Indigenous food ingredients for complementary food formulations to combat infant malnutrition in Benin: a review.

This paper reviews indigenous Beninese food resources as potential ingredients for complementary infant foods with the aim to develop affordable formulations for low-income households in each agro-ecological zone of the country. Potential ingredients were selected on their documented nutritional value. The selected foods encompass 347 food resources, namely 297 plant products from home gardens or collected from natural vegetation and 50 animals, either domesticated or from the wild. The compiled data reveal that the distribution of the available food resources was unbalanced between agro-ecological zones. Only a few animal ingredients are obtainable in northern Benin. Most resources are seasonal, but their availability may be extended. A high variation was observed in energy and nutrient contents. Antinutritional factors were identified in some resources, but processing techniques were reported to reduce their presence in meals. In general, ingredients from local tree foods (Adansonia digitata, Parkia biglobosa) were adequate as sources of nutrients for complementary infant foods. Based on this review, local foods for the development of complementary food formulas for Beninese infants and children may be selected for each agro-ecological zone. The approach used is exemplary for other sub-Saharan African countries in need of complementary infant foods. © 2017 Society of Chemical Industry.

Assessment of Regression Models for Adjustment of Iron Status Biomarkers for Inflammation in Children with Moderate Acute Malnutrition in Burkina Faso.

BACKGROUND: Biomarkers of iron status are affected by inflammation. In order to interpret them in individuals with inflammation, the use of correction factors (CFs) has been proposed. OBJECTIVE: The objective of this study was to investigate the use of regression models as an alternative to the CF approach. METHODS: Morbidity data were collected during clinical examinations with morbidity recalls in a cross-sectional study in children aged 6-23 mo with moderate acute malnutrition. C-reactive protein (CRP), α1-acid glycoprotein (AGP), serum ferritin (SF), and soluble transferrin receptor (sTfR) were measured in serum. Generalized additive, quadratic, and linear models were used to model the relation between SF and sTfR as outcomes and CRP and AGP as categorical variables (model 1; equivalent to the CF approach), CRP and AGP as continuous variables (model 2), or CRP and AGP as continuous variables and morbidity covariates (model 3) as predictors. The predictive performance of the models was compared with the use of 10-fold crossvalidation and quantified with the use of root mean square errors (RMSEs). SF and sTfR were adjusted with the use of regression coefficients from linear models. RESULTS: Crossvalidation revealed no advantage to using generalized additive or quadratic models over linear models in terms of the RMSE. Linear model 3 performed better than models 2 and 1. Furthermore, we found no difference in CFs for adjusting SF and those from a previous meta-analysis. Adjustment of SF and sTfR with the use of the best-performing model led to a 17% point increase and <1% point decrease, respectively, in estimated prevalence of iron deficiency. CONCLUSION: Regression analysis is an alternative to adjust SF and may be preferable in research settings, because it can take morbidity and severity of inflammation into account. In clinical settings, the CF approach may be more practical. There is no benefit from adjusting sTfR. This trial was registered at www.controlled-trials.com as ISRCTN42569496.

Effect of fetal and infant malnutrition on metabolism in older age.

BACKGROUND: While malnutrition is an important concern in the developing world, Western countries are experiencing a pandemic of obesity and metabolic diseases. OBJECTIVE: This work reviews the current state of knowledge of the effects of malnutrition during early life on metabolism in older age. METHODS: The impact of early-life determinants on diabetes and related metabolic diseases in later life is elucidated by three different methodological approaches. First, results from animal studies in dietary manipulation models are reviewed. Second, findings from epidemiological studies that often use natural experiments to determine the effects of famines on the health status of the population are discussed. Finally, the relation between maternal or childhood malnutrition and diabetes in adulthood is explored in a big-data study using the entire population of a country across a century. RESULTS: We present overwhelming evidence that the maternal or early childhood nutritional status negatively affects both the short- and long-term health status and development of the offspring, thereby providing starting points to formulate intervention and prevention strategies. In particular, it was found that in the case of early-life exposure to famine, the risk of the offspring to develop type 2 diabetes in older age is up to 125% higher than without famine exposure. CONCLUSION: Due to its inherent complexity, an understanding of the long-term effects of maternal and childhood malnutrition on metabolism in older age necessitates interdisciplinary and big-data approaches. Only then can we hope to prevent chronic diseases at their earliest beginning.

Effects of neonatal programming on hypothalamic mechanisms controlling energy balance.

The prevalence of overweight and obesity in most developed countries has markedly increased during the last decades. In addition to genetic, hormonal, and metabolic influences, environmental factors like fetal and neonatal nutrition play key roles in the development of obesity. Interestingly, overweight during critical developmental periods of fetal and/or neonatal life has been demonstrated to increase the risk of obesity throughout juvenile life into adulthood. In spite of this evidence, the specific mechanisms underlying this fetal/neonatal programming are not perfectly understood. However, it is clear that circulating hormones such as insulin and leptin play a critical role in the development and programming of hypothalamic circuits regulating energy balance. Here, we review what is currently known about the impact of perinatal malnutrition on the mechanisms regulating body weight homeostasis. Understanding these molecular mechanisms may provide new targets for the treatment of obesity.

Metabolomics and fetal-neonatal nutrition: between "not enough" and "too much".

Metabolomics is a new analytical technique defined as the study of the complex system of metabolites that is capable of describing the biochemical phenotype of a biological system. In recent years the literature has shown an increasing interest in paediatric obesity and the onset of diabetes and the metabolic syndrome in adulthood. Some studies show that fetal malnutrition, both excessive and insufficient, may permanently alter the metabolic processes of the fetus and increase the risk of future chronic pathologies. At present then, attention is being focused mainly on the formulation of new hypotheses, by means of metabolomics, concerning the biological mechanisms to departure from fetal-neonatal life that may predispose to the development of these diseases.

[Fecal calprotectin levels in preterm infants during the early neonatal period].

OBJECTIVE: To explore whether fecal calprotectin (f-calprotectin, FC) may be an early marker for the identification of gastrointestinal injury in preterm infants by measuring FC concentration and changes of FC concentration in infants with different perinatal factors. METHODS: FC concentration was measured using ELISA in 76 samples (50-100 mg) obtained from 38 preterm infants (gestation 29 to 33 weeks), at birth and on the third day after birth (the 1st and the 2nd FC levels). The infants were classified into three groups according to the reason for preterm birth: premature rupture of membranes (PROM; n=13), spontaneous preterm birth (SPB; n=5) and indicated preterm birth (IPB; n=20). RESULTS: There were no significant differences between the 1st and 2nd FC levels in the 38 infants. The 1st FC level in the PROM group was significantly higher than that in the IPB group (P<0.05). The 1st FC level in infants whose mothers received antenatal antibiotics treatment was significantly lower. Infants born by cesarean section had a significantly lower 1st FC level than those born by vaginal delivery (P<0.05). Both the 1st and 2nd FC levels in infants with feeding intolerance were significantly higher than in infants with feeding tolerance (P<0.05). The 2nd FC level was negatively correlated with 1 min Apgar score (r=-0.3, P<0.05). CONCLUSIONS: Premature rupture of membranes and perinatal asphyxia may lead to an increase in the excretion of FC in preterm infants. FC may be used as a marker for early evaluation of gastrointestinal conditions in preterm infants.

Peptides from adipose tissue in monitoring energy balance in infants.

BACKGROUND/AIM: Overnutrition as well as undernutrition is a serious problem in hospitalized patients, especially in infants. Routine laboratory tests detecting disturbances in energy balance are not specific or accurate. The aim of this study was to evaluate adiponectin and leptin as markers of short-time energy malnutrition. METHODS: Forty-five infants fed orally and parenterally were included in the study. Plasma glucose, leptin and adiponectin were measured in a fasting state and postprandially (1 h after the meal), after a minimum of 24 h of total parenteral nutrition (TPN) and after a minimum of 8 h of intravenous infusion of glucose and crystalloids. RESULTS: Postprandial glucose levels in children fed orally was similar to that observed in children who received intravenous infusion of glucose. The TPN children had slightly higher glucose concentration in contrast to leptin levels which were significantly lower in this group (1.08 mg/mL +/- 0.43) as compared to the others (p < 0.05 in both cases). The mean postprandial levels of the adiponectin in orally fed children were significantly higher (10.7 microg/mL +/- 2.4) than in children with TPN (5.8 microg/mL +/- 2.4; p < 0.001) and in children hydrated intravenously (3.3 microg/mL +/- 2.3; p < 0.001). The concentration of adiponectin correlated significantly with calorie intake. CONCLUSIONS: Oral meal does not affect the plasma concentrations of leptin and adiponectin in infants. Adiponectin is a good short-time marker of energy malnutrition in infants.

Weight gain and metabolic complications in preterm infants with nutritional support.

OBJECTIVE: To analyze the weight gain and to describe the metabolic complications in preterm newborns with nutritional support (NS) and to describe nutritional practices in the first month of hospitalization for 52 preterm newborns. MATERIAL AND METHODS: Descriptive and prospective study of preterm infants (30-36 gestational weeks), with birth weight > 1 kg, hospital stay > 12 days, without respiratory support or complications, conducted at a public hospital in Leon, Guanajuato, Mexico from January to November 2006. Weight, serum glucose, insulin, cholesterol, triglycerides, gamma-glutamyltransferase, creatinine, urea nitrogen, type of NS (parenteral PN, enteral EN, mixed MN), energy content, and macronutrient intake were measured weekly. To obtain representative data, nutritional practices were not altered by the study protocol. One way ANOVA and Wilcoxon tests were used in data analyses. RESULTS: Overall, 52 newborns were included, averaging 33 gestational weeks and 1,590 g of weight. The NS was started by the fourth day on average. Parenteral nutrition was the most frequent NS during the first 2 weeks (75%). Energy and macronutrient supply was 50% less than the recommended. Weight gain ranged from -100 to 130 g/week. Parenteral nutrition showed better weekly weight gain, followed by EN. The metabolic complication rate per person-day was greater for MN (0.56), than for EN (0.16) or PN (0.09). Routine surveillance of weight and metabolic complications was deficient. CONCLUSIONS: Late onset of NS, insufficient energy supply, and deficient surveillance were obstacles to weight gain and to prevent the metabolic complications in these newborns.

Neurochemical changes in the developing rat hippocampus during prolonged hypoglycemia.

Hypoglycemia is common during development and is associated with the risk of neurodevelopmental deficits in human infants. The effects of hypoglycemia on the developing hippocampus are poorly understood. The sequential changes in energy substrates, amino acids and phosphocreatine were measured from the hippocampus during 180 min of insulin-induced hypoglycemia (blood glucose < 2.5 mmol/L) in 14-day-old rats using in vivo(1)H NMR spectroscopy. Hypoglycemia resulted in neuroglycopenia (brain glucose < 0.5 micromol/g). However, the phosphocreatine/creatine (PCr/Cr) ratio was maintained in the physiological range until approximately 150 min of hypoglycemia, indicating that energy supply was sufficient to meet the energy demands. Lactate concentration decreased soon after the onset of neuroglycopenia. Beyond 60 min, glutamine and glutamate became the major energy substrates. A precipitous decrease in the PCr/Cr ratio, indicative of impending energy failure occurred only after significant depletion of these amino acids. Once glutamate and glutamine were significantly exhausted, aspartate became the final energy source. N-acetylaspartate concentration remained unaltered, suggesting preservation of neuronal/mitochondrial integrity during hypoglycemia. Correction of hypoglycemia normalized the PCr/Cr ratio and partially restored the amino acids to pre-hypoglycemia levels. Compensatory neurochemical changes maintain energy homeostasis during prolonged hypoglycemia in the developing hippocampus.

Perinatal copper deficiency alters rat cerebellar purkinje cell size and distribution.

Copper is required for activity of several key enzymes and for optimal mammalian development, especially within the central nervous system. Copper-deficient (CuD) animals are visibly ataxic, and previous studies in rats have demonstrated impaired motor function through behavioral experiments consistent with altered cerebellar development. Perinatal copper deficiency was produced in Holtzman rat dams by restricting dietary copper during the last two thirds of gestation and lactation. Male offspring were evaluated at postnatal day 25. Compared to cerebella from copper-adequate pups, the CuD pups had larger Purkinje cell (PC) size and irregularities in the Purkinje cell monolayer. These results suggest that the ataxic behavioral phenotype of CuD rats may result from disrupted inhibitory pathways in the cerebellum. A similar PC phenotype is seen in Menkes disease and in mottled mouse mutants with genetic copper deficiency, suggesting that copper deficiency and not just specific loss of ATP7A function is responsible.

Tyrosine requirement during the rapid catch-up growth phase of recovery from severe childhood undernutrition.

The requirement for aromatic amino acids during the rapid catch-up in weight phase of recovery from severe childhood undernutrition (SCU) is not clearly established. As a first step, the present study aimed to estimate the tyrosine requirement of children with SCU during the catch-up growth phase of nutritional rehabilitation using a diet enriched in energy and proteins. Tyrosine requirement was calculated from the rate of excretion of ¹³CO2 (F ¹³CO2) during [¹³C]phenylalanine infusion in thirteen children with SCU, five females and eight males, at about 19 d after admission when the subjects were considered to have entered their rapid catch-up growth phase and were consuming 627.3 kJ and about 3.5 g protein/kg per d. Measurements of F ¹³CO2 during [¹³C]phenylalanine infusion were made on two separate days with a 1 d interval. Three measurements at tyrosine intakes of 48, 71 and 95 mg/kg per d were performed on experimental day 1 and measurements at tyrosine intakes of 148, 195 and 241 mg/kg per d were performed on experimental day 2. An estimate of the mean requirement was derived by breakpoint analysis with a two-phase linear regression cross-over model. The breakpoint, which represents an estimate of the mean tyrosine requirement, is a value of 99 mg/kg per d when the children were growing at about 15 g/kg per d. The result indicates that the mean requirement for tyrosine during the catch-up growth phase of SCU is about 99 mg/kg per d under similar conditions to the present study.

Perinatal malnutrition programs sustained alterations in nitric oxide released by activated macrophages in response to fluoxetine in adult rats.

OBJECTIVE: Nutritional restriction during lactation has long-term consequences on the functioning of neuroimmune systems. Receptors and transporter serotonin (5-HT) are present in macrophages and may influence their role. This study evaluated nitric oxide release by alveolar macrophages (AMs) in adult control rats and rats malnourished during lactation in response to different fluoxetine (FLX) concentrations and 5-HT(1A) and 5-HT(1B) agonists at different times. METHODS: Male Wistar rats were distributed into two groups according to maternal diet during lactation: a control group of 12 rats whose dams had received a 23% protein diet and a malnourished group of 12 rats whose dams had received an 8% protein diet. After weaning, all rats received a 23% protein diet. On the 90th day after birth, nitric oxide (NO) release kinetics was measured in supernatants of AMs cultured with FLX. The NO release following the adjunction of serotoninergic agonists was also quantified. RESULTS: The malnourished rats weighed less at weaning (control rats = 15.3 +/- 0.4 g, malnourished rats = 11.8 +/- 0.4 g); this difference persisted until 90 days of life (control rats = 355.4 +/- 8.6 g; malnourished rats = 267.8 +/- 7.9 g). In the presence of 10(-6)M FLX, NO release by AMs in control rats was lower. The addition of agonists did not interfere with NO release by AMs in control rats. NO release by AMs from malnourished rats was modified neither by FLX nor by agonists. As a consequence of malnutrition, there were lower numbers of cells and AMs in the bronchoalveolar lavage fluid, and cell viability and NO release by AMs were impaired. CONCLUSIONS: Nutritional manipulation in the perinatal period seems to interfere with the functional programming of macrophages; it also seems to affect their serotoninergic regulation through adulthood.

[Biologic profile in Tunisian infants (0-2 years), malnourished]. / Profil biologique d'une population de nourrissons Tunisiens (0-2 ans), malnutris.

BACKGROUND: The malnutrition of the infants could be explained by a delay of the growth and the perturbation of biological parameters. AIM: To establish the nutritional profile of the Tunisian infant of less than two years. To specify the principal deficiencies and the possible origins of these deficiencies. METHODS: In our transverse exploratory study, carried out in period of 9 month. This study was conducted in two groups of Tunisian young children less than two years old: a control group and a malnourished group (Z score < or = 2SD). RESULTS: Our data consolidate the important impact of pregnant women nutritional state and of breastfeeding on the foetus ant infant growth.Compared to control infants, the malnourished young showed a significant alteration of different biologic parameters. This alteration appeared positively linked to the gravity of malnutrition as indicated by the positive relation obtained between the weight/height ratio and many studied parameters. The malnourished infants showed, notably, a significant reduction of the average values of Chol-HDL, apo AI, Vit E, TSH and TF4 levels and Chol-HDL/Chol LDL ratio. Chol-HDL, apo AI and HDL/Chol-LDL are found positively and significantly correlated with TF4. So, their reduction in ill children would be, at least in part, a side effect of the thyroid function reduction. CONCLUSION: Our results confirm the existence of an important change of biological profile in malnourished young children. Besides, they emphasize that studies about young children could be helpful, notably, in the prevention and the fight against atherosclerosis.

Animal Models of Undernutrition and Enteropathy as Tools for Assessment of Nutritional Intervention.

: Undernutrition is a major public health problem leading to 1 in 5 of all deaths in children under 5 years. Undernutrition leads to growth stunting and/or wasting and is often associated with environmental enteric dysfunction (EED). EED mechanisms leading to growth failure include intestinal hyperpermeability, villus blunting, malabsorption and gut inflammation. As non-invasive methods for investigating gut function in undernourished children are limited, pre-clinical models are relevant to elucidating the pathophysiological processes involved in undernutrition and EED, and to identifying novel therapeutic strategies. In many published models, undernutrition was induced using protein or micronutrient deficient diets, but these experimental models were not associated with EED. Enteropathy models mainly used gastrointestinal injury triggers. These models are presented in this review. We found only a few studies investigating the combination of undernutrition and enteropathy. This highlights the need for further developments to establish an experimental model reproducing the impact of undernutrition and enteropathy on growth, intestinal hyperpermeability and inflammation, that could be suitable for preclinical evaluation of innovative therapeutic intervention.

Nutritional tryptophan restriction and the role of serotonin in development and plasticity of central visual connections.

Tryptophan is an essential amino acid and metabolic precursor of serotonin. Serotonin is both a classical neurotransmitter and a signaling molecule that plays crucial roles in the development of neural circuits and plasticity. The specification of neural circuits in rodents occurs during the postnatal period with conspicuous influence of environmental factors including the nutritional status. Sensory, motor and cognitive systems develop during a critical period, a time window that is crucial to the use-dependent organization of neuronal circuits. This review presents recent experimental findings that disclose some mechanism of tryptophan- and serotonin-dependent plasticity in the developing and adult brain.

Arginine flux and intravascular nitric oxide synthesis in severe childhood undernutrition.

BACKGROUND: Although nutritionally dispensable amino acids are not essential in the diet, adequate synthesis is necessary for maintenance of good health. Whereas children with edematous severe childhood undernutrition (SCU) can maintain production rates of glycine and serine despite a slower body protein breakdown rate, it is unknown whether the same is true for the semidispensable amino acid arginine. OBJECTIVE: We aimed to measure arginine flux and intravascular nitric oxide synthesis in children with SCU. DESIGN: Arginine flux and the fractional and absolute synthesis rates of plasma nitrite plus nitrate were measured postabsorptively by using a 6-h infusion of [(15)N(2)]-arginine in 2 groups of children with edematous (n = 14) or nonedematous (n = 7) SCU when they were infected and malnourished (postadmission day approximately 3; clinical phase 1), when they were no longer infected (postadmission day approximately 15; clinical phase 2), and when they were recovered (postadmission day approximately 55; clinical phase 3). RESULTS: Arginine flux was slower (P < 0.01) and plasma arginine concentrations were lower in the edematous group than in the nonedematous group at clinical phase 1. At clinical phase 2, flux doubled to a value that was not significantly different from the value at clinical phase 3. There were no significant differences in the plasma concentration or fractional or absolute synthesis rate of plasma nitrite plus nitrate between the groups at any clinical phase and among clinical phases within each group. CONCLUSION: Whereas children with nonedematous SCU can maintain arginine flux at the same rate as when recovered, children with edematous SCU cannot. The slower arginine flux was not, however, associated with slower nitric oxide synthesis.

Studies with 15N-labeled ammonia and urea in the malnourished child.

Investigations using ammonium citrate-(15)N and urea-(15)N showed that children in the acute stage of kwashiorkor and marasmus receiving a diet of adequate protein content retained a considerable percentage of the label from both compounds. Excretion of both total (15)N and urea-(15)N was subnormal and elimination was virtually completed 36 hr after administration of the isotope. During recovery from kwashiorkor total (15)N excretion had approached normal a month after commencement of rehabilitation. Urea-(15)N excretion was still slightly subnormal after 3 months. In marasmus urea-(15)N formed a normal proportion of total (15)N excretion after 1 month, although total (15)N excretion then was still low. Ammonia nitrogen was retained to a greater extent than urea nitrogen in all cases. As it is known that a considerable amount of urea is degraded to ammonia in the gastrointestinal tract, it seems probable that urea nitrogen became available for use after this degradation. Examination of blood from one marasmic child after feeding ammonia-(15)N and from another after intravenous injection of urea-(15)N showed incorporation of the label into blood cells and plasma proteins. This did not occur in well nourished controls. It is concluded that ammonia and urea as sources of nonessential nitrogen may play an important part in protein metabolism in the malnourished child.

Stress/aggressiveness-induced immune changes are altered in adult rats submitted to neonatal malnutrition.

BACKGROUND/AIMS: Neonatal malnutrition induces metabolic and endocrine changes that have beneficial effects on the neonatal in the short term but, in the longer term, these alterations lead to maladaptations. We investigated the effect of neonatal malnutrition on immune responses in adult rats submitted or not to an aggressiveness test. METHODS: Male Wistar rats were distributed to one of two groups according to their mothers' diet during lactation: the well-nourished group (group C, n = 42, receiving 23% of protein) and the malnourished group (group MN, n = 42, receiving 8% of protein). After weaning, all rats received normoproteic diet. Ninety days after birth, each group was subdivided into three subgroups: control rats (n = 14, respectively), aggressive rats (n = 14, respectively) and rats receiving foot shock (FS; n = 14, respectively). Plasma corticosterone concentration was measured after FS sessions. Leukocyte counts and humoral immunity were evaluated. RESULTS: In neonatal malnourished animals, FS-induced stress reduced plasma corticosterone concentration. Intraspecific aggressiveness induced alterations in leukocyte counts and antibody titers 7 and 15 days after immunization. Neonatal malnourished animals showed no changes in the immune parameters evaluated. CONCLUSIONS: Expression of intraspecific aggressiveness activates the immune system. Neonatal malnutrition seems to have a long-lasting effect on components of both neuroendocrine and immune functions.

Stable C and N isotope analysis of hair suggest undernourishment as a factor in the death of a mummified girl from late 19th century San Francisco, CA.

The chance discovery of a 1.5-3.5 years old mummified girl presents a unique opportunity to further our understanding of health and disease among children in 19th Century San Francisco. This study focuses on carbon and nitrogen stable isotope signatures in serial samples of hair that cover the last 14 months of her life. Results suggest an initial omnivorous diet with little input from marine resources or C4 plants. Around six months before death δ15N starts a steady increase, with a noticeable acceleration just two months before she died. The magnitude of δ15N change, +1.5‰ in total, is consistent with severe undernourishment or starvation. Cemetery records from this time period in San Francisco indicate high rates of infant and child mortality, mainly due to bacterial-borne infectious diseases, about two orders of magnitude higher than today. Taken together, we hypothesize that the girl died after a prolonged battle with such an illness. Results highlight the tremendous impacts that modern sanitation and medicine have had since the 1800s on human health and lifespan in the United States.

Sulfur amino acid metabolism in children with severe childhood undernutrition: cysteine kinetics.

BACKGROUND: Children with edematous but not nonedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentrations of cysteine, the rate-limiting precursor of glutathione synthesis. We propose that these lower cysteine concentrations are due to reduced production secondary to slower de novo synthesis plus decreased release from protein breakdown. OBJECTIVE: We aimed to measure cysteine production, de novo synthesis, and the rate of cysteine release from protein breakdown in children with SCU. DESIGN: Cysteine flux, de novo synthesis, and release from protein breakdown were measured in 2 groups of children with edematous (n = 11) and nonedematous (n = 11) SCU when they were infected and malnourished (clinical phase 1), when they were still severely malnourished but no longer infected (clinical phase 2), and when they had recovered (clinical phase 3). RESULTS: In clinical phase 1, cysteine production and its release from protein breakdown were slower in both groups of children than were the values in the recovered state. These kinetic variables were significantly slower, however, in the children with edematous SCU than in those with nonedematous SCU. De novo cysteine synthesis in clinical phase 1 was faster than the rate at recovery in the edematous SCU group, and there were no significant differences between the groups at any clinical phase. CONCLUSION: These findings suggest that cysteine production is reduced in all children with SCU because of a decreased contribution from protein breakdown and not from decreased de novo synthesis. The magnitude of this reduction, however, is much greater in children with edematous SCU than in those with nonedematous SCU.