Abstract
Autism spectrum disorder (ASD) has a long-standing history of being strongly associated with multiple psychiatric comorbidities, including substance use disorders (SUDs) and eating disorders (EDs) like anorexia nervosa (AN). ASD-specific features, including repetitive behaviors, constricted interests, cognitive rigidity, and obsessive fixations, are believed to make patients with ASD vulnerable to SUD and ED development. However, little research attempts to understand the interconnection between ASD and these comorbidities. We present a case of a 26-year-old man with a long-standing diagnosis of ASD who developed SUD and restrictive food intake, culminating in the patient meeting the AN criteria. This patient voluntarily admitted himself to the inpatient psychiatric unit with worsening depression and suicidal ideation following a car accident resulting from sleep deprivation and acute cannabis intoxication. Further investigation revealed a problematic, obsessive pattern of initial alcohol use associated with weight gain, followed by profound food restriction and subsequent transition to daily, near-constant cannabis use. On presentation, he appeared anxious with overt signs of sleep deprivation and malnutrition from substantial weight loss with a body mass index (BMI) decline from 23.6 to 16.98 over the last year. A urine drug screen was positive for cannabinoids, and imaging was unremarkable. Over an 11-day hospitalization, a multidisciplinary team initiated anxiolytics, antidepressants, sleep aids, and cannabis-withdrawal management combined with nutritional rehabilitation under dietitian supervision until acute suicidality was resolved with an improved BMI to 18.75. At discharge, the patient reported eagerness to engage with outpatient psychotherapy, ongoing psychiatric follow-up, and ASD-adapted cognitive behavioral therapy. This case underscores the diagnostic and management implications associated with co-occurring ASD, SUD, and ED. Obsessive fixation and rigidity potentiate maladaptive coping, which, if unaddressed in therapy, may increase the risk of future SUD and ED relapse. Though rapid inpatient stabilization is possible, gaps in both specialty care and ASD-adapted programs may compound relapse risk, especially in underserved regions. Additionally, this case necessitates a comprehensive assessment of patients with neurodevelopmental disorders for more informed and integrated therapeutic intervention. The nuanced interplay between ASD, SUD, and ED has synergistic effects on caloric restriction, requiring multidisciplinary treatment strategies to achieve sustained recovery and reduce morbidity in a vulnerable population.