plasma
born when CRIP is extremely low? In any case, this research adds a new dimension to our understanding of zinc metabolism. 1. Cousins RJ. Absorption, transport, and hepatic metabolism of copper and zinc: special reference to metallothionein and ceruloplasmin. Physiol Rev
1985;65:238-309 2. Hoadley JE, Leinart AS, Cousins RJ. Relationship of YT-Zn
Trans cellular
Figure 1. Proposed model of zinc absorption by an enterocyte involving CRIP, metallothionein, and nonspecific zinc binding (NSB). A paracellular pathway of absorption is also indicated. 0 J Nutr (122:8%95).
ing competitive binding of zinc by metallothionein and CRIP. When the luminal concentration of zinc was increased progressively, there was no change in total zinc bound to CRIP, but there was a decreased proportion of 65Zn bound to CRIP, suggesting that the protein exhibits saturation kinetics. According to this model, upregulation of metallothionein would decrease zinc absorption, which agrees with most evidence. The hypothesis that CRIP serves as a zinc transport protein, analogous to the purported role of calbindin in calcium transport ,8 requires additional verification. Among the questions to be answered are: 1) Is CRIP regulated by zinc or other substances? and 2) How is zinc transported in the new-
65Zn absorption kinetics to intestinal metallothionein in rats: effects of zinc depletion and fasting. J Nutr 1988;118:497-502 3. Hempe JM, Carlson JM, Cousins RJ. Intestinal metallothionein gene expression and zinc absorption in rats are zinc-responsive but refractory to dexamethasone and interleukin la. J Nutr 1991;121:
138S96 4. Hempe JM, Cousins RJ. Cysteine-rich intestinal protein binds zinc during transmucosal zinc transport. Proc Natl Acad Sci USA 1991;88:9671-4 5. Hempe JM, Cousins RJ. Cysteine-rich intestinal protein and intestinal metallothionein: an inverse relationship as a conceptual model for zinc absorption in rats. J Nutr 1992;122:8%95 6. Hempe JM, Cousins RJ. Effect of EDTA and zincmethionine complex on zinc absorption by rat intestine. J Nutr 1989;119:117!3-87 7. Berkenmeier EH, Gordon JI. Developmental regulation of a gene that encodes a cysteine-rich intestinal protein and maps near the murine immunoglobulin heavy chain locus. Proc Natl Acad Sci USA
1986;83:2516-20 8. Bronner F. Intestinal calcium absorption: mechanisms and applications. J Nutr 1987;117:1347-52
Calcium Supplementation Prevents Hypertensive Disorders of Pregnancy Preeclampsia, a hypertensive disorder of pregnancy, is a major cause of fetal and maternal morbidity and mortality. Epidemiologic studies have shown an inverse relationship between dietary calcium intake and gestational hypertension. A recent large-scale, randomized, doubleblind, placebo-controlled clinical trial has shown that supplementation of pregnant women with 2 g calcium per day from the twentieth week of gestation to term can significantly lower the incidence of hypertensive disorders of pregnancy. The beneficial effect of calcium supplementation was apparent as early as the twenty-eighth week of gestation. The mechanism responsible for the effects of calcium on gestational hypertension is unknown.
Preeclampsia is a major cause of fetal and maternal morbidity and mortality. The clinical signs of preNutrition Reviews, Vol. 50, No. 8
eclampsia usually appear in late gestation in nulliparous pregnant women as hypertension, edema, proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, abnormalities in liver function or coagulation, and elevated serum uric acid levels. Major pathophysiologic aspects of preeclampsia include decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; significantly increased peripheral vascular resistance; and exaggerated pressor responses to endogenous angiotensin I1 and catecholamines.' Preeclampsia occurs in 5-10% of all pregnancies and can rapidly progress to a convulsive phase (eclampsia). Preeclampsia usually occurs after the twentieth week of gestation, most frequently near term. Epidemiologic studies have found an inverse relationship between calcium intake and preeclampsia.2 Moreover, calcium supplementation has been 233
reported to lower blood pressure in pregnant and nonpregnant women.3 The possible importance of calcium metabolism in the pathogenesis of preeclampsia is supported by observations that the largest reduction in blood pressure in pregnant women given calcium supplementation was seen in those with low pretreatment serum calcium levels .4 Other reports indicate that urinary calcium excretion is reduced in women with preeclampsia.’ Until recently, however, the efficacy of calcium supplementation in the prevention of preeclampsia had not been demonstrated in a large, randomized, controlled trial. Recently, Belizan et aL6reported the findings of a multicenter, double-blind, randomized controlled trial that examined the effects of calcium supplementation on the incidence of hypertensive disorders of pregnancy. The study was conducted in three hospitals in Argentina between 1987 and 1989. Eligibility requirements for the study subjects included initiation of prenatal care before the twentieth week of gestation; a nulliparous, singleton pregnancy; blood pressure less than 140/90 mmHg, absence of clinical or laboratory evidence of disease, including glucose intolerance; and absence of medications. Women (n = 1194) were entered into the study and were randomized to receive either placebo or 2 g/day of elemental calcium (as calcium carbonate tablets). Hospital visits were scheduled so that the initial visit occurred before 20 weeks of gestation, with subsequent visits at 23, 25, 27, 31, and 35 weeks, and then weekly until delivery. A battery of measurements was made at each hospital visit, including a 24-hour dietary recall (subjects recruited during the first four months of the study only); fasting urinary calcium; blood pressure (five measurements per visit); and serum calcium, magnesium, phosphorus, and uric acid. No eclampsia occurred during the study. When gestational hypertension (blood pressure 140/90 mmHg or above) or preeclampsia [defined in this study as gestational hypertension with proteinuria (protein more than 0.3 g/L)] developed, the patient received medical treatment and her participation in the incidence study ended, although pregnancy outcome and neonatal outcome were followed. Only 2.3% of the initial study group was lost to follow-up, with equal losses reported in each treatment group. Forty-six women in the placebo group and 52 in the calcium group were also excluded from the analysis due to incomplete follow-up. The final number of women in each treatment group was 588 receiving placebo and 579 receiving calcium. The mean age of the women in the study was 23.7 -+ 5.5 years. The initial blood pressure was 104/66 mmHg, and the urinary ca1cium:creatinine ratio 234
(mmo1:mmol) was 0.75. Mean calcium intake, determined in 87 women in the placebo group, was 642 ? 448 mg/day, which was similar to the 646 -+ 396 mg/day observed in 86 women in the calcium group. Overall compliance, assessed by pill count, was reported to be about 85%, with 69% of the subjects taking more than 80% of their calcium supplements. This high degree of compliance was also reflected in urinary calcium and creatinine excretion. The primary hypothesis tested in this study was that calcium supplementation would reduce the incidence of gestational hypertensive disorders. The beneficial effects of calcium supplementation on hypertensive disorders of pregnancy are illustrated in Figure 1. The incidence of gestational hypertension in the placebo group was 10.7%, which was significantly greater than the 7.2% incidence reported in the group taking calcium supplements (odds ratio 0.64, 95% confidence interval 0.43-0.93). The incidence of preeclampsia was 2.6% in the calciumsupplemented group vs. 3.9% in the placebo group (odds ratio 0.65, 95% confidence interval 0.351.25). The overall rates of hypertensive disorders of pregnancy were 14.8% in the placebo group and 9.8% in the calcium-supplemented group (odds ratio 0.63, 95% confidence interval 0.44-0.90). The effects of calcium on gestational hypertension were evident as early as the twenty-eighth week of gestation (Figure 2). The calcium supplementation appeared to be less effective in subjects with higher urinary calcium losses. The study subjects were stratified according to their baseline urinary ca1cium:creatinine ratio into one group having low calcium excretion
=
PLACEBO
Ca-TREATED
Gestational HT
Preeclampsia
Total
I 0
I
5
10
15
20
Incidence of Hypertensive Disorders, % Figure 1. Effect of calcium supplementation on the incidence of hypertensive disorders of pregnancy. Gestational hypertension was defined as a blood pressure greater than or equal to 140/90 mmHg. Preeclampsia was defined as the presence of both gestational hypertension and proteinuria. Calcium supplementation significantly reduced the risk of developing hypertensive disorders of pregnancy. Figure was made from data presented in Beliz6n et al. (ref. 6). Nutrition Reviews, Vol. 50, No. 8
/
//' /
;
Placebo
20
22
24
26
28
30
32
34
36
38
40
Weeks of Gestation
Figure 2. Percentage of women in the calcium-treated
and placebo groups in whom hypertensive disorders of pregnancy (gestational hypertension and preeclampsia) developed, according to the week of gestation. Figure is reprinted with permission from N Engl J Med (1991;325: 1399-1465).
(less than 0.62 mmol calcium per mmol creatinine) and a second group having high urinary calcium excretion (more than 0.62 mmol calcium per mmol creatinine). The incidence of gestational hypertension in the low urinary calcium group receiving calcium supplements was significantly lower (7.8%) compared to their placebo controls (13.2%). However, the incidence of gestational hypertension was not significantly different between placebo and calcium-treated groups in subjects with initially high levels of urinary calcium excretion (11% in the placebo group and 9.4% in the calcium-treated subjects). This well-designed, double-blind, placebocontrolled trial clearly demonstrates that the risk of hypertensive disorders of pregnancy can be reduced significantly by administration of 2 g/day of elemental calcium after the twentieth week of gestation. The findings of Belizan et a1.6are consistent with those obtained from several other studies, completed in different population groups, which demonstrated a tendency for calcium supplementation to protect against hypertensive disorders of pregnancy. The mechanism by which calcium supplementation reduces the risk for gestational hypertension is not known. Disturbances in calcium metabolism have been reported in hypertensive subjects,' and erythrocyte and platelet calcium levels are higher in women with gestational hypertension.*^^ In addition, several studies have reported that women with Nutrition Reviews, Vol. 50, No. 8
preeclampsia are hypocalciuric. lo-'* Low urinary calcium excretion may result from the elevated parathyroid hormone levels observed in preeclampsia.I3 It has been speculated that calcium supplementation during gestation may lower parathyroid hormone levels, and that this may, in turn, reduce intracellular calcium concentrations in vascular smooth muscle cells and diminish their responsiveness to pressure stimuli, thereby reducing blood p r e ~ s u r e . 'Other ~ possible effects of calcium supplementation include changes in renal sodium handling and changes in sodium retention. These intriguing possibilities should be investigated, as well as the possible involvement of abnormal vitamin D metabolism. l 3 , I 5 It should be noted, however, that pregnancy is associated with absorptive hypercalciuria. The addition of 2 g calcium to the diet will increase the degree of hypercalciuria and may increase the risk of developing renal calculi, which occur in one in 1500 pregnancies. Caution needs to be exercised before large-scale implementation of calciumsupplementation programs for pregnant women is initiated. 1. Lindheimer MD, Katz Al. Preeclampsia: pathophysiology, diagnosis, and management. Annu Rev Med 1989;40:233-50 2. Villar J, Belizan JM, Fischer PJ. Epidemiologic observations on the relationship between calcium intake and eclampsia. Int J Gynaecol Obstet 1983; 21 :271-8 3. Villar J, Repke J, Belizan JM, Pareja G. Calcium supplementation reduces blood pressure during pregnancy: results of a randomized controlled clinical trial. Obstet Gynecol 1987;70:317-22 4. Repke JT, Villar J, Anderson C, Pareja G, Dubin N, Belizan JM. Biochemical changes associated with blood pressure reduction induced by calcium supplementation during pregnancy. Am J Obstet Gynecol 1989;160:684-90 5. Taufield PA, Ales KL, Resnick LM, Druzin ML, Gertner JM, Laragh JH. Hypocalciuria in preeclampsia. N Engl J Med 1987;316:715-8 6. Belizan JM, Villar J, Gonzalez L, Campodonico, Bergel E. Calcium supplementation to prevent hypertensive disorders of pregnancy. N Engl J Med 1991;325:1399-405 7. McCarron DA. Dietary calcium in the pathogenesis and therapy of human and experimental hypertension. In: Rubin RP, Weiss GB, Putney JW Jr., eds. Calcium in biological systems. New York: Plenum Press, 1985:561-8 8. Sowers JR, Zemel MB, Bronsteen RA, et al. Erythrocyte cation metabolism in preeclampsia. Am J Obstet Gynecol 1989;161:441-5 9. Haller H, Oeney T, Hauck U, Distler A, Philipp T. Increased intracellular free calcium and sensitivity to angiotensin II in platelets of preeclamptic women. Am J Hypertens 1989;2:238-43 235
10. Rodriguez MH, Masaki DI, Mestman J, Kumar D, Rude R. Calcium-creatinine ratio and microalbuminuria in the prediction of preeclampsia. Am J Obstet Gynecol 1988;159:1452-5 11. Maclntosh MC, Hutchesson AC, Duncan SL, Forrest AR. Hypocalciuria and hypertension in pregnancy: a prospective study. Br J Obstet Gynaecol 1989;96:1243-4 (abstract) 12. Frenkel Y, Barkai G, Mashiach S, Dolev E, Zimlichman R, Weiss M. Hypocalciuria of preeclampsia is independent of parathyroid hormone level. Obstet Gynecol 1991;77:689-91 13. Mochizuki M, Morikawa H, Yamasaki M, Maruo T.
Vascular reactivity in normal and abnormal gestation. Am J Kidney Dis 1991;17:139-43 14. BelizAn JM, Villar J, Repke J. The relationship between calcium intake and pregnancy-induced hypertension: up-to-date evidence. Am J Obstet Gynecol 1988;158:898-902 15. Seely EW, Wood RJ, Brown EM, Graves SW. Lower serum ionized calcium and abnormal calciotrophic hormone levels in preeclampsia. J Clin Endocrinol Metab 1992;74:430-4 16. Ferris TF. Pregnancy, preeclampsia, and the endothelial cell. N Engl J Med 1991;325:1439-40
Women on the Short End of the Loaf: lntrahousehold Food Allocation Among Members of Poor Nepalese Families Intensive and structured intrahousehold observations of the pattern of food allocation in poor rural Nepalese households indicate no difference in the distribution of nutrients between male and female children. In contrast, preferential food distribution patterns among adults show that women are less likely to achieve recommended levels of some nutrients than are men of the same age.
As both population and poverty increase in developing countries, estimates are that, by the year 2000, four of five persons will live in less-developed nations, and that 90% of these will be classified as poor. Such widespread poverty places certain groups, especially young children, women of childbearing age, and the elderly, at increased risk for malnutrition, although studies’ indicate that factors other than poverty also contribute to malnutrition. Within the same poor community, some families produce healthy, normally growing children, while others have malnourished children. Successful child rearing under adverse conditions has been termed “positive deviance.”’ Conversely, based on national per capita food balance or nutrient availability, some nations appear to have sufficient resources to prevent widespread nutritional deficiencies, yet stunting, wasting, and even clinical malnutrition can be common. One possible explanation for both situations is that the distribution of food is selective and unequal, either favoring or disfavoring the groups susceptible to nutritional compromise. This has been a comfortable explanation for differential survival and growth and development within or among families in less-privileged societies, but ways to measure the differential distribu-
236
tion of food within the home have not been forthcoming. Understanding the patterns of unequal intrahousehold food allocation is important not only to determine the causes of undernutrition, but also to design and implement interventions aimed at improving nutritional status. Nutritional anthropologists have attempted to open the “black box” that surrounds the system of intrahousehold food allocation that control the size and distribution of serving portions, the patterns of second helpings, and the provision of prime or inferior food morsels to individual family members. Until recently, more theory than practice has been devoted to the issue of intrahousehold but a recent study from Nepal by Gittelsohn’ provides solid methods for observing household interactions and for analyzing the data. Gittelsohn’ examined five elements related to intrahousehold food allocation, including the identity of the food server; the order in which individuals were served; what was served to whom; how much was served to whom; and how individuals were served (e.g., automatically, on request, or by force). Field-workers trained to categorize and quantify feeding behaviors randomly observed a total of three to four main meals in the homes and compounds of 105 rural highland Nepalese families (767 individuals) during a four-month period. Based on these observations, the following variables were developed: 1. Serving order (relative to all served) 2. Serving method (relative autonomy of server or served) 3. Second helpings (multiple offerings to an individual) 4. Refusals (rejection of a food by the person requesting it)
Nutrition Reviews, Vol. 50, No. 8
born when CRIP is extremely low? In any case, this research adds a new dimension to our understanding of zinc metabolism. 1. Cousins RJ. Absorption, transport, and hepatic metabolism of copper and zinc: special reference to metallothionein and ceruloplasmin. Physiol Rev
1985;65:238-309 2. Hoadley JE, Leinart AS, Cousins RJ. Relationship of YT-Zn
Trans cellular
Figure 1. Proposed model of zinc absorption by an enterocyte involving CRIP, metallothionein, and nonspecific zinc binding (NSB). A paracellular pathway of absorption is also indicated. 0 J Nutr (122:8%95).
ing competitive binding of zinc by metallothionein and CRIP. When the luminal concentration of zinc was increased progressively, there was no change in total zinc bound to CRIP, but there was a decreased proportion of 65Zn bound to CRIP, suggesting that the protein exhibits saturation kinetics. According to this model, upregulation of metallothionein would decrease zinc absorption, which agrees with most evidence. The hypothesis that CRIP serves as a zinc transport protein, analogous to the purported role of calbindin in calcium transport ,8 requires additional verification. Among the questions to be answered are: 1) Is CRIP regulated by zinc or other substances? and 2) How is zinc transported in the new-
65Zn absorption kinetics to intestinal metallothionein in rats: effects of zinc depletion and fasting. J Nutr 1988;118:497-502 3. Hempe JM, Carlson JM, Cousins RJ. Intestinal metallothionein gene expression and zinc absorption in rats are zinc-responsive but refractory to dexamethasone and interleukin la. J Nutr 1991;121:
138S96 4. Hempe JM, Cousins RJ. Cysteine-rich intestinal protein binds zinc during transmucosal zinc transport. Proc Natl Acad Sci USA 1991;88:9671-4 5. Hempe JM, Cousins RJ. Cysteine-rich intestinal protein and intestinal metallothionein: an inverse relationship as a conceptual model for zinc absorption in rats. J Nutr 1992;122:8%95 6. Hempe JM, Cousins RJ. Effect of EDTA and zincmethionine complex on zinc absorption by rat intestine. J Nutr 1989;119:117!3-87 7. Berkenmeier EH, Gordon JI. Developmental regulation of a gene that encodes a cysteine-rich intestinal protein and maps near the murine immunoglobulin heavy chain locus. Proc Natl Acad Sci USA
1986;83:2516-20 8. Bronner F. Intestinal calcium absorption: mechanisms and applications. J Nutr 1987;117:1347-52
Calcium Supplementation Prevents Hypertensive Disorders of Pregnancy Preeclampsia, a hypertensive disorder of pregnancy, is a major cause of fetal and maternal morbidity and mortality. Epidemiologic studies have shown an inverse relationship between dietary calcium intake and gestational hypertension. A recent large-scale, randomized, doubleblind, placebo-controlled clinical trial has shown that supplementation of pregnant women with 2 g calcium per day from the twentieth week of gestation to term can significantly lower the incidence of hypertensive disorders of pregnancy. The beneficial effect of calcium supplementation was apparent as early as the twenty-eighth week of gestation. The mechanism responsible for the effects of calcium on gestational hypertension is unknown.
Preeclampsia is a major cause of fetal and maternal morbidity and mortality. The clinical signs of preNutrition Reviews, Vol. 50, No. 8
eclampsia usually appear in late gestation in nulliparous pregnant women as hypertension, edema, proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, abnormalities in liver function or coagulation, and elevated serum uric acid levels. Major pathophysiologic aspects of preeclampsia include decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; significantly increased peripheral vascular resistance; and exaggerated pressor responses to endogenous angiotensin I1 and catecholamines.' Preeclampsia occurs in 5-10% of all pregnancies and can rapidly progress to a convulsive phase (eclampsia). Preeclampsia usually occurs after the twentieth week of gestation, most frequently near term. Epidemiologic studies have found an inverse relationship between calcium intake and preeclampsia.2 Moreover, calcium supplementation has been 233
reported to lower blood pressure in pregnant and nonpregnant women.3 The possible importance of calcium metabolism in the pathogenesis of preeclampsia is supported by observations that the largest reduction in blood pressure in pregnant women given calcium supplementation was seen in those with low pretreatment serum calcium levels .4 Other reports indicate that urinary calcium excretion is reduced in women with preeclampsia.’ Until recently, however, the efficacy of calcium supplementation in the prevention of preeclampsia had not been demonstrated in a large, randomized, controlled trial. Recently, Belizan et aL6reported the findings of a multicenter, double-blind, randomized controlled trial that examined the effects of calcium supplementation on the incidence of hypertensive disorders of pregnancy. The study was conducted in three hospitals in Argentina between 1987 and 1989. Eligibility requirements for the study subjects included initiation of prenatal care before the twentieth week of gestation; a nulliparous, singleton pregnancy; blood pressure less than 140/90 mmHg, absence of clinical or laboratory evidence of disease, including glucose intolerance; and absence of medications. Women (n = 1194) were entered into the study and were randomized to receive either placebo or 2 g/day of elemental calcium (as calcium carbonate tablets). Hospital visits were scheduled so that the initial visit occurred before 20 weeks of gestation, with subsequent visits at 23, 25, 27, 31, and 35 weeks, and then weekly until delivery. A battery of measurements was made at each hospital visit, including a 24-hour dietary recall (subjects recruited during the first four months of the study only); fasting urinary calcium; blood pressure (five measurements per visit); and serum calcium, magnesium, phosphorus, and uric acid. No eclampsia occurred during the study. When gestational hypertension (blood pressure 140/90 mmHg or above) or preeclampsia [defined in this study as gestational hypertension with proteinuria (protein more than 0.3 g/L)] developed, the patient received medical treatment and her participation in the incidence study ended, although pregnancy outcome and neonatal outcome were followed. Only 2.3% of the initial study group was lost to follow-up, with equal losses reported in each treatment group. Forty-six women in the placebo group and 52 in the calcium group were also excluded from the analysis due to incomplete follow-up. The final number of women in each treatment group was 588 receiving placebo and 579 receiving calcium. The mean age of the women in the study was 23.7 -+ 5.5 years. The initial blood pressure was 104/66 mmHg, and the urinary ca1cium:creatinine ratio 234
(mmo1:mmol) was 0.75. Mean calcium intake, determined in 87 women in the placebo group, was 642 ? 448 mg/day, which was similar to the 646 -+ 396 mg/day observed in 86 women in the calcium group. Overall compliance, assessed by pill count, was reported to be about 85%, with 69% of the subjects taking more than 80% of their calcium supplements. This high degree of compliance was also reflected in urinary calcium and creatinine excretion. The primary hypothesis tested in this study was that calcium supplementation would reduce the incidence of gestational hypertensive disorders. The beneficial effects of calcium supplementation on hypertensive disorders of pregnancy are illustrated in Figure 1. The incidence of gestational hypertension in the placebo group was 10.7%, which was significantly greater than the 7.2% incidence reported in the group taking calcium supplements (odds ratio 0.64, 95% confidence interval 0.43-0.93). The incidence of preeclampsia was 2.6% in the calciumsupplemented group vs. 3.9% in the placebo group (odds ratio 0.65, 95% confidence interval 0.351.25). The overall rates of hypertensive disorders of pregnancy were 14.8% in the placebo group and 9.8% in the calcium-supplemented group (odds ratio 0.63, 95% confidence interval 0.44-0.90). The effects of calcium on gestational hypertension were evident as early as the twenty-eighth week of gestation (Figure 2). The calcium supplementation appeared to be less effective in subjects with higher urinary calcium losses. The study subjects were stratified according to their baseline urinary ca1cium:creatinine ratio into one group having low calcium excretion
=
PLACEBO
Ca-TREATED
Gestational HT
Preeclampsia
Total
I 0
I
5
10
15
20
Incidence of Hypertensive Disorders, % Figure 1. Effect of calcium supplementation on the incidence of hypertensive disorders of pregnancy. Gestational hypertension was defined as a blood pressure greater than or equal to 140/90 mmHg. Preeclampsia was defined as the presence of both gestational hypertension and proteinuria. Calcium supplementation significantly reduced the risk of developing hypertensive disorders of pregnancy. Figure was made from data presented in Beliz6n et al. (ref. 6). Nutrition Reviews, Vol. 50, No. 8
/
//' /
;
Placebo
20
22
24
26
28
30
32
34
36
38
40
Weeks of Gestation
Figure 2. Percentage of women in the calcium-treated
and placebo groups in whom hypertensive disorders of pregnancy (gestational hypertension and preeclampsia) developed, according to the week of gestation. Figure is reprinted with permission from N Engl J Med (1991;325: 1399-1465).
(less than 0.62 mmol calcium per mmol creatinine) and a second group having high urinary calcium excretion (more than 0.62 mmol calcium per mmol creatinine). The incidence of gestational hypertension in the low urinary calcium group receiving calcium supplements was significantly lower (7.8%) compared to their placebo controls (13.2%). However, the incidence of gestational hypertension was not significantly different between placebo and calcium-treated groups in subjects with initially high levels of urinary calcium excretion (11% in the placebo group and 9.4% in the calcium-treated subjects). This well-designed, double-blind, placebocontrolled trial clearly demonstrates that the risk of hypertensive disorders of pregnancy can be reduced significantly by administration of 2 g/day of elemental calcium after the twentieth week of gestation. The findings of Belizan et a1.6are consistent with those obtained from several other studies, completed in different population groups, which demonstrated a tendency for calcium supplementation to protect against hypertensive disorders of pregnancy. The mechanism by which calcium supplementation reduces the risk for gestational hypertension is not known. Disturbances in calcium metabolism have been reported in hypertensive subjects,' and erythrocyte and platelet calcium levels are higher in women with gestational hypertension.*^^ In addition, several studies have reported that women with Nutrition Reviews, Vol. 50, No. 8
preeclampsia are hypocalciuric. lo-'* Low urinary calcium excretion may result from the elevated parathyroid hormone levels observed in preeclampsia.I3 It has been speculated that calcium supplementation during gestation may lower parathyroid hormone levels, and that this may, in turn, reduce intracellular calcium concentrations in vascular smooth muscle cells and diminish their responsiveness to pressure stimuli, thereby reducing blood p r e ~ s u r e . 'Other ~ possible effects of calcium supplementation include changes in renal sodium handling and changes in sodium retention. These intriguing possibilities should be investigated, as well as the possible involvement of abnormal vitamin D metabolism. l 3 , I 5 It should be noted, however, that pregnancy is associated with absorptive hypercalciuria. The addition of 2 g calcium to the diet will increase the degree of hypercalciuria and may increase the risk of developing renal calculi, which occur in one in 1500 pregnancies. Caution needs to be exercised before large-scale implementation of calciumsupplementation programs for pregnant women is initiated. 1. Lindheimer MD, Katz Al. Preeclampsia: pathophysiology, diagnosis, and management. Annu Rev Med 1989;40:233-50 2. Villar J, Belizan JM, Fischer PJ. Epidemiologic observations on the relationship between calcium intake and eclampsia. Int J Gynaecol Obstet 1983; 21 :271-8 3. Villar J, Repke J, Belizan JM, Pareja G. Calcium supplementation reduces blood pressure during pregnancy: results of a randomized controlled clinical trial. Obstet Gynecol 1987;70:317-22 4. Repke JT, Villar J, Anderson C, Pareja G, Dubin N, Belizan JM. Biochemical changes associated with blood pressure reduction induced by calcium supplementation during pregnancy. Am J Obstet Gynecol 1989;160:684-90 5. Taufield PA, Ales KL, Resnick LM, Druzin ML, Gertner JM, Laragh JH. Hypocalciuria in preeclampsia. N Engl J Med 1987;316:715-8 6. Belizan JM, Villar J, Gonzalez L, Campodonico, Bergel E. Calcium supplementation to prevent hypertensive disorders of pregnancy. N Engl J Med 1991;325:1399-405 7. McCarron DA. Dietary calcium in the pathogenesis and therapy of human and experimental hypertension. In: Rubin RP, Weiss GB, Putney JW Jr., eds. Calcium in biological systems. New York: Plenum Press, 1985:561-8 8. Sowers JR, Zemel MB, Bronsteen RA, et al. Erythrocyte cation metabolism in preeclampsia. Am J Obstet Gynecol 1989;161:441-5 9. Haller H, Oeney T, Hauck U, Distler A, Philipp T. Increased intracellular free calcium and sensitivity to angiotensin II in platelets of preeclamptic women. Am J Hypertens 1989;2:238-43 235
10. Rodriguez MH, Masaki DI, Mestman J, Kumar D, Rude R. Calcium-creatinine ratio and microalbuminuria in the prediction of preeclampsia. Am J Obstet Gynecol 1988;159:1452-5 11. Maclntosh MC, Hutchesson AC, Duncan SL, Forrest AR. Hypocalciuria and hypertension in pregnancy: a prospective study. Br J Obstet Gynaecol 1989;96:1243-4 (abstract) 12. Frenkel Y, Barkai G, Mashiach S, Dolev E, Zimlichman R, Weiss M. Hypocalciuria of preeclampsia is independent of parathyroid hormone level. Obstet Gynecol 1991;77:689-91 13. Mochizuki M, Morikawa H, Yamasaki M, Maruo T.
Vascular reactivity in normal and abnormal gestation. Am J Kidney Dis 1991;17:139-43 14. BelizAn JM, Villar J, Repke J. The relationship between calcium intake and pregnancy-induced hypertension: up-to-date evidence. Am J Obstet Gynecol 1988;158:898-902 15. Seely EW, Wood RJ, Brown EM, Graves SW. Lower serum ionized calcium and abnormal calciotrophic hormone levels in preeclampsia. J Clin Endocrinol Metab 1992;74:430-4 16. Ferris TF. Pregnancy, preeclampsia, and the endothelial cell. N Engl J Med 1991;325:1439-40
Women on the Short End of the Loaf: lntrahousehold Food Allocation Among Members of Poor Nepalese Families Intensive and structured intrahousehold observations of the pattern of food allocation in poor rural Nepalese households indicate no difference in the distribution of nutrients between male and female children. In contrast, preferential food distribution patterns among adults show that women are less likely to achieve recommended levels of some nutrients than are men of the same age.
As both population and poverty increase in developing countries, estimates are that, by the year 2000, four of five persons will live in less-developed nations, and that 90% of these will be classified as poor. Such widespread poverty places certain groups, especially young children, women of childbearing age, and the elderly, at increased risk for malnutrition, although studies’ indicate that factors other than poverty also contribute to malnutrition. Within the same poor community, some families produce healthy, normally growing children, while others have malnourished children. Successful child rearing under adverse conditions has been termed “positive deviance.”’ Conversely, based on national per capita food balance or nutrient availability, some nations appear to have sufficient resources to prevent widespread nutritional deficiencies, yet stunting, wasting, and even clinical malnutrition can be common. One possible explanation for both situations is that the distribution of food is selective and unequal, either favoring or disfavoring the groups susceptible to nutritional compromise. This has been a comfortable explanation for differential survival and growth and development within or among families in less-privileged societies, but ways to measure the differential distribu-
236
tion of food within the home have not been forthcoming. Understanding the patterns of unequal intrahousehold food allocation is important not only to determine the causes of undernutrition, but also to design and implement interventions aimed at improving nutritional status. Nutritional anthropologists have attempted to open the “black box” that surrounds the system of intrahousehold food allocation that control the size and distribution of serving portions, the patterns of second helpings, and the provision of prime or inferior food morsels to individual family members. Until recently, more theory than practice has been devoted to the issue of intrahousehold but a recent study from Nepal by Gittelsohn’ provides solid methods for observing household interactions and for analyzing the data. Gittelsohn’ examined five elements related to intrahousehold food allocation, including the identity of the food server; the order in which individuals were served; what was served to whom; how much was served to whom; and how individuals were served (e.g., automatically, on request, or by force). Field-workers trained to categorize and quantify feeding behaviors randomly observed a total of three to four main meals in the homes and compounds of 105 rural highland Nepalese families (767 individuals) during a four-month period. Based on these observations, the following variables were developed: 1. Serving order (relative to all served) 2. Serving method (relative autonomy of server or served) 3. Second helpings (multiple offerings to an individual) 4. Refusals (rejection of a food by the person requesting it)
Nutrition Reviews, Vol. 50, No. 8
