Bariatric surgery increases the risk of alcohol and substance use disorders by altering ethanol metabolism and reward pathways, leading to nutritional deficiencies and weight regain.
Metabolic and bariatric surgery increases long-term vulnerability to alcohol and substance use disorders, necessitating lifelong multidisciplinary screening and targeted nutritional supplementation.
Metabolic and bariatric surgery (MBS) has evolved into a highly effective neurohormonal intervention for severe obesity; however, it introduces unique long-term vulnerabilities, particularly regarding alcohol (AUD) and substance use disorders (SUD). This review synthesizes the epidemiological, pharmacokinetic, and neurobiological drivers of postoperative substance misuse. Procedures like Roux-en-Y gastric bypass (RYGB) radically alter ethanol metabolism, eliminating first-pass metabolism and accelerating gastric emptying, while simultaneously recalibrating reward pathways, creating a “reward gap” that facilitates addiction transfer. These physiological shifts exacerbate critical micronutrient deficiencies (thiamine, B12, iron), increase the risk of post-bariatric hypoglycemia, and correlate with higher rates of liver cirrhosis and suicide. Furthermore, substance use is a primary driver of suboptimal weight loss trajectories and weight regain. Mitigation requires a lifelong, multidisciplinary framework involving preoperative risk stratification, validated screening (e.g., AUDIT-C), and targeted nutritional supplementation to safeguard the long-term metabolic and psychological benefits of MBS.
Campuzano-Donoso et al. (2026) studied this question. Bariatric surgery increases the risk of alcohol and substance use disorders by altering ethanol metabolism and reward pathways, leading to nutritional deficiencies and weight regain.