Rachael Morkem, Scott Patten, John Queenan, and David Barber

Journal of Attention Disorders 1 –8 , 2017 DOI: 10.1177/1087054717720719

This study describes trends the incidence and prevalence of prescribing ADHD medication in a large Canadian Primary Care Physician (PCP) Network over a ten year period from 2005-2015. Canada has public funded health care, creating a system that the provision for chronic disorders (such as ADHD) is often provided by PCPs, who serve as gatekeepers to specialty referrals only when necessary. A population-based retrospective cohort was derived from EMR data from the Canadian Primary Care Sentinel Surveillance Network, which has 11 practice-based research networks (PBRNs) composed of 1,100 primary care practitioners throughout Canada. Total number of prescriptions, type of medication, age group were assessed by year throughout the ten-year span. The annual prevalence was determined by establishing the number of patients prescribed at least one ADHD medication, divided by total number of patients with a PCP visit that year. Annual incidence rates were established using a similar formula for patients who were receiving their initial treatment with ADHD medication. The authors found over the decade a 2.5 and 2.6 fold increase in the prescribing prevalence in preschool and school age children, respectively and a 4 fold increase in prescribing prevalence in adults. Methylphenidate was the most commonly prescribed medication over the decade (65%), with a slight decrease in the later years of the decade, presumably due to the introduction of the long-acting amphetamine lisdexamphetamine. The authors noted that although ADHD disease prevalence was stable, the prescribing prevalence was increasing over the decade. Also gender differences of higher prescribing rates of boys:girls in children and adolescents were not seen in adults. The investigators posit that since the ADHD disease prevalence was noted to be relatively stable in Canada (Hauck et al. 2017), and the frequency of medication prescription remains below ADHD prevalence, the increased prevalence of prescriptions may reflect improved long-term treatment. Several caveats should be noted to this study: 1) the most common annual frequencies of taking medications were in the 20% range for once or >=10/year; this bimodal distribution may indicate ongoing issues with adherence to medications in Canadanian ADHD patients, 2) the authors were unclear as to how they handled patients who switched between medication preparations and 3) as the authors note, the study is only able to examine what was prescribed, but not what was taken. One take home point for US clinicians is the higher utilization of methylphenidate products in the Canadian population as compared to what has been described in US adult ADHD populations.

REFERENCES:
Hauck, T. S., Lau, C., Wing, L. L. F., Kurdyak, P., & Tu, K. (2017). ADHD treatment in primary care: Demographic factors, medication trends, and treatment predictors. Canadian Journal of Psychiatry, 62, 393-402.

Yan He, Jian Chen, Li-Hua Zhu, Ling-Ling Hua, and Fang-Fang Ke

Journal of Attention Disorders 1 –11 , 2017 DOI: 10.1177/1087054717696766

This article describes a meta-analyses of studies which examined the potential effects of maternal smoking on the risk of childhood ADHD. A prior meta-analysis in 2005 (Langley, Rice, Van den Bree, & Thapar, 2005) found a strong association between maternal smoking and subsequent development of childhood ADHD in exposed offspring. Several recent individual studies also found an association be, tween maternal smoking and childhood ADHD, but one prospective study (Ball et al., 2010) did not find such an association. Therefore, given the length of time since the last meta-analysis and the one negative study noted above, highlighted the need for an updated meta-analysis. The authors employed fairly standard meta-analysis guidelines via the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement, which included a selection of studies, data extraction and assessment of study quality. The risk ratios (RRs) and 95% CIs reported in the individual studies were pooled across studies to examine the potential association of maternal smoking during pregnancy and childhood ADHD risk. The authors also examined for presence of publication bias and changing association over time. 265 studies were originally identified, with 12 meeting the stringent criteria to be included in the meta-analysis. The main finding of the analysis was the maternal smoking was modestly association with an increased risk of ADHD in children (pooled RR = 1.58, 95% CI = [1.33, 1.88]) and this association seemed to increase over time (by examining publication year); no significant publication bias was seen. The authors that the association they observed was not as robust as the one seen by Langley et al. for several reasons: their including a larger number of trials, which were limited to those with prospective and not case-controlled desi This meta-analysis is important for clinicians as it highlights the importance of the need to caution their patients as to potential risks of offspring developing ADHD in mothers who smoke during pregnancy.

REFERENCES:
Ball, S. W., Gilman, S. E., Mick, E., Fitzmaurice, G., Ganz, M. L., Seidman, L. J., & Buka, S. L. (2010). Revisiting the association between maternal smoking during pregnancy and ADHD. Journal of Psychiatric Research, 44, 1058-10

Langley, K., Rice, F., Van den Bree, M. B., & Thapar, A. (2005). Maternal smoking during pregnancy as an environmental risk factor for attention deficit hyperactivity disorder behaviour. A review. Minerva Pediatrica, 57, 359-37

Stephen V. Faraone, Michael J. Silverstein , Kevin Antshel, Joseph Biederman, David W. Goodman, Oren Mason, Andrew A. Nierenberg, Anthony Rostain, Mark A. Stein and Lenard A. Adler

Journal of Attention Disorders, 1–15, 2018, DOI: 10.1177/1087054718804354

Lenard Adler, MD ADHD in AdultsThis manuscript reviews the results of the first phase of Quality Measures (QM) Initiative of the American Professional Society of ADHD and Related Disorders (APSARD). QMs (sometimes described as Quality Indicators) are critical metrics to the delivery and assessment of state-of-the-art health care; QMs numerically describe outcomes, patient perceptions, processes quantify health care processes, outcomes, patient perceptions, and systems. The authors followed the pathway outlined by the U.S. Agency for Healthcare Research and Quality (AHRQ) for the development of QMs; the manuscript describes the first phase, the development of draft QMs. This was a four-step process: 1) a literature search for adult ADHD QMs; (2) having experts develop a “wide net” of potential QMs in the areas of screening, diagnosis, treatment, follow-up, care coordination, and patient experience; (3) cross-referencing this “wide-net” of QMs to existing adult ADHD guidelines; (4) have ADHD experts rate the importance, reliability, validity, feasibility, and usability of the QMs via an online survey. The top 10 QMs from the expert survey were: Screening: % high-risk patients screened (e.g., depressed patients, family history of ADHD), Diagnosis: % patients treated for ADHD having documented DSM-5 diagnosis of ADHD, % patients with ADHD with review of other psychiatric disorders, % patients with ADHD with documentation of impairment, Treatment initiation: % patients receiving ADHD medications for whom treatment alternatives, benefits and risks have been discussed, % patients with ADHD assessed for vitals prior to medication treatment, % patients with ADHD for whom warnings and contraindications for medication were reviewed, Treatment follow-up: % patients with ADHD where validated measure of symptom change used to assess treatment efficacy at least annually, % patients stabilized on an ADHD medication seen at least once per year, % patients prescribed medication for ADHD seen within 1 month of initial prescription. This manuscript is important for clinicians because it is the first step toward the development of QMs for adult ADHD, which have not existed to date; if validated through field testing in the second phase of the initiative, these QM may be important metrics of health care quality in the care of patients with ADHD.

Journal of Attention Disorders 1 –7 DOI: 10.1177/1087054718763736 journals.sagepub.com/home/jad

Benjamin J. Lovett and Alexander H. Jordan

Lenard Adler MD - ADHD in Adults FacultyRates of ADHD in college students have been increasing somewhat in recent years, as has use of screening tools to help identify individuals at risk for disorders such as ADHD. These investigators designed a trial to examine whether screening for adult ADHD, in essence creating some positive expectation bias of having the disorder in leading to increased reporting of ADHD symptoms and altered performance on cognitive tests. One group was screened for ADHD using the ASRS v.1.1 Screener and received feedback if they screened positive for the disorder and then completed a self ADHD symptom checklist (CAARS: S Long version) and a batter of psychological tests (three subtests on the Woodcock– Johnson IV Tests of Cognitive Abilities (WJ-IV) (processing speed), a mathematical test and Letter-Pattern Matching (LPM)/Number-Pattern Matching (NPM), and Pair Cancelation (PC) for general cognitive efficiency. The control group received the same interventions except were not screened for ADHD. There were no significant differences in the two groups in terms of ADHD symptoms or neuropsychological measures. The authors note that while there was concern that screening positive for ADHD might result in increased expectation of having more ADHD symptoms, these effects were limited and did not significantly affect reporting ADHD symptoms. Several limitations of the trial include the constraint of the sample to only college students which limits the generalizability of the results, the absence of a comparison intervention (ie. Mock screening) in the control group and the use of DSM-IV version of the adult ADHD screener, instead of the most recently validated DSM-5 version. The important take-home point for clinicians seeing college students is the lack of increased reporting of ADHD symptoms and absence of effects on neuropsychological tests introduced by the process of screening for ADHD.

Journal of Attention Disorders 1 –10 © The Author(s) DOI: 10.1177/1087054718787894 journals.sagepub.com/home/jad

Jessica R. Lunsford-Avery, Scott H. Kollins, and John T. Mitchell

Lenard Adler MD - ADHD in Adults FacultySluggish cognitive tempo is a constellation of symptoms including sluggishness, daydreaming, being slow to react, easily bored and fogginess in thinking, which has been shown to exist in several disorders, but commonly in children with ADHD (Barkley 2014). This investigation is important as the authors characterize the psychometric properties of self and collateral report of the Barkley SCT scale (BAARS-IV: SCT subscale – nine items) versus the Conners Adult ADHD Scale in 124 adults (80 of whom had ADHD). The Barkley SCT scale had high internal consistency (self-report Cronbach’s α = .79, collateral-report Cronbach’s α = .82). The self and collateral versions of the Barkley SCT scale were significantly, moderately correlated after covarying for age and sex (r = .41, p < .001). Factor analyses supported the same three factors generally found in studies of childhood SCT: Slow/Daydreamy, Sleepy/Sluggish and Low Initiation/Persistence Symptoms. The Barkley SCT scale was fairly highly correlated with ADHD symptoms in the CAARS, except for the Sleepy/Sluggish factor not correlating with Hyperactivity/Restlessness or Impulsivity and lower association with Emotional Lability. The lack of association of the Sleepy/Sluggish factor with Restlessness and Impulsivity appears to have some face validity given the differential nature of the symptoms. This article is important to clinicians because it highlights the importance of assessing adult ADHD patients for symptoms of sluggish cognitive tempo and how these SCT symptoms may relate to DSM-5 ADHD symptoms.

REFERENCES
Barkley, R. A. (2014). Sluggish cognitive tempo (concentration deficit disorder?): Current status, future directions, and a plea to change the name. Journal of Abnormal Child Psychology, 42, 117-125. doi:10.1007/s10802-013-9824-y

Our genes are very important for the development of mental disorders – including ADHD, where genetic factors capture up to 75% of the risk. Until now, the search for these genes had yet to deliver clear results. In the 1990s, many of us were searching for genes that increased the risk for ADHD because we know from twin studies that ADHD had a robust genetic component. Because I realized that solving this problem required many DNA samples from people with and without ADHD, I created the ADHD Molecular Genetics Network, funded by the US NIMH. We later joined forces with the Psychiatric Genomics Consortium (PTC) and the Danish iPSYCH group, which had access to many samples.

The result is a study of over 20,000 people with ADHD and 35,000 who do not suffer from it – finding twelve locations (loci) where people with a particular genetic variant have an increased risk of ADHD compared to those who do not have the variant. The results of the study have just been published in the scientific journal Nature Genetics, https://www.nature.com/articles/s41588-018-0269-7.

These genetic discoveries provide new insights into the biology behind developing ADHD. For example, some of the genes have significance for how brain cells communicate with each other, while others are important for cognitive functions such as language and learning.

We study used genomewide association study (GWAS) methodology because it allowed us to discover genetic loci anywhere on the genome. The method assays DNA variants throughout the genome and determines which variants are more common among ADHD vs. control participants. It also allowed for the discovery of loci having very small effects. That feature was essential because prior work suggested that, except for very rare cases, ADHD risk loci would individually have small effects.

The main findings are:

  1. A) we found 12 loci on the genome that we can be certain harbor DNA risk variants for ADHD. None of these loci were traditional ‘candidate genes’ for ADHD, i.e., genes involved in regulating neurotransmission systems that are affected by ADHD medications. Instead, these genes seem to be involved in the development of brain circuits.
  2. B) we found a significant polygenic etiology in our data, which means that there must be many loci (perhaps thousands) having variants that increase risk for ADHD. We will need to collect a much larger sample to find out which specific loci are involved;

We also compared the new results with those from a genetic study of continuous measures of ADHD symptoms in the general population. We found that the same genetic variants that give rise to an ADHD diagnosis also affect inattention and impulsivity in the general population. This supports prior clinical research suggesting that, like hypertension and hypercholesteremia, ADHD is a continuous trait in the population. These genetic data now show that the genetic susceptibility to ADHD is also a quantitative trait comprised of many, perhaps thousands, of DNA variants

The study also examined the genetic overlap with other disorders and traits in analyses that ask the questions: Do genetic risk variants for ADHD increase or decrease the likelihood a person will express other traits and disorders.  These analyses found a strong negative genetic correlation between ADHD and education. This tell us that many of the genetic variants which increase the risk for ADHD also make it more likely that persons will perform poorly in educational settings. The study also found a positive correlation between ADHD and obesity, increased BMI and type-2 diabetes, which is to say that variants that increase the risk of ADHD also increase the risk of overweight and type-2 diabetes in the population.

This work has laid the foundation for future work that will clarify how genetic risks combine with environmental risks to cause ADHD. When the pieces of that puzzle come together, researchers will be able to improve the diagnosis and treatment of ADHD.

 

 

A Danish team recruited 29,489 participants from among voluntary blood donors between the ages of 17 and 67, ensuring a large sample size. Participants were asked to complete two simple questionnaires on digital tablets. One asked two questions: “Have you ever had migraine?” and “Have you ever had visual disturbances lasting 5-60 min followed by headache?” A yes to either was considered positive for migraine. The other used the ADHD Self-Report Scale, with 18 ADHD symptoms evaluated on a five-point scale.

Excluding those who did not answer all questions left 26,456 participants. The risk for migraines among those with ADHD was nearly twice the risk for others. The odds ratio (OR) was 1.8, with a 95 percent confidence interval from 1.53 to 2.12 (p < 0.001). The OR was higher among females (2.01) than males (1.64). For those with visual disturbances, the OR was higher (1.98) than for those without (1.52). The association disappeared in those over 60, with an OR essentially equal to one (0.98, 95% CI = 0.84 – 1.15, p = 0.8).

Although the authors concluded, “We demonstrate a significant comorbidity between migraine and ADHD in adults, and this is most prominent for participants with migraine with visual disturbances,” the significance to which they refer are of the p-values, and should not be misinterpreted as an indication of a strong association, as the odds ratios point variably to weak, and weak-to-moderate associations, depending on subpopulations. The work is, however, important as it points to another somatic comorbidity of ADHD. That list is growing and now includes obesity, eczema and asthma.

REFERENCES
Thomas Folkmann Hansen, Louise K. Hoeffding, Lisette Kogelman, Thilde Marie Haspang, Henrik Ullum, Erik Sørensen, Christian Erikstrup, Ole Birger Pedersen, Kaspar René Nielsen, Henrik Hjalgrim, Helene M. Paarup, Thomas Werge, and Kristoffer Burgdorf, “Comorbidity of migraine with ADHD in adults,” BMC Neurology (2018), 18:147.

A German team recruited 104 adults with ADHD at both inpatient and outpatient ADHD clinics, and from ADHD self-help groups. Just under two-thirds were being treated with ADHD drugs, most with methylphenidate.

Just under a quarter reported high internalized stigma. Two in five reported high levels of alienation, meaning a sense of “not being a fully functioning, valuable member of society.” Three in ten reported high levels of social withdrawal.

On the other hand, only two participants reported high levels of stereotype endorsement, meaning personal acceptance of stereotypes associated with mental illness. And more than two-thirds reported high stigma resistance, meaning they were internally resistant to stigmatization. Thus, while most were free of significant internalized stigma, a still substantial minority were not.

Most of the participants expected to be discriminated against and treated unfairly by employers, colleagues at work, neighbors, and teachers should they reveal that they have ADHD. Relatively few expected to be discriminated against by health professionals, family, and friends. Almost half expected discrimination if they confided to strangers they were dating.

Over two-thirds of participants reported they had encountered public stereotypes concerning ADHD. But, on balance, they rated these at low levels of intensity. Nevertheless, among those perceiving such stereotypes, eight out of nine sensed some degree of public doubt about the validity of ADHD as a genuine ailment (“ADHD does not exist in adults”), and three out of four had at some point encountered the argument that “ADHD is invented by drug companies.” More than four out of five had heard allegations that ADHD results from bad parenting, and almost three in four had heard the claim that it results from watching too much television or playing too many video games.

These data call for more education of the public about the nature and causes of ADHD. Information reduces stigmatization so the widespread dissemination of the facts about ADHD is warranted.

REFERENCES
Theresa Vera Masuch, Myriam Bea, Barbara Alm, Peter Deibler, Esther Sobanski, “Internalized stigma, anticipated discrimination and perceived public stigma in adults with ADHD,” ADHD Attention Deficit and Hyperactivity Disorders (2018), doi.org/10.1007/s12402-018-0274-9.

All Swedish residents have their health records tracked through unique personal identity numbers. That makes it possible to identify psychiatric and medical disorders with great accuracy across an entire population, in this case encompassing more than five and a half million adults aged 18 to 64. A subgroup of more than 1.6 million persons between the ages of 50 and 64 enabled a separate examination of disorders in older adults.

Slightly over one percent of the entire population (about 61,000) were diagnosed with ADHD at some point as an adult. Individuals with ADHD were nine times as likely to suffer from depression as were adults not diagnosed with ADHD. They were also more than nine times as likely to suffer from anxiety or a substance use disorder, and twenty times as likely to be diagnosed with bipolar disorder. These findings are very consistent with reports from clinical samples in the USA and Europe.

Adults with ADHD also had elevated levels of metabolic disorders, being almost twice as likely to have high blood pressure, and more than twice as likely to have type 2 diabetes. Persons with ADHD but without psychiatric comorbidities were also almost twice as likely to have high blood pressure, and more than twice as likely to have type 2 diabetes.
Similar patterns were found in men and women with ADHD, although comorbid depression, bipolar disorder, and anxiety were moderately more prevalent in females than in males, whereas substance use disorder, type 2 diabetes, and hypertension were more prevalent in males than in females.

ADHD was less than a third as prevalent in the over-50 population as in the general adult population. Nevertheless, individuals in this older group with ADHD were twelve times as likely to suffer from depression, anxiety, or substance use disorders, and more than 23 times as likely to be diagnosed with bipolar disorder as their non-ADHD peers. They were also 63% more likely to have high blood pressure, and 72% more likely to have type 2 diabetes.

The authors noted, “Although the mechanisms underlying these associations are not well understood, we know from both epidemiologic and molecular genetic studies that a shared genetic predisposition might account for the co¬existence of two or more psychiatric conditions. In addition, individuals with ADHD may experience increased difficulties as the demands of life increase, which may contribute to the development of depression and anxiety.” As for associations with hypertension and type 2 diabetes, these “might reflect health ¬risk behaviors among adult patients with comorbid ADHD in addition to a shared biological substrate. As others have noted, inattention, disinhibition, and disorganization associated with ADHD could make it difficult for patients to adhere to treatment regimens for metabolic disorders.” They concluded that “Clinicians should remain vigilant for a wide range of psychiatric and metabolic problems in ADHD affected adults of all ages and both sexes.”

REFERENCES
Qi Chen, Catharina A. Hartman, Jan Haavik, Jaanus Harro, Kari Klungsøyr, Tor¬Arne Hegvik, Rob Wanders, Cæcilie Ottosen, Søren Dalsgaard, Stephen V. Faraone, Henrik Larsson, “Common psychiatric and metabolic comorbidity of adult attention-deficit/hyperactivity disorder: A population-based cross-sectional study,” PLoS ONE (2018), 13(9): e0204516. https://doi.org/10.1371/journal.pone.0204516.

Stephen V. Faraone, PhDThere has been much interest in omega-3 Polyunsaturated fatty acids (PUFAs) as treatments for ADHD. Humans are unable to synthesize omega-3 PUFA alpha-linolenic acid (ALA) and the omega-6 PUFA linoleic acid (LA), and must therefore obtain these through food, which is why they are known as essential fatty acids. Because cells in the brain need omega-3 PUFAs, they have been studied as a treatment for ADHD by many researchers. In fact, several meta-analyses are available.

A 2014 meta-analysis by Elizabeth Hawkey and Joel Nigg combined nine studies involving 586 participants. It found mean blood levels of omega-3 PUFAs in persons with ADHD to be lower than in controls. The standardized mean difference (SMD) effect size was medium (SMD = .42, 95% CI = .26-.59), with less than a one in one thousand probability of such a result being obtained by chance alone. Adjusting for publication bias reduced the effect size slightly to .36 with a 95% CI of .21-.51, in the small-to-medium range. The authors then examined whether omega-3 supplementation could help alleviate ADHD symptoms. Combining 16 studies with 1,408 participants, they found improvements, but this time with a small effect size (SMD = .26, 95% CI = .15-.37), again with less than a one in a thousand probability of such a result being observed by chance. Adjusting for publication bias reduced the effect size to .16 with a 95% CI of .03-.28. For comparison, the SMD for stimulants is about 0.9.

Another meta-analysis conducted in the same year by Basant Puri and Julian Martins combined 18 PUFA supplementation studies involving 1,640 participants. They also found a small effect size for reduced ADHD symptoms (SMD = .19, 95% CI = .09-.30, p<.001). Adjusting for publication bias further reduced the effect size to a paltry and statistically insignificant level (SMD = .12, 95% CI = -.01-.25). It should be noted that while 16 of the studies involved omega-3 supplementation, two involved only omega-6 supplementation. Yet the results for the latter did not differ noticeably from the former. When the authors limited the analysis to the 11 studies specifically including both the omega-6 GLA and the omega-3 EPA, the effect size for reducing inattention symptoms was a bit higher (SMD = .31, 95% CI = .16-.46, p<.0001). But the results were not significantly different than those for the studies without the GLA+ALA combination (.012; 95% CI: .161-.137; p=.875). Publication bias was not addressed, and the hunt for a highly specific subset with positive results may have produced a false positive finding. The authors conceded, “Weaknesses of this study include the following: although the pooled effect was statistically significant, only two studies showed a significant effect by themselves; the funnel plot showed evidence of publication bias; there was evidence of reporting bias; few studies were formally registered; study methodological quality was variable; and the placebo used across studies varied.”

A 2016 meta-analysis by Laura Lachance et al. tried looking for differences in the ratio of omega-6 to omega-3 PUFAs, and more specifically, AA to EPA, in the blood of persons with ADHD versus normally developing persons. Pooling five studies with 485 participants, it found the omega-6 to omega-3 ratio to be significantly higher in persons with ADHD, and pooling three studies with 279 participants, it likewise found the AA to EPA ratio significantly higher.

A 2017 meta-analysis by Jane Pei-Chen Chang et al. reexamined comparative levels of omega-3 PUFAs in ADHD patients versus normally developing controls. Combining six studies with 396 participants, ADHD patients had lower levels in blood and mouth tissue, with a medium effect size (SMD = .38) that was not statistically significant (p=.14). Omega-6 levels were indistinguishable (SMD = .03) in the two groups. AA (SMD = .18, p=.33) and EPA (SMD = .25, p=.17) levels were slightly lower, but once again statistically not significant. DHA levels were lower as well, this time with a medium effect size (SMD = .56), but at the outer margin of significance (p=.05). Only by dropping one study were the authors able to claim significance for EPA, AA, and omega-3 differences.

Chang et al. also performed a meta-analysis of supplementation studies. Combining seven studies with 534 participants, they found a small to medium reduction in ADHD symptoms with omega-3 supplementation (SMD = .38, 95% CI = .2-.56, p<.0001). Corrections for publication bias were not reported. The authors also reported large reductions in both omission errors (SMD = 1.09, 95% CI = .43-.1.75, p<.001) and commission errors (SMD = 2.14, 95% CI = 1.24-3.03, p<.00001) on a neuropsychological test of attention. But the former involved only 3 studies with 214 participants, and the latter only two studies with 85 participants.

Also in 2017, Pelsser et al. published a systematic review that identified only two meta-analyses of double-blind, placebo-controlled trials of PUFA supplementation. One of those, a 2012 meta-analysis by Gillies et al., found no statistically significant declines in either parent-rated ADHD symptoms (five trials, 413 participants, SMD = -.17, 95% CI = -.38-.03) or teacher-rated ADHD symptoms (four trials, 324 participants, SMD = .05, 95% CI = -.18-.27). The other, a 2013 meta-analysis by Sonuga-Barke et al., found only a slight and barely statistically significant reduction in symptoms (11 trials, 827 participants, SMD = .16, 95% CI = .01-.31). Pelsser et al. concluded, “Considering the small average ESs [effect sizes] PUFA supplementation is unlikely to provide a tangible contribution to ADHD treatment.”

Putting all of this together, there are indications that individuals with ADHD may have lower levels of omega-3 PUFAs, and that omega-3 supplementation may slightly reduce symptoms of ADHD, but the evidence remains inconclusive, with at best small effect sizes. It is possible, but not yet demonstrated, that omega-3 PUFAs might produce good outcomes in a small subset of patients.

REFERENCES
Jane Pei-Chen Chang, Kuan-Pin Su, Valeria Mondelli, and Carmine M Pariante, “Omega-3 Polyunsaturated Fatty Acids in Youths with Attention Deficit Hyperactivity Disorder: a Systematic Review and Meta-Analysis of Clinical Trials and Biological Studies,” Neuropsychopharmacology (2017), 43(3): 534–545.

Donna Gillies, John KH Sinn, Sagar S Lad, Matthew J Leach, Melissa J Ross, “Polyunsaturated fatty acids (PUFA) for attention deficit hyperactivity disorder (ADHD) in children and adolescents,” Cochrane Database of Systematic Reviews (2012), DOI:10.1002/14651858.CD007986.pub2.

Elizabeth Hawkey and Joel T. Negg, “Omega−3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials,” Clinical Psychology Review (2014), 34(6), 496-505.

Laura LaChance, Kwame McKenzie, Valerie H. Taylor, and Simone N. Vigod, “Omega-6 to Omega-3 Fatty Acid Ratio in Patients with ADHD: A Meta-Analysis,” Journal of the Canadian Academy of Child and Adolescent Psychiatry (2016), 25(2), 87-96.

Lidy M. Pelsser, Klaas Frankena, Jan Toorman, Rob Rodrigues Pereira, “Diet and ADHD, Reviewing the Evidence: A Systematic Review of Meta-Analyses of Double-Blind Placebo-Controlled Trials Evaluating the Efficacy of Diet Interventions on the Behavior of Children with ADHD,” PLOS ONE (January 25, 2017), 1-25.

Basant K. Puri and Julian G. Martins, “Which polyunsaturated fatty acids are active in children with attention-deficit hyperactivity disorder receiving PUFA supplementation? A fatty acid validated meta-regression analysis of randomized controlled trials,” Prostaglandins, Leukotrienes and Essential Fatty Acids (2014), 90, 179-189.

Edmund J.S. Sonuga-Barke et al., “Nonpharmacological Interventions for ADHD: Systematic Review and Meta-Analyses of Randomized Controlled Trials of Dietary and Psychological Treatments,” American Journal of Psychiatry (2013), 170:275-289.