Essential fatty acids and attention-deficit/hyperactivity disorder

by Joey Day
LAT1, Language and Communications
Western Governors University
August 7, 2010

Introduction

Attention-deficit/hyperactivity disorder (commonly abbreviated ADHD or AD/HD), characterized by symptoms of inattention, hyperactivity, and impulsivity, is one of the most commonly studied and diagnosed disorders in children. Although stimulant drugs such as Ritalin (Methylphenidate) are known to treat AD/HD effectively, these drugs have a number of side-effects and patients can develop dependencies (addictions) and/or tolerances to them over time. For these reasons and others, researchers have long sought alternative and safer means of treating AD/HD (“Attention-deficit,” 2010).

One interesting observation in AD/HD subjects is a relatively low level of certain essential fatty acids (EFAs) in the blood stream (Colter, Cutler, & Meckling, 2008). The essential fatty acids are the ω-3 (also called omega-3 or n-3) and ω-6 (also called omega-6 or n-6) fatty acids, which humans need to stay healthy, but which cannot be synthesized from other fatty acids inside the body. Instead, they must be obtained from diet. Common food sources of EFAs include fish oils, vegetable oils, seeds, and nuts (“Essential,” 2010).

Since low levels of EFAs are common in AD/HD sufferers, it’s been hypothesized that supplementation with EFAs could be an effective treatment for the disorder, and, in fact, some groups and authors have advocated their use to the general public. However, caution is important here. Although there seems to be a verifiable correlation between levels of EFAs in the bloodstream and symptoms related to AD/HD, clinical research has shown that EFA supplementation is not an effective treatment for AD/HD.

The link between EFAs and AD/HD

The link between levels of essential fatty acids in the bloodstream and symptoms of AD/HD has been well established in clinical research. In an article recently published in Nutrition Journal, researchers studied adolescent subjects to see if they could corroborate what many preceding papers had shown in children, namely that sufferers of AD/HD symptoms tend to have lower levels of docosahexaenoic acid (DHA, an ω-3 fatty acid) than normal peers. The six-week study concluded that the AD/HD diagnosed group indeed “presented with significantly lower DHA . . . and total n-3 fatty acids.” Additionally, “The ratio of n-3 fatty acids to n-6 fatty acids was also significantly lower” (Colter, Cutler, & Meckling, 2008, p. 8) than that of the non-AD/HD control group. If a deficiency of DHA is common to AD/HD sufferers of all ages, this naturally leads to the question of whether supplementation of DHA or other essential fatty acids can be an effective treatment of AD/HD symptoms.

One important thing to note is that, although AD/HD sufferers consume more calories, protein, carbohydrates, and fat than normal controls, they do not consume a significantly different (lower or higher) amount of essential fatty acids, which at first seems inconsistent with the fact that AD/HD sufferers present with lower levels of EFAs in their systems. The key seems to be the way the body metabolizes the EFAs, not in how many are consumed. Indeed, Colter, Cutler, & Meckling (2008) go on to say that their finding of low DHA levels in AD/HD patients, despite consuming just as much DHA as normal peers, suggests “a higher rate of oxidation of this fatty acid [DHA] in these patients” (p. 8). Correlation doesn’t imply causation, and it may certainly be true that low DHA in the bloodstream is simply a symptom of AD/HD, not a root cause, and that therefore, supplementation of DHA won’t do anything to solve the problem.

Some authors advocate the use of EFAs as treatment for AD/HD

Despite this caution, some have jumped to the conclusion that DHA and other essential fatty acids can effectively treat the symptoms of AD/HD. Irresponsibly, some have even advocated the use of DHA as an AD/HD cure to the general public, such as the editors of The Duke Encyclopedia of New Medicine (Liebowitz, 2006) and Prescription for Drug Alternatives (Balch, 2008). The former resource cites only a single source in support of its claim, a randomized double-blind, placebo-controlled study of the effects of EFAs on children with specific learning disabilities. The latter similarly cites only two sources, one an open-label pilot study of high doses of EFAs, the other a double-blind, placebo-controlled trial on the effects of EFAs on patients with Developmental Coordination Disorder. A critical look at these three sources seems in order.

In their randomized double-blind, placebo-controlled study, which is used as direct support for treating AD/HD symptoms with EFAs by The Duke Encyclopedia of New Medicine, Alexandra Richardson and Basant Puri (2002) conducted a trial with 41 children who presented with “specific learning disabilities (mostly dyslexia)” (p. 234). But, the authors admit, “None of these subjects had been formally diagnosed with ADHD” (p. 234). Raz and Gabis (2009), in a survey of all extant AD/HD- and EFA-related research, state about this study that, “The applicability of the study to children with ADHD is highly questionable; the children were not diagnosed, and the authors state that most of them showed subclinical levels of ADHD symptoms” (p. 588). Though the study showed more favorable results for EFA than placebo on all 14 of the standard questionnaires administered, there was a high dropout rate (only 29 subjects completed the study), which meant that a statistically significant difference could only be shown in 3 of the 14 scales.

An open-label trial conducted by Paul Sorgi et. al. (2007) is cited by Prescription for Drug Alternatives as direct support for EFA supplementation for AD/HD symptoms. This trial studied the effects of high doses of EFAs on nine subjects. There was no placebo group, and the nine subjects knew they were taking active supplements. Raz and Gabis (2009) rightly point out that this study and others like it “cannot separate the biological effects from the placebo effects on behavioral endpoints” (p.587). Futher, the hypothesis of the authors of this study wasn’t that EFAs could effectively treat the symptoms of AD/HD. Instead they conducted their research to see, firstly, if children can handle higher doses of EFAs without adverse side effects and, secondly, if AA:EPA ratios in the bloodstream could be brought closer to the levels found in non-AD/HD peers through supplementation. Though they do assess behavior on AD/HD rating scales, that assessment was secondary to their primary purpose in the study. The only real conclusion the authors reached was that additional research seemed warranted. As such, the use of this study as direct support for EFA supplementation seems premature.

In a randomized double-blind, placebo-controlled study also used as direct support for EFA supplementation in Prescription for Drug Alternatives, Alexandra Richardson and Paul Montgomery (2005) conducted a 6-month one-way crossover trial of 117 children. For the first three months, the children were divided into active and control groups, and for the last three months, all subjects received active treatment. Like the previous Richardson and Puri (2002) study, the subjects were not confirmed to have a diagnosis of AD/HD, but instead, had been formally diagnosed with Developmental Coordination Disorder. Though DCD is highly comorbid with AD/HD, the authors of the study admit that, “To the best of our knowledge, no child had a formal ADHD diagnosis,” (p. 1363) and that only 32 of the 117 subjects had questionnaire scores that would place them within the range to be clinically diagnosed with AD/HD. The study did conclude that EFA treatment lowered these AD/HD test scores significantly in the active treatment group after 3 months, but given that only 16 of the 50 subjects in the active treatment group had clinically significant levels of AD/HD symptoms in the first place, it’s hard to interpret exactly why this is an important finding. Raz and Gabis (2009) concede that “This study corrected some of the methodological difficulties that appeared in Richardson and Puri,” but ultimately conclude that, “Owing to the inclusion of children without ADHD, the applicability of this trial to ADHD is questionable” (p. 588).

Further research shows EFAs are not an effective treatment for AD/HD symptoms

In addition to the research already surveyed, there is a larger body of research which shows that EFAs are not effective treatement for AD/HD. First, a double-blind randomized placebo-controlled study was published by Hirayama, Hamazaki, and Terasawa (2004). The authors conducted a 2-month trial with 40 children, who “had been diagnosed or suspected as AD/HD” (p. 468) using standardized questionnaires. The authors admit that “in a strict sense, eight subjects [20%] might not be AD/HD” (p. 468), but this is a far cry from, for example, the 69% who were undiagnosed in the Richardson & Montgomery (2005) study. The authors administered DHA and EPA to the active group by mixing it into bread and milk. The control group received identical foods with no EFAs mixed in. Both at baseline and at the end of the study, the subjects were rated according to standard AD/HD questionnaires, and were also tested for visual perception and visual and audio short-term memory by having to point out identical shapes and memorize sequences of numbers. By the end of this trial the only significant differences between the control and active groups was that the control group had improved visual short-term memory and made fewer errors of commission. The authors note this was probably due to increased familiarity with the tests administered, but this can’t explain why the active group didn’t improve similarly. The authors conclude that “DHA supplementation did not improve any AD/HD symptoms,” (p. 472) though they do suggest that treatment of AD/HD with EFAs should be studied further.

Johnson, Östlund, Fransson, Kadesjö, and Gillberg (2009) conducted a 6-month randomized, placebo-controlled trial of 75 children and adolescents. The authors hoped to reproduce the results of the Richardson & Montgomery (2005) study and, to that aim, used the same dosages of EFAs and the same one-way crossover format. However, Johnson et al. were more careful than Richardson & Montgomery to choose only subjects who were formally diagnosed with AD/HD at the clinic where they conducted the trial. The authors conclude that “the overall outcome was negative. More than half of all children with clinically impairing ADHD did not respond to 6 months of treatment with omega 3/6 fatty acids” (p. 400).

Raz, Carasso, and Yehuda (2009) conducted a 7-week randomized, double-blind, placebo-controlled study with 73 children with verified diagnoses of AD/HD. This study utilized questionnaires filled out by parents and teachers along with an objective performance test. At the end of the trial, the authors found no significant differences in symptoms or behaviors between the active group and the placebo group, and thus failed to show positive support for EFAs as supplementation for AD/HD.

After summarizing the results of seven different randomized, placebo-controlled trials, Raz and Gabis (2009) concluded that “randomized controlled trials of EFA in ADHD have generally been unsuccessful in demonstrating treatment effects, and some of them even displayed better results for the placebo group” (p. 589).

Conclusion

In conclusion, it’s unquestioned that there is a link between essential fatty acid deficiency and the symptoms of attention-deficit/hyperactivity disorder. However, it need not be assumed this relationship is a causal one. It’s entirely plausible, as Colter, Cutler, & Meckling (2008) speculated, that there is simply “a higher rate of oxidation of this fatty acid in these patients” (p. 8), or as Raz and Gabis (2009) speculated, that “children with ADHD might suffer from slower conversion” (p. 583) of some EFAs to others. Whatever the cause of EFA deficiency in AD/HD patients, it’s clear from the larger body of clinical research that EFA supplementation is not a viable cure for AD/HD symptoms. 

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