What would you like to find today?

An international team of mental health professionals used a nationally representative sample of English adults over age 16 to explore this question. Of 13,671 households selected, 7,461 were a little more than half participated.

Participants used the Adult ADHD Self-Report Scale (ASRS) Screener to assess symptoms of ADHD on a scale ranging from 0 to 24. Those scoring ≥ 14 were considered as having high levels of ADHD symptoms. They also responded to a computer-assisted self-interview that asked, "Have you been unfairly treated in the last 12 months … because of your mental health," requiring a yes or no answer.

The raw data showed an exponential relationship between levels of ADHD symptoms and mental health discrimination. Respondents scoring0-9 on the ASRS reported negligible discrimination (prevalence of 0.3%).  Among those scoring 10-13, the prevalence was 2.3%, rising to 5.5% of those with scores in the 14-17 range, and 18.8% among those in the 18-24 range.

After adjusting for sociodemographic variables (sex, age, ethnicity, marital status, educational attainment, and income), those with high levels of ADHD symptoms were nearly 10 times more likely to have experienced discrimination than others.  After adjusting for other psychopathology and stressful life events, this increased risk fell to 2.8.

The authors concluded, "This is an important finding given that mental health discrimination has been associated with detrimental consequences in individuals with mental health disorders and therefore might also be a factor in the negative outcomes that have been noted in adults with ADHD/ADHD symptomatology. As ADHD continues to be underdiagnosed and untreated in adults, the results of this study highlight the importance of identifying and treating these individuals and suggest that interventions to inform the public about ADHD may be important for reducing the stigma and discrimination associated with this condition."

Many college students truly have ADHD and deserve to be treated, but some attempt to fake ADHD symptoms to get stimulant medications for nonmedical uses, such as studying and getting high.  Some students who fake ADHD also seek to gain accommodations that would give them additional time to complete exams. To address this issue, two psychologists examined data from 514 university students being assessed for ADHD to evaluate the ability of assessment tools to detect students who fake ADHD symptoms.

All participants had asked to be assessed to determine whether they could qualify for disability services. This was therefore by no means a random sample of university students, and could be expected to include some non-ADHD individuals seeking the benefits of an ADHD diagnosis. But this offered a good opportunity to explore which combination of tools would yield the best accuracy, and be best at excluding malingerers.

That was achieved by using both multiple informants and multiple assessment tools and comparing results. Self-assessment was supplemented by assessment by other informants (e.g. parent, partner, friend, or another relative). These were supplemented with symptom validity tests to check for telltale highly inconsistent symptom reporting, or symptom exaggeration, which could signal false positives.

On the other hand, some individuals with ADHD have executive functioning problems that may make it difficult for them to reliably appraise their symptoms on self-assessment tests, which can lead to false negatives. Performance validity tests were therefore also administered, to detect poor effort during evaluation, which could lead to false negatives.

Observer reporting was found to be more reliable than self-reporting, with significantly lower inconsistency scores (p < .001), and significantly higher exaggeration scores (p < .001). More than twice as many self-reports showed evidence of symptom exaggeration as did observer reports. This probably understates the problem when one considers that the observer reports were performed not by clinicians but by parents and partners who may themselves have had reasons to game the tests in favor of an ADHD diagnosis.

Even so, the authors noted, "External incentives such as procurement of a desired controlled substance or eligibility for the desired disability accommodation are likely to be of more perceived value to those who directly obtain them." They suggested compensating for this by making ADHD diagnoses only based on positive observer tests in addition to self-reports: "Applying an 'and' rule-one where both self-and observers reports were required to meet the diagnostic threshold-generally cut the proportions meeting various thresholds at least in half and washed out the differences between the adequate and inadequate symptom validity groups."

They also recommended including formal tests of response validity, using both symptom validity tests and performance validity tests. Overall, they found that just over half of the sub-sample of 410 students administered performance validity tests demonstrated either inadequate symptom or performance validity.

Finally, they recommended "that clinicians give considerable weight to direct, objective evidence of functional impairment when making decisions about the presence of ADHD in adults. The degree to which symptoms cause significant difficulty functioning in day-to-day life is a core element of the ADHD diagnostic criteria (American Psychiatric Association,2013), and it cannot be assumed that significant symptoms cause such difficulty, as symptoms are only moderately associated with such functional impairment. ... we urge clinicians to procure objective records (e.g., grade transcripts, work performance evaluations, disciplinary and legal records) to aid in determining functional impairment in adults assessed for ADHD."

ADHD is far more prevalent among persons with AUD (roughly20 percent) than it is in the general population. The most accurate way of identifying ADHD is through structured clinical interviews. Given that this is not feasible in routine clinical settings, ADHD self-report scales offer a less reliable but much less resource-intensive alternative. Could the latter be calibrated in a way that would yield diagnoses that better correspond with the former?

A German team compared the outcomes of both methods on 404 adults undergoing residential treatment for AUD. All were abstinent while undergoing evaluations. First, to obtain reliable ADHD diagnoses, each underwent the Diagnostic Interview for ADHD in Adults, DIVA. If DIVA indicated probable ADHD, two expert clinicians conducted successive follow-up interviews. ADHD was only diagnosed when both experts concurred with the DIVA outcome.

Participants were then asked to use two adult ADHD self-report scales, the six-item Adult ADHD Self Report Scale v1.1 (ASRS) and the 30-item Conner's Adult ADHD Rating Scale (CAARS-S-SR). The outcomes were then compared with the expert interview diagnoses.

Using established cut-off values for the ASRS, less than two-thirds of patients known to have ADHD were scored as having ADHD by the test. In other words, there was a very high rate of false negatives. Lowering the cut-off to a sum score ≥ 11 resulted in an incorrect diagnosis of more than seven out of eight. But the rate of false positives shared to almost two in five. Similarly, the CAARS-S-SR had its greatest sensitivity (ability to accurately identify those with ADHD) at the lowest threshold of ≥ 60, but at a similarly high cost in false positives (more than a third).

The authors found it was impossible to come anywhere near the precision of the expert clinical interviews. Nevertheless, they judged the best compromise to be to use the lowest thresholds on both tests and then require positive determinations from both. That led to successfully diagnosing more than three out of four individuals known to have ADHD, with a false positive rate of just over one in five.

Using this combination of the two self-reporting questionnaires with lower thresholds, they suggest, could substantially reduce the under-diagnosis of ADHD in alcohol-dependent patients.

Autism spectrum disorder (ASD) is frequently comorbid with ADHD. Among adults with ADHD, as many as half are reported to also have ASD.

A Dutch team set out to answer two questions:

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1)    Do adults with ADHD and comorbid ASD experience less effectiveness in pharmacological treatment for ADHD than adults with only ADHD
2)    Do adults with ADHD and comorbid ASD experience different or more severe side effects of pharmacological treatment for ADHD than adults with only ADHD, as measured in side effect scores, blood pressure, heart rate, and weight?

This was a retrospective study, using well-documented medical records, of the effects of drug treatment with methylphenidate (MPH), dexamphetamine (DEX), atomoxetine (ATX), bupropion, or modafinil.

The researchers compared 60 adults with comorbid ASD and ADHD to 226 adults with only ADHD. ADHD symptoms were scored using the Conner's ADHD Rating Scale: Self Report-Short Version (CAA RS: S-S). Side effects of ADHD medication were measured using either a 13-item or 20-item checklist with 4-point scales for item response. Researchers also tracked changes in body weight, blood pressure, and heart rate.

Following treatment, ADHD symptoms among the comorbid group declined by a quarter, and among the ADHD-only group by almost a third. There was no significant difference between men and women. Controlling for age, gender, and ADHD subtype, a comorbid diagnosis of ASD also did not significantly affect ADHD symptom reduction.

Turning to side effects, in the ADHD+ASD group, there were significant increases in decreased appetite and weight loss, and decreases in agitation, anxiety, and sadness/unhappiness. In the ADHD-only group, there were significant increases in decreased appetite, weight loss, and dry mouth, and decreases in sleeping disorder, nervousness, agitation, anxiety, and sadness/unhappiness. Yet there were no significant differences between the two groups. Side effects increased and decreased similarly in both. Likewise, there were no significant differences between the groups in changes in heart rate and blood pressure. The only significant difference in medication dosage was for bupropion, which was higher in the ADHD+ASD group, though without any sign of the difference in side effects.

The authors concluded that this retrospective study "showed pharmacological treatment of adults with diagnoses of ADHD and ASD to be just as successful as the pharmacological treatment of adults with only ADHD," but cautioned that "randomized controlled trial should be conducted to evaluate the effectiveness and possible side effects of pharmacological treatment for ADHD in patients with ASD more reliably."

A team of Iranian researchers recently published a meta-analysis seeking to determine what, if any, association there may be between low vitamin D levels and ADHD in children and adolescents.
Combining the results from thirteen studies with 10,334participants, they found that youth with ADHD had "modest but significant" lower serum concentrations of 25-hydroxyvitamin D than normally developing children. The weighted mean difference was just under 7 nanograms per milliliter. The odds of obtaining such a result by chance would be less than one in a thousand(p < .001). There was little to no sign of publication bias. Between-study heterogeneity, however, was very high (I2 = 94).
These results suggest an association. But are low serum levels of vitamin D a cause or effect of ADHD? Causation is vastly more difficult to establish than an association. To begin to tease this out, the researchers identified four prospective studies that compared maternal vitamin D levels with the subsequent development of ADHD symptoms in their children. Two of these used maternal serum levels, and two used umbilical cord serum levels. Together, these studies found that low maternal vitamin D levels were associated with a 40% higher risk of ADHD in their children. Whether maternal serum or umbilical cord serum measurements were used had little or no effect on the outcome. Study heterogeneity was negligible. But the authors noted that this result "should be considered with caution" because it was heavily dependent on one of the prospective studies included in the analysis. All of which suggest a need for further prospective studies
In the meantime, the authors suggest it would be prudent to increase sun exposure and vitamin D supplementation, given the prevalence of vitamin D deficiency.

A Spanish team of researchers recently completed a comprehensive review of studies looking for links between compulsive video gaming (both online and offline) and a variety of psychological disorders, including anxiety, depression, social phobia, and ADHD. The focus was on behavior "of sufficient severity to result in significant impairment in personal, family, social, educational, occupational or other important areas of functioning."

The team identified 24 studies, of which eight with a combined total of 16,786 participants looked for associations with either ADHD or its hyperactivity component. Participants included children, adolescents, and adults. One large longitudinal study, with 3,034 participants, found no association. Another study with 1,095 participants found a small effect. Two more, with a combined total of 11,868 found medium effect sizes. Four studies found large associations, but their combined total number of participants, was789, comprising less than a twentieth of the combined participants.

The authors concluded, "The relationship between Internet Gaming Disorder and ADHD and hyperactivity symptoms were analyzed in eight studies. Seven of them reported full association, with four finding large, two finding small, and one reporting moderate, effect sizes. The studies comprised two case-control, five cross-sectional and one longitudinal design; they later found no association between the two variables."[1]They also emphasized that 87 percent "of the studies describe significant correlations ... with ADHD or hyperactivity symptoms."[2]

Yet they did not note that all the studies with large effect sizes were comparatively small. And while they presented funnel charts evaluating publication bias for anxiety and depression, they did not do so for ADHD, where the small studies with very large effect sizes suggest publication bias (i.e., that evidence for association is exaggerated due to the early publication of positive findings).

Leaving out these small studies, the four high-powered studies with 15,997 participants reported effect sizes ranging from none to medium. Overall, that suggests that there is an association between ADHD and video gaming, though not a particularly strong one.  Moreover, due to the nature of the study designs, this work cannot conclude that the small effect observed is due to playing video games being a risk factor for ADHD or to the possibility that ADHD youth are more attracted to video games than others.

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.

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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.

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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.

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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.

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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.

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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.

We are only beginning to explore how ADHD affects sleep in adults. A team of European researchers recently published the first meta-analysis on the subject, drawing on thirteen studies with 1,439 participants. They examined both subjective evaluations from sleep questionnaires and objective measurements from actigraphy and polysomnography. However, due to differences among the studies, only two to seven could be combined for any single topic, generally with considerably fewer participants (88 to 873).

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Several patterns emerged. Looking at results from sleep questionnaires, they found that adults with ADHD were far more likely to report general sleep problems (very large SMD effect size 1.55). Getting more specific, they were also more likely to report frequent night awakenings(medium effect size 0.56), taking longer to get to sleep (medium-to-large effect size 0.67), lower sleep quality (medium-to-large effect size 0.69), lower sleep efficiency (medium effect size 0.55), and feeling sleepy during the daytime(large effect size 0.75).

There was little to no sign of publication bias, though considerable heterogeneity on all but night awakenings and sleep quality.

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Actigraphy readings confirmed some subjective reports. On average, adults with ADHD took longer to get to sleep (large effect size 0.80) and had lower sleep efficiency (medium-to-large effect size 0.68). They also spent more time awake (small-to-medium effect size 0.40). There was little to no sign of publication bias and there was little heterogeneity among studies.

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None of the polysomnography measurements, however, found any significant differences between adults with and without ADHD. All effect sizes were small (under 0.20), and none came close to being statistically significant.

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There were four instances where measurement criteria overlapped those from actigraphy and self-reporting, with varying degrees of agreement and divergence. There was no significant difference in total sleep time, matching findings from both the questionnaires and actigraphy. On percent time spent awake, polysomnography found little to no effect size with no statistical significance, whereas actigraphy found a small-to-medium effect size that did not quite reach significance, and self-reporting came up with a medium effect size that was statistically significant. Sleep onset latency and sleep efficiency, for which questionnaires and actigraphy found medium-to-large effects, the polysomnography measurements found little to none, with no statistical significance.

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Polysomnography found no significant differences in stage 1-sleep, stage 2-sleep, slow-wave sleep, and REM sleep. Except for slow-wave sleep, there was no sign of publication bias. Heterogeneity was generally minimal.

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One problem with the extant literature is that many studies did not take medication status into account.

The authors concluded, "future studies should be conducted in medicatio- naïve samples of adults with and without ADHD matched for comorbid psychiatric disorders and other relevant demographic variables."

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In summary, these findings provide robust evidence that ADHD adults report a variety of sleep problems.  In contrast, objective demonstrations of sleep abnormalities have not been consistently demonstrated.   More work in medication-naïve samples is needed to confirm these conclusions.