Early-Life Nutritional Ecologies and Perinatal Outcomes among Immigrants
H Cebolla Boado, A Suárez Vergne, MB LundAbstract
Research on migrant perinatal health has primarily focused on immigrants’ protection against low birth weight, often overlooking their elevated risk of fetal macrosomia. We propose a multi-sited, life-course framework linking early-life nutritional environments in mothers’ countries of origin to perinatal outcomes after migration. Using unconditional quantile regressions on Spanish birth registry microdata (2016–2021) linked to historical FAO nutritional series, we document a monotonically increasing immigrant birth-weight differential across quantiles: immigrant status is associated with protection at the lower tail of the birthweight distribution but progressively higher birth weight toward the upper tail. Adjusting for early-life nutritional environments in the origin country, proxied by the share of calories from fat, substantially attenuates this differential, reducing the immigrant coefficient by about half at the 95th percentile and explaining most of the observed attenuation. By contrast, alternative indicators of origin-country conditions—including caloric availability, protein share, GDP per capita, HDI, and infant mortality—are associated primarily with the lower tail of the distribution and provide little explanation for upper-tail differences. Additional analyses show that the upper-tail birth-weight differential is largest among immigrants whose mothers grew up in nutritional environments characterized by lower fat availability. This directional pattern is consistent with a nutritional mismatch mechanism, whereby women exposed to earlier stages of the nutrition transition encounter substantially more energy-dense nutritional environments after migration, increasing the likelihood of fetal overgrowth.
Key messages
• Migrant perinatal health should be assessed beyond low birth weight, as fetal overgrowth may be an overlooked risk.
• Early-life nutritional environments before migration may shape macrosomia risk after migration.