Long-term use of GLP-1 receptor agonists (semaglutide, liraglutide) and dual GIP/GLP-1 agonists (tirzepatide) generates micronutrient vulnerability through at least five converging mechanisms: reduced caloric intake, diminished dietary diversity, gastrointestinal intolerance, delayed gastric emptying, and rapid weight-loss-driven metabolic shifts. The most clinically significant signals cluster around iron, vitamin B12, vitamin D, calcium, magnesium, zinc, thiamine, folate, and fat-soluble vitamins A, E, and K. Most documented abnormalities remain subclinical, but high-risk subgroups — post-bariatric patients, older adults, those with GI disorders or prolonged nausea — face meaningful clinical consequences.
This narrative review arrives at a critical inflection point. With semaglutide and tirzepatide prescriptions surging globally, the field has focused heavily on glycemic and cardiovascular outcomes while nutritional surveillance has lagged. The micronutrient risk profile here closely mirrors what bariatric surgery literature documented a decade ago — and that community learned costly lessons about thiamine-related neuropathy and iron-deficiency anemia from delayed monitoring protocols. The mechanistic overlap with post-surgical physiology is not coincidental; both reduce gastric acid exposure and nutrient transit time. Clinicians should treat prolonged incretin therapy with the same nutritional vigilance applied to sleeve gastrectomy patients. This review's primary limitation is its narrative design — no pooled effect sizes, no incidence rates, and no causal hierarchy among mechanisms. Prospective cohort data are urgently needed. Incrementally confirmatory in framing, but practically important given the scale of current prescribing.
