Iodine status and thyroid function of Boston-area vegetarians and vegans.

CONTEXT: Adequate dietary iodine is required for normal thyroid function. The iodine status and thyroid function of U.S. vegetarians and vegans have not been previously studied. Environmental perchlorate and thiocyanate (inhibitors of thyroid iodine uptake) exposures may adversely affect thyroid function. OBJECTIVE: The objective of the study was to assess the iodine status and thyroid function of U.S. vegetarians (consume plant based products, eggs, milk; abstain from meat, poultry, fish, shellfish) and vegans (avoid all animal products) and whether these may be affected by environmental perchlorate and thiocyanate exposures. DESIGN AND SETTING: This was a cross-sectional assessment of urinary iodine, perchlorate, and thiocyanate concentrations and serum thyroid function in Boston-area vegetarians and vegans. SUBJECTS: One hundred forty-one subjects (78 vegetarians, 63 vegans) were recruited; one vegan was excluded. RESULTS: Median urinary iodine concentration of vegans (78.5 µg/liter; range 6.8-964.7 µg/liter) was lower than vegetarians (147.0 µg/liter; range 9.3-778.6 µg/liter) (P < 0.01). Adjusted for cigarette smoking (confirmed by urinary cotinine levels) and thiocyanate-rich food consumption, median urinary thiocyanate concentration of vegans (630 µg/liter; range 108-3085 µg/liter) was higher than vegetarians (341 µg/liter; range 31-1963 µg/liter) (P < 0.01). There were no between-group differences in urinary perchlorate concentrations (P = 0.75), TSH (P = 0.46), and free T(4) (P = 0.77). Urinary iodine, perchlorate, and thiocyanate levels were not associated with TSH (P = 0.59) or free T(4) (P = 0.14), even when adjusted for multiple variables. CONCLUSIONS: U.S. vegetarians are iodine sufficient. U.S. vegans may be at risk for low iodine intake, and vegan women of child-bearing age should supplement with 150 µg iodine daily. Environmental perchlorate and thiocyanate exposures are not associated with thyroid dysfunction in these groups.

Iodine in enteral and parenteral nutrition.

Iodine deficiency (ID) has multiple adverse effects on growth and development due to inadequate thyroid hormone production. Methods for assessment of iodine nutrition in individuals include the urinary iodine concentration (UI), thyroid size and thyroid function tests. The UI measured in several repeat 24-h urine samples can detect inadequate iodine intake in individuals receiving enteral or parenteral nutrition (PN) and allow for iodine supplementation before the onset of hypothyroidism. A daily dose of 1 microg iodine/kg body weight is currently recommended for children receiving PN, but this is far below their requirements. Daily iodine requirements in adults receiving enteral nutrition or PN are estimated to be 70-150 microg, but most PN formulations do not contain iodine. Despite this, ID has been unlikely because absorption from iodine-containing skin antiseptics and other adventitious sources can provide sufficient iodine. However, if chlorhexidine replaces iodine-containing antiseptics for catheter care, ID may occur during long-term PN, and periodic testing of UI and thyroid function may be prudent. Infants may be particularly vulnerable to ID because of their small thyroidal iodine store. In this review, we describe three recent patients (an infant, a child and an adult) who developed ID and thyroid hypofunction during PN.

Nutritional deficiencies in German middle-class male alcohol consumers: relation to dietary intake and severity of liver disease.

OBJECTIVE: The purpose of the present study was to compare the nutrient intake and the nutritional status between German middle-class alcohol consumers and non-drinkers. DESIGN: Cross-sectional study using patients with different stages of alcoholic liver disease (ALD) and healthy volunteers. SETTING: Southern Germany. SUBJECTS: Seventy-six hospitalized German middle-class alcohol consumers with different stages of alcoholic liver disease (ALD) and 22 healthy control subjects. METHODS: Subjects and controls were nutritionally assessed and mineral and vitamin content was measured in blood and urine. RESULTS: When compared with controls, alcohol consumers had significantly higher intakes of total calories, but intake of non-alcoholic calories did not differ between groups (P<0.05). Among drinkers, there was a decrease in percentage of energy derived from protein and fat and a significant increase in carbohydrates (P<0.05). With the exception of vitamin E, micronutrient intake of alcoholics was equal to that of controls; however, blood vitamin (vitamin C, retinol, lycopene, alpha- and gamma-carotene) and trace element (selenium, zinc) concentrations of alcohol-drinking patients were lower than those of non-drinkers. CONCLUSION: From the results of this study it is concluded that in German middle-class male alcohol consumers the status of several micronutrients is disturbed, although dietary intake hardly differs from that in non-alcoholic controls.

Nutrition indices in obese continuous peritoneal dialysis patients with inadequate and adequate urea clearance.

OBJECTIVE: To test whether better nutrition is associated more with adequate urea clearance than with inadequate urea clearance in obese patients on continuous peritoneal dialysis (CPD). DESIGN: Retrospective analysis of clearance and nutrition indices in obese CPD patients. Only obese patients were analyzed. Obesity was defined as a ratio of actual weight to desired weight (W/DW) > or = 1.2. The dose of dialysis was considered adequate at weekly Kt/V urea > or = 2.0. Small solute clearances and nutrition indices were compared between patients with weekly Kt/V urea < 2.0 and patients with weekly Kt/V urea > or = 2.0 at the first clearance study. SETTING: Four university-affiliated and two private dialysis units in Canada and the United States. PATIENTS: A total of 270 CPD patients with W/DW > or = 1.2 at the first clearance study. RESULTS: Among the 270 obese CPD patients, 157 (58.1%) were underdialyzed (weekly Kt/V urea 1.66 +/- 0.22) and 113 (41.9%) had adequate dialysis (weekly Kt/V urea 2.51 +/- 0.47) at the first clearance study. Creatinine clearance values also differed between the underdialyzed and adequately dialyzed obese groups (55.6 +/- 15.2 vs 87.6 +/- 29.8 L/1.73 m2 weekly, respectively, p < 0.001). The underdialyzed group contained fewer women (39.5% vs 60.2%, p < 0.001) and more patients with anuria (35.0% vs 8.8%, p < 0.001), and had higher serum urea (20.7 +/- 6.9 vs 18.2 +/- 5.3 mmol/L, p = 0.001) and serum creatinine (974 +/- 283 vs 734 +/- 275 micromol/L, p < 0.001), marginally lower serum albumin (35.8 +/- 5.2 vs 37.2 +/- 6.4 g/L, p = 0.082), lower urea nitrogen excretion (5778 +/- 2290 vs 7085 +/- 2238 mg/24 hr, p < 0.001) and indices derived from urea nitrogen excretion (protein nitrogen appearance and normalized protein nitrogen appearance), and lower creatinine excretion (1034 +/- 349 vs 1217 +/- 432 mg/24 hr, p < 0.001) and indices derived from creatinine excretion (lean body mass normalized to actual or desired weight) than the adequately dialyzed group. CONCLUSION: Nutrition indices derived from urea nitrogen and creatinine excretion are worse in underdialyzed than in adequately dialyzed obese CPD patients. This finding may have clinical importance, despite the mathematical coupling between small solute clearances and excretion rates in cross-sectional studies, because of evidence from other studies that small solute excretion rate in cross-sectional studies is a robust Independent predictor of outcome in CPD.

Serum and urinary magnesium in young diabetic subjects in Bangladesh.

BACKGROUND: Magnesium imbalance, implicated in diabetes mellitus both as a cause and a consequence, has not yet been investigated in subgroups of subjects with malnutrition-related diabetes mellitus. which is prevalent in young patients in tropical developing countries such as Bangladesh. OBJECTIVE: The present study evaluated the serum and urinary magnesium concentrations in groups of young diabetic subjects in Bangladesh. DESIGN: Forty patients newly diagnosed with diabetes [13 with fibrocalculus pancreatic diabetes (FCPD), 13 with protein-deficient diabetes (PDDM), and 14 with type 2 diabetes mellitus] were studied along with 13 healthy control and 13 malnourished control subjects [body mass index (in kg/m2) < 19]. Magnesium was measured by atomic absorption spectrophotometry. RESULTS: Malnutrition itself was not related to the serum glucose (fasting: 3.68+/-0.74 and 4.11+/-0.29 mmol/L; postprandial: 6.30+/-0.41 and 6.00+/-0.24 mmol/L for healthy and malnourished control subjects, respectively) or serum or urinary magnesium (serum: 0.73+/-0.03 and 0.75+/-0.05 mmol/L: urinary: 232+/-124 and 243+/-88 mmol Mg/mol creatinine for healthy and malnourished control subjects, respectively) concentration. Subjects with FCPD and PDDM had significantly lower serum magnesium concentrations (PDDM: 0.68+/-0.06 mmol/L, FCPD: 0.66+/-0.07 mmol/L) than those in both control groups. In contrast with 0% of healthy and 7.7% of malnourished control subjects, 42.85% of type 2 diabetic subjects, 61.54% of those with PDDM, and 69.23% of those with FCPD were hypomagnesemic. Subjects with FCPD and PDDM had significantly higher urinary excretion of magnesium than the healthy and malnourished control subjects and the type 2 diabetic subjects. Hypermagnesuria paralleled hypomagnesemia. CONCLUSIONS: Malnutrition may not itself give rise to glucose intolerance, and serum magnesium deficiency seems to be a consequence rather than a cause of diabetes mellitus.

Urinary retinol excretion and kidney function in children with shigellosis.

BACKGROUND: Acute infections, including diarrhea, are associated with an increased risk of vitamin A deficiency. Urinary retinol excretion during such infections may contribute to this risk. The mechanism accounting for urinary retinol loss has not been clearly defined. OBJECTIVE: This study attempted to determine whether urinary retinol loss in children with acute infection is associated with impaired kidney function, particularly impaired tubular protein reabsorption. DESIGN: Urinary retinol excretion and kidney function were examined in 66 hospitalized children 5 mo to 5 y of age with acute Shigella dysentery. RESULTS: Urinary retinol loss occurred in 59% of children and was substantial (>0.1 micromol/d) in 8% of them. Children with more severe disease excreted higher concentrations of urinary retinol; those with a body temperature > or =40 degrees C excreted a mean of 0.10 +/- 0.18 micromol/d compared with 0.005 +/- 0.008 micromol/d for other children (P < 0.0001). Children with more severe disease also had impaired tubular reabsorption of low-molecular-weight proteins beta2-microglobulin and retinol binding protein (RBP)], although other measures of tubular and glomerular function were not similarly impaired. In multiple regression analysis, severity of disease indicators were the best predictors of tubular reabsorption of beta2-microglobulin (R2 = 0.53) whereas tubular reabsorption of beta2-microglobulin and RBP were found to be the best predictors of urinary retinol loss (R2 = 0.69). CONCLUSIONS: A significant amount of retinol was excreted in the urine in children with shigellosis: 8% excreted >0.10 micromol/d (15% of the daily metabolic requirement). Impaired tubular reabsorption of low-molecular-weight proteins, such as RBP transporting retinol, appeared to be the cause of this urinary retinol loss.

Urinary organic acids in infant malnutrition.

The metabolic derangements in severe protein-energy malnutrition (PEM) are only partially known, due to the limitations of blood collection in these patients. Urinary excretion of organic acids was studied by gas chromatography-mass spectrometry in 39 infants with four types of PEM: 1) upon hospital admission, as soon as eventual infections had been cleared, and salt and water deficits corrected, but before oral feeding was started; 2) after start of protein alimentation; 3) on the day of discharge. All of the patients showed an increased excretion of various organic acids at some point of their hospital stay, regardless of the clinical type of PEM. In nearly half of the malnourished children, results were suggestive of blocks in the pathways of propionate (15.4% with increased methylmalonate and 25.6% with 2-methylcitrate), of fatty acid beta-oxidation (30.8% with raised dicarboxylic acids with low or low normal 3-hydroxybutyrate), or of both pathways (12.8%). These abnormalities may have been caused by cofactor deficiencies (biotin, vitamin B12, riboflavin, carnitine, niacin). Dicarboxylic acids were excreted in high amounts since the initial sample, probably due to increased mobilization of fatty acids. Increased 2-methylcitrate and methylmalonate excretion was observed more frequently once patients started to be orally fed. The accumulation of potentially toxic acyl-CoA precursors of these compounds could contribute to the known clinical worsening of some malnourished infants after suddenly increased protein intake. Other less specific metabolites, such as 3-hydroxybutyrate, lactate, 4-hydroxyphenyllactate, fumarate, succinate, and 4-hydroxyphenylacetate, were also abnormally excreted in some patients. The analysis of urinary organic acids provides a new approach for the metabolic study of PEM and may have diagnostic and therapeutic implications.

Urinary excretion of 5-L-oxoproline (pyroglutamic acid) is increased during recovery from severe childhood malnutrition and responds to supplemental glycine.

We hypothesized that a limitation in the endogenous formation of glycine might constrain catch-up growth during recovery from severe childhood malnutrition. The urinary excretion of 5-L-oxoproline is increased when the glycine available for glutathione synthesis is limited. Urinary excretion of 5-L-oxoproline was measured throughout recovery in 12 children (aged 16 +/- 6 mo) with severe malnutrition. Urinary 5-L-oxoproline was similar at admission and after recovery, but was increased significantly during rapid catch-up growth. There was a significant relationship between the rate of weight gain and 5-L-oxoproline excretion in urine. In nine children (aged 15 +/- 5 mo), the effect of oral supplementation with glycine, [1.7 mmol/(kg x d) for 48 h] during rapid catch-up growth on 5-L-oxoprolinuria and blood glutathione concentration was determined. In seven of the nine children weight gain was less than 17 g/(kg x d) and following oral glycine supplements 5-L-oxoproline excretion was reduced up to 64% and blood glutathione concentration increased up to 100%. In the two children who were gaining weight at a rate > 17 g/(kg x d), glycine supplementation was associated with a further increase in 5-L-oxoproline excretion and a decrease in blood glutathione. If 5-L-oxoproline is an index of the relative availability of glycine, then the data indicate that glycine may be limiting during rapid catch-up growth. This would have important implications for repletion of muscle and gain in height.

Murine acariasis: I. Pathological and clinical evidence suggesting cutaneous allergy and wasting syndrome in BALB/c mouse.

We describe here a disease related to mite-associated ulcerative dermatitis in BALB/c mice, a strain previously classified as resistant to this condition. The disease was recognized by pruritic cutaneous pathology and wasting. Pathologic studies showed a marked allergic-type inflammation in the skin. The dominant histologic feature was extensive mast cell infiltration in cutaneous lesions and in lymphoid tissues, associated with a greatly elevated serum IgE concentration. The disease was secondary to infestation with an acarian ectoparasite Myocoptes musculinus, and seemed to represent an allergic reaction to the parasite-derived substances, with an associated wasting syndrome. This condition may be a useful experimental model for allergic diseases.

Failure of anabolism in malnourished cancer patients receiving growth hormone: a clinical research center study.

Previous work demonstrated that the provision of adequate or even excessive nutritional support is unable to reverse the negative nitrogen balance in many cancer patients. Our goal in a preliminary, short term study was to determine whether three daily GH injections (0.125 mg/kg.day, im) in cancer patients would increase insulin-like growth factor I concentrations and reverse the catabolic metabolic response to cancer, as indicated by reduced urinary nitrogen loss. Three days of GH therapy were associated with a significant increase in mean circulating GH (1.6 +/- 0.4 vs. 15.4 +/- 3.0 micrograms/L; P < 0.01), insulin-like growth factor I (112 +/- 15 vs. 329 +/- 54 micrograms/L; P < 0.01), insulin (57 +/- 11 vs. 184 +/- 46 pmol/L; P < 0.01), glucagon (63 +/- 11 vs. 77 +/- 11 ng/L; P < 0.05), and glucose (5.4 +/- 0.1 vs. 6.2 +/- 0.2 mmol/L; P < 0.05) concentrations. Twenty-four-hour urinary urea nitrogen (6.7 +/- 0.9 vs. 4.9 +/- 0.5 g; P < 0.05) and total nitrogen (7.8 +/- 1.2 vs. 6.0 +/- 1.2 g; P < 0.05) were significantly reduced. GH treatment in the group overall failed to alter leucine appearance (77.3 +/- 4.0 vs. 76.1 +/- 5.4 mumol/kg.h), leucine oxidation (11.8 +/- 1.5 vs. 9.6 +/- 1.0 mumol/kg.h), hepatic glucose production (13.5 +/- 0.8 vs. 14.2 +/- 0.8 mumol/kg.min), or estimated mean nitrogen balance (-0.24 +/- 0.97 vs. 0.85 +/- 0.75 g/day; t = 1.56; P = 0.10). Nitrogen balance was directly correlated with the percentage of the patient's ideal body weight (r = 0.776; P < 0.01). Seven of the 10 cancer patients were at or above 90% of ideal body weight, and they had a significant improvement in nitrogen balance (-1.46 +/- 0.99 vs. 0.60 +/- 1.03 g/day; P < 0.01). These patients also demonstrated a significant reduction in leucine oxidation (14.1 +/- 1.3 vs. 10.0 +/- 1.4 mumol/kg.h) and leucine appearance (81.2 +/- 3.8 vs. 72.9 +/- 3.3 mumol/kg.h; P < 0.05). This suggests that those most severely malnourished cancer patients may not respond anabolically to short term GH administration. We conclude that GH administration may be anabolic in cancer patients if there is not severe preexisting malnutrition.

Marked elevation of urinary 3-hydroxydecanedioic acid in a malnourished infant with glycogen storage disease, mimicking long-chain L-3-hydroxyacyl-CoA dehydrogenase deficiency.

An infant with glycogen storage disease and prolonged malnourishment showed a urinary organic acid profile during an episode of fasting hypoglycaemia with inappropriate hypoketotic dicarboxylic aciduria that was indistinguishable from that reported in long-chain L-3-hydroxyacyl-CoA dehydrogenase deficiency. Although there was a striking elevation of urinary 3-hydroxydecanedioic acid, the ratios between hydroxydicarboxylic acids were consistent with values reported to be indicate of medium-chain acyl-CoA dehydrogenase deficiency. We suspect that the fasting 3-hydroxydicarboxylic aciduria was attributable to secondarily impaired enzyme activities, the consequence of malnutrition, early infancy, and/or glycogen storage disease. Caution is advised in the interpretation of urinary organic acid patterns that indicate a 3-hydroxydicarboxylic aciduria, as well as an inappropriate hypoketotic dicarboxylic aciduria, as they may represent non-specific findings.

The effect of the level of dietary protein, carbohydrate and fat on urea kinetics in young children during rapid catch-up weight gain.

The kinetics of urea metabolism were measured in children recovering from severe malnutrition. For a period of up to 10 d they received one of four diets which provided 711 kJ (170 kcal)/kg per d. Two groups received a diet with a high protein:energy (P:E) ratio of 10-6% (HP), enriched with either fat (HP/F) or maize starch and sucrose (HP/C). Two groups received a diet with a low P:E ratio of 8.8% (LP), enriched with either fat (LP/F) or maize starch and sucrose (LP/C). The rate of weight gain on the HP diets was significantly greater than on the LP diets. There was no difference in urea production between any of the four diets: HP/F 1.23 (SE 0.12), HP/C 1.37 (SE 0.14), LP/F 1.64 (SE 0.22), LP/C 1.15 (SE 0.15) mmol nitrogen/kg per h. On the HP diets urea excretion was 0.77 (SE 0.07) mmol N/kg per h, 61% of production. There was significantly less urea excreted in the urine on diet LP/C than on LP/F (0.36 (SE 0.05) and 0.64 (SE 0.04) mmol N/kg per h respectively). A significantly greater percentage of the urea production was hydrolysed on the LP diets (61%) compared with the HP diets (39%), with the consequence that 50% of urea-N produced was available for synthetic activity on the LP diets compared with 30% on the HP diets. The increase in the urea hydrolysed on the LP diets was equivalent in magnitude to the decreased intake of N, so that overall intake plus hydrolysis did not differ between the LP and the HP diets. Crude N balance was similar on diets HP/F, HP/C and LP/C, but was significantly reduced on diet LP/F. These results show that there is an accommodation in urea kinetics during rapid catch-up weight gain, which becomes evident when the P:E ratio of the diet falls to 8.8%. It is proposed that, for a P:E ratio of 8.8%, protein is limiting for catch-up growth. When the intake has a P:E ratio of 8.8% the pattern of urea kinetics can be modified by the relative proportions of fat and carbohydrate in the diet. The measurement of urea kinetics provides a useful approach to the definition of the adequacy of the protein in the diet.

The effect of the level of dietary protein, carbohydrate and fat on urea kinetics in young children during rapid catch-up weight gain

The kinetics of urea metabolism were measured in children recovering from severe malnutrition. For a period of up to 10 d they receive one of four diets which provided 711 kj (170 kcal)/kg per d. Two groups received a diet with a high protein:energy (P:E) ratio of 10.6 percent (HP), enriched with either fat (HP/F) or maize starch and sucrose HP/C). Two groups received a diet with a low P:E ratio of 8.8 percent (LP), enriched with either fat (LP/F) or maize starch and sucrose (LP/C). The rate of weight gain on the HP diets was significsntly greater than on the LP diets. There was no difference in urea production between any of the four diets: HP/F 1.23 (se 0.12), HP/C 1.37 (se 0.14), LP/F 1.64 (se 0.22) LP/C 1.15 (se 0.15) mmol nitrogen/kg per h. On the HP diets urea excretion was 0.77 (se0.07) mmol N/kg per h, 61 percent of production. There was significantly less urea excreted in the urine on diet LP/C than on LP/F (0.36 (se0.05) and 0.64 (se 0.04)mmol N/kg per h respectively). A significantly greater percentage of the urea production was hydrolysed on the LP diets (61 percent) compared with the HP diets (39 percent), with the consequence that 50 percent of urea-N produced was available for synthetic activity on the LP diets compared with 30 percent on the HP diets. The increase in the urea hydrolysed on the LP diets was equivalent in magnitude to the decreased intake of N, so that overall intake plus hydrolysis did not differ between the LP and HP diets. Crude N balance was similiar on diets HP/F, HP/C and LP/C, but was significantly reduced on diet LP/F. These results show that there is an accommodation in urea kinetics during rapid catch-up weight gain, which becomes evident when the P:E ratio of 8.8 percent, protein is limiting for catch-up growth. When the intake has a P:E ratio of 8.8 percent the pattern of urea kinetics can be modified by the relative proportion of fat and carbohydrate in the diet. The measurement of urea kinetics provides a useful approach to the definition of the adequacy of the protein in the diet. (AU)

Urine collection as an alternative to blood sampling: a noninvasive means of determining isotopic enrichment to study amino acid flux in neonates.

The validity of measuring isotopic enrichment of amino acids in urine was tested in neonates during different feeding regimens and tracer administration protocols, and with different amino acid tracers. Twenty infants, fed enterally or parenterally, were given primed, constant infusions of 15N-glycine, L-[1-13C]leucine, and L-[1-13C]phenylalanine. Urine was collected every 2 h for 16 h. Blood was sampled only when required clinically. At baseline, enrichment in plasma and urine did not differ for any amino acid. At isotopic steady state, leucine enrichment was similar in plasma and urine, while the agreement was slightly weaker for glycine and phenylalanine, probably because of problems inherent in drawing blood samples from neonates. Study protocol did not affect the agreement. Since urine collection involves minimal invasive procedures, this approach could facilitate more indepth tracer studies in infants and children.

Increased urinary excretion of cortisol and catecholami-NES in malnourished cancer patients.

Excretion of cortisol and catecholamines were measured from 24-hour urine samples collected over a period of 3 days from hospitalized cancer patients suffering from malnutrition and were compared with those of control patients equally malnourished and having a similar degree of inflammation. Compared with control patients, cancer patients had a higher excretion of cortisol, adrenaline, and noradrenaline, although noradrenaline excretion reached statistical significance only when normalized to creatinine excretion. Plasma glycerol concentrations after an overnight fast were significantly higher in cancer patients as compared with control patients, in keeping with an increased adrenal and adrenergic activity. This study demonstrates evidence of simultaneously elevated catecholamine and cortisol excretion in cancer patients, which could not be ascribed to alteration in body composition. The results may, in part, explain the mechanisms behind ongoing tissue breakdown in progressive cancer disease.

Effects of increasing glucose intake on nitrogen balance and energy expenditure in malnourished adult patients receiving parenteral nutrition.

The effects of increasing glucose intake on nitrogen balance, energy expenditure and fuel utilization were measured in malnourished adult patients receiving parenteral nutrition with constant nitrogen intake and high or low glucose intakes for 8 day periods. Energy balance, nitrogen balance, weight and temperature were determined daily. Blood samples taken at admission and at the end of days 7 and 8 of each diet were analysed for glucose, fatty acids, urea, insulin, glucagon and thyroid hormones. The effect of increasing glucose intake was to increase nitrogen balance by 0.28 +/- 0.08 (SEM) mg/kJ. A scheme is proposed, based on present and previous findings, of the separate effects of nitrogen and energy intake on nitrogen balance, permitting calculation of rates of repletion of fat and lean body mass from estimates of nitrogen intake and energy balance. Malnourished patients are shown to attain markedly positive nitrogen balances at zero or negative energy balances. Large errors in estimation of energy requirements have little effect on nitrogen balance. Changes in nitrogen balance were entirely due to changes in urea excretion. Creatinine excretion increased 12% with high glucose intake, attributed mainly to increased muscle mass (7%) and body temperature (4%). A 12% increase in resting energy expenditure was only partly due to costs of glycogen storage and lipogenesis; the remainder, about one-half, is probably due to glucose and insulin mediated increases in sympathetic activity. There were marked increases in 3,5,3'-triiodothyronine (T3) concentrations with time, but no difference between the high and low glucose diets. The T3/thyroxine ratio, an index of free T3 concentration, increased much more rapidly on the high than on the low glucose diet. Changes in T3 could not account for the effect of glucose, under these conditions, to increase resting energy expenditure.

The maintenance energy requirement for children: an estimate based on a study of children with infection associated underfeeding.

An estimate of the maintenance energy requirement (MER) has been based on energy balance data from children fed at different levels of intake during and after acute measles. The relationship between apparent energy balance (B) and the metabolizable energy intake (ME) was investigated by regression analysis. The relationship between B and ME in 34 balance studies is given by B = 0.79 ME -211.9 (r = 0.91). The ME at zero B [268.3 kJ (64.1 kcal)/kg X 24 h] is equivalent to the maintenance energy requirement (MER). Paired data on 16 children were used to study the relationship between MER and the resting metabolic rate (RMR). The relationship between MER and RMR during measles, ie at low levels of energy intake, is given by MER = 1.52 RMR -140.9 kJ/kg X 24 h (r = 0.79). The factorial relationship between MER and mean RMR was estimated, and also the safe level of intake to supply the MER when ME represents between 76% and 84% of gross energy (GE). The safe level of GE intake, between 381 and 416 kJ/kg X 24 h (ie between 91.1 and 99.4 kcal/kg X 24 h), is very close to the WHO/FAO (1973) recommendations for growing children.

[Zinc balance in malnourished children given prolonged total parenteral feeding]. / Balance de zinc en niños desnutridos con alimentación parenteral total prolongada.

Zinc balances were performed in five different occasions in three children receiving prolonged total parenteral nutrition (TPN) for 4 or more weeks. Excessive urinary zinc loss was a constant finding and one patient also presented increased fecal loss. It is concluded that TPN solutions when administered for long periods must be supplemented with zinc in order to obtain positive balances and a retention of zinc between 50-100 micrograms kg/day. In children without abnormal losses supplements recommended by the American Medical Association (100 micrograms/kg/day up to 5 years and from 2.5 to 4 mg/day in old children) seem adequate. In case of deficit in Zn and/or high digestive losses supplement of Zn in TPN must be increased up to 200 to 500 micrograms/kg/day.