinose in two brothers with autistic features. Clinical Chemistry 41 1094-1104
Stevens L., Zentall S., Deck J., Abate M., Watkins B., Lipp S., and Burgess J. 1995
Essential fatty acid metabolism in boys with attention deficit hyperactivity disorder. American Journal of Clinical Nutrition 62 761-768
Taylor D. (undated) Essential fatty acids, diet, and developmental disorders. Positive Health Publications.
© Mike Connor 2004.
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