Abstract Background Low and high birth weight and accelerated postnatal weight gain are associated with an increased risk of obesity. Perinatal effects on energy intake and eating behavior have been proposed as underlying mechanisms. This study aimed to examine the independent associations of birth weight and postnatal weight and height gain with childhood energy intake and satiety response. Methods In a birth cohort study, we used data from 2227 children (52 % male), mean age 5.6 (±0.4) years. Mean daily energy intake and satiety response were parent-reported through validated questionnaires. Exposures were birth weight z-score and conditional weight and height gain between 0–1, 1–3, 3–6, 6–12 months and 12 months to 5 years. Conditional weight and height are residuals of current weight and height regressed on prior growth data, to represent deviations from expected growth. Analyses were adjusted for a set of potential confounding variables. Results Conditional weight gain between 1–3, 3–6 months and 12 months to 5 years was significantly associated with energy intake, with 29.7 (95 %-CI: 4.6; 54.8), 24.0 (1.8; 46.1) and 79.5 (29.4; 129.7) kcal/day more intake for each Z-score conditional weight gain between 1–3, 3–6 months and 12 months to 5 years, respectively. Conditional height gain between 0–1, 1–3 months and 12 months to 5 years was negatively associated with energy intake (β: −42.0 [66.6; –17.4] for 0–1 months, −35.1 [−58.4; −11.8] for 1–3 months and −37.4 [−72.4; −2.3] for 12 months to 5 years). Conditional weight gain in all periods was negatively associated with satiety response, with effect sizes from − 0.03 (−0.06; −0.002) in early infancy to −0.12 (−0.19; −0.06) in childhood. Birth weight was not associated with energy intake or satiety response. Conclusions Our findings suggest that accelerated infant and childhood weight gain are associated with increased energy intake and diminished satiety response at 5 years. Accelerated height gain seems to be beneficial for childhood energy intake. This perinatal ‘programming’ of energy intake and eating behavior provide a potential mechanism linking early life influences with later obesity and cardiovascular disease.