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Old 01-10-04, 12:40 AM
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Long-Chain Polyunsaturated Fatty Acids

... which is (unless I've been mislead) found in fish oil and flax seed oil, and is in other food too; still checking up on that! Also can be taken through supplements. It's about small studies done on it's effect to ADHD, and then some! I found this interesting, and pretty straight forward- I think I need to read it a second time though, too much to sink in all at once! [Copywrite to The Hospital for Sick Children noted].


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.

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.

Belzung, C., et al. (1998). Alpha-linolenic acid deficiency modifies distractibility but not anxiety and locomotion in rats during aging. Journal of Nutrition, 128(9), 1537-1542.

Burgess, J.R., Stevens, L., Zhang, W., & Peck, L. (2000). Long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, 71(1), 327-330.

Colquhoun, I., & Bunday, S. (1981). A lack of essential fatty acids as a possible cause of hyperactivity in children. Medical Hypotheses, 7, 673-679.

Gamoh, S., et al., (1999). Chronic administration of docosahexaenoic acid improves reference memory-related learning ability in young rats. Neuroscience, 93, 237-241.

Hamazaki, T., et al., (1996). The effect of docosahexaenoic acid on aggression in young adults: a placebo-controlled double-blind study. Journal of Clinical Investigation, 97, 1129-1133.

Mitchell, E.A., Aman, M.G., Turbott, S.H., & Manku, M. (1987). Clinical characteristics and serum essential fatty acid levels in hyperactive children. Clinical Pediatrics, 26, 406-411.

Richardson, A.J. & Puri, B.K. (2002). A randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning difficulties. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 26, 233-239.

Stevens, L.J., Zentall, S.S., Deck,J.L. Abate, M.L., Watkins, B.A., Lipp, S.R., & Burgess. (1995). Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, 62, 761-768.

Stevens, L.J., Zentall, S.S., Abate, M.L., Kuczek, T., & Burgess, J.R. (1996). Omega-3 fatty acids in boys with behavior, learning, and health problems. Physiology and Behavior, 59(4/5), 915-920.

Stordy, J. (2000). Dark adaptation, motor skills, docosahexaenoic acid, and dyslexia. American Journal of Clinical Nutrition, 71(1), 323-326.

Copyright 2002 The Hospital for Sick Children, All rights reserved You are free to duplicate this document. We request that you acknowledge The Hospital for Sick Children copyright.
"And I get to tend the rabbits!"

Last edited by SubtleMuttle; 01-10-04 at 12:46 AM..
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