Asian Journal of Pediatric Research

Giardiasis in childhood ranges from self-limited gastroenteritis to persistent, recurrent, or clinically silent intestinal infection. Its contribution to growth faltering remains difficult to isolate because exposure is concentrated in settings where dietary insufficiency, repeated enteric infection, environmental enteric dysfunction, and socioeconomic deprivation coexist. This critical narrative review evaluates how acute and chronic giardiasis affect ponderal and linear growth, nutritional status, intestinal function, and the growth hormone–insulin-like growth factor-1 axis in children. PubMed/MEDLINE, PubMed Central, Crossref metadata, DOI records, and citation-linked sources were searched for eligible literature published from January 1980 to 26 May 2026. Evidence was appraised according to temporality, exposure measurement, anthropometric quality, control of confounding and co-infection, and mechanistic coherence. Acute symptomatic giardiasis can cause short-term weight loss through diarrhoea, reduced intake, dehydration, maldigestion, and secondary carbohydrate intolerance, but evidence that a single treated episode independently produces sustained stunting is limited. The stronger signal concerns early, persistent, recurrent, or high-density infection: longitudinal cohorts associate these phenotypes with increased intestinal permeability and modest decrements in length-for-age, although site heterogeneity and reverse causality remain important. Mechanistic evidence increasingly indicates that Giardia duodenalis may impair growth without the overt inflammatory pattern typical of other enteropathogens. Nutrient malabsorption, amino-acid depletion, microbial co-metabolism, epithelial injury, and reduced circulating insulin-like growth factor-1 may form a low-inflammatory pathway from intestinal infection to impaired skeletal growth. Direct human evidence for the insulin-like growth factor-1 link is nevertheless recent and derives mainly from one small birth-cohort analysis; broader infection and environmental enteric dysfunction studies support plausibility but are not parasite-specific. Treatment can promote catch-up growth when symptomatic or persistent infection and nutritional deficits are corrected, yet evidence does not justify assuming that eradication of asymptomatic carriage alone will restore growth. Future studies require repeated quantitative diagnostics, standardised persistence definitions, dense anthropometry, diet and co-pathogen measurement, and longitudinal growth-axis biomarkers. The evidence supports a conditional causal model in which timing, duration, parasite burden, diet, microbiota, and host vulnerability determine whether giardiasis becomes growth-limiting.