Cookie Preferences
By clicking, you agree to store cookies on your device to enhance navigation, analyze usage, and support marketing. More Info
Thank you! Your submission has been received!
Oops! Something went wrong while submitting the form.
April 27, 2021
ADHD is a serious disorder that requires treatment to prevent many adverse outcomes. But, because the diagnosis of ADHD is based on how the patient responds to questions, people can pretend that they have ADHD when they do not. If you Google "fake ADHD" you'll get many pages of links, including a Psychology Today article on the topic and bloggers describing how they were able to fool doctors into giving them ADHD medications. Is fake ADHD a serious problem? Not really. The Internetseems to be faking an epidemic of fake ADHD.I say that because we have decades of research that show many objective measures of abnormality and impairment in people who say they have ADHD. These include traffic accidents, abnormalities in brain imaging, and molecular genetic differences. Some studies even suggest that ADHD adults downplay their ADHD symptoms. For example, one study diagnosed ADHD in children and then contacted them many years later when they were young adults.When they were interviewed as young adults, their responses to questions about ADHD suggested that they did not have the disorder. But when the same questions about the patient were asked to someone who lived with the patient as a young adult, it was clear that they still had ADHD. So rather than faking ADHD, many ADHD adults do not recognize that they have symptoms of the disorder. That said, we also know from research studies that, when asked to pretend that they have ADHD, adults can fake the disorder. That means that they can learn about the symptoms of the disorder and makeup examples of how they have had them when they have not. The research discussed above suggests that this is not common, but we do know that some people have motives for faking ADHD.For example, some college students seek special accommodations for taking tests; others may want stimulants for abuse, misuse, or diversion. Fortunately, doctors can detect fake ADHD in several ways. If an adult itself-referred for ADHD and asks specifically for stimulant medication, that raises the possibility of fake ADHD and drug-seeking. Because the issue of stimulant misuse has been mostly a concern on college campuses, many doctors treating college students will require independent verification of the patient's ADHD symptoms by speaking with a parent, even over the phone if an in-person visit is not possible. Using ADHD rating scales will not detect fake ADHD, and it is easy to fake poor performance on tests of reading or math ability. Neuropsychological tests can sometimes be used to detect malingering, but require referral to a specialist. Researchers are developing methods to detect faking ADHD symptoms. These have shown some utility in studies of young adults, but are not ready for clinical practice. So, currently, doctors concerned about fake ADHD should look for objective indicators of impairment (e.g., documented traffic accidents; academic performance below expectation) and speak to a parent of the patient to document that impairing symptoms of the disorder were present before the age of twelve. Because the issue of fake ADHD is of most concern on college campuses, it can also be helpful to speak with a teacher who has had frequent contact with the patient. In an era of large lecture halls and broadcast lectures, that may be difficult. And don't be fooled by the Internet. We don't want to deny treatment to ADHD patients out of undocumented reports of an epidemic of fake ADHD.
Harrison, A. G., Edwards, M. J. & Parker, K. C. (2007).Identifying students faking ADHD: Preliminary findings and strategies fordetection. Arch Clin Neuropsychol 22, 577-88.
Sansone, R. A. & Sansone, L. A. (2011). Faking attentiondeficit hyperactivity disorder. Innov Clin Neurosci 8, 10-3
Loughan, A., Perna, R., Le, J. & Hertza, J. (2014). C-88Abbreviatingthe Test of Memory Malingering: TOMM Trial 1 in Children with ADHD. Arch ClinNeuropsychol 29, 605-6.
Loughan, A. R. & Perna, R. (2014). Performance andspecificity rates in the Test of Memory Malingering: an investigation intopediatric clinical populations. Appl Neuropsychol Child 3, 26-30.
Quinn, C. A. (2003). Detection of malingering in the assessmentof adult ADHD. Arch Clin Neuropsychol 18, 379-95.
Suhr, J., Hammers, D., Dobbins-Buckland, K., Zimak, E. &Hughes, C. (2008). The relationship of malingering test failure toself-reported symptoms and neuropsychological findings in adults referred forADHD evaluation. Arch Clin Neuropsychol 23, 521-30.
Greve, K. W. & Bianchini, K. J. (2002). Using theWisconsin card sorting test to detect malingering: an analysis of thespecificity of two methods in non malingering normal and patient samples. J ClinExp Neuropsychol 24, 48-54.
Killgore, W. D. & Della Pietra, L. (2000). Using theWMS-III to detect malingering: empirical validation of the rarely missed index(RMI). J Clin Exp Neuropsychol 22, 761-71.
Ord, J. S., Greve, K. W. & Bianchini, K. J. (2008).Using the Wechsler Memory Scale-III to detect malingering in mild traumaticbrain injury. Clin Neuropsychol 22, 689-704.
Wisdom, N. M., Callahan, J. L. & Shaw, T. G.(2010). Diagnostic utility of the structured inventory of malingeredsymptomatology to detect malingering in a forensic sample. Arch ClinNeuropsychol 25, 118-25.
Exercise has attracted growing attention as an intervention for ADHD. As a potential treatment option for ADHD, it is, of course, highly appealing because it can be low- to no-cost, widely accessible, and free of the side effects that can accompany medication. From previous studies, we know that certain types of exercise may be more effective than others, but do we actually know enough for clinicians to prescribe physical activity as a treatment for ADHD?
The First Study: Effects on Core ADHD Symptoms
Despite encouraging findings in individual studies, researchers have lacked clear guidance on which types of exercise work best, at what intensity, and for how long. A meta-analysis by Chen et al. set out to address this by pooling data from 20 randomized controlled trials (RCTs) involving 841 children and adolescents aged 4–18, all of which compared exercise interventions against non-exercising control groups.
The results were cautiously optimistic. Across standardized symptom scales, exercise produced a small improvement in ADHD symptoms overall. Objective cognitive tests showed a moderate improvement. Emotional and behavioral outcomes, however, showed no significant change.
To understand what was driving differences between studies, the researchers broke results down by exercise type. Therapeutic and alternative exercises (targeted movements and specific techniques such as those prescribed by physical therapists) were associated with moderate symptom improvements. Mind-body practices (such as yoga or tai chi) showed small-to-moderate gains. Conventional aerobic exercise yielded smaller effects, while skill-based competitive sports showed no measurable benefit. Notably, the variability between individual studies remained high throughout, meaning these categories should be interpreted with some caution.
Results:
The authors recommend that clinicians and parents consider incorporating therapeutic or alternative exercise sessions twice a week, each lasting 60–90 minutes, as a supplemental strategy alongside existing ADHD treatment. They stop short of calling this definitive, noting that future research should clarify how exercise produces its effects and how it might best be combined with medication or behavioral therapy.
The Second Study: Effects on Inhibitory Control
A second meta-analysis, by Zhang et al., zoomed in on a specific and particularly relevant cognitive challenge in ADHD: inhibitory control. Inhibitory control refers to the ability to suppress impulsive responses and tune out irrelevant distractions. This capacity underlies much of the restlessness, interrupting, and difficulty staying on task that characterize the condition.
This analysis drew on 34 studies with over 1,300 participants spanning all age groups, making it broader in scope than the Chen et al. review. Overall, exercise was associated with a moderate improvement in inhibitory control. When the analysis was restricted to RCTs alone, this finding held up. When studies with a high risk of bias were excluded, however, the effect size dropped to small-to-moderate.
One notable null result: three studies that used EEG to measure brain activity during inhibitory tasks found no significant effects on the neural signatures most closely tied to this process. This suggests exercise may influence behavior without necessarily changing the underlying brain mechanisms researchers expected, or that current methods aren't yet sensitive enough to detect such changes.
The dosing question produced some of the more practically useful findings. Single exercise sessions yielded only borderline small improvements. Sustained exercise programs, by contrast, showed moderate improvements, and programs with sessions three times per week produced large gains and had the strongest effect between the two meta-analyses. Exercise intensity and total program duration, perhaps interestingly, were not significant factors.
Results:
The authors are measured in their conclusions: exercise shows a real but modest benefit for inhibitory control, and frequency appears to matter more than intensity. They caution against overstating the case for exercise as treatment for ADHD overall, as it did not significantly affect hyperactivity or impulsivity as standalone outcomes, and its neural effects remain unclear.
The Broader Picture :
Ultimately, these two meta-analyses support exercise as a meaningful supplemental intervention for ADHD, particularly for attention and cognitive control, while urging realistic expectations. Neither suggests exercise should replace established treatments. Both are limited by high variability across the underlying studies, and both call for better-designed research to sharpen the guidance available to clinicians and families.
Boredom is more than just feeling restless or under-stimulated. It’s a negative emotional state that arises when activities feel meaningless or dull and, for those with ADHD, this negative emotional state might be markedly more intense. Researchers increasingly view boredom as functional: an internal signal pushing people to seek more rewarding and meaningful experiences. But for some, that signal becomes chronic and overwhelming.
People who are highly prone to boredom face a range of psychological and behavioral consequences, including anxiety, depression, difficulty identifying their own emotions (alexithymia), impulsivity, and physical complaints. These struggles often surface in harmful behaviors: overeating, substance use, compulsive internet use, and gambling.
For people with ADHD, boredom can cross into genuine distress. Many describe it as “torture” or “an itchy coat you can’t scratch”, language that conveys not mild discomfort but an urgent, almost unbearable need to escape. This makes sense given that ADHD involves core difficulties with attention, arousal regulation, and motivation, all of which make sustained engagement harder and boredom far more likely.
The Study:
A recent meta-analysis of 18 studies involving more than 22,000 participants confirmed a moderately strong and consistent positive association (an overall effect size of r = 0.40) between ADHD and self-reported boredom. All but one study found significant results, and there was no evidence of publication bias.
“While the relationship between ADHD and boredom may seem obvious,” the authors state, “this has paradoxically led to the phenomenon being understudied.”
Despite how significant this connection appears to be, the researchers noted it has attracted surprisingly little scientific attention; a gap they attribute to a widespread assumption that boredom in ADHD is simply a byproduct of inattention or impulsivity, and therefore not worth studying on its own terms. They push back on that view, arguing that boredom may be a more fundamental part of the ADHD experience: a bridge between atypical brain function and the behavioral, emotional, and cognitive difficulties that shape long-term outcomes.
The Take-Away:
Ultimately, addressing the profound boredom experienced by individuals with ADHD requires a multifaceted approach that goes beyond simply treating inattention. Researchers emphasize the need for rigorous studies to determine if stimulant medications actively reduce this intense boredom by repairing underlying brain mechanisms, rather than just as a side effect of improved focus. Beyond medication, tailored psychological therapies may offer promise; psychoeducation can help individuals reframe boredom as a biological signal rather than a personal failure or character flaw.
Additionally, another approach suggests that rather than solely focusing on treating the individual, systemic issues must be addressed, such as the effects of low-stimulation environments. For example, prioritizing a better "person-environment fit" through smaller class sizes, flexible academic pacing, and/or offering highly stimulating, novel tasks, schools and workplaces can offer meaningful relief from the chronic distress of ADHD-related boredom.
A new study from Japan suggests that infants born with craniosynostosis are significantly more likely to be diagnosed with ADHD later in childhood. Craniosynostosis is a condition in which the bony plates of the skull fuse prematurely, leading to increased intracranial pressure.
The Background:
Craniosynostosis affects roughly one in every 2,000 births. When the skull’s natural seams close prematurely, it can restrict brain growth and increase intracranial pressure, potentially reducing blood flow to the brain. Because the condition is relatively rare, it has been difficult to study at scale until now.
The Study:
To overcome this, researchers tapped into a large Japanese insurance database compiled by JMDC, Inc., which holds records on around 20 million people, or about 15% of Japan’s population. Drawing on two decades of data, the team tracked over 338,000 mother-child pairs. Children with related genetic syndromes or chromosomal conditions such as Down syndrome were excluded to keep the focus on craniosynostosis itself.
Of the children studied, around 1,145 had craniosynostosis, and 7,325 were diagnosed with ADHD. After accounting for factors like sex, birth year, maternal age, mental health history, pregnancy infections, and birth complications, children with craniosynostosis were found to have roughly 2.4 times the risk of a subsequent ADHD diagnosis compared to those without it.
To test whether shared family genetics or home environment might be driving the association rather than the skull condition itself, the researchers conducted a separate analysis among siblings. The elevated risk remained at 2.2 times. The consistency of the finding across both analyses strengthens the case for a genuine biological link.
The Results:
The results point to raised intracranial pressure and restricted cerebral blood flow as plausible mechanisms, though the study’s observational design means causation cannot be confirmed. Ultimately, these findings highlight the need for proactive, long-term care strategies for those born with craniosynostosis. By establishing a solid link between premature skull fusion and a significantly higher risk of ADHD, the research demonstrates that medical care for this condition should not end once the skull's physical structure is addressed.
The Takeaway:
Pediatricians, neurologists, and parents can use this data to implement early, routine behavioral and developmental screening for these children as they grow. This additional support would ensure that those who do develop ADHD can receive timely interventions, educational aids, and therapies, ultimately improving their long-term developmental outcomes.
_logo%201.svg)
