Weight Gain

The grounding supports medication-associated weight gain, especially with second-generation antipsychotics, and weight regain after discontinuation of glucagon-like peptide-1 receptor agonists. It also supports weight regain or insufficient weight loss after metabolic bariatric surgery, with changes in endogenous GLP-1 levels implicated in that setting.

The literature describes weight gain as part of broader metabolic dysregulation, including disturbances in glucose homeostasis, lipid regulation, and adipose tissue function. Proposed mechanisms include antipsychotic-induced metabolic changes that may occur before overt weight gain, and altered gut GLP-1 signaling after bariatric surgery or after stopping GLP-1 receptor agonists, affecting appetite, energy expenditure, and weight maintenance.

Risk is increased by exposure to second-generation antipsychotics, which are associated with metabolic disturbance and body weight gain. The grounding also supports prior metabolic bariatric surgery with subsequent weight regain, and discontinuation of GLP-1 receptor agonist therapy as contexts in which weight gain can occur.

The supplied grounding supports treatment at the modality level with glucagon-like peptide-1 receptor agonists for obesity and for weight regain after bariatric surgery. It also supports that antipsychotic-associated weight gain is managed in the context of choosing among antipsychotics with differing metabolic side-effect profiles, but it does not provide a specific treatment regimen for weight gain itself.