Neonatal Diuretic Therapy may not Alter Children's Preference for Salt Taste

Leshem, Micah; Maroun, Mouna; Weintraub, Zalman

doi:10.1006/appe.1997.0111

Cited by 19 publications

(14 citation statements)

References 24 publications

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“…This is reminiscent of our previous finding with children treated neonatally with diuretics who showed no preference for salt, although fractional excretion of sodium measured in five children was almost twice that of matched controls, suggesting higher consumption of sodium (30). Explaining increased sodium intake without increased preference is awkward (51).…”

Section: Discussionsupporting

confidence: 76%

“…Maternal vomiting during gestation, infantile diuresis, diarrhea, vomiting, and inadequate infant formula electrolytes, have all been linked to long-term increased sodium appetite in humans (9,10,23,27,30,44) and are consistent with findings in animals (4,16,26,29,48).…”

Section: Discussionsupporting

confidence: 68%

“…Whether similar relationships to neonatal serum sodium pertain to normal weight and term neonates requires urgent pursuit, these findings accentuate the importance of monitoring and balancing sodium levels in premature babies. Taken together with other recent evidence (4,9,10,16,23,26,27,30,44,48), it is now clear that perinatal sodium loss, from a variety of causes, is a consistent and significant contributor to long-term sodium intake.…”

Section: Discussionmentioning

confidence: 83%

“…In an earlier attempt, we tested children who had received neonatal diuretic therapy, and found that five children who had received neonatal diuretics had a greater fractional excretion of sodium than their matched controls, suggesting greater sodium intake (30). In the present study, using data from neonatal medical records, we investigated whether neonatal serum sodium loss might be related to salt appetite in the children 8 -15 yr later.…”

mentioning

confidence: 93%

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Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Shirazki

Weintraub²,

Reich³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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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...

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Section: Discussionsupporting

confidence: 76%

Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 83%

mentioning

confidence: 93%

See 2 more Smart Citations

Lowest neonatal serum sodium predicts sodium intake in low birth weight children

Shirazki

Weintraub²,

Reich³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

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show abstract

“…It apparently is not learned because, although preference for salt in a specific food can be learned, there is no generalization to other foods (12,40). One contributing factor to adult sodium appetite is perinatal sodium loss (3,20,21,23,39).…”

mentioning

confidence: 99%

Increased salt appetite in patients with congenital adrenal hyperplasia 21-hydroxylase deficiency

Kochli¹,

Tenenbaum‐Rakover²,

Leshem³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Salt appetite was investigated in 14 patients with congenital adrenal hyperplasia of the salt-wasting form (SW group), 12 patients with the simple virilized form who are not salt losing, and 18 healthy siblings. Salt appetite was evaluated by questionnaire, preference tests, and dietary analyses. The findings showed that SW who were not therapeutically normalized showed increased salt appetite but no change in sweet preference. Their salt appetite correlated with symptoms of salt wasting, namely, plasma renin activity, plasma K(+), and urine Na(+) and (inversely) with blood pressure. Sensitivity to the taste of NaCl was not altered. Factor analyses of a larger group confirmed the distinction between salt appetite and sweet preference, but intake of dietary Na(+) and sweet carbohydrates and intake of salty and sweet snacks did not reflect distinct salt or sweet preferences. We confirm that putative perinatal dehydration, due to maternal nausea and vomiting during pregnancy, childhood vomiting, and diarrhea with occasional saline infusion, was related to increased salt appetite in adolescence. The findings suggest that salt appetite in humans is determined by interdependent, innate, physiological, and acquired attributes. Salt appetite in SW patients is an adaptive response mediated by the renin-angiotensin system, an innate predisposition to acquire salt preference (in anticipation of both sodium loss and its consequence), and imprinting by perinatal hyponatremic occurrences. Our findings contribute to understanding human salt intake, provide insight into the motivation for salt in patients with congenital adrenal hyperplasia 21-OH deficiency, and may point the way to improvements in therapeutic compliance in these patients.

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