Why Emotion Regulation Travels With ADHD Remains Unsettled

The state of the argument

Researchers who study ADHD hold three different positions on the emotional volatility that so often accompanies it, and each has serious people behind it. The first treats that volatility as a core feature of ADHD, as intrinsic to the condition as distractibility. The second treats it as the mark of a separate condition travelling alongside ADHD rather than belonging to it. The third treats emotional volatility and ADHD as distinct but correlated dimensions, arising from processes the two share.

Philip Shaw and his co-authors named those camps lumpers, splitters and diplomats in a 2014 review for The American Journal of Psychiatry, written with Argyris Stringaris, Joel Nigg and Ellen Leibenluft across the National Human Genome Research Institute, the National Institute of Mental Health, King’s College London and Oregon Health and Science University. They pooled effect sizes where the literature allowed it and reviewed the rest narratively. Emotion dysregulation, throughout, refers to feeling that arrives faster and larger than the situation warrants and subsides more slowly than the child would choose.

How common it is depends on who is counted and how. The review reports emotion dysregulation in around 25 to 45 percent of children and between 30 and 70 percent of adults with ADHD. A population study of 5,326 youth found mood lability in 38 percent of children with ADHD, a ten-fold increase over the rate in the general population, while clinic-based studies of young people produce estimates between 24 and 50 percent. Sobanski and colleagues found emotional lability more than three standard deviations above population norms in a quarter of their ADHD sample; Spencer and colleagues found 44 percent of an ADHD group meeting a dysregulation profile against 2 percent of controls.

Three effects could be pooled, and all three were substantial. Aggression was consistently elevated in ADHD populations, with an effect size of 1.92. Difficulty labelling emotion in others showed moderate impairment, 0.65. Delay aversion, the preference for a smaller reward now over a larger one later, was moderately associated with ADHD at 0.6, with considerable heterogeneity across studies.

None of that settles the question of origin. The dysregulation profile on the Child Behavior Checklist is 67 percent heritable, and among 424 children with ADHD and their siblings, the link between neuropsychological measures and emotional lability ran almost entirely through the severity of ADHD symptoms. Each finding is compatible with more than one of the three models. Almost no study has been designed to ask the question directly, and the authors decline to choose among them.

What a parent can do with an open question

The consequences have been measured, whatever their origin. In a study of 1,500 children, emotional problems bore more heavily on well-being and self-esteem than hyperactivity and inattention did, and young people with ADHD plus emotion dysregulation were significantly more impaired in peer relationships, family life, occupational attainment and academic performance than those with ADHD alone. That difference held after controlling for co-occurring conditions, oppositional defiant disorder included. Among adults, those whose ADHD persisted showed higher rates of emotion dysregulation, 42 to 72 percent depending on the symptom, than those whose ADHD had remitted, at 23 to 45 percent, though both groups differed from healthy comparison subjects.

Treatment is where the picture grows thinnest. Two randomized placebo-controlled trials in children found psychostimulants reduced emotional lability and irritability; two randomized trials of amphetamine against placebo found no benefit across a broad range of emotional problems, and some studies report amphetamine preparations increasing irritability. A lithium trial for severe mood dysregulation was negative. In 30 children whose aggression had not responded to stimulant and behavioural treatment, adding divalproex produced significantly higher remission than placebo, a single small trial rather than a course of action, and one that belongs in conversation with a clinician.

The review’s literature search closed at the start of January 2013, so the treatment evidence in particular has moved since, and any parent reading it should assume the specifics have changed. The neural picture has not consolidated either. Results across imaging work are mixed, though dysfunction is implicated in a network linking the striatum, amygdala and medial prefrontal cortex, with amygdala hyperactivation in the larger studies.

A parent watching a child come apart over a maths worksheet is being asked to live with an argument the field has not finished. The impairment attached to that volatility is documented well enough to justify addressing it now, in school plans and clinical conversations, without waiting on the explanation. You are entitled to know that the explanation is genuinely open, and to say so to anyone who tells you otherwise.