ADHD and Obesity

ADHD is a neurobiological psychiatric disorder in children, adults, and older people with a prevalence of between 2.5% and 5% in the general population (2). ADHD is characterized by lifetime symptoms of inattentiveness, forgetfulness, impulsive behavior, mood swings, and restlessness. Binge eating is one of the manifestations of impulsivity in ADHD. Difficulty in planning as a consequence of inattentiveness in ADHD is often expressed by skipping breakfast and lunch (3). In addition, ADHD is highly comorbid with other psychiatric disorders, including (seasonal) depression, anxiety, and circadian rhythm disturbances. Children and adults with ADHD usually suffer from short sleep duration due to insomnia, which has been associated with delayed onset of melatonin (4). Short sleep duration, binge eating, and skipping meals are all associated with obesity (5).

Obesity rates are increasing worldwide and constitute a huge public health concern because of the relationship with chronic diseases like diabetes, hypertension, cardiovascular disease, and cancer. Public health initiatives aim to prevent and reduce the incidence of obesity in order to prevent potential epidemics of chronic disease in the general population. As a dose-response relationship between the severity of ADHD and obesity has been established, it may be time we pay attention to this specific combination of mental and physical disorders (6, 7).

Behavior abnormalities in both ADHD and obesity may be related to addictive behaviors. Disturbance of the neurotransmitter dopamine plays an important role in all three conditions. Treatment of eating disorders and obesity is no longer considered to be “brainless.” Changes in behavior can be related to brain-plasticity changes induced by obesity and are observed in both animal models and human subjects (8). Functional magnetic resonance imaging studies have identified three shared neurobehavioral circuits in ADHD, obesity, and abnormal eating behavior; these circuits are associated with reward processing, response inhibition, and emotional processing and regulation (9).

The interrelatedness of sleep debt by circadian disturbances, melatonin, and appetite hormones is a subject of current research (10, 11). Ongoing studies on the gut-brain connection and on the microbiome in psychiatric disorders and eating behavior may bring us closer to the necessary next steps to improve mental and physical health in patients with ADHD and in the increasing number of obese individuals in the general population.

The association between ADHD and obesity is highly relevant for the beginning of a better understanding of psychiatric symptoms that may drive the development of obesity. New research questions in this domain may be formulated and studied. Public health projects aiming to reduce the severity of obesity and the number of people with obesity worldwide may now target people with ADHD as a potential group for preventive measures. From a clinical perspective, the relationship between ADHD and obesity is well known. Increasing numbers of patients with ADHD are obese, and in obesity clinics, the chance of having ADHD increases with body mass index (6). The current study by Cortese et al. adds meta-analytic confirmation. In clinics for bariatric surgery, where the most severe and chronic obesity patients are seen, standard screening for ADHD would help to identify affected patients and initiate treatment for ADHD, in an effort to improve patient outcomes before and after bariatric surgery.

Treatment of obesity in ADHD patients can be complex and involves careful assessment of all disorders and risk factors to determine the best order of treatment. Common comorbidity patterns are ADHD, delayed sleep phase disorder, binge eating, obesity, and depression or anxiety. Treatment starts with psychoeducation on the interrelatedness of late and short sleep, skipping meals, binge eating, and obesity. In addition, depressed mood often increases the craving for carbohydrate-rich food, especially in winter.

The ADHD symptoms of forgetfulness, bad planning, and impulsivity add to the chronicity of these behaviors. A patient’s understanding of the relationship between factors may facilitate compliance for each step of treatment, which consists of treatment of the most severe disorder first, usually the mood disorder, with a selective serotonin reuptake inhibitor or, in case of seasonal depression, bright light therapy in the morning. Melatonin may be added for the delayed sleep phase disorder to help reset the biological clock and lead to an earlier sleep onset and thus longer sleep duration. Sufficient sleep may improve mood and reduce carbohydrate craving, as well as the severity of ADHD symptoms. Finally, ADHD is treated with a stimulant with the aim of improving the ability to plan and oversee the consequences of erratic eating patterns during the day. Usually, the patient is able for the first time to keep to a diet, aided by the decrease in appetite, which in this case is a welcome side effect of the stimulant medication. However, weight loss while using a stimulant is usually limited to 2–3 kg. To lose more weight, a diet and a change of lifestyle are needed. The improved planning of meals and the ability to keep to a diet seem to be the most important contributions of the stimulant treatment for weight loss. In the meta-analysis by Cortese et al., medical treatment of ADHD brought the risk of obesity back to normal, showing not only that untreated ADHD symptoms drive obesity but also that combined treatment of ADHD and obesity may be more effective than treatment of obesity alone.