Significant weight gain following discontinuation of extended-release methylphenidate in an adult with ADHD: a case report

Abstract ADHD in adults is frequently associated with impulsivity, reward dysregulation, and maladaptive eating behaviors. Stimulant medications, including extended-release methylphenidate, improve executive functioning and suppress appetite. We report a 30-year-old male with ADHD who developed severe binge eating and rapid weight gain following methylphenidate discontinuation. Despite a previously favorable clinical response, the patient became non-adherent and experienced substantial weight gain within two months. This case highlights the potential for dopaminergic rebound and dysregulation of appetite following stimulant discontinuation.

Introduction ADHD in adulthood involves impairments in impulse control and reward processing, which are closely linked to maladaptive eating behaviors and obesity [1,2]. Extended-release methylphenidate exerts therapeutic effects through dopaminergic and noradrenergic pathways, improving executive control, reducing impulsivity, and suppressing appetite via modulation of reward circuitry [1,3]. Discontinuation may lead to a rebound increase in appetite and reward-seeking behaviors due to abrupt changes in dopaminergic tone [4].

Case Presentation A 30-year-old male presented with persistent attention difficulties and dysregulated eating behavior. His developmental history included limited social engagement and a preference for solitary activities; comorbid autism spectrum disorder was considered clinically. Previously diagnosed with ADHD, he was initially treated with immediate-release methylphenidate, discontinued due to withdrawal-like symptoms, then prescribed extended-release methylphenidate, resulting in significant improvement in attention and daily functioning.

Despite this benefit, he chose to discontinue treatment and remained non-adherent for approximately six months. Over the following two months, he developed recurrent binge eating episodes with marked weight gain. His BMI increased from 37.5 to 43.8 kg/m², indicating a transition from class II to class III obesity. He also reported low energy, fluctuating mood, and increased impulsivity. Prior trials with fluoxetine, escitalopram, and bupropion were discontinued due to adverse effects with no sustained benefit. Extended-release methylphenidate remained the only agent associated with meaningful improvement, including appetite regulation.

Discussion This case demonstrates a clear temporal association between methylphenidate discontinuation and severe eating dysregulation resulting in rapid, clinically significant weight gain. Methylphenidate enhances dopaminergic neurotransmission, improving executive functioning, reducing impulsivity, and decreasing the reinforcing value of food [5]. Following discontinuation, dopaminergic rebound may occur, characterized by reduced synaptic dopamine availability and increased reward sensitivity. In individuals with ADHD, who already exhibit baseline reward deficiency and impaired inhibitory control, this shift may lead to compensatory reward-seeking through highly palatable foods. Epidemiological studies support a strong association between ADHD and obesity, reflecting shared neurobiological mechanisms involving dopaminergic dysfunction and impaired self-regulation [2]. The rapid BMI transition is more plausibly explained by loss of pharmacological modulation of reward and appetite than by lifestyle factors alone [3,4].

Conclusion This case highlights the behavioral and metabolic consequences of stimulant discontinuation in adults with ADHD. Stimulant medications play an important role not only in improving cognitive symptoms but also in regulating appetite and reward-related behaviors. Clinicians should be aware of dopaminergic rebound risk following treatment cessation and should emphasize adherence alongside close monitoring of eating patterns and weight trajectory.

References

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