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The potential role of fatty acids in developmental dyspraxia – can dietary supplementation help?

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Abstract

Summary 1. Dyspraxia or developmental coordination disorder (DCD) shows substantial overlap with other developmental and psychiatric conditions both within individuals and within families – notably dyslexia, ADHD and autistic spectrum disorders, but also mood disorders and schizophrenia spectrum disorders. This indicates some common predisposing factors at the biological level. The proposal considered here is that these could involve aspects of fatty acid metabolism. 2. Certain HUFA of the omega-3 and omega-6 series are essential for normal brain development and function. Together they should make up around 20% of the dry mass of the brain, and adequate supplies are also crucial for efficient information processing within the brain and nervous system, as well as for many aspects of general health. 3. These key HUFA are often lacking from modern diets and must therefore be manufactured within the body from simpler essential fatty acids (EFA). However, this process is inefficient in humans, and can also be blocked by dietary and lifestyle factors. Furthermore, dietary intake of the necessary omega-3 EFA in particular is often low. 4. The predisposition to dyspraxia and related conditions may involve mild constitutional inefficiencies of fatty acid metabolism that increase the usual dietary requirements for HUFA. These could include (a) poor EFA-HUFA conversion, (b) difficulties in incorporating HUFA into brain cell membranes and/or (c) unusually high rates of HUFA breakdown and loss, although there are other possible mechanisms. 5. Many features associated with dyspraxia are consistent with HUFA deficiencies or imbalances. These include the core difficulties with motor coordination, attention and sensory processing, as well as the excess of males affected, proneness to allergic or autoimmune conditions, disturbances in temperature regulation and sleep, and irregularities of mood. 6. There is already some experimental evidence for fatty acid abnormalities in ADHD, dyslexia and the autistic spectrum. Although dyspraxia has never been ‘factored out’ in studies of these related conditions, no studies of dyspraxia per se have yet been reported although these are now underway. 7. If fatty acid deficiencies were a contributory factor in these developmental conditions then dietary supplementation with HUFA might be of benefit. In ADHD, a few controlled treatment studies have been reported, with mixed results; and in dyslexia, the first controlled trial has shown that treatment with omega-3 and omega-6 HUFA can reduce attentional problems, anxiety, and disruptive behaviour. 8. In dyspraxia, no properly controlled trials of HUFA supplementation have yet been reported. One small open study indicated possible benefits, but without a placebo control group these cannot be attributed to the treatment itself. A large-scale randomised controlled trial of HUFA treatment in dyspraxic children is now underway. 9. As yet there is therefore no firm evidence of benefits from HUFA supplementation in dyspraxia, although many people are already trying this approach. HUFA are generally safe and have many general health benefits, but medical advice is recommended before taking any food supplement. Furthermore, fatty acid supplements vary widely in their composition and quality. Available evidence indicates that omega-3 fatty acids – and particularly EPA – may be most effective, but this still requires confirmation. 10. Other aspects of diet may also merit attention, but nutritional intervention is obviously only one aspect to consider in the management of dyspraxia, and cannot be expected to benefit more a subset of affected individuals. Some features that may indicate a good response to HUFA supplementation have already been identified, but further research is needed to verify their predictive power.
The potential role of fatty acids in
developmental dyspraxia – can dietary
supplementation help?
Alexandra J. Richardson, D.Phil (Oxon), PCGE
Senior Research Fellow, University Lab. of Physiology
and Mansfield College, Oxford.
This article was written at the request of the Dyspraxia Foundation UK,
and appeared in their Professional Journal, 2002.
Correspondence address:
University Lab. of Physiology
Parks Road
Oxford
OX1 3PT
Email: alex.richardson@physiol.ox.ac.uk
Acknowledgements:
The author’s work in this area is supported by the Dyslexia Research
Trust, Food And Behaviour Research and Mansfield College, Oxford.
Further information on research in this area can be found at
www.fabresearch.org
Fatty acids in developmental dyspraxia – can dietary supplementation help?
© A.J. Richardson 2002
Summary
1. Dyspraxia or developmental coordination disorder (DCD) shows substantial overlap with other
developmental and psychiatric conditions both within individuals and within families – notably
dyslexia, ADHD and autistic spectrum disorders, but also mood disorders and schizophrenia
spectrum disorders. This indicates some common predisposing factors at the biological level.
The proposal considered here is that these could involve aspects of fatty acid metabolism.
2. Certain HUFA of the omega-3 and omega-6 series are essential for normal brain development
and function. Together they should make up around 20% of the dry mass of the brain, and
adequate supplies are also crucial for efficient information processing within the brain and
nervous system, as well as for many aspects of general health.
3. These key HUFA are often lacking from modern diets and must therefore be manufactured
within the body from simpler essential fatty acids (EFA). However, this process is inefficient in
humans, and can also be blocked by dietary and lifestyle factors. Furthermore, dietary intake of
the necessary omega-3 EFA in particular is often low.
4. The predisposition to dyspraxia and related conditions may involve mild constitutional
inefficiencies of fatty acid metabolism that increase the usual dietary requirements for HUFA.
These could include (a) poor EFA-HUFA conversion, (b) difficulties in incorporating HUFA
into brain cell membranes and/or (c) unusually high rates of HUFA breakdown and loss,
although there are other possible mechanisms.
5. Many features associated with dyspraxia are consistent with HUFA deficiencies or imbalances.
These include the core difficulties with motor coordination, attention and sensory processing, as
well as the excess of males affected, proneness to allergic or autoimmune conditions,
disturbances in temperature regulation and sleep, and irregularities of mood.
6. There is already some experimental evidence for fatty acid abnormalities in ADHD, dyslexia
and the autistic spectrum. Although dyspraxia has never been ‘factored out’ in studies of these
related conditions, no studies of dyspraxia per se have yet been reported although these are now
underway.
7. If fatty acid deficiencies were a contributory factor in these developmental conditions then
dietary supplementation with HUFA might be of benefit. In ADHD, a few controlled treatment
studies have been reported, with mixed results; and in dyslexia, the first controlled trial has
shown that treatment with omega-3 and omega-6 HUFA can reduce attentional problems,
anxiety, and disruptive behaviour.
8. In dyspraxia, no properly controlled trials of HUFA supplementation have yet been reported.
One small open study indicated possible benefits, but without a placebo control group these
cannot be attributed to the treatment itself. A large-scale randomised controlled trial of HUFA
treatment in dyspraxic children is now underway.
9. As yet there is therefore no firm evidence of benefits from HUFA supplementation in dyspraxia,
although many people are already trying this approach. HUFA are generally safe and have many
general health benefits, but medical advice is recommended before taking any food supplement.
Furthermore, fatty acid supplements vary widely in their composition and quality. Available
evidence indicates that omega-3 fatty acids – and particularly EPA – may be most effective, but
this still requires confirmation.
Further information: Food And Behaviour Research www.fabresearch.org 2
Fatty acids in developmental dyspraxia – can dietary supplementation help?
© A.J. Richardson 2002
10. Other aspects of diet may also merit attention, but nutritional intervention is obviously only one
aspect to consider in the management of dyspraxia, and cannot be expected to benefit more a
subset of affected individuals. Some features that may indicate a good response to HUFA
supplementation have already been identified, but further research is needed to verify their
predictive power.
Introduction
Dyspraxia or developmental co-ordination disorder (DCD)1 remains one of the least studied of a
range of common and interrelated developmental disorders of childhood. Conditions showing
substantial overlap include dyslexia, attention-deficit / hyperactivity disorder (ADHD) and autistic
spectrum disorders (ASD). Dyslexia refers to specific difficulties in the acquisition of written
language skills, but these are part of a developmental syndrome involving a much broader range of
features (Miles, 1994). The ADHD diagnosis involves hyperactive and impulsive behaviours,
attentional difficulties, or both; but controversy still surrounds this diagnosis and its treatment (NIH
Consensus Statement 1998). In autistic spectrum disorders, the central features are specific
difficulties in social interaction and communication and a restricted range of behaviours, but again,
diagnosis is fraught with difficulties and the clinical picture includes many other features (Jones,
2000). In practice, therefore, there is substantial variability within each of these diagnostic
categories, and most affected individuals show features of more than one of these conditions, i.e.
‘pure’ cases are the exception, not the rule.
Between them these developmental conditions affect more than 10% of the school-age population;
and as they all have a dimensional aspect, milder difficulties are even more common. Although they
often go unrecognised, the earlier these kinds of behavioural and learning difficulties can be
identified, the better are the chances of successful management and remediation. However, because
the formal diagnoses of dyspraxia, dyslexia, ADHD, and ASD all involve different sets of
operational criteria, each tends to involve specialists from different professional disciplines and
therefore different management approaches. Unfortunately, practitioners dealing with any one of
these conditions may be unfamiliar with at least some of the others, and thus unaware of co-
morbidity issues and their implications.
In none of these conditions is the possible role of nutrition considered as part of standard evaluation
and management, despite its obvious and fundamental importance for optimal functioning of the
brain. A whole range of micronutrients is essential in this respect, but in particular, there is
mounting evidence – summarised here - that deficiencies or imbalances in certain highly
unsaturated fatty acids (HUFA) of the omega-3 and omega-6 series may contribute to both the
predisposition and the developmental expression of dyspraxia and related conditions (Richardson
and Ross, 2000). This raises the possibility that dietary supplementation with the relevant HUFA
might help in their management, but further research is needed to investigate this. Very few
properly controlled treatment trials have yet been carried out, and these have involved children with
a primary diagnosis of either ADHD or dyslexia, although a trial involving dyspraxic children is
now in progress (Richardson and Portwood, in preparation). What evidence there is from trials of
fatty acid treatment in related conditions is therefore considered here, followed by a discussion of
the potential practical implications.
1 In neuropsychology, dyspraxia refers to specific problems in the planning and execution of complex, sequenced
actions - the most obvious of which involve motor co-ordination difficulties. The DCD diagnosis adopted by the DSM-
IV (American Psychiatic Association, 1994) is much broader, but developmental dyspraxia has come to be used by
many in a similarly general way, as it will be here for convenience.
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
© A.J. Richardson 2002
Associations between dyspraxia and other behavioural and learning difficulties
The overlap between dyspraxia and dyslexia is between 30-50% in both directions, depending on
the exact criteria and ‘cut-off’ points used in each diagnosis. Individuals with both conditions often
show more difficulties with spelling, handwriting and written expression than they do with reading
per se, and other common features include directional confusions, weaknesses in working memory
and the sequential organisation of ideas, and inefficient automatisation of skills. It seems likely that
dyspraxia may involve the same kinds of difficulties in rapid visual processing that have already
been well-documented in dyslexia (Stein and Walsh, 1997), although this has not yet been formally
investigated. Within dyslexia, poor motor coordination has also been particularly associated with
attentional difficulties (Denckla et al, 1985), suggesting that the interface between dyslexia and
dyspraxia also overlaps into the broad territory of ADHD. However, motor abnormalities in early
development appear to be fundamental to dyslexia (Haslum,1989), as are general difficulties in the
automatisation of skills; hence the cerebellum has become a focus of recent study. This brain region
is crucially involved in motor control, but also plays a key role in cognition; it is especially
important for the acquisition of any new skills (including language) as well as the smooth
performance of previously mastered skills. Cerebellar activation in dyslexic adults was found to be
dramatically lower than that of non-dyslexic adults during both acquisition of new skills and the
performance of previously learned skills (Nicolson et al, 1999), and metabolic differences in
cerebellar activity in dyslexia have also been reported (Rae et al, 1998). Dyspraxia has not usually
been considered in studies of dyslexia, but this – as well as separate studies of dyspraxia - is clearly
long overdue; and anomalies of cerebellar function seem more than likely in this condition
(Nicolson, 2000).
The mutual overlap between dyspraxia and ADHD can also be as high as 50%. Population studies
indicate that this combination syndrome, involving deficits in attention, motor control and
perception (DAMP), may actually identify a much more homogeneous group than does the ADHD
diagnosis. Furthermore, long-term follow-up studies indicate that these children – who meet criteria
for both DCD and ADHD at primary school entry - have a particularly poor prognosis in terms of
later achievement and social adjustment (Hellgren et al, 1994; Rasmussen and Gillberg, 2000).
Within ADHD, different underlying factors probably contribute to the two dimensions of attentional
difficulties and hyperactivity-impulsivity, and the former seem more fundamentally associated with
dyspraxia. Such attentional problems are often associated with emotional sensitivity, mood swings
and anxiety, which may be ‘internalised’ and thus not always obvious to others. By contrast,
hyperactive and impulsive behaviour is more ‘externalised’ and overtly disruptive, but this can be
associated either with apparent ‘carelessness’ and a remarkable lack of anxiety, or with powerful
emotional frustration and a tendency to cycle between a tense, overaroused state and periods of
apparent apathy and fatigue. There is mounting evidence that in many cases, apparent ‘ADHD’
symptoms of either variety may actually reflect an underlying mood disorder – either depression, or
even bipolar (manic-depressive) traits. This issue is emphasised by Papolos and Papolos (1999) in
their excellent book on bipolar disorders in children; and it has very important implications for
management, because the stimulant medications typically used to control ADHD symptoms can
have disastrous consequences for children with a bipolar temperament. The fact that omega-3 fatty
acids have been found to stabilise mood swings in adult bipolar disorder (Stoll et al, 1999) make
this an approach well worth exploring in either children or adults with an ‘ADHD’/bipolar profile.
The overlap between dyspraxia and autistic spectrum disorders is also substantial, particularly for
milder forms of the latter such as Asperger’s syndrome. Early difficulties with feeding are common
in both cases, often associated with digestive problems that may reflect food allergies or
intolerances. These - together with the so-called ‘leaky gut’ syndrome - still remain a source of
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
© A.J. Richardson 2002
controversy that will only be resolved by further investigation, but sensitivity to cow’s milk appears
to be a real issue for some individuals, and the predisposition to dyspraxia and related conditions
may well involve overactive immune responses, as discussed later. Other features common to
dyspraxia and the autistic spectrum include sleep problems, poor temperature regulation, physical
anhedonia and/or hypersensitivity to touch, and excitability or instability of mood. These physical
features are well known to both clinicians and those directly affected by these conditions, but
unfortunately most research to date has largely neglected these kinds of physiological aspects,
focusing rather on the behavioural or cognitive features of each condition.
In summary, diagnostic criteria for the four conditions considered here are completely different, and
yet the evidence shows that boundaries between them are far from clear-cut. This is not surprising
when we remember that the diagnostic labels used to classify developmental disorders simply
describe patterns of behaviour. They do not provide any explanation of the causes of that behaviour
– which are almost always multifactorial, and may differ substantially between individuals with
exactly the same clinical diagnosis. When it comes to management, it therefore makes sense for
practitioners to focus on treating the individual concerned, and to attempt to identify any factors that
may be relevant to their particular difficulties. An excellent case study of a boy with ‘dyslexia’
exemplifies this approach (Baker, 1985). Biochemical investigations of this child revealed fatty acid
deficiencies as well as other imbalances that were easily corrected via nutritional management, and
improvements in schoolwork followed. As the author acknowledges, single case studies of this kind
cannot provide definitive evidence, and this approach is likely to help only a subset of children with
the ‘dyslexia’ label. However, it is hard to disagree with his statement that ‘when the stakes are
high, and the risk or cost is low, it makes sense to consider any factor that has reasonable odds of
playing a role’.
The perspective taken here is that dyspraxia, dyslexia, ADHD and autistic spectrum disorders are all
highly complex developmental syndromes with a constitutional basis. As readers of this journal will
already be aware, the developmental dyspraxia label itself can encompass a very broad and varied
range of features. However, some of this variation undoubtedly reflects the high clinical overlap
with these other developmental conditions, and the many associated features they share point to
some common underlying factors at the level of biological predisposition. These could plausibly
include anomalies of fatty acid metabolism, acting to increase the usual dietary requirement for
certain highly unsaturated fatty acids that are essential for optimal brain development and function,
but are unfortunately lacking from many modern diets.
Familial associations and genetic factors
Dyspraxia, dyslexia, ADHD and autistic spectrum disorders not only overlap within the same
individuals, but also cluster within the same families, as do many of the associated physical features
(such as elevated rates of non-right-handedness, and an apparent increased susceptibility to allergic
or autoimmune disorders). Some psychiatric conditions also appear to be associated with these
developmental ones, including depression, bipolar (manic-depressive) disorder, substance abuse,
antisocial or other personality disorders and schizophrenia. It has been proposed that ‘phospholipid
spectrum disorders’ might better describe this diverse range of interrelated conditions than do the
current diagnostic labels (Peet, Glen and Horrobin, 1999), because there is now mounting evidence
that abnormalities of fatty acid and phospholipid metabolism play at least some part in each case,
and could perhaps help to explain some of their overlap.
In all these conditions there is a clear genetic component, but the evidence indicates several if not
many different genes acting together to increase or reduce risk; and the very high prevalence of
dyspraxia and related developmental conditions indicates that the predisposing genes for these are
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
© A.J. Richardson 2002
widely distributed in the general population. No specific genes have yet been identified, but it
seems likely that some will be found to play a part in more than one of these conditions.2 A review
of proposed sites of genetic linkage to this range of developmental and psychiatric conditions shows
many commonalities, and many of these sites also contain genes known to be important in
phospholipid and fatty acid metabolism (Bennett and Horrobin, 2000).
In discussing genetic factors it is crucial to emphasise that ‘genetic’ does not mean ‘fixed’ or ‘pre-
determined’. Environmental factors (both physical and social) are constantly acting to regulate gene
expression, such that genes are actually being switched on and off every millisecond in response to
a whole array of ‘environmental’ stimuli. These include what we experience through our senses as
well as what we take in through our skin, via the air that we breathe, and also – most relevant to the
topic under discussion here – from the food that we eat. Thus genetic and environmental influences
are inextricably linked, and the tedious ‘nature versus nurture’ issue so beloved of journalists is
largely meaningless. Environmental factors (including other genes) influence gene expression; and
conversely, genetic factors can lead individuals to select certain aspects of their environments. It is
also worth emphasising that most environmental factors can usually be modified rather more easily
than can genes.
Fatty acid metabolism actually lies at the interface of gene-environment interactions, because
individual differences exist for many genes that influence the absorption, transport and utilisation of
fatty acids; and the expression of individual genetic differences of all kinds depends heavily on
dietary intake of fatty acids, both during development and throughout life. These points are
discussed further in a recent book containing a wealth of accessible information on the importance
of lipids in the evolution of the modern human brain, and the relevance of this for developmental
and psychiatric conditions, particularly schizophrenia (Horrobin, 2001). The central proposal is that
the individual differences underlying these conditions are actually as old as humanity, but that their
developmental expression will depend crucially on dietary fatty acid intake.
The role of fatty acids in adult psychiatric conditions has now started to receive considerable
attention, not least because omega-3 fatty acids (found naturally in fish oil, but often seriously
lacking from modern diets) appear to be a very promising new line of treatment. Benefits from
omega-3 supplementation – and particularly the fatty acid EPA - have now been demonstrated in
controlled trials of schizophrenia (Peet et al 2001; Peet and Horrobin, 2002a) bipolar (manic-
depressive) disorder (Stoll et al, 1999), and most recently, treatment-resistant depression (Nemets et
al, 2002; Peet and Horrobin, 2002b). Similar research concerning the developmental conditions is
still in its early stages, but the evidence from these studies will be discussed later. Meanwhile, an
overview of the nature and importance of highly unsaturated fatty acids is first provided, followed
by the background evidence for fatty acid deficiencies or imbalances in dyspraxia and related
conditions.
Fats and the brain – essential fatty acids (EFA) and highly unsaturated fatty acids (HUFA)
It is not widely appreciated (particularly by those who choose to adopt ‘low-fat’ or even ‘no-fat’
diets) that 60% of the non-water content of the human brain is actually fat. Moreover, just four
highly unsaturated fatty acids should make up around 20% of the brain’s dry mass: EPA and DHA
2 It is important to make clear that there are not - and never will be - any genes ‘for’ behaviourally-defined conditions
such as dyspraxia, dyslexia, ADHD, or autism – because genes simply do not operate at that level. Genes provide coded
information for making different kinds of proteins - the basic building blocks for bodies and brains, and for the enzymes
that constantly regulate the innumerable complex biological processes involved in living. Therefore genes cannot
possibly account directly for any complex, socially-learned behaviours, although they can certainly help to shape the
predisposition to such behaviours.
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
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from the omega-3 series, and DGLA and AA from the omega-6 series. What makes these fats so
special is the number of ‘double-bonds’ in their long carbon chains, which give them unique
biological properties. By contrast, saturated fats have no such double bonds (the carbon atoms are
literally ‘saturated’ with hydrogen atoms) while ‘monounsaturated’ fats such as oleic acid, found in
olive oil, have just one double-bond.
Table 1: Omega-6 and omega-3 fatty acids
The truly essential fatty acids (EFA) that cannot be synthesised within the body are linoleic
acid (LA) of the omega-6 series and alpha-linolenic acid (ALA) of the omega-3 series.
The longer-chain, highly unsaturated fatty acids (HUFA) that the brain needs can in theory
be synthesised from these EFA precursors - via processes of desaturation (insertion of a double-
bond) and elongation (adding two carbon atoms to the fatty acid chain).
However: the conversion of EFA to HUFA is relatively slow and inefficient in humans, so
p
re-formed HUFA from dietary sources may be needed to ensure an adequate supply of these vital
nutrients.
OMEGA-6 series Enzymes involved in
HUFA synthesis OMEGA-3 series
Linoleic Acid (LA) 18:2 Alpha-linolenic Acid (ALA) 18:3
Delta 6- desaturase
Gamma-linolenic Acid (GLA) 18:3 Octadecatetraenoic Acid 18:4
Elongase
Dihomogamma-linolenic Acid
(DGLA)
20:3 Eicosatetraenoic Acid 20:4
Delta 5-desaturase
Arachidonic Acid(AA) 20:4 Eicosapentaenoic Acid (EPA) 20:5
Elongase
Adrenic Acid 22:4 Docosapentaenoic Acid (DPA) 22:5
Elongase, Delta 6-
Docosapentaenoic Acid (DPA) 22:5 desaturase, Beta-
oxidation
Docosahexaenoic Acid (DHA) 22:6
Four HUFA are particularly important for brain development and function: DGLA and AA from
the omega-6 series, and EPA and DHA from the omega-3 series.
AA and DHA are major structural components of neuronal membranes (making up 20% of the
dry mass of the brain and more than 30% of the retina).
EPA and DGLA are also crucial, but they play functional rather than structural roles.
EPA, DGLA and AA (but not DHA) are needed to manufacture eicosanoids - hormone-like
substances including prostaglandins, leukotrienes, and thromboxanes - that play a critical role
in the moment-by-moment regulation of a very wide range of brain and body functions.
Fatty acids from one series cannot be converted into the other within the bod
y
. However,
both are essential, and the balance of omega-3 and omega-6 fatt
y
acids is ver
y
important, as
they play complementary roles in many biological functions.
For example, derivatives of AA include the ‘pro-inflammatory’ series 2 prostaglandins, while
DGLA and EPA give rise to ‘anti-inflammatory’ prostaglandins (series 1 and series 3
respectively). Similarly, thromboxanes derived from AA act to constrict blood vessels while those
derived from EPA act to relax blood vessels and improve blood flow.
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
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If these four key HUFA are not directly available in the diet, they can in theory be manufactured
within the body from simpler ‘essential’ fatty acids (EFA), as shown in Figure 1. However, it has
only recently become clear that this EFA-HUFA conversion process is actually very slow and
inefficient in humans (Salem et al, 1999; Pawloski et al, 2001; Brenna, 2002), probably reflecting
the fact that we evolved on a ‘hunter-gatherer’ diet that was very rich in pre-formed HUFA. To
make matters worse, this pathway for HUFA synthesis is further impeded by a wide range of
dietary, lifestyle or chance factors that can act to block the enzymes required (Brenner, 1981).
These inhibiting factors include:
a high dietary intake of saturated fats, hydrogenated or ‘trans’ fatty acids (the artificial fats
found in most margarines and processed foods),
lack of the necessary vitamin and mineral co-factors (particularly zinc, magnesium and
vitamins B3, B6 and C)
heavy use of caffeine (found not only in coffee and tea, but in a wide range of soft drinks
including coca-cola)
viral infections
high levels of the hormones released in response to stress.
Other relevant lifestyle factors include heavy consumption of alcohol, and smoking, although these
primarily appear to act by destroying HUFA rather than preventing their synthesis. Their effects in
depleting HUFA levels are so reliable and pronounced that these factors need to be carefully
controlled whenever HUFA status is under experimental investigation.
Why HUFA are essential for normal brain development and function
Structurally, AA and DHA are key components of brain cell membranes, making up 15-20% of the
brain’s dry mass and more than 30% of the retina. Adequate supplies of these HUFA are therefore
essential during prenatal development, and the placenta has been shown to double the levels
circulating in maternal plasma in order to meet the needs of the growing baby’s brain (Crawford et
al, 2000). Severe HUFA deficiencies can have permanent effects if they occur during critical
periods of neural development, but milder deficiencies are likely to give rise to more subtle
developmental difficulties (Crawford, 1992). The omega-6 fatty acid AA is crucial to brain growth,
and mild deficiencies are associated with low birth weight and reduced head circumference, while
the structural omega-3 fatty acid DHA is particularly concentrated in highly active sites such as
synapses and photoreceptors, and is essential for normal visual and cognitive development
(Neuringer et al, 1994).
In early life, HUFA are essential in supporting further brain growth and maturation and are
therefore found in breast milk, although they are still not present in many formula feeds. Carefully
controlled studies comparing the effects of infant formula with and without pre-formed HUFA have
shown clear advantages for both visual and cognitive development from their addition (Makrides et
al, 1995; Willatts and Forsyth, 2000)
Throughout life, adequate supplies of HUFA remain crucial for optimal brain function. They are
essential for maintaining the fluidity or elasticity of neuronal membranes (while saturated,
hydrogenated or trans fats and cholesterol act to reduce this). This fluidity is key to the proper
functioning of the membrane-bound and membrane-associated proteins that carry the chemical or
electrical signals underlying all information processing in the brain. Certain HUFA – notably AA
and EPA - also play key roles as ‘second messengers’ in chemical neurotransmitter systems, as well
as contributing to many other aspects of cell signalling (Nunez, 1993).
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Fatty acids in developmental dyspraxia – can dietary supplementation help?
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Functionally, three HUFA are particularly important in the brain: the omega-6 fatty acids DGLA
and AA and the omega-3 fatty acid EPA. In the body these give rise to a very wide range of
substances collectively known as the ‘eicosanoids’, highly bioactive hormone-like substances
including prostaglandins, leukotrienes and thromboxanes. These HUFA derivatives can exert
profound influences on brain development and function, as they play key roles in regulating blood
flow, hormonal systems and immune function. Their effects on the immune system may be
particularly relevant to dyspraxia and related conditions, and it is therefore worth noting that while
AA’s derivatives tend to be pro-inflammatory, the substances produced from both DGLA and EPA
have powerful natural anti-inflammatory effects.
In summary, adequate supplies of all four key HUFA (the omega-3 fats EPA and DHA and the
omega-6 fats DGLA and AA) are required for normal brain development, and for efficient
information processing within the brain and nervous system throughout life. Unfortunately, there
are many possible reasons why their availability may be less than optimal, and these will briefly be
considered next.
Possible reasons for HUFA deficiencies or imbalances
a) Inadequate dietary intake of HUFA (and/or the relevant EFA)
Oily fish and seafood provide the only significant direct dietary source of the crucial omega-3 fatty
acids that the brain needs (EPA and DHA), and this fact supports the traditional wisdom that ‘fish is
good for the brain’. The ‘parent’ essential fatty acid of the omega-3 series (ALA) is found in dark
green leafy vegetables and certain nuts and seeds (walnuts, pumpkin seeds and linseed (flax) are
particularly rich sources), but levels of both ALA and the more important omega-3 HUFA tend to
be very low in many modern diets. The dramatic increase in the ratio of omega-6 to omega-3 fats in
our diet over the last century (from around 3:1 to over 100:1 by some estimates) is believed by
many experts to present serious health problems, although in reality, it is likely to be the HUFA
ratio that matters most. Together with the increase in total fat (particularly from saturated and
artificial fats), abundant evidence suggests that a relative lack of omega-3 HUFA may underlie the
equally dramatic increase in many ‘modern’ disorders of physical and mental health, including heart
disease and stroke, inflammatory and other immune system disorders (including cancer) and
depression (Holman, 1998; Alexander, 1998; Hibbeln, 1998; Horrobin and Bennett, 1999).
The ‘parent’ omega-6 fatty acid (LA) is very unlikely to be lacking from the diet, as this is found in
most vegetable oils. However, as noted above, conversion of EFA to HUFA appears to be
inefficient in many people. One of the key omega-6 HUFA, AA, is found in meat and dairy
products, so this is also fairly abundant in modern diets (although vegetarians and vegans may need
to take steps to ensure an adequate intake). However, an excess of AA in relation to EPA and
DGLA - which by contrast are often lacking from the diet - can increase tendencies to
inflammation. The only food known to contain significant quantities of the other crucial omega-6
fatty acid, DGLA, is human breast milk; but this fatty acid is very easily synthesised from its
immediate precursor, GLA, which is found in some seed oils such as evening primrose,
blackcurrant and borage oils. Supplementation with GLA can therefore bypass the initial ‘delta-6-
desaturase’ enzyme step in EFA-HUFA conversion, which is usually the limiting factor.
b) Difficulties in EFA-HUFA conversion
Various dietary and lifestyle factors that can impair the (already limited) synthesis of HUFA from
EFA have already been noted earlier, but difficulties in EFA-HUFA conversion can also occur for
constitutional reasons. Atopic conditions such as eczema are associated with impaired HUFA
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synthesis (Manku et al, 1984; Wright and Bolton, 1989), and the same appears to be true in diabetes
(Arisaka et al, 1986; Horrobin, 1988). Of particular interest in relation to the excess of males
affected by dyspraxia and related conditions is the fact that males are particularly vulnerable to
HUFA deficiency, because oestrogen helps to conserve HUFA under conditions of dietary
deprivation, while testosterone can inhibit HUFA synthesis (Huang and Horrobin, 1978; Marra and
de Alaniz, 1989).
c) Difficulties in recycling HUFA
Other possible constitutional reasons for HUFA deficiencies or imbalances include inefficiencies in
the enzymes responsible for recycling them within the brain and body. HUFA are constantly
replaced and recycled, both during the normal turnover and remodelling of cell membranes, and in
the chemical cascades triggered by normal cell signalling processes. Particular enzymes from the
phospholipase A2 (PLA2) group act to remove HUFA from membrane phospholipids, and this
creates free fatty acids and other products that are highly vulnerable to destruction by oxidation, and
therefore have to be rapidly recycled in at least two further enzyme steps. The efficiency of these
processes will differ between individuals, and there is some evidence for both excessive HUFA
breakdown and recycling problems in developmental conditions related to dyspraxia, as discussed
below.
Features of dyspraxia consistent with fatty acid deficiencies
Difficulties in motor coordination are obviously the fundamental issue in dyspraxia, and evidence
from other areas indicates that these are often associated with fatty acid deficiencies. The movement
disorders that develop in many elderly people were found to be robustly associated with HUFA
deficiencies in a carefully controlled general population study (Nilsson et al, 1996). The same
appears to be true of the movement abnormalities in Huntington’s disease and those that can result
from antipsychotic drug treatment in schizophrenia (Vaddadi, 1996). Furthermore, preliminary
evidence shows that treatment with fatty acids may be beneficial in both of these conditions (Peet et
al, 2001; Peet and Horrobin, 2002b; Puri et al, 2002), and recent studies have also shown that DHA
– one of the key omega-3 HUFA - is particularly concentrated in brain regions involved in motor
control.
HUFA deficiencies could also contribute to some of the developmental difficulties in visual
processing that are characteristic of dyspraxia. The omega-3 fatty acids are likely to be most
relevant here: DHA makes up 30-50% of the retina and when omega-3 fatty acids are lacking from
the diet this is replaced by 22:5 omega-6. However, despite the fact that this fatty acid differs from
DHA by only one double bond, the effect of this substitution is a dramatic reduction in the
efficiency of signal transduction in the retina – the very first stage of visual information processing
(Litman et al, 2001). An enormous research literature now testifies to the essentiality of omega-3
fatty acids for other aspects of visual development and function, (Neuringer et al, 1994; Uauy et al,
2001), and deficits in visual selective attention and spatial learning are among the classic
consequences of omega-3 deficiency.
With respect to the more general difficulties with attention and arousal that are common in many
dyspraxic individuals, the existing evidence for fatty acid deficiencies in ADHD is obviously
relevant, and this is considered in the following section. However, in terms of possible mechanisms,
it is noteworthy that chronic omega-3 deficiency is associated with reduced levels of dopamine (and
its binding to D2 receptors) in frontal cortex (Delion et al, 1994), and this is of course the main
neurotransmitter boosted by the stimulant medications used to treat ADHD. Moreover, detailed
studies indicate that the reduced storage of dopamine in these regions following omega-3 deficiency
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may be insufficient to maintain the high release needed during ‘stimulated cognitive processes’
such as sustained attention to a demanding task (Zimmer et al, 1998). Animal studies have also
shown that the behavioural effects of n-3 HUFA deficiency include changes in attention,
motivation, and reactivity to stimuli and rewards, but not necessarily locomotion (Francàs et al,
1995). This is interesting in view of our own clinical impressions that omega-3 supplements may
perhaps have more effect on the ‘attentional’ aspects of ADHD than on hyperactivity per se,
although this still awaits confirmation.
Many other features associated with dyspraxia are also consistent with HUFA deficiencies,
including:
The excess of males affected. Sex hormones appear to increase vulnerability to HUFA
deficiency in males, as noted above.
An apparent susceptibility to allergic or autoimmune disorders. This may reflect constitutional
inefficiencies of EFA-HUFA conversion, and would be exacerbated by an excess of AA relative
to EPA and DGLA, both of which have anti-inflammatory effects.
Disturbances in temperature regulation and sleep. These are also consistent with a less than
optimal balance of eicosanoids (produced from AA, DGLA and EPA), as these help to regulate
the hormonal and other systems involved in these functions.
Irregularities of mood and arousal. HUFA can have profound effects on the neural systems
governing arousal, and as noted earlier, recent evidence shows that the omega-3 fatty acids –
particularly EPA – can help to stabilise mood swings and counteract depression.
Experimental evidence for fatty acid abnormalities in related conditions
Unfortunately, no studies of fatty acid metabolism in dyspraxia per se have yet been reported,
although research of this kind is now underway. However, there is already experimental evidence
for fatty acid abnormalities in related conditions including ADHD, dyslexia and the autistic
spectrum. It is also worth noting that dyspraxia has never yet been ‘factored out’ in these studies,
hence many of the participants may have had dyspraxic-type difficulties in addition to their primary
diagnosis.
Physical signs of fatty acid deficiency
Mild physical signs consistent with fatty acid deficiency were first reported in connection with
ADHD (Colquhoun and Bunday, 1981; Stevens et al, 1995, 1996). These include excessive thirst,
frequent urination, rough, dull or dry skin and hair, dandruff, soft or brittle nails, and ‘follicular
keratosis’ (a build-up of hard skin around the hair follicles that gives the skin a ‘bumpy’ appearance
and feel). Although each of these signs can have other possible causes, their association with fatty
acid deficiency has been well-studied in animals; and in children with ADHD, when scored on a
simple questionnaire scale their presence and severity has been shown to relate to HUFA status as
assessed via blood biochemical measures (Stevens et al, 1995).
These fatty acid deficiency signs were very marked in the dyslexic boy studied by Baker (1985),
and their association with dyslexia has been confirmed in subsequent studies. Ratings of these signs
were significantly higher in dyslexic than non-dyslexic adults (Taylor et al, 2000); and within the
dyslexic group they were associated with visual symptoms when reading, other visual problems,
auditory and language confusions and motor problems. Their occurrence and severity was also
found to correlate with the severity of difficulties with reading, spelling and working memory in
dyslexic children (Richardson et al, 2000).
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In members of the autistic spectrum, recent studies indicate that these physical signs of fatty acid
deficiency are even more prevalent than they appear to be in ADHD or dyslexia (Bell et al 2000,
2002). In dyspraxia, no studies have yet been reported but these are now underway, and clinical
experience and anecdotal evidence suggest that the same physical signs will also be associated with
this condition. Given that the checklist first developed by Stevens et al. (1995) for rating these signs
is a very simple instrument that could potentially be used with minimal guidance by parents,
teachers or other professionals, further studies to validate this against objective biochemical
measures of fatty acid status are also in progress.
Evidence from biochemical and brain imaging studies.
In ADHD, several biochemical studies have now shown reduced concentrations of HUFA in the
blood of ADHD children compared with matched controls (Mitchell et al, 1987; Bekaroglu et al,
1996; Arnold et al, 1994; Stevens et al, 1995, 1996; Burgess et al, 2000).
The most detailed studies (Stevens et al, 1995, 1996) revealed no deficiencies of the ‘parent’ EFA –
either in the blood samples or in these children’s diets. This observation is consistent with
difficulties in EFA-HUFA conversion, as first suggested by Colquhoun and Bunday (1981), but it
would also be explicable in terms of an unusually rapid rate of HUFA breakdown and loss in
children with ADHD.
Further analyses of the combined sample of ADHD boys and controls revealed that irrespective of
clinical diagnosis, HUFA deficiencies were significantly associated with a range of behavioural,
learning and health problems (Stevens et al, 1996). These findings are in keeping with a
dimensional view of ADHD, at least with respect to fatty acid deficiencies as a possible
contributory factor. Of particular note is that low levels of omega-6 fatty acids were related only to
some physical health measures (such as dry skin and hair, frequency of colds, and antibiotic use),
but not to parental ratings of behaviour or learning. By contrast, low omega-3 fatty acid status was
associated not only with physical signs of fatty acid deficiency (particularly excessive thirst,
frequent urination and dry skin) but also with both behavioural problems (including conduct
disorder, hyperactivity-impulsivity, anxiety, temper tantrums and sleep problems) as well as
learning difficulties in these children. This is consistent with substantial evidence from other
sources that the omega-3 fatty acids play a particularly key role in brain function.
Blood biochemical studies of individuals with autistic spectrum disorders have also shown
reductions in HUFA concentrations relative to controls in both plasma (Vancassel et al, 2001) and
red cell membranes (Bell et al, 2000, 2002). In the latter case, differences did not reach significance
in the small number of subjects studied to date, as wide individual variation was observed even
within ASD groups separated into ‘classical’ or ‘regressive’ autism (according to whether
symptoms were present from birth, or developed after the age of 18 months). However, a significant
elevation in both groups relative to controls was found in the ratio of AA to EPA, a potential index
of ‘pro-inflammatory’ tendencies. The studies by Bell and colleagues have also revealed that red
cell membrane HUFA of individuals with a regressive form of autism are unusually vulnerable to
further breakdown during storage unless the blood samples are kept at extremely low temperatures.
Possible explanations for this include an excess of a PLA2 enzyme that removes HUFA from
membrane phospholipids, as very low storage temperatures are required to inactivate this enzyme.
High levels of PLA2 have previously been reported in both schizophrenia and dyslexia (Macdonell
et al, 2000), consistent with an unusually rapid rate of breakdown and potential loss of HUFA via
oxidation.
In dyslexia, blood biochemical evidence confirmed the clinical picture of fatty acid deficiency in
the case study reported by Baker (1985), but further blood biochemical evidence in this condition is
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still awaited, as is also the case with dyspraxia. However, in dyslexic adults, brain imaging with
cerebral 31-phosphorus magnetic resonance spectroscopy (a non-invasive method of assessing the
chemical composition of brain tissue) has revealed anomalies of membrane lipid turnover that
would be consistent with HUFA deficiency (Richardson et al, 1997).
Can dietary supplementation with highly unsaturated fatty acids help?
The suggestive evidence for HUFA deficiencies or imbalances in dyspraxia and related conditions
has raised the possibility that dietary supplementation with HUFA might be of some benefit.
Anecdotal evidence suggests that this is true in at least some cases, but carefully designed and
properly controlled studies are needed to establish whether or not this is really the case.
Randomised, double-blind, placebo-controlled trials are regarded as the ‘gold standard’ in this
respect: participants are allocated at random to either the treatment under study or a placebo, and
no-one is permitted to know which treatment any individual is receiving until all study data have
been collected and verified. While controlled trials of this kind remain the only reliable way to
eliminate the influence of expectations, they do have their limitations (Slade and Priebe, 2001).
They are most suited to evaluating single treatments for physical medical conditions involving clear
diagnostic criteria and homogeneous study populations. They are much less suited to behaviourally-
defined developmental conditions such as dyspraxia, dyslexia, ADHD or the autistic spectrum (or
any psychiatric conditions), where the causes are likely to be complex and multifactorial, and
standard diagnostic criteria will identify a very heterogeneous population.
In ADHD, several controlled treatment trials have been reported to date, with somewhat mixed
results. The first such studies involved supplementation with evening primrose oil, supplying the
omega-6 fatty acid GLA, and these indicated only marginal if any clear benefits (Aman et al, 1987;
Arnold et al, 1989). However, mounting evidence now indicates that omega-3 fatty acids are likely
to be more important than omega-6 in their effects on behaviour and learning, and these are also
more likely to be lacking from modern diets.
In another randomised controlled trial of fatty acid treatment in ADHD children, a supplement of
fish oil and evening primrose oil was therefore used, supplying mainly the omega-3 fatty acids
(EPA and DHA) as well as a little omega-6 (GLA and AA). An early report of this study indicated
blood fatty acid changes in the treated children that were associated with reduced ADHD symptoms
(Burgess, 1998), but a full publication of the results has not yet appeared at the time of writing.
Meanwhile, supplementation with DHA alone was recently found to be completely ineffective in
ADHD (Voigt et al, 2001). These findings are consistent with other evidence that EPA, not DHA, is
the important omega-3 fatty acid for improving attention and mood and reducing perceptual or
cognitive disturbances, as discussed further below.
In dyslexia, several randomised controlled trials have now been carried out involving both children
and adults, although only one of these has so far reached full publication (Richardson and Puri,
2002). This was a small pilot study involving dyslexic children from a special school who also
showed features of ADHD, although none of them had a formal ADHD diagnosis. Results showed
that compared with placebo treatment, HUFA supplementation for three months led to significant
reductions in attentional problems, anxiety, and disruptive behaviour as assessed by the Conners’
Parent Rating Scales (CPRS-L). When the placebo group were then given HUFA supplementation
(without the children or their parents and teachers being aware of the switch) they showed a similar
reduction in ADHD-related symptoms over the next three months, in stark contrast to their earlier
lack of improvement on placebo (Richardson et al, in preparation). In a different, larger study of
clinic-referred dyslexic children, preliminary results suggest that HUFA treatment may also
improve reading progress (Richardson et al, in preparation). Full analyses of the data from this trial
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are still in progress, but treatment effects seem to be particularly pronounced in children showing
either physical signs of fatty acid deficiency or visual symptoms before treatment.
As yet, there have been no properly controlled trials concerning either dyspraxia or the autistic
spectrum. One small open study of dyspraxic children has been reported, involving supplementation
for three months with both omega-3 and omega-6 HUFA from a combination of fish oil and
evening primrose oil (Stordy 2000). Reductions were found in both motor difficulties (as assessed
via parental report and the Movement ABC) and ADHD symptoms (as assessed by the Conners
Parent Rating Scales). However, without a placebo control group it is not possible to ascribe these
changes to the treatment itself, as expectations can obviously play a significant role.
The first randomised, double-blind, placebo-controlled trial of HUFA treatment in dyspraxic
children is now underway, involving 120 children aged 8-12 years. Measures of motor function,
visuomotor skills and ratings of ADHD-related features are being assessed before and after
treatment with either a HUFA supplement (containing 80% high-EPA fish oil and 20% evening
primrose oil, supplying mainly omega-3 but some omega-6 HUFA) or a placebo (containing olive
oil, and carefully matched for both appearance and flavour with the active treatment). This study
also includes a new biochemical measure in the form of a ‘breath test’ designed to measure levels of
ethane, the final breakdown product of omega-3 fatty acids (Ross, 2002). High levels of expired
ethane would suggest that these fatty acids are being lost more rapidly than usual (rather than being
recycled), and the breath test may therefore help to identify those individuals who may need a
higher dietary intake of these key fatty acids.
In summary, only a few properly controlled trials of HUFA supplementation in ADHD and dyslexia
have yet been carried out. The balance of evidence suggests that this may have benefits in at least
some cases, but differences in the populations studied, the supplements used, and the outcome
measures as well as the trial designs make clear interpretation difficult. Many of these early studies
have involved only small numbers of participants – and while this obviously makes generalisation
difficult, it also means that much larger treatment effects are required in order to show statistically
significant group differences. Further studies are therefore needed, but given the heterogeneity
within dyspraxia and related conditions, a focus on subsets of individuals defined by specific
features - rather than these broad diagnostic labels - may be the most fruitful approach.
Practical guidance
As noted above, there is not yet any firm evidence that dietary supplementation with HUFA is
beneficial for dyspraxia. However, as a result of increasing public awareness and the many positive
anecdotal reports that have been circulating both within support groups and via the media, many
people are already trying this approach for themselves. Unfortunately, accurate information on how
to go about this is often lacking, and there are actually many important factors to consider.
First, prior consultation with a medical practitioner is always advisable before taking any food
supplement, and this is clearly essential for anyone undergoing medical treatment or supervision. If
possible, guidance from a well-qualified nutrition practitioner is also recommended, as there may
well be other aspects of diet that require attention. Dietary and lifestyle changes alone can
substantially increase the availability of HUFA, although if individual needs are unusually high then
supplements may be the only practicable option. It must also be firmly emphasised that this
approach cannot be expected to help every individual with the ‘dyspraxic’ label. However, provided
that some basic precautions are taken, HUFA supplements are very unlikely to do any harm, and
furthermore, they are already known to have a wide range of general health benefits. The only
known negative effects involve mild digestive upset, although this is relatively uncommon and can
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usually be minimised with attention to other aspects of the diet. Allergies to any food substance are
of course possible in some individuals, and if this possibility is suspected, medical advice and/or
supervision should always be sought in advance.
Choosing Supplements
It is crucial to recognise that although many different fatty acid supplements are available, these
vary widely in both their composition and their quality. With respect to quality, it is an unfortunate
fact that some fish and fish oils may contain pollutants such as mercury, PCBs or dioxins. Although
EU regulations set strict limits on this, food supplements are unfortunately not monitored as strictly
as pharmaceutical products. However, information on this – and on quality control procedures –
should be available from reputable suppliers on request. The quality (and therefore the efficacy) of
both omega-3 and omega-6 oils is also affected by the methods of manufacturing, processing and
storage used. In brief, they are destroyed by exposure to light, heat or air,3 so the packaging and
storage conditions should minimise any such exposure, and consumers should take every care both
to keep this to a minimum and to abide by the ‘use by’ dates, which should be clearly marked.
Ideally, information on quality and safety issues should be obtained from an independent source
(such as a suitably qualified practitioner) before choosing any supplement. At the very least, it
should definitely not be assumed that the cheapest supplements provide the ‘best value’; but
equally, a high price should not be taken as a guarantee that the product is of high quality, as sadly
there are many cases when this may instead reflect expensive packaging and marketing and/or high
profit margins. With respect to the composition of supplements, several points are relevant:
1. Omega-3 HUFA appear more relevant than omega-6 to these developmental
conditions, and these are also the ones more likely to be lacking from modern diets.
The ‘parent’ omega-6 EFA (LA) is plentiful in most vegetable oils, and the important
omega-6 HUFA arachidonic acid (AA) is supplied directly by most meat and dairy products.
However, if EFA-HUFA conversion is inefficient there might still be a relative lack of the
omega-6 fatty acid DGLA. If so, additional evening primrose oil to supply GLA (easily
converted to DGLA) may be helpful.
2. Within the omega-3 HUFA, the latest research indicates that it is EPA, not DHA, that
is likely to be most effective. Both are essential for optimal brain function, but while DHA
is important in brain structure (hence adequate supplies are particularly needed during early
brain development), EPA plays important roles in the moment-by-moment regulation of
brain function. Substances produced within the body from EPA are crucial for regulating
immune function, hormonal balance and blood flow, which can all affect brain function as
well as many other aspects of health. Pure DHA has been found ineffective in treating both
depression and schizophrenia, while pure EPA has shown significant benefits in these
conditions (Peet et al, 2001; Peet and Horrobin 2002a,b). Pure DHA was also found to be
completely ineffective in reducing ADHD symptoms (Voigt et al, 2001), while preliminary
evidence suggests that supplements containing both EPA and DHA may help to do this
(Burgess, 1998; Richardson and Puri, 2002). Standard fish oils contain both EPA and DHA
in ratio of around 3:2, but supplements containing higher proportions of EPA are now
available.
3. Fish liver oils are not generally suitable for these purposes owing to their high Vitamin
A content, because this vitamin is stored by the body and can be toxic in excess. As noted
above, any HUFA supplements for which premium quality cannot be guaranteed should also
3 See Erasmus (1993) for a full and extremely readable explanation of the implications of this for the manufacturing of
all fats and oils, as well as the importance of omega-3 and omega-6 oils for general health.
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be avoided. These may not only be ineffective, but could contain harmful residues (from
environmental pollution or from extraction and processing methods), as noted above.
4. Antioxidant intake should be considered, because HUFA are particularly susceptible to
breakdown via oxidation. Supplementation with Vitamin E in particular can help to protect
them, but its efficiency in this role depends on other nutrients including Vitamin C, so a
good intake of these and other antioxidants is advisable. Some specialist fatty acid
supplements include a little Vitamin E, but few contain any other antioxidants.
5. Vitamin and mineral intake is important. Essential co-factors for the synthesis of HUFA
from EFA include zinc, magnesium, and vitamins B3, B6 and C among others. These and
other vitamins and minerals are required in any case for the proper functioning of the brain
and body, but available evidence indicates that many individuals do not receive an adequate
intake of these essential micronutrients. These should ideally be obtained from the diet, but
could also be provided by a multivitamin and mineral supplement if required.
6. Other aspects of diet may also merit attention, and this may well be the best place to
start. Advice from a well-qualified nutrition practitioner may be useful, as well as consulting
with the GP (which is essential if any serious allergies or food intolerances are suspected).
However, some sensible basic steps for most people would include:
eating plenty of fresh fruit and vegetables, nuts and seeds, fish and seafood and
unrefined carbohydrates (i.e. those found in whole grains and vegetables);
drinking plenty of water (and avoiding too much tea, coffee, or drinks that contain
caffeine or other stimulants);
reducing the intake of saturated fats (particularly from fried foods), and avoiding highly
processed foods with artificial fats (hydrogenated and 'trans' fatty acids);
cutting down on sugar and refined starch (i.e. non-wholemeal bread, cakes, pastries,
biscuits, sweets and soft drinks, which often have a high sugar content and/or artificial
sweeteners, which may also be best avoided);
If food allergies or intolerances are suspected, it may also be worth exploring these,
preferably with professional assistance. Some people have difficulties in properly
digesting wheat and/or dairy products in particular, but many other common foods have
been implicated in individual cases. Removing some foods from the diet can be very
helpful in some cases, although restrictive diets should not be undertaken without
specialist advice to ensure that basic nutritional needs are being met.
Dosage, duration, and monitoring of response
Dietary HUFA requirements will differ between individuals and can also differ in the same
individual over time, as they will depend on other aspects of diet, stress levels or illness, among
other things. Optimal dosage is therefore best determined from careful monitoring, with attention
paid to any changes in other factors that may be relevant.
In our ongoing studies of dyslexia and dyspraxia, a high-EPA fish oil supplying around 500mg EPA
daily is used. However, it is clear that some individuals may need more than this (particularly those
with severe mood swings, emotional sensitivity and/or behavioural problems such as temper
tantrums). It may be relevant that recent studies have found doses of 1g/day of EPA or more to be
effective in reducing symptoms of depression (Puri et al, 2001, 2002a; Peet and Horrobin, 2002;
Nemets et al, 2002), and daily doses of 2-4g pure EPA have been used successfully in disorders
such as schizophrenia and bipolar (manic depressive) disorder (Puri and Richardson, 1998; Puri et
al, 1999; Stoll et al, 1999; Peet et al, 2001, Peet and Horrobin, 2002).
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As discussed above, supplementation with omega-3 fatty acids appears to be more important than
omega-6 for these purposes, but an adequate dietary supply of both series is always needed. If an
individual appears to need any additional omega-6 (e.g. there are still signs of dry skin conditions
and/or possible hormonal imbalance), consultation with a suitably qualified practitioner may be
helpful. For general usage, evening primrose oil supplying 50-100mg of GLA daily should be a
sufficient dose, although a higher dose might be appropriate for individuals who also suffer from
atopic conditions such as eczema.
It is very important to recognise that HUFA are foodstuffs and do not act as rapidly as most
medications, so any effects will take time to appear. In our experience, most individuals who
respond to supplementation usually report noticeable benefits within one or two weeks, but in other
cases changes seem to be more gradual. The minimum trial period should be at least three months,
as studies have shown that it takes 10-12 weeks for HUFA levels in brain cell membranes to return
to normal levels after a long-standing deficiency (Bourre et al, 1988).
After a few months, reducing the initial dose to half or even one-third of these levels may be
possible without loss of benefits, and some manufacturers advise this. Unfortunately, there is not
yet any published research even comparing different doses within the same study, let alone
changing the dose over time, so this remains speculative. Clinical experience suggests that many
people do appear to need to maintain the initial dosage on a long-term basis in order to prevent
symptoms from re-appearing, but personal experimentation is likely to be the only way to determine
what may be optimal for a given individual. Any dose changes should be made as systematically as
possible, and the effects of each change should be monitored carefully for at least 1-2 weeks before
further changes are made.
Predicting the response to HUFA supplementation?
Given the variability that exists within dyspraxia and related conditions, fatty acid supplementation
cannot be expected to benefit more a subset of affected individuals, and many people who consume
a balanced and healthy diet will already be obtaining all the HUFA they need. Nonetheless, some
possible indicators of a good response to HUFA supplementation have emerged from our clinical
experience and research to date, and these include the following features:
Physical signs of fatty acid deficiency (excessive thirst, frequent urination, rough or dry skin
and hair, dandruff, and soft or brittle nails)
Atopic tendencies (especially eczema)
Visual symptoms (such as poor night vision or sensitivity to bright light, and visual disturbances
when reading - e.g. letters and words move, swim or blur on the page)
Attentional problems (including distractibility, difficulties with sustained concentration,
working memory problems and feelings often described as like ‘brain fog’)
Emotional sensitivity or lability (especially undue anxiety/tension, excessive mood swings, or
temper tantrums arising from ‘low frustration tolerance’)
Sleep problems (particularly if these involve difficulties in both falling asleep at night and
waking up in the morning)
Further research is still needed to establish which of these features – if any – may respond to dietary
supplementation with HUFA, but results from controlled trials in both dyspraxia and related
conditions should help to elucidate this. It must also be emphasised that nutritional intervention is
obviously only one aspect to consider in the management of developmental dyspraxia. Other
interventions – and most important of all, understanding, appropriate support and encouragement –
are likely to be needed for dyspraxic individuals to achieve their full potential.
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Further information: Food And Behaviour Research www.fabresearch.org 21
... As mentioned above, dyspraxia, or developmental coordination disorder, and other overlapping neurodevelopmental disorders are associated with highly polyunsaturated fatty acid deficiency. Dyspraxia affects approximately 5 per cent of school-aged children and results in impairments of motor function, independent of general ability (Richardson, 2002). Dyslexia and dyspraxia share many common characteristics. ...
... Both manifest difficulties with spelling, handwriting and written expression. Additionally, ADHD and dyspraxia are implicated in deficits in attention and poor motor control and coordination (Richardson, 2002). Research in Durham, UK with 117 children between the ages of 5 and 12 diagnosed with dyspraxia found marked improvements in reading, spelling, and behaviour after 3 months of dietary fatty acid supplements, but no effect on motor skills (Richardson and Montgomery, 2005). ...
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This study utilized a sample of 313 eight- to sixteen-year-old same-sex twin pairs (183 monozygotic, 130 dizygotic) to assess the etiology of comorbidity between reading disability (RD) and attention-deficit/hyperactivity disorder (ADHD). RD was assessed by a discriminant function score based on the Peabody Individual Achievement Test, a standardized measure of academic achievement. The DSM-III version of the Diagnostic Interview for Children and Adolescents was used to assess symptoms of ADHD, and separate factor scores were computed for inattention and hyperactivity/impulsivity (hyp/imp). Individuals with RD were significantly more likely than individuals without RD to exhibit elevations on both symptom dimensions, but the difference was larger for inattention than hyp/imp. Behavior genetic analyses indicated that the bivariate heritability of RD and inattention was significant (h2g(RD/Inatt) = 0.39), whereas the bivariate heritability of RD and hyp/imp was minimal and nonsignificant (h2g(RD/Hyp) = 0.05). Approximately 95% of the phenotypic covariance between RD and symptoms of inattention was attributable to common genetic influences, whereas only 21% of the phenotypic overlap between RD and hyp/imp was due to the same genetic factors. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:293–301, 2000. © 2000 Wiley-Liss, Inc.