Giardia lamblia (Giardia)is among the most common intestinal pathogens in children in low- and middle-income countries (LMICs). AlthoughGiardiaassociates with early-life linear growth restriction, mechanistic explanations forGiardia-associated growth impairments remain elusive. Unlike other intestinal pathogens associated with constrained linear growth that cause intestinal or systemic inflammation or both,Giardiaseldom associates with chronic inflammation in these children. Here we leverage the MAL-ED longitudinal birth cohort and a model ofGiardiamono-association in gnotobiotic and immunodeficient mice to propose an alternative pathogenesis of this parasite. In children,Giardiaresults in linear growth deficits and gut permeability that are dose-dependent and independent of intestinal markers of inflammation. The estimates of these findings vary between children in different MAL-ED sites. In a representative site, whereGiardiaassociates with growth restriction, infected children demonstrate broad amino acid deficiencies, and overproduction of specific phenolic acids, byproducts of intestinal bacterial amino acid metabolism. Gnotobiotic mice require specific nutritional and environmental conditions to recapitulate these findings, and immunodeficient mice confirm a pathway independent of chronic T/B cell inflammation. Taken together, we propose a new paradigm thatGiardia-mediated growth faltering is contingent upon a convergence of this intestinal protozoa with nutritional and intestinal bacterial factors.