Intake and hedonics of calcium and sodium during pregnancy and lactation in the rat $ M. Leshem a, * , T. Levin a , J. Schulkin b a Department of Psychology, University of Haifa, Haifa, 31905 Israel b Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC, USA Received 19 July 2001; received in revised form 9 October 2001; accepted 8 November 2001 Abstract These experiments sought to distinguish whether increased calcium intake during pregnancy and lactation in the rat is due to arousal of a specific calcium appetite, with altered taste hedonics, as occurs with sodium depletion, to reduced taste sensitivity, or to the hyperdipsia of reproduction. We find that, during pregnancy and lactation, CaCl 2 intake is not increased more (in fact less) than intakes of control tastants, MgCl 2 and quinine HCl, and multiparous dams do not have a greater calcium intake than primaparous dams. Changes in taste reactivity to CaCl 2 and to NaCl do not correlate with changes in intake of these minerals during pregnancy or lactation, suggesting that alterations in hedonics or sensitivity do not explain the increased intake of these minerals. Taken together with the increased intake of all the tastants, it may be that the increased intakes of calcium and sodium during reproduction are not due to respective specific appetites or to a general mineral appetite but rather to the reproduction-increased ingestion that may meet all the dam’s increased mineral and nutrient requirements. Differences in the degree of increased intakes of tastes may be due to specific alterations in their transduction during reproduction. D 2002 Elsevier Science Inc. All rights reserved. Keywords: Appetite; Calcium; Ingestion; Lactation; Pregnancy; Rat; Sodium; Taste reactivity; Taste 1. Introduction Changes in ingestive behavior in a variety of species during reproduction have been attributed to adaptive changes in nutrient requirements, e.g. to obtain metabolic fuels and minerals or to avoid toxins [14,33,34,37,46]. Increased calcium intake, like sodium intake, during preg- nancy and lactation is believed to be due to the elicitation of specific appetites [14,48,49]. For calcium, this seems especially likely since with restricted dietary calcium the dam decalcifies her bones significantly, presumably to supply calcium to her fetal and nursing litter [13]. How- ever, in nursing women, this is true even without restriction of calcium intake [21,30,35,38]. The evidence for a specific calcium appetite during reproduction is equivocal. Where increased calcium intake during pregnancy and lactation has been reported, control tastes were not examined [29,32,48,49] so the increase may not be specific to calcium. Indeed, in cafeteria tests of ingestion during reproduction, intakes of other nutrient min- erals, such as potassium, also increased, which was inter- preted as showing that other specific appetites for minerals are also aroused during reproduction [14,33,34,37]. Clearly, comparisons with intakes of nonnutritive tastants are required to establish specificity. The issue is whether the reproducing dam has a repro- duction-aroused specific spontaneous appetite to preempt the deficit, as distinct from the calcium hunger that is aroused in the wake of calcium deficiency in nonreproducing rats [23,37,45]. In dietary depletion, it takes about 2 weeks for the appetite to emerge in rats (e.g. Refs. [9,44,45]), perhaps too long for it to be of much use during a 3-week pregnancy or lactation, but it is possible that the hormonal constellation of reproduction arouses the appetite more rapidly [14,31]. While increased ingestion of calcium during reproduc- tion may be an appropriate behavioral adaptation (though 0031-9384/02/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved. PII:S0031-9384(01)00668-0 $ Experiment 4 in this paper is part of Tamy Levin’s MAThesis. Parts of these data were presented at the Israel Society for Neuroscience, Eilath, December 1999 and at the Society for the Study of Ingestive Behavior, Dublin, June 2000. * Corresponding author. Tel.: +972-48-249175; fax: +972-48-240966. E-mail address: micah.leshem@psy.haifa.ac.il (M. Leshem). Physiology & Behavior 75 (2002) 313 – 322