with low birth weight of 1,218.2 Ϯ 36.6 g (range, 765-1,580 g) were selected from hospital archives on the basis of whether they had received neonatal diuretic treatment or as healthy matched controls. The children were tested for salt appetite and sweet preference, including rating of preferred concentration of salt in tomato soup (and sugar in tea), ratings of oral spray (NaCl and sucrose solutions), intake of salt or sweet snack items, and a food-seasoning, liking, and dietary questionnaire. Results showed that sodium appetite was not related to neonatal diuretic treatment, birth weight, or gestational age. However, there was a robust inverse correlation (r ϭ Ϫ0.445, P Ͻ 0.005) between reported dietary sodium intake and the neonatal lowest serum sodium level (NLS) recorded for each child as an index of sodium loss. The relationship of NLS and dietary sodium intake was found in both boys and girls and in both Arab and Jewish children, despite marked ethnic differences in dietary sources of sodium. Hence, low NLS predicts increased intake of dietary sodium in low birth weight children some 8 -15 yr later. Taken together with other recent evidence, it is now clear that perinatal sodium loss, from a variety of causes, is a consistent and significant contributor to long-term sodium intake. dietary sodium; humans; hyponatremia; neonates; perinatal programming; sodium appetite THE SOURCE OF INDIVIDUAL VARIATION in salt appetite and why many people ingest an excess of salt are not known. Early development is considered to be a crucial period for establishing individuality in behavior and may similarly determine individual differences in salt preference. Yet attempts in rats to relate early sodium intake to long-term salt preference have yielded inconsistent results (11,29,37). Similarly, in humans, studies on the determinants of individual variability in salt preference and intake that have concentrated on exposure, acculturation, and learning, particularly in infancy and childhood, have not revealed the determinants of individual variability in salt preference (7, 18, 34) although they have shown how a particular salty food becomes preferred (47).On the other hand, in rats, long-term increases in salt intake have been found consequent on varied instances of perinatal mineralofluid loss: offspring of dams that during pregnancy were dehydrated, lost sodium, or had their hormones of sodium conservation activated, or rats that were acutely sodium deprived postnatally, all show increased sodium intake in adulthood (4,16,26,29,48). Similarly, in humans, maternal vomiting during pregnancy increases offspring salt preference, as do childhood vomiting, diarrhea, salt wasting, and electrolyte deficient feeding (9,10,23,27,42).Much of the human data are based on recall, and it thus remains to be proven that confirmed neonatal sodium deficit increases salt appetite enduringly in humans. In an earlier attempt, we tested children who had received neonatal diuretic therapy, and found that five children who had received neonatal di...