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.
* * * * * *
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Converse J. 2002 Diet, supplements, and autism spectrum. info@nutritioncare.net
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.
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© Mike Connor 2004.
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