prepared for
Community Health Systems Resource Group
Hospital for Sick Children
April 29th, 2002
Long-Chain Polyunsaturated Fatty Acids
and Learning Disabilities
- Introduction
- The evidence
- Limitations of the LCP research
- Unanswered Questions
- The final word
- LCP research
- LCP promotions
- Conclusion
Introduction
Researchers first recognized a connection between long-chain polyunsaturated
fatty acid (LCP) deficiency and learning disabilities (LD) over twenty years
ago. From this association a potential new LD treatment involving LCP
supplementation is evolving. There is a compelling evidence base in support of
an LCP/LD link as well as preliminary support for LCP supplementation as an
effective treatment for some LD symptoms.
Recently, a number of sources have reported impressive LCP research findings in
conjunction with LCP treatment promotions. However, none provide any critical
analysis of the research or caution consumers with respect to possible
limitations of the data. The present report will provide a more rounded view
of the evidence and highlight some shortcomings of the LCP data.
The purpose of this report is neither to promote nor discredit LCP as a
treatment for LD. Rather, it is to provide a very brief critical review of the
LCP/LD research findings and to address some concerns regarding recent LCP
promotions. A proper critical review of the LCP research goes well beyond the
scope of this report. Of more relevance here, is the overall strength of the
case for fatty acid supplementation. Specifically, this paper will reveal how
the actual findings compare to recent claims of LCP efficacy.
The evidence
A link between essential fatty acids levels and hyperactivity was first
hypothesized in 1981. Excessive thirst, frequent urination, dry hair and skin,
all symptoms of essential fatty acid deficiency, were observed in a group of
hyperactive children. Clinical support for this theory was not obtained until
1987 when a study by Mitchel and colleagues confirmed low blood plasma levels
of certain LCPs in children with hyperactivity.
In 1995, a research team lead by John Burgess at Purdue University, discovered
that a group of ADHD boys had significantly lower concentrations of essential
fatty acids in their blood even though their diets were not LCP deficient. The
ADHD boys were also less likely to have been breast fed than boys without ADHD.
Among the ADHD boys who were breast fed, longer breast feeding duration was
associated with less severe ADHD symptoms. Breast milk contains high
concentrations of docosahexaenoic acid (DHA) one of the essential fatty acids.
In the UK. Jacqueline Stordy hypothesized that low LCP levels in dyslexics would
result
in poor dark adaptation. Rod cells of the retina are responsible for night
vision and contain high concentrations of DHA. Results confirmed the
hypothesis with dyslexics demonstrating poorer dark adaptation than controls.
Further, following DHA treatment, dyslexics showed significant improvement in
dark adaptation. Stordy also examined the effect of 4 months of LCP
supplementation on symptoms of dyspraxia. Following treatment, dyspraxic
children improved on measures of motor skills and behavior.
Research with animals adds yet another dimension to the evidence base for a
fatty acid/LD link. Of particular relevance to behaviors associated with ADHD,
rats who are fed an LCP deficient diet are more distractible than rats fed a
lipid balanced diet. Other animal studies link LCP deficiencies with learning
and memory deficits.
Research with human non-LD subjects provides support for a possible link between
LCP levels and behavior. In Japan, university students were given LCP
supplements or an inactive placebo for 3 months prior to the onset of exams.
Measures of hostility were taken before and after treatment. While the
controls showed an expected increase in hostility at exam time (presumably due
to the stress of exams), the LCP group showed no change in hostility ratings.
The most recently published findings involving LCP supplementation in LD were
conducted at Oxford by Alexandra Richardson and her team. Children with
specific learning difficulties and symptoms of ADHD who were given LCP
supplements over a 12 week period demonstrated a reduction in behavioral and
learning problems.
The most recent ADHD/LCP research is being carried out by Burgess and colleagues
at the Mayo Medical School in Rochester, Minnesota and Baylor College of
Medicine in Houston Texas. Sixty-three children with ADHD are being
supplemented with pure DHA or placebo in combination with stimulant medication.
Measures of inattention, impulsivity and hyperactivity are being taken before
and after treatment.
In other ongoing research, Richardson and colleagues at Oxford are collaborating
on 2 large double-blind, placebo-controlled trials one involving adults with
dyslexia and one involving children. Subjects are being supplemented with LCP
for 6 months. Follow-up tests will be carried out at 3-month intervals. Final
results of these trials are pending but preliminary results are promising and
in favor of LCP efficacy.
Limitations of the LCP research
If the LCP findings are indiscriminately reviewed, promotions for LCP appear
justified. However, even a cursory look at the original research reveals a
less convincing case. Consider Stordy's study on the effects of LCP on
symptoms of dyspraxia. Only 15 dyspraxic children participated in the trial
and no control group was included. Children and their parents were aware that
they were receiving active supplements and parents were responsible for rating
their children's behavior. Researchers acknowledge the significant placebo
effects associated with supplementation trials. With no controls, it cannot be
determined whether observed improvements in behavior were due to LCP, placebo
effects or possible bias introduced by parent ratings.
In the most recently published LCP study led by Richardson, participants
included children with specific learning problems and "ADHD-related" symptoms
rather than formal diagnoses of ADHD or other LDs. This means that results
based on this particular sample do not necessarily generalize to all children
with LD or even to children with formal diagnoses of ADHD who may differ in
their response to LCP supplementation.
A more serious limitation of many LCP studies is that of small sample size. For
research findings to be meaningful, they must be based on adequate numbers of
study participants. The appropriate sample size differs for every study and
depends on several factors. Small samples make sense for preliminary research
or "pilot" studies but results from such trials are not sufficiently powerful
to support firm conclusions.
The most recent Richardson study described above is in fact only a pilot study.
Follow-up analysis involved only 15 treatment and 14 placebo controls. Also,
Stordy's dark adaptation study included only 10 dyslexic children and 10
controls. The second part of the study involving supplementation compared only
5 dyslexic to 5 control children.
Pilot studies are an essential part of the research process and allow for
relatively fast answers to complex questions. Results from pilots determine
whether the time and expense of a full-scale trial is warranted. The fact that
some of the LCP studies are pilots is not at issue. What is questionable is
the practice of conveying pilot results with no mention of sample size and the
limitations associated with small trials.
Unaswered questions
In addition to the methodological shortcomings of the LCP research are a number
of unanswered questions regarding LCP treatment and LD. For example, the
available research tells us little about the long-term effects of
supplementation use. Also, the optimum formulation and dosage of LCP has not
been fully explored. Future LCP research must also determine whether all LD
children or only certain subtypes will benefit from LCP treatment. Finally,
the precise mechanism by which LCP supplements affect LD is not yet known.
The final word
LCP research
A diverse but as yet incomplete research base supports the potential for LCP
supplementation as a viable LD treatment. Results from numerous studies point
to a definite link between LCP deficiency and LD and the possible benefits of
LCP treatment in alleviating LD symptoms. The case for LCP treatment is
strengthened by the fact that support comes from a variety of sources involving
a range of subject samples. The most serious criticism of the LCP literature
is that the majority of studies to date have used insufficient subject numbers
to make firm conclusions about efficacy. Strictly speaking, this is not really
a criticism in that small-scale studies are a necessary part of preliminary
research and are not meant to be conclusive in their findings. At issue is not
the size of these trials but how they are interpreted and presented.
In practical terms this means that more research is required before LCP can
confidently be prescribed as an effective LD treatment. The evidence base is
still lacking large-scale studies with proper follow-up. As well, more
research is needed to determine the most effective formulation and dosage of
LCP as well as the target population which will most benefit from
supplementation. If the results of ongoing research by Burgess and Richardson
concur with preliminary data, the case for LCP will be further strengthened
especially given the scale of these most recent trials. Positive results will
have to be confirmed through replication by independent researchers before they
will be considered well established. Even then, many unanswered questions
regarding the possible role of LCP in the development, maintenance and
treatment of LD will need to be addressed in future research.
Potential side effects are a major consideration for any treatment choice. Not
only do fatty acid supplements appear to be safe, medical research continues to
build an extensive evidence base in support of the major health benefits of LCP
enriched diets. These safety and nutritional factors must be considered
together with the evidence for LD treatment efficacy when determining the merit
of LCP supplementation as an intervention for LD.
LCP promotions
In general, some recent promotions for LCP treatment of LD are overstated,
premature and misleading. To begin with, the association between LCP
deficiency and LD is not a new discovery, although some sources give the
impression that it is. Presenting longstanding ideas as recent discoveries is
nothing more than a marketing tactic to attract consumer interest. Overzealous
promotions do little to encourage consumer confidence and ultimately set back
the case for fatty acid supplementation. Some LD treatment consumers, wary of
treatment hype, might be discouraged by flashy LCP promotions and discount a
treatment actually worthy of consideration.
A more serious concern is that some LCP findings are presented as proof of
efficacy when in fact they are based on preliminary small-scale trials. It is
simply too early to predict with any certainty whether LCP supplementation will
help all LD children and to what extent. There is also little data on the
long-term efficacy of LCP or the best formulation, dosage, and course of
supplementation. The main objection to premature claims of treatment efficacy
is that they encourage unrealistic expectations in an already vulnerable group
of children and parents. Promoters of LCP should not underestimate the impact
of disappointment and failure should the treatment not work for some.
It is always unfortunate when invalid claims of treatment efficacy are made but
it is especially discouraging when misleading promotions occur in relation to a
truly promising treatment with credible preliminary research such as LCP
supplementation.
Conclusion
It is hoped that recent overstatements in relation to LCP efficacy do not
undermine the case for LCP as a potential LD treatment. It is safe to say that
there is enough evidence to argue a case for LCP supplementation as a possible
future treatment for LD and definitely enough to warrant more large-scale
research. In general, consumers should remain patient and cautiously
optimistic while the results of ongoing more substantial trials are gathered.
References
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Copyright © 2002 The Hospital for Sick Children, All rights reserved You are
free to duplicate this document. We request that you acknowledge The Hospital
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