A team at the University of California at Los Angeles (UCLA) has just reported on the first-ever, double-blinded, sham-controlled study of trigeminal nerve stimulation (TNS) for treating ADHD. The trigeminal nerve is the largest cranial nerve. It enables facial sensation, as well as biting and chewing.

Over a four-week period, researchers fitted 62 eight-to-twelve-year-old children with electrodes while they slept; 32 got an active low current, the rest none at all. The active and sham setups were identical in appearance. The children were told, “pulses may come so fast or so slowly that the nerves in the forehead might or might not detect a sensation.” At the conclusion of the four weeks, there was an additional blinded week without intervention.

The primary efficacy outcome measure was the clinician-completed ADHD-RS total score, derived from parent interviews and available clinical information. It was completed at the onset of the study, and repeated over subsequent weeks. The Clinical Global Impression (CGI) score was used as a secondary outcome measure.

Both groups of children showed significant reductions in ADHD symptoms over the first week. But scores leveled off during the remaining three weeks for the group with sham treatment, while scores continued to decline for those in the group with actual stimulation. The standardized mean difference (SMD) between groups was 0.5.

By the conclusion of week 4, 52 percent for those in active treatment were improved or very much improved as indicated by CGI scores; only 14 percent did as well with the sham treatment. The number needed to treat was just 3.

After discontinuation of treatment, total scores in both groups rose at similar rates. At the end of week 5, CGI ratings for active treatment showed 13 percent improvement over baseline, versus 7 percent for sham treatment. The SMD was 0.46, once again indicating persistence of a medium effect size a week after treatment cessation.

The effect sizes computed for TNS are roughly comparable to effect sizes for nonstimulant medication, but less than those for stimulants.

Though the active group had significant gains in weight and pulse over the sham group, there were no serious adverse events in either group.

The authors concluded: “Results from the Early Impressions Questionnaire showed no differences in outcome expectations between treatment groups after 1 week using the randomized device, suggesting that our sham procedures successfully accomplished double blinding of group assignment. Improvements seen in the active and sham groups at week 1 likely reflect some placebo response secondary to the high level of parental involvement in administering treatment. Nonetheless, further improvement over subsequent weeks with active TNS suggests the emergence of true treatment effects … TNS is a non-medication minimal risk intervention with proven efficacy in alleviating ADHD symptoms. Although the present study finds that only slightly more than half of those receiving therapy have clinically meaningful improvement, the virtual lack of significant side effects should make it a popular treatment choice for many patients with ADHD, particularly for parents who prefer to avoid psychotropic medication.”

Nevertheless, one must keep in mind that this is a single un-replicated study with a small sample size. Further studies with larger numbers of participants are needed, both to confirm efficacy and to further explore the weight gains and higher pulse rates in the treatment group.

REFERENCES
James J. McGough, MD, Alexandra Sturm, PhD, Jennifer Cowen, PhD, Kelly Tung, BS, Giulia C. Salgari, MS, Andrew F. Leuchter, MD, Ian A. Cook, MD, Catherine A. Sugar, PhD, Sandra K. Loo, PhD, “Double-Blind, Sham-Controlled, Pilot Study of Trigeminal Nerve Stimulation for Attention-Deficit/ Hyperactivity Disorder,” Journal of the American Academy of Child & Adolescent Psychiatry, Vol. 58, No. 4 (April 2019), 403-411.

Many college students truly have ADHD and deserve to be treated but some attempt to fake ADHD symptoms with the goal of getting stimulant medications for non-medical 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 other 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 own symptoms on self-assessment tests, which can lead to false negatives. Performance validity tests were therefore also administered, in order 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 a 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 on the basis of positive observer tests in addition to self-reports: “Applying an ‘and’ rule—one where both self- and observer 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 the subsample 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 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.”

REFERENCES
Jason M. Nelson and Benjamin J. Lovett, “Assessing ADHD in College Students: Integrating Multiple Evidence Sources With Symptom and Performance Validity Data,” Psychological Assessment, published online January 31, 2019 http://dx.doi.org/10.1037/pas0000702.

Behavioral disinhibition is a trait associated with both ADHD and several genes that affect dopamine signaling. A new study by three American medical researchers set out to examine how these ADHD risk genes – DRD4 (dopamine 4 receptor density), DAT1 (dopamine 1 transporter), and DBH (dopamine beta-hydroxylase) – affect estimated life expectancy in young adulthood.

The method used was a longitudinal study of 131 hyperactive children and 71 matched controls through early adulthood. The original evaluations were done in 1979-1980, when both groups were children in the 4 to 12 age range. They were reevaluated in 1987-1988 as adolescents aged 12 to 20. The next follow-up was in 1992-1996 in early adulthood, aged 19 to 25. The final follow-up was in 1998-2004, as adults aged 24 to 32. All agreed to physical examinations that formed the basis for calculating estimated life expectancy using actuarial tables that factor in the effects of smoking, body mass index, alcohol, and other risk factors on expected longevity. Participants also provided blood samples that enabled gene typing.

For the DAT1 gene, participants who had the homozygous nine-repeat allele (9/9) had a five-year reduction in estimated life expectancy relative to those with the ten-repeat allele (10/10). Those with the intermediate (9/10) configuration had a three-year reduction in estimated life expectancy.

For the DBH Taq1 gene, those with a heterozygous (A1/A2) combination had almost a three-year reduction in estimated life expectancy relative to those with homozygous (A1/A1 or A2/A2) configurations.

For DRD4, on the other hand, no significant differences were found for estimated life expectancy.

In a related study, several background traits were found to be significantly predictive of variance in estimated life expectancy. The largest of these was behavioral disinhibition, followed by verbal IQ, self-rated hostility, and a nonverbal fluency test. But no significant differences were found between any of the gene polymorphisms on any of these four measures, indicating that the present gene associations were independent of the background traits.

The researchers next sought to determine which variables used in the estimated life expectancy calculations were associated with the two significant genes. For DBH, one variable stood out. Those with the A1/A2 heterozygous pairings had almost twice the alcohol consumption of those with homozygous pairings (p = 0.023).

For DAT1, two variables stood out. Overall, the 9/9 pairings smoked two and a half times as much as the 10/10 pairings, with the 9/10 pairings midway between the extremes (p = 0.036). They were also 73 percent more likely to be smokers relative to the 10/10 pairings, and 61 percent more likely relative to the 9/10 pairings. They also had significantly less education than the 10/10 pairings, with the 9/10 pairings again being intermediate (p = 0.027).

An obvious limitation of the study was its small sample size. The authors cautioned, “our findings should be considered quite preliminary and in need of much greater research before being given much weight in the literature or in public policy.”

“With these limitations in mind,” they concluded, “the present study demonstrated that two ADHD risk genes (DBH and DAT1) independently contributed to a reduction in ELE [estimated life expectancy] beyond the second order variables of behavioral disinhibition, IQ, hostility, and nonverbal fluency that contributed in the related study to variation in ELE. The gene polymorphisms seemed to be influencing ELE through their affiliation with first-order or more proximal factors related to ELE such as education, smoking, alcohol use, and possibly exercise.”

REFERENCES
Russell A. Barkley, Karen Müller Smith, and Mariellen Fischer, “ADHD risk genes involved in dopamine signaling and metabolism are associated with reduced estimated life expectancy at young adult follow-up in hyperactive and control children,” American Journal of Medical Genetics (2019), DOI: 10.1002/ajmg.b.32711.

ADHD is far more prevalent among persons with AUD (roughly 20 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 Conners’ 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 correct diagnosis of more than seven out of eight. But the rate of false positives soared 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.

REFERENCES
Mathias Luderer, Nurcihan Kaplan-Wickel, Agnes Richter, Iris Reinhard, Falk Kiefer, Tillmann Weber, “Screening for adult attention-deficit/hyperactivity disorder in alcohol dependent patients: Underreporting of ADHD symptoms in self-report scales,” Drug and Alcohol Dependence (2019), 195:52-58.

Mindfulness has been defined as “intentionally directing attention to present moment experiences with an attitude of curiosity and acceptance.” Mindfulness-based interventions (MBIs) aim to improve mindfulness skills.

A newly-published meta-analysis of randomized controlled trials (RCTs) by a team of British neurologists and psychiatrists explores the effectiveness of MBIs in treating a variety of mental health conditions in children and adolescents. Among those conditions is the attention deficit component of ADHD.

A comprehensive literature search identified studies that met the following criteria:

  1. The effects of mindfulness were compared against a control condition – either no contact, waitlist, active, or attention placebo. Waitlist means the control group receives the same treatment after the study concludes. Active control means that a known, effective treatment (as opposed to a placebo) is compared to an experimental treatment. Attention placebo means that controls receive a treatment that mimics the time and attention received by the treatment group but is believed not to have a specific effect upon the subjects. Participants were randomly assigned to the control condition.
  2. The MBI was delivered in more than one session by a trained mindfulness teacher, involved sustained meditation practice, and it was not mixed in with another activity such as yoga.

Eight studies evaluating attention deficit symptoms, with a combined total of 1,158 participants, met inclusion criteria. The standardized mean difference (SMD) was 0.19, with a 95% confidence range of 0.04 to 0.34 (p = .02). That indicates a small effect size for MBIs in reducing attention deficit symptoms. Heterogeneity was low (I2 = 35, p = .15), and the Egger test showed little sign of publication bias (p = 0.42).

When looking only at studies with active controls, five studies with a total of 787 participants yielded an SMD of 0.13, with a 95% confidence interval of -0.01 to 0.28 (p = .06), indicating a tiny effect size that failed to reach significance. Active controls most commonly received health education, with a few receiving social responsibility trainings or Hatha yoga.

Overall, this meta-analysis suggests limited effectiveness, especially when compared with active controls. If MBIs are effective for ADHD, there effect on symptoms is very small. Thus, such treatments should not be used in place of the many well-validated, evidenced-based therapies available. Whether longer periods of MBI (training times varied between 2 and 18 hours spread out over 2 to 24 weeks) might result in greater effect sizes remains unexplored.

REFERENCES
Darren L. Dunning, Kirsty Griffiths, Willem Kuyken, Catherine Crane, Lucy Foulkes, Jenna Parker, and Tim Dalgleish, “Research Review: The effects of mindfulness-based interventions on cognition and mental health in children and adolescents – a meta-analysis of randomized controlled trials,” Journal of Child Psychology and Psychiatry (2018), doi:10.1111/jcpp.12980.

A newly-published systematic review by a British team identified 48 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 229 South 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 less developed countries. A 2001 U.K. survey of 150 general practitioners found that only 6 percent of them had received formal ADHD training. In a 2002 study of 499 Finnish PCPs, only half felt confident in their ability to diagnose ADHD. A 2005 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 723 U.S. PCPs found only 44 percent used DSM criteria. In a 2006 UK study of 40 general 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 use of APA (American Psychological Association) guidelines by PCPs had expanded markedly between 1999 and 2005, from one in eight to one in two.

Given these facts, it is unsurprising that many PCPs expressed 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 and 138 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 in 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 of 380 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 consumption of sugary food and drink. Others reported a gender bias. A 2002 U.S. study of 395 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 57 French 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 2012 study in the Netherlands found that 74 physicians and 154 non-medical professionals matched by age, sex, and education showed no differences in 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 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 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 in 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 a 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 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 service provider and local authorities.”

REFERENCES
B. French, K. Sayal, D. Daley, “Barriers and facilitators to understanding of ADHD in primary care: a mixed‐method systematic review,” European Child & Adolescent Psychiatry (2018), https://doi.org/10.1007/s00787-018-1256-3.

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.