Stunting is a major global health issue, affecting 165 million children under 5 years of age, with a height-for-age Z-score (HAZ) below -2. It is a complex condition with long-term consequences, including increased morbidity and mortality, reduced physical and cognitive development, and a higher risk of metabolic diseases in adulthood. Stunting is cyclical, as women who were stunted in childhood tend to have stunted offspring, creating an intergenerational cycle of poverty. The review discusses the mechanisms of linear growth failure at different ages, the short-, medium-, and long-term consequences of stunting, and the evidence for windows of opportunity during the life cycle to target interventions. Stunting begins in utero and continues for at least the first 2 years of life, making the first 1000 days the most critical period for interventions. Environmental factors such as maternal nutrition, feeding practices, hygiene, and access to healthcare are major determinants of growth in the first 2 years of life. Socioeconomic factors significantly influence stunting prevalence, and improving these factors is crucial for reducing stunting. Antenatal factors, such as maternal undernutrition, short stature, and poor weight gain during pregnancy, contribute to stunting. Maternal height is associated with offspring height and stunting prevalence. Prenatal interventions, such as multiple micronutrient supplementation and iron and zinc supplementation, can reduce stunting. However, the effectiveness of antenatal interventions varies, and not all have shown long-term benefits. In the first 6 months of life, exclusive breastfeeding is recommended to prevent stunting, but evidence for its impact on linear growth is limited. Complementary feeding practices, particularly in the 6–24 months period, are critical for preventing stunting. Interventions such as lipid-based nutrient supplements (LNS) have shown some effectiveness in improving linear growth. However, the impact of micronutrient deficiencies, such as vitamin A, zinc, iron, and iodine, on stunting is complex and requires further research. Infections, inflammation, and gut damage are significant contributors to stunting. Recurrent infections, such as malaria and helminths, are associated with increased stunting risk. Environmental enteric dysfunction (EED), a condition characterized by chronic inflammation and malabsorption in the small intestine, is a key factor in stunting. Interventions targeting EED, such as antibiotics and probiotics, show some promise but require further study. Stunting has long-term consequences, including reduced cognitive development, lower educational attainment, and poorer economic outcomes. It is also associated with an increased risk of metabolic diseases in adulthood, such as hypertension, cardiovascular disease, and type 2 diabetes. The 'Developmental Origins of Health and Disease' hypothesis suggests that early-life nutritional deprivation can lead to permanent epigenetic changes that increase the risk of these diseases. Policy and program implications highlight the need for aStunting is a major global health issue, affecting 165 million children under 5 years of age, with a height-for-age Z-score (HAZ) below -2. It is a complex condition with long-term consequences, including increased morbidity and mortality, reduced physical and cognitive development, and a higher risk of metabolic diseases in adulthood. Stunting is cyclical, as women who were stunted in childhood tend to have stunted offspring, creating an intergenerational cycle of poverty. The review discusses the mechanisms of linear growth failure at different ages, the short-, medium-, and long-term consequences of stunting, and the evidence for windows of opportunity during the life cycle to target interventions. Stunting begins in utero and continues for at least the first 2 years of life, making the first 1000 days the most critical period for interventions. Environmental factors such as maternal nutrition, feeding practices, hygiene, and access to healthcare are major determinants of growth in the first 2 years of life. Socioeconomic factors significantly influence stunting prevalence, and improving these factors is crucial for reducing stunting. Antenatal factors, such as maternal undernutrition, short stature, and poor weight gain during pregnancy, contribute to stunting. Maternal height is associated with offspring height and stunting prevalence. Prenatal interventions, such as multiple micronutrient supplementation and iron and zinc supplementation, can reduce stunting. However, the effectiveness of antenatal interventions varies, and not all have shown long-term benefits. In the first 6 months of life, exclusive breastfeeding is recommended to prevent stunting, but evidence for its impact on linear growth is limited. Complementary feeding practices, particularly in the 6–24 months period, are critical for preventing stunting. Interventions such as lipid-based nutrient supplements (LNS) have shown some effectiveness in improving linear growth. However, the impact of micronutrient deficiencies, such as vitamin A, zinc, iron, and iodine, on stunting is complex and requires further research. Infections, inflammation, and gut damage are significant contributors to stunting. Recurrent infections, such as malaria and helminths, are associated with increased stunting risk. Environmental enteric dysfunction (EED), a condition characterized by chronic inflammation and malabsorption in the small intestine, is a key factor in stunting. Interventions targeting EED, such as antibiotics and probiotics, show some promise but require further study. Stunting has long-term consequences, including reduced cognitive development, lower educational attainment, and poorer economic outcomes. It is also associated with an increased risk of metabolic diseases in adulthood, such as hypertension, cardiovascular disease, and type 2 diabetes. The 'Developmental Origins of Health and Disease' hypothesis suggests that early-life nutritional deprivation can lead to permanent epigenetic changes that increase the risk of these diseases. Policy and program implications highlight the need for a