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Several meta-analyses have assessed this question by computing the standardized mean difference or SMD statistic.  The SMD is a measure that allows us to compare different studies. For context, the effect of stimulant medication for treating ADHD is about 0.9.  SMDs less than 0.3 are considered low, between 0.3 to 0.6 medium, and anything greater than high.
A 2004 meta-analysis by Schab and Trinh combined the results of fifteen studies with a total of 219 participants and found a small association(SMD = .28, 95% CI .08-.49) between consumption of artificial food colors by children and increased hyperactivity. Excluding the smallest and lowest quality studies further reduced the SMD to .21, and a lower confidence limit of .007 also made it barely statistically significant. Publication bias was indicated by an asymmetric funnel plot. No effort was made to correct the bias.
A 2012 meta-analysis by Nigg et al. combined twenty studies with a total of 794 participants and again found a small effect size (SMD =.18, 95% CI .08-.29). It likewise found evidence of publication bias. Correcting for the bias led to a tiny effect size at the outer margin of statistical significance (SMD = .12, 95% CI .01-.23). Restricting the pool to eleven high-quality studies with 619 participants led to a similarly tiny effect size that fell just outside the 95% confidence interval (SMD = .13, CI =0-.25, p = .053). The authors concluded, "Overall, a mixed conclusion must be drawn. Although the evidence is too weak to justify action recommendations absent a strong precautionary stance, it is too substantial to dismiss."
In 2013 a European ADHD Guidelines Group consisting of 21 researchers (Sonuga-Barke et al.) performed a meta-analysis of eight studies involving 294 participants that examined the efficacy of excluding artificial colors from the diets of children and adolescents as a treatment for ADHD. It found a small-to-medium effect size (SMD = .32, 95% CI .06-.58), with less than one in fifty probability that such a result would occur by chance. Yet "Restricting the probably blinded assessment analysis to the four no/low medication trials reduced the standardized mean difference (0.32) to non-significant levels (95%CI=-0.13, 0.77)."
On balance, the research to date suggests a small effect of artificial food colors in aggravating symptoms of hyperactivity in children, and a small beneficial effect of excluding these substances from the diets of children and adolescents, but the evidence is not very robust. More studies with greater numbers of participants, and better control for the effects of ADHD medications, will be required for a more definitive finding.
In the meantime, given that artificial food colors are not an essential part of the diet, parents should consider excluding them from their children's meals, since doing so is risk-free, and the cost (reading labels) negligible.

A study conducted at Auburn University in Alabama recruited 54 college students to address this question. All had previously been diagnosed with ADHD. All lived independently, and all were taking prescribed ADHD medication. Students with severe comorbid psychiatric conditions were excluded. Three students dropped out, leaving a final sample size of 51.
Each student completed a total of four half-hour assessments, scheduled at monthly intervals. At each first assessment, researchers counted the participant's ADHD medication pills and transferred them to an electronic monitoring bottle-a bottle with a microchip sensor in the cap that automatically tracks the date and time of every opening. This enabled them to compare students' subjective estimates at subsequent assessments with the objective evidence from pill counts and the data output from the electronic monitoring bottles.
Overall, students reported missing about one in four (25 percent) of their prescribed doses. But the objective measures showed they were skipping closer to half their doses. According to pill counts, they were missing 40 percent of their doses, and according to the electronic monitoring bottles, 43 percent. The odds of obtaining such a result due to chance with a sample of size were less than one in a hundred (p < 0.01).
In other words, college students with ADHD significantly overestimate their adherence rates to their medications. The authors concluded, "without additional strategies in place, expecting adolescents and young adults with ADHD to remember a daily task that requires no more than a few seconds to accomplish, such as medication taking, is unrealistic. They suggest using smartphone reminder applications ("apps") and text messaging services.
The authors caution that this was the first such study and that it had a small sample size. Moreover, the study was not randomized. Students responded to advertisements posted on campus, and thus self-selected.
Pending the outcome of larger studies with randomization, the authors suggest that wherever possible, prescribing physicians adopt objective measures of medication adherence, as an aid in ensuring greater efficacy of treatment.

Roughly one in thirty adult women have ADHD. Research results indicate that psychostimulants (methylphenidate and amphetamines) offer the most effective course of treatment in most instances. But during pregnancy, such treatment also exposes the fetus to these drugs. Several studies have set out to determine whether such exposure is harmful.

The largest comparison was 5,571 infants exposed to amphetamines and 2,072 exposed to methylphenidate with unexposed infants. It found no increased risks for adverse outcomes due to amphetamine or methylphenidate exposures. Another study studied 3,331 infants exposed to amphetamines, 1,515 exposed to methylphenidate, and 453 to atomoxetine. Comparing these infants to unexposed infants, it found a slightly increased risk of preeclampsia, with an adjusted risk ratio of 1.29 (95% CI 1.11-1.49), but no statistically significant effect for placental abruption, small gestational age, and preterm birth. When assessing the two stimulants, amphetamine, and methylphenidate, together, it found a small increased risk of preterm birth, with an adjusted risk ratio of 1.3 (95% CI 1.10-1.55). There was a statistically significant effect for preeclampsia, placental abruption, or small gestational age. Atomoxetine use was free of any indication of increased risk.

Another study involving 1,591 infants exposed to ADHD medication (mostly methylphenidate) during pregnancy, reported increased risks associated with exposure. The adjusted odds ratio for admission to a neonatal intensive care unit was 1.5 (95% CI 1.3-1.7), and for the central nervous system, disorders were 1.9 (95% CI 1.1-3.1). There was no increased risk for congenital malformations or perinatal death.

Six studies focused on methylphenidate exposure. Two, with a combined total of 402 exposed infants, found no increased risk for malformations. Another, with 208 exposed infants, found a slightly greater risk of cardiovascular malformations, but it was not statistically significant. A fourth, with 186 exposed infants, found no increased risk of malformations but did find a higher rate of miscarriage, with an adjusted hazard ratio of 1.98(95% CI 1.23-3.20). A fifth, with 480 exposed infants, also found a higher rate of miscarriage, with an odds ratio of 2.07 (95% CI 1.51-2.84). But although the sixth, with 382 exposed infants, likewise found an increased risk of miscarriage (adjusted relative risk 1.55 with 95% CI1.03-2.06), it also found an identical risk for women with ADHD who were not on medication during their pregnancies (adjusted relative risk 1.56with 95% CI 1.11-2.20). That finding suggests that all women with ADHD have a higher risk of miscarriage, and that methylphenidate exposure is not the causal factor.

Summing up, while some studies have shown increased adverse effects among infants exposed to maternal ADHD medications, most have not. There are indications that higher rates of miscarriage are associated with maternal ADHD rather than fetal exposure to psychostimulant medications. One study did find a small increased risk of central nervous system disorders and admission to a neonatal intensive care unit. But, again, we do not know whether that was due to exposure to psychostimulant medication or associated with maternal ADHD. If there is a risk, it appears to be a small one.

The question then becomes how to balance that as yet uncertain risk against the disadvantage of discontinuing the effective psychostimulant medication. As the authors of this review conclude. It [ADHD] is associated with significant psychiatric comorbidities for women, including depression, anxiety, substance use disorders, driving safety impairment, and occupational impairment. The gold standard treatment includes behavioral therapy and stimulant medication, namely methylphenidate and amphetamine derivatives. Psychostimulant use during pregnancy continues to increase and has been associated with a small increased relative risk of a range of obstetric concerns. However, the absolute increases in risks are small, and many of the best studies to date are confounded by other medication use and medical comorbidities.

Thus, women with moderate-to-severe ADHD should not necessarily be counseled to suspend their ADHD treatment based on these findings. They advise that when functional impairment from ADHD is moderate to severe, the benefits of stimulant medications may outweigh the small known and unknown risks of medication exposure, and that "If a decision is made to take ADHD medication, women should be informed of the known risks and benefits of the medication use in pregnancy, and take the lowest therapeutic dose possible."

A newly-published systematic review by a British team identified48 qualitative and quantitative studies that explored "ADHD in primary care, including beliefs, understanding, attitudes, and experiences." The studies described primary care experiences in the U.S., Canada, Europe, Australia, Singapore, Iran, Pakistan, Brazil, and South Africa.

More than three out of four studies identified deficits in education about ADHD. Of particular concern was the training of primary care providers (PCPs), most of whom received no specific training on ADHD. In most places, a quarter or less of PCPs received such training. Even when such training was provided, PCPs often rated it as inadequate and said they did not feel they could adequately evaluate children with ADHD.

There was even less training for adult ADHD. A 2009 survey of 194 PCPs in Pakistan found that ADHD was not included at all in medical training there and that most learned from colleagues. Half readily admitted to having no competence, and less than one in five were shown to have adequate knowledge about ADHD. In a 2009 survey of 229South African PCPs, only 7 percent reported adequate training in childhood ADHD, and a scant one percent in adult ADHD.

These problems were by no means limited to fewer developed countries. A 2001 U.K. survey of 150 general practitioners found that only 6percent of them had received formal ADHD training. In a 2002 study of 499Finnish PCPs, only half felt confident in their ability to diagnose ADHD. A2005 survey of 405 Canadian PCPs likewise found that only half reported skill and comfort in diagnosis. In a 2009 survey of 400 U.S. primary care physicians, only 13 percent said they had received adequate training. A 2017 study of Swiss PCPs found that only five of the 75 physicians in the sample expressed competence in diagnosis.

Eight studies explored knowledge of DSM (Diagnostic and Statistical Manual of Mental Disorders) criteria and clinical guidelines among PCPs. Only a quarter of PCPs were using DSM criteria, and only one in five were using published guidelines. In a 1999 survey of 401 pediatricians in the U.S.and Canada, only 38 percent reported using DSM criteria. A 2004 survey of 723U. S. PCPs found only 44 percent used DSM criteria. In a 2006 UK study of 40general practitioners, only 22 percent were aware of ADHD criteria. In the same year, a survey of 235 U.S. physicians found that only 22 percent were familiar with ADHD guidelines, and 70 percent used child behavior in the office to make a diagnosis. More encouragingly, a 2010 U.S. study reported that the use of APA (American Psychological Association) guidelines by PCPs had expanded markedly between1999 and 2005, from one in eight to one in two.

Given these facts, it is unsurprising that many PCPs expressed a lack of confidence in treating ADHD. In a 2003 survey of 143 South African general practitioners, two-thirds thought it was difficult to diagnose ADHD in college students. A 2012 U.S. study of 1,216 PCPs found that roughly a third lacked confidence in diagnosis and treatment. More than a third said they did not know how to manage adult ADHD. In a 2015 survey of 59 physicians and138 nurses in the U.S., half lacked confidence in their ability to recognize ADHD symptoms. This was especially pronounced among the nurses. A 2001 U.K.survey of 150 general practitioners found that nine out of ten wanted further training on drug treatment, and more than one out of ten were unwilling to prescribe due to insufficient knowledge.

Misconceptions about ADHD were widespread. In a survey of380 U.S. PCPs, almost half thought ADHD medications were addictive, one in five thought ADHD was "caused by poor diet," more than one in seven thought "the child does it on purpose," and one in ten thought medications can cure ADHD. Some studies reported that many PCPs believed ADHD was related to the consumption of sugary food and drink. Others reported a gender bias. A 2002 U.S. study of395 PCPs found that when presented with boys and girls with parent-reported problems, they were significantly more likely to diagnose ADHD in boys.

A 2010 Iranian study of 665 PCPs found that 82 percent believed children adopted ADHD behavior patterns as a strategy to avoid obeying rules and doing assignments. One-third believed sugary food and drink contributed to ADHD. Only 6 percent believed it could be a lifelong condition. Half blamed dysfunctional families. The aforementioned large 2012 U.S. study similarly found that almost half of PCPs believed ADHD was caused by absent or bad parenting. More than half of 399 Australian PCPs surveyed in 2002 believed inadequate parenting played a key role. In a 2003 study of 48 general practitioners in Singapore, a quarter blamed sugar for ADHD. A 2014 survey of 57French pediatricians found that a quarter thought ADHD was a foreign construct imported into France, and 15 percent attributed it to bad parenting. In all, ten studies reported a widespread belief that ADHD was due to bad parenting, with ratios varying from over one in seven PCPs to more than half. They were particularly likely to attribute hyperactivity to dysfunctional families and to dismiss parents' views of hyperactivity as a medical problem as a way to deflect attention from inadequate parenting. While a third of the studies reported on stigma, the surprise was that it did not seem to play as big a role as expected. A 2012study in the Netherlands found that 74 physicians and 154 non-medical professionals matched by age, sex, and education showed no differences in the level of stigmatization toward ADHD.

On the other hand, the studies identified significant resource constraints limiting more effective understanding, diagnosis, and treatment. Given the complex nature of ADHD, the time required to gain relevant information, especially in the context of competing demands on the attention of PCPs, was a limiting factor. Many studies identified a need for better assessment tools, especially for adults.

Another major constraint was PCP's uneasiness about medication. Studies found a widespread lack of knowledge about treatment options, and more specifically the pros and cons of medication relative to other options. This often led to an unwillingness to prescribe.

Yet another limitation was the difficulties PCPs had in communicating with mental health specialists. One study found that less than one in six PCPs received communications from psychiatrists. Much of this was ascribed to "system failure": discontinuity of care, no central accountability, limited resources, buck-passing. Many PCPs were unsure who to turn to. Another problem is often faulty interactions between schools, parents, children, and providers. Parents often fail to keep appointments. Schools and parents often are less than cooperative in providing information. In a 2004 survey of 786 U.S. school nurses, less than half reported good levels of communication between schools and physicians. Schools and parents often apply pressure on PCPs to issue a diagnosis. In the U.S. survey of 723 PCPs, more than half reported strong pressure from teachers to diagnose ADHD, and more than two-thirds said they were under pressure to prescribe medication.

The authors noted, "The need for education was the most highly endorsed factor overall, with PCPs reporting a general lack of education on ADHD. This need for education was observed on a worldwide scale; this factor was discussed in over 75% of our studies, in 12 different countries, suggesting that lack of education and inadequate education was the main barrier to the understanding of ADHD in primary care.

"In addition, "time and financial constraints affect the opportunities for PCPs to seek extra training and education but also affect the communication with other professionals such as secondary care workers, teachers, and parents." The authors cautioned that only eleven of the 48 studies were published since 2010. Also, because it was a systematic review and not a meta-analysis, there was no way to evaluate publication bias.

They concluded, "Better training of PCPs on ADHD is, therefore, necessary but to facilitate this, dedicated time and resources towards education needs to be put in place by the service providers and local authorities."

A working group of the International League Against Epilepsy(ILAE), consisting of twenty experts spanning the globe (U.S., U.K., France, Germany, Japan, India, South Africa, Kenya, Brazil), recently published "consensus paper" summarizing and evaluating what is currently known about comorbid epilepsy with ADHD, and best practices.

ADHD is two to five times more prevalent among children with epilepsy. The authors suggest that ADHD is underdiagnosed in children with epilepsy because its symptoms are often attributed either to epilepsy itself or to the effects of antiepileptic drugs (AEDs).

The working group did a systematic search of the English-language research literature. It then reached a consensus on practice recommendations, graded on the strength of the evidence.

Three recommendations were graded A, indicating they are well-established by evidence:
·        Children with epilepsy with comorbid intellectual and developmental disabilities are at increased risk of ADHD.
·        There is no increased risk of ADHD in boys with epilepsy compared to girls with epilepsy.
·        The anticonvulsant valproate can exacerbate attentional issues in children with childhood absence epilepsy (absence seizures look like staring spells during which the child is not aware or responsive). Moreover, a single high-quality population-based study indicates that valproate use during pregnancy is associated with inattentiveness and hyperactivity in offspring.

Four more were graded B, meaning they are probably useful/predictive:
·        Poor seizure control is associated with an increased risk of ADHD.
·        Data support the ability of the Strengths and difficulties questionnaire (SDQ) to predict ADHD diagnosis in children with epilepsy: "Borderline or abnormal SDQ total scores are highly correlated with the presence of a validated psychiatric diagnosis (93.6%), of which ADHD is the most common (31.7%)." The SDQ can therefore be useful as a screening tool.
·        Evidence supports the efficacy of methylphenidate in children with epilepsy and comorbid ADHD.
·        Methylphenidate is tolerated in children with epilepsy.

At the C level of being possibly useful, there is limited evidence that supports that atomoxetine is tolerated in children with ADHD and epilepsy and that the combined use of drugs for ADHD and epilepsy (polytherapy) is more likely to be associated with behavioral problems than monotherapy. In the latter instance, "Studies are needed to elucidate whether the polytherapy itself has resulted in the behavioral problems, or the combination of polytherapy and the underlying brain problem reflects difficult-to-control epilepsy, which, in turn, has resulted in the prescription of polytherapy."

All other recommendations were graded U (for Unproven), "Data inadequate or conflicting; treatment, test or predictor unproven." These included three where the evidence is ambiguous or insufficient:
·        Evidence is conflicted on the impact of early seizure onset on the development of ADHD in children with epilepsy.
·        Tolerability for amphetamine in children with epilepsy is not defined.
·        Limited evidence exists for the efficacy of atomoxetine and amphetamines in children with epilepsy and ADHD.

There were also nine U-graded recommendations based solely on expert opinion. Most notable among these:
·        Screening of children with epilepsy for ADHD beginning at age 6.
·        Reevaluation of attention function after any change in antiepileptic drug.
·        Screening should not be done within 48 hours following a seizure.
·        ADHD should be distinguished from childhood absence epilepsy based on history and an EEG with hyperventilation.
·        Multidisciplinary involvement in transition and adult ADHD clinics is essential as many patients experience challenges with housing, employment, relationships, and psychosocial wellbeing.

An international team of researchers has carefully examined the best current evidence and found strong evidence for an association between asthma and ADHD by combining a meta-analysis of prior data with a new analysis of the Swedish population.

The meta-analysis identified 46 datasets with a total of more than 3.3 million persons.  It computed an unadjusted (odds)'s ratio (OR) of 1.7, which indicates that ADHD patients have about twice the risk of developing asthma compared with people without ADHD. Limiting the meta-analysis to studies that adjusted for confounding factors, 30 datasets with more than a third of a million participants still led to an adjusted (odds)' ratio of 1.5 (95% CI 1.4 - 1.7). The likelihood of obtaining this result by chance in such a large sample would be less than one in ten thousand.

When the team further checked this result against the results for the Swedish population of more than one and a half million persons, the (odds)  ratio was almost identical to 1.6. Adjusting for confounding factors reduced it to 1.5 (95% CI 1.41 - 1.48). That means the findings are very robust: asthma and ADHD are associated, with an (odds)'ratio of 1.5, after adjusting for confounding factors.

What does this small but statistically very reliable association between asthma and ADHD mean? For researchers, it suggests that the two disorders may have common risk factors and that the search for these shared risk factors might lead to improved treatments.  These risk factors might also be shared with two other somatic conditions for which ADHD patients are at increased risk: obesity and eczema.  Common inflammatory processes may account for this overlap among disorders.  Clinicians should be aware that children with asthma have an increased risk for ADHD, although, given the small association, systematic screening may not be warranted.  But given that ADHD might interfere with asthma medication compliance, the disorder should be considered among noncompliant youth, especially among those who show other evidence of inattention, poor memory, or disorganization.

Swedish researchers examined outcomes for adult women who sought treatment at the Stockholm Center for Eating Disorders over two years and nine months. Out of 1,517 women who came to the clinic, 1,143remained eligible for the study, after excluding women whose symptoms did not fulfill the DSM-IV criteria for eating disorders or had incomplete records.

Of these, seven hundred patients could not be reached or declined to participate, leaving 443 for follow-up. To guard against the possibility that the follow-up group might not be representative of the overall treatment group, researchers compared to age, body mass index, and scores on tests for depression, anxiety, compulsively, inattention, and hyperactivity. The only statistically significant differences were small ones. The median age of the group lost to follow-up was one year younger, they were less likely to be living alone, and on average scored a single point higher on the depression test. Otherwise, they were broadly similar.

The one-year follow-up on the study group found a substantial difference in the rate of recovery from eating disorders between those with and without comorbid ADHD. Almost three out of four patients (72%) who scored lower (between 0-17) on the World Health Organization adult ADHD self-report scale had recovered from their eating disorder. Among those scoring18 and higher, on the other hand, it was less than half (47%). This difference was extraordinarily unlikely (one chance in one thousand) to be due to chance(p=.001).

Another way of expressing this is through odds ratios. Those scoring 18 and up on the ADHD self-report scale were about two and a half times less likely to recover from their eating disorders following treatment. More specifically, thy were about three times less likely to recover from the loss of control and binging, and almost three and a half times less likely to recover from purging.

To improve outcomes, the researchers suggest "identifying concomitant ADHD symptoms and customizing treatment interventions based on this." They specifically propose controlled clinical trials to explore the effect of combining stimulant medications with standard treatment for eating disorders

A Dutch study compared the efficacy of mindfulness-based cognitive therapy (MBCT) combined with treatment as usual (TAU), with TAU-only as the control group. MBCT consisted of an eight-week group therapy consisting of meditation exercises (body scan, sitting meditation, mindful movement), psychoeducation about ADHD, and group exercises. TAU consisted of usual treatment in the Netherlands, including medications and other psychological treatments. Sixty individuals were randomly assigned to each group. MBCT was taught in subgroups of 8 to 12 individuals. Patients assigned to TAU were not brought together in small groups. Baseline demographic and clinical characteristics were closely matched for both groups.

Outcomes were evaluated at the start, immediately following treatment, and again after 3 and 6 months using well-validated rating scales. Following treatment, the MBCT + TAU group outperformed the TAU group by an average of 3.4points on the Conner's Adult Rating Scale, corresponding to a standardized mean difference of .41. Thirty-one percent of the MBCT + TAU group made significant gains, versus 5% of the TAU group. 27% of MBCT +TAU patients scored a symptom reduction of at least 30 percent, as opposed to only 4% of TAU patients. Three and six-month follow-up effects were stable, with an effect size of .43.

The authors concluded, "that MBCT has significant benefits to adults with ADHD up to 6 months after post-treatment, about both ADHD symptoms and positive outcomes." Yet in their section on limitations, they overlook a potentially important one. There was no active placebo control. Those who were undergoing TAU-only were aware that they were not doing anything different from what they had been doing before the study. Hence, no substantial placebo response would be expected from this group during the intervention period (post-treatment they were offered an opportunity to undergo MBCT). Moreover, MBCT + TAU participants were gathered into small groups, whereas TAU participants were not. We, therefore, have no way of knowing what effect group interaction had on the outcomes because it was not controlled for. So, although these results are intriguing and suggest that further research is worthwhile, the work is not sufficiently rigorous to definitively conclude that MBCT should be prescribed for adults with ADHD.

Though there have been numerous studies on the efficacy of cognitive-behavioral therapy (CBT) for ADHD symptoms in children, adolescents, and adults, few have examined efficacy among adults over 50. A new study begins to fill that void.

Psychiatric researchers from the New York University School of Medicine, Massachusetts General Hospital, and Pfizer randomly assigned 88 adults diagnosed with elevated levels of ADHD to one of two groups. The first group received 12 weeks of CBT targeting executive dysfunction - a deficiency in the ability to properly analyze, plan, organize, schedule, and complete tasks. The second group was assigned to a support group, intended to serve as a control for any effects arising from participating in group therapy. Each group was split into subgroups of six to eight participants. One of the CBT subgroups was run concurrently with one of the support-only subgroups and matched on the percent receiving ADHD medications.

Outcomes were obtained for 26 adults aged 50 or older (12 in CBT and 14 in support) and compared with 55 younger adults (29 in CBT and 26 in support). The mean age of the younger group was 35 and of the older group 56. Roughly half of the older group, and 3/5ths of the younger group, were on medication. Independent("blinded") clinicians rated symptoms of ADHD before and after treatment.

In the blind structured interview, both inattentive scores and executive function scores improved significantly and almost identically for both older and younger adults following CBT. When compared with the controls(support groups), however, there was a marked divergence. In younger adults, CBT groups significantly outperformed support groups, with mean relative score improvements of 3.7 for inattentive symptoms and 2.9 for executive functioning. In older adults, however, the relative score improvements were only 1.1 and0.9 and were not statistically significant.

Given the non-significant improvements over placebo, the authors' conclusion that "The results provide preliminary evidence that CBT is an effective intervention for older adults with ADHD" is premature. As they note, a similar large placebo effect was seen in adults over 50 in a meta-analysis of CBT for depression, rendering the outcomes non-significant. Perhaps structured human contact is the key ingredient in this age group. It may also be, as suggested by the positive relative gains on six of seven measures, that CBT has a small net benefit over placebo, which cannot be validated with such a small sample size. Awaiting results from studies with larger sample sizes, it is, for now, impossible to reach any definitive conclusions about the efficacy of CBT for treating adults over 50.

A two-year study examined the effect of digital media use on ADHD symptoms in over 2500 adolescents. An earlier meta-analysis found that traditional media use (TV and video console games) was modestly associated with ADHD-like behaviors (Nikkelen et al 2014). The current study extends the examination to a large sample, with modern digital media delivery of high-intensity stimuli, including mobile platforms.

The authors used the Current Symptom Self-Report Scale (Barkley R 1998) to establish ADHD symptoms at baseline and six-month assessments over 24 months. None of the subjects reported having ADHD, study entry. Subjects were considered to be ADHD symptom-positive (the primary binary outcome) if they had greater than or equal to six inattentive and/or hyperactive-impulsive symptoms rated on this frequency-based scale (0-3). Modern digital media use was surveyed on a frequency basis for 14 media activities(including checking social media sites, texting, browsing, downloading or streaming music, posting pictures, online chatting, playing games, online shopping, and video chatting). The most common media activity was the high-frequency checking of social media. Of note, high-frequency engagement in each of the digital media activities was significantly, but moderately, associated with having ADHD symptoms at each six-month follow-up (OR 1.10), even after adjusting for covariates. High-frequency media use at baseline seemed to be associated with the development of ADHD symptoms.

Among the 495 students who reported no high-frequency media use at baseline, 4.6% met ADHD symptom criteria at follow-up. Among 114 students scoring 7 for high-frequency media use at baseline, 9.5% met the symptoms criteria. For the 51 students with a score of 14 for high-frequency media use at baseline, the rate was 10.5% (both comparisons were statistically significant).

This study is important in that it notes that an association between high-frequency digital media use (in current platforms and modalities) may be associated with the development of ADHD-like symptoms. A significant limitation of the study, as noted by the authors, is that ADHD-like symptoms do not establish a diagnosis of ADHD and do not assess impairment; therefore, these results must be interpreted with some caution. It does highlight that even with the current level of understanding, it might be prudent for clinicians to recommend limiting high-frequency media use for adolescent patients.