Misconceptions about ADHD stigmatize affected people, reduce credibility of providers, and prevent/delay treatment. To challenge misconceptions, we curated findings with strong evidence base. We reviewed studies with more than 2000 participants or meta-analyses from five or more studies or 2000 or more participants. We excluded meta-analyses that did not assess publication bias, except for meta-analyses of prevalence. For network meta-analyses we required comparison adjusted funnel plots. We excluded treatment studies with waiting-list or treatment as usual controls. From this literature, we extracted evidence-based assertions about the disorder. We generated 208 empirically supported statements about ADHD. The status of the included statements as empirically supported is approved by 80 authors from 27 countries and 6 continents. The contents of the manuscript are endorsed by 366 people who have read this document and agree with its contents. Many findings in ADHD are supported by meta-analysis. These allow for firm statements about the nature, course, outcome causes, and treatments for disorders that are useful for reducing misconceptions and stigma.

Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobiological condition in Germany and Australia, with a prevalence of 5.9% to 9.9% in children and adolescents and 2.5% to 5% in adults.^1-3 The disorder is characterized by inattention, impulsive behavior, and hyperactivity across a variety of settings, resulting in functional and developmental impairment,⁴ and can progress into psychosocial, educational, and neuropsychological dysfunction in adulthood.⁵ Quiz Ref ID However, stimulant medication for treatment of ADHD is often highly effective, with an observed effect size of close to 1.0 for methylphenidate hydrochloride.⁶ In the longer term, effective stimulant treatment may lead to improvement in self-esteem, academic performance, and social outcomes.⁷

In a cohort of 65 boys aged 12–16 years at recruitment, treatment for more than 3 years with stimulant medication was associated with a slower rate of physical development during puberty, compared with boys not taking stimulants.

Children treated with stimulant medication for attention deficit hyperactivity disorder (ADHD) often lose weight. It is important to understand the implications of this during growth. This prospective study was designed to quantify the changes in body composition and markers of bone metabolism on starting treatment. 34 children (29 boys) aged 4.7 to 9.1 years newly diagnosed with ADHD were treated with dexamphetamine or methylphenidate, titrating the dose to optimise the therapeutic response. Medication was continued for as long as clinically indicated. Body composition and bone density (dual-energy X-ray absorptiometry) were measured at baseline, 6 months and 3 years; changes were analysed in Z-scores based on data from 241 healthy, local children. Markers of bone turnover were measured at baseline, 3 months and 3 years. Fat loss of 1.4±0.96kg (total fat 5.7±3.6 to 4.3±3.1kg, p<0.001) occurred in the first 6 months. There were significant reductions over 3 years in the sex and height corrected Z-scores for lean tissue, bone mineral content, bone mineral density and ratio of central to total fat (-0.84±0.86, p=0.003; -0.55±0.31, p<0.0001; -0.41±0.28, p<0.0001 and -0.55±0.62, p=0.006 respectively). Propeptide of type I collagen indicated a significant reduction in bone turnover after 3 months (564±202 to 458±96ng/ml, p=0.019), which was fully recovered after 3 years (619±276ng/ml). Stimulant medication was associated with early fat loss and reduced bone turnover. Lean tissue including bone increased more slowly over 3 years of continuous treatment than would be expected for growth in height. There was long-term improvement in the proportion of central fat for height. This study shows that relatively minor reductions in weight on stimulant medication can be associated with long-term changes in body composition. Further study is required to determine the effects of these changes on adult health.

Stimulant medication is known to cause transient weight loss and slowing down of growth, but whether it delays physical maturation is unclear. We studied growth and bone age over the first 3 years of treatment in children with attention-deficit/hyperactivity disorder (patients) compared with healthy siblings (controls). Bone age was estimated blindly by two independent radiologists using Tanner and Whitehouse version 3. Dexamphetamine or methylphenidate was titrated and continued when clinically indicated. Forty out of 73 patients, together with 22 controls, completed the study. There were no significant growth differences between the two groups at baseline. Despite slower growth on treatment [5.1 cm/year, 95% confidence interval (CI): 4.7–5.5, vs. 6.3 cm/year, 95% CI: 5.7–6.8, P=0.002; and 2.7 kg/year, 95% CI: 2.1–3.3, vs. 4.4 kg/year, 95% CI: 3.5–5.3, P=0.005], the patients showed no significant maturational delay (RUS score: 49 U/year, 95% CI: 44–55, vs. 55 U/year, 95% CI: 47–63, P=0.27). A subgroup of patients underwent serial biochemistry and dual-energy X-ray absorptiometry, recording a significant reduction in fat (5.61±3.56–4.22±3.09 kg, P<0.001) and leptin (3.88±2.87–2.57±1.94 ng/ml, P=0.017). The pattern of change in height z-score over time was modified by the dose of medication (P for interaction=0.024). We found no medication effect on the rate of maturation, which was instead predicted by baseline leptin (P=0.035 controlling for age and sex).