Inadequate nutrient intakes are common and are associated with low diet variety in rural, community-dwelling elderly.

Poor dietary habits and inadequate nutrient intakes are of concern in the elderly. The nutritional characteristics of those who survive to become the oldest are not well defined. Our goal was to describe dietary habits, nutrient intakes and nutritional risk of community-dwelling, rural Iowans, 79 y of age and older. Subjects were interviewed (n = 420) using a standardized format on one occasion in their homes and instructed to complete 3-d diet records (n = 261) after the in-home interview. Standardized interviews assessed demographic information, cognitive function and dietary habits (Nutrition Screening Initiative Checklist). Adequate nutrient intake was defined as consumption of the nutrient's estimated average requirement, 67% adequate intake or 67% recommended dietary allowance. Mean age was 85.2 y, 57% lived alone and 58% were widowed. Subjects completing 3-d diet records were younger, more cognitively intact and less likely to be at nutritional risk than subjects not completing diet records. The percentage of subjects with inadequate intakes of selected nutrients was 75% for folate, 83% for vitamin D and 63% for calcium. Eighty percent of subjects reported inadequate intakes of four or more nutrients. Diet variety was positively associated with the number of nutrients consumed at adequate intakes (r = 0.498), total energy (r = 0.522) and dietary fiber (r = 0.421). Our results suggest that rural, community-dwelling old have inadequate intakes of several nutrients. Recommendations to increase diet variety and consume a nutrient supplement may be necessary for elderly people to achieve adequate nutrient intakes.

Effect of vitamin E on resistance vessel endothelial dysfunction induced by methionine.

We tested if vitamin E, a fat-soluble antioxidant, prevents resistance vessel endothelial dysfunction caused by methionine-induced hyperhomocysteinemia in humans. Moderate elevations in plasma homocysteine concentrations are associated with atherosclerosis and hypertension. Homocysteine causes endothelial dysfunction possibly through several mechanisms. No previous study has tested if a fat-soluble antioxidant can prevent endothelial dysfunction caused by experimental hyperhomocysteinemia. Ten healthy subjects participated in a 2 x 2 factorial, double-blind crossover study, receiving L-methionine (100 mg/kg at -6 hours) or vehicle, with and without vitamin E (1,200 IU at -13 hours). Endothelial function of forearm resistance vessels was assessed using forearm blood flow responses to brachial artery administration of endothelium-dependent and endothelium-independent agents. Forearm resistance vessel dilatation to acetylcholine was significantly impaired 7 hours after methionine (placebo, 583 +/- 87% vs methionine 30 +/- 68%; p <0.05). Dilatation to bradykinin was also impaired (placebo, 509 +/- 54% vs methionine 289 +/- 48%; p <0.05). Methionine did not alter vasodilatation to the endothelium-independent vasodilators, nitroprusside, and verapamil. Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p <0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone). Experimentally increasing plasma homocysteine concentrations by oral methionine rapidly impairs resistance vessel endothelial function in healthy humans and this effect is reversed with administration of the fat-soluble antioxidant, vitamin E.

Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia.

A single high-fat meal transiently impairs conduit vessel endothelial function. We tested the hypothesis that transient moderate hypertriglyceridemia by consumption of a high-fat meal impairs forearm resistance vessel endothelial function. Fifteen healthy persons consumed isocaloric high- and low-fat meals (900 calories, 50 and 4 g of fat, respectively) on 2 separate days. Endothelial function in forearm resistance vessels was assessed using blood flow responses to local intra-arterial infusion of nitroprusside, acetylcholine, bradykinin, and verapamil from 1 to 3 hours after the meal. Serum triglycerides increased from 112 +/- 15 mg/dl preprandially to 165 +/- 20 mg/dl 4 hours after the high-fat meal, which was a significantly larger increase than levels after the low-fat meal (p = 0.01). Total cholesterol, high-density lipoprotein, low-density lipoprotein, and very low density lipoprotein (VLDL) cholesterol concentrations did not change. There was no difference between high- and low-fat meals in vasodilation to the endothelium-dependent agents acetylcholine (low fat, 337 +/- 47%; high fat, 356 +/- 88%; p = 0.81) and bradykinin (low fat, 312 +/- 39%; high fat, 403 +/- 111%; p = 0.28), or to the endothelium-independent vasodilators nitroprusside (low fat, 313 +/- 27%; high fat, 355 +/- 42%; p = 0.31) and verapamil (low fat, 292 +/- 48%; high fat, 299 +/- 36%; p = 0.18). Thus, transient hypertriglyceridemia due to a high-fat meal does not impair resistance vessel endothelial function. These data contrast with previous studies in conduit vessels that showed substantial endothelial dysfunction. Therefore, although high-fat intake may contribute to large artery atherosclerosis, it probably does not predispose to hypertension or ischemia through resistance vessel dysfunction. The results suggest that the mechanism by which triglyceride-rich lipoproteins impair endothelial function in conduit vessels is not operative in resistance vessels.

Effects of fat and carbohydrate meals on colonic motor response.

BACKGROUND: Ingestion of a meal stimulates colonic motility. It is unclear whether the nutrient composition of a meal affects colonic motor response. AIMS: To investigate and compare the effects of a predominantly fat or carbohydrate meal on colonic motility. METHODS: In 18 healthy subjects, ambulatory colonic manometry was performed by placing a six sensor, solid state probe from the mid-transverse colon to the rectum. In a randomised, crossover design, 10 and 27 hours after probe placement, subjects received 4.18 MJ meals containing 60% calories from fat or carbohydrate sources. Preprandial and postprandial pressure activity and motor patterns were evaluated. RESULTS: Both meals induced phasic activity with a greater area under the curve (p<0.03) in the first postprandial hour, compared with the control period. Fat induced motor activity persisted longer (p<0.05) than that of the carbohydrate meal, but the onset of motor response was slower (p<0.001). Although both meals induced more (p<0.001) propagating pressure waves, only the fat meal induced more (p<0.05) simultaneous and retrograde waves. After both meals, 50% of subjects exhibited high amplitude (more than 103 mm Hg), prolonged duration (more than 13 seconds) propagating waves. Both meals induced greater activity (p<0.05) in the transverse/descending colon than in the rectosigmoid colon. CONCLUSIONS: Carbohydrate meals induce colonic motor response, but the effects are short lived when compared with fat meals. The prolonged, segmental, and retrograde phasic activity induced by the fat meal may delay colon transit. Thus meal composition influences colonic motor response.

Drug and environmental factors associated with adverse pregnancy outcomes. Part III: Folic acid: pharmacology, therapeutic recommendations, and economics.

OBJECTIVE: To review folic acid's mechanism of action, adverse effects, therapeutic recommendations, compliance, and cost. DATA SOURCES: A MEDLINE search was conducted through December 1997. Additional sources were obtained from Current Contents and citations from the references obtained. Search terms included folate, folic acid, neural tube defect, homocysteine, and methylenetetrahydrofolate reductase. STUDY SELECTION: Animal and human studies examining the effects of folate were reviewed. DATA EXTRACTION: Data collected included mechanism of action, safety issues, dosing recommendations, compliance with recommendations, and economics. DATA SYNTHESIS: Folic acid decreases neural tube defect risk through an effect on methionine-homocysteine metabolism. In addition, increased folate intake may reduce cardiovascular morbidity and mortality. Since toxicity is minimal, everyone can potentially benefit from increased folate consumption. To help achieve this, the Food and Drug Administration has mandated that cereal grain be fortified with 140 micrograms of folic acid per 100 g of grain, which will add approximately 0.1 mg of folate to the average diet. Studies recommend supplementing with 0.2 mg to promote optimal homocysteine concentrations and for preventing neural tube defects. CONCLUSIONS: Despite fortification, most women will still receive less folate than the 0.4 mg/d recommended by the Public Health Service. All population groups would benefit from increased folate intake. Current studies indicate 200 micrograms/d may be the minimum effective amount of fortification needed for normalizing homocysteine concentrations and preventing a significant number of neural tube defects; thus, a higher level of food fortification may be warranted.

Drug and environmental factors associated with adverse pregnancy outcomes. Part II: Improvement with folic acid.

OBJECTIVE: To provide a comprehensive review of periconceptional folic acid supplementation and factors affecting folate supplementation trials. DATA SOURCES: A MEDLINE search was conducted through December 1997. Additional sources were obtained from Current Contents and citations from the references obtained. Search terms included folate, folic acid, neural tube defect, spina bifida, and anencephaly. STUDY SELECTION: Relevant animal and human studies examining the effects of folate were reviewed. DATA EXTRACTION: Data collected included: type of study, folate dosing, dietary folate intake, serum and red blood cell folate concentrations, type of defect(s) studied, vitamin usage, parental risk factors, factors affecting trial results. DATA SYNTHESIS: Nine key factors have been identified that affect outcomes of folic acid supplementation trials. Daily doses of 0.8 mg decreased the occurrence and doses of 4 mg decreased the recurrence of neural tube defects in randomized clinical trials. Since lower folic acid doses were effective in nonrandomized trials, research is needed to determine the lowest effective dosage. Other benefits involving pregnancy outcome are suggested. CONCLUSIONS: Women of childbearing age should take a daily folic acid supplement to reduce the risk of pregnancies resulting in infants with a neural tube defect and other potential adverse pregnancy outcomes. Further health benefits from folic acid supplementation are reviewed in Part III of this series.

Drug and environmental factors associated with adverse pregnancy outcomes. Part I: Antiepileptic drugs, contraceptives, smoking, and folate.

OBJECTIVE: Part I of this review examines the relationship between antiepileptic drugs (AEDs) and pregnancy outcomes. Drug-induced folate deficiency and the role of AED metabolism are emphasized. Part II will discuss periconceptional folate supplementation for prevention of birth defects. Part III will discuss the mechanism of folate's protective effect, therapeutic recommendations, compliance, and cost. DATA SOURCES: A MEDLINE search was conducted for journal articles published through December 1997. Additional sources were obtained from Current Contents and citations from the references obtained. Search terms included phenytoin, carbamazepine, phenobarbital, primidone, valproic acid, oral contraceptives, clomiphene, drug-induced abnormalities, spina bifida, anencephaly, neural tube defect, folate, folic acid, and folic acid deficiency. STUDY SELECTION: Relevant animal and human studies examining the effects of AEDs, smoking, and oral contraceptives on folate status and pregnancy outcome are reviewed. DATA EXTRACTION: Studies and case reports were interpreted. Data extracted included dosing, serum and red blood cell folate concentrations, teratogenicity of anticonvulsant medications, metabolism of AEDs and folate, and genetic susceptibility to AED-induced teratogenicity. DATA SYNTHESIS: Low serum and red blood cell folate concentrations are associated with adverse pregnancy outcomes. Decreases in serum folate are seen with AEDs, oral contraceptives, and smoking. Since similar birth defects are observed with multiple AEDs, metabolism of aromatic AEDs to epoxide metabolites and genetic factors may play a role in teratogenesis. CONCLUSIONS: Adequate prepregnancy planning is essential for women who have epilepsy. Women receiving folate-lowering drugs may be at increased risk of adverse pregnancy outcomes. Therefore, epileptic women contemplating pregnancy should be treated with the minimum number of folate-lowering drugs possible and receive folic acid supplementation.

Is coffee a colonic stimulant?

BACKGROUND: It is unclear if ingestion of coffee affects colonic function and if this effect is due to its caffeine content. We investigated the effects of coffee on colonic motor activity in healthy humans. METHODS: We performed ambulatory colonic manometry by placing a six-sensor solid-state probe up to the mid-transverse colon in 12 healthy subjects. The following day, over a 10 h period, subjects received four stimuli: 240 ml of three drinks at 45 degrees C in random order: black Colombian coffee (150 mg caffeine), decaffeinated coffee or water and 1000 kcal meal. We analyzed the effects of each stimulant on colonic motor responses. RESULTS: Caffeinated coffee, decaffeinated coffee and meal induced more activity in the colon with a greater area under the curve of pressure waves (P < 0.01) and a greater number of propagated contractions (P < 0.05) when compared with water. Caffeinated coffee, decaffeinated coffee and meal induced greater (P < 0.05) motor activity in the transverse/descending colon when compared with the rectosigmoid colon. The effects of decaffeinated coffee on colonic motility were not significantly different from those of water or caffeinated coffee and were lower (P < 0.05) than that of a meal. CONCLUSION: Caffeinated coffee stimulates colonic motor activity. Its magnitude is similar to a meal, 60% stronger than water and 23% stronger than decaffeinated coffee.

Increased urinary excretion of 3-hydroxyisovaleric acid and decreased urinary excretion of biotin are sensitive early indicators of decreased biotin status in experimental biotin deficiency.

To assess the utility of various indicators of biotin status, marginal biotin deficiency was induced experimentally in normal adults. Ten subjects consumed a diet that contained enough avidin to bind seven times more biotin than that in the diet. Blood and 24-h urine samples were collected before the diet began and twice weekly thereafter for 20 d. The urinary excretion and serum concentration of biotin and its two principal inactive metabolites bisnorbiotin and biotin sulfoxide were determined after HPLC separation with an avidin-binding assay. The urinary concentration of 3-hydroxyisovaleric acid, an indicator of reduced activity of a biotin-dependent enzyme, was quantitated by gas chromatography-mass spectrometry. The urinary excretion of 3-hydroxyisovaleric acid increased significantly (P < 0.0001). For all subjects, the urinary excretion of both biotin and bisnorbiotin decreased significantly (P < 0.0001 for each). In contrast, the mean serum concentration of biotin did not decrease significantly (P = 0.06). These data provide evidence that the urinary excretion of 3-hydroxyisovaleric acid and the urinary excretion of biotin are early and sensitive indicators of biotin deficiency and that the serum concentration of biotin is not.

Does increased nitrate ingestion elevate nitrate levels in human milk?

OBJECTIVE: To determine whether the nitrate content of human milk is influenced by maternal ingestion of water containing elevated nitrate levels. DESIGN: Prospective, nonrandomized, volunteer study. SETTING: Clinical Research Center at the University of Iowa Hospitals and Clinics, Iowa City. PATIENTS: Twenty healthy lactating women with infants older than 6 months. INTERVENTIONS: The mothers were asked to consume a minimum of 1500 mL of water containing 0 mg of nitrate per liter on day 1, 45 mg on day 2, and 100 mg on day 3 in addition to consuming and recording their dietary intake. Breast-feeding was permitted during days 1 and 2, but milk was expressed on day 3 and the infants were given alternate food sources. After each 24-hour study day, maternal urine and milk samples were collected and frozen. A modified cadmium column reduction method was used to determine spot urinary and milk nitrate content. RESULTS: The meant total nitrate intake from diet and water on days 1,2, and 3, respectively, was 46.6, 168.1, and 272.0 mg. Spot urine nitrate content on days 1, 2, and 3, respectively, was 36.0, 66.0, and 84.0 mg. Nitrate concentration of human milk on days 1,2, and 3, respectively, was 4.4, 5.1 and 5.2 mg/L. CONCLUSION: Women who consume water with a nitrate concentration of 100 mg/L or less do not produce milk with elevated nitrate levels.

Erythrocyte L-aspartyl-L-phenylalanine hydrolase activity and plasma phenylalanine and aspartate concentrations in children consuming diets high in aspartame.

A deficit of alpha-aspartyl-phenylalanine (alpha-Asp-Phe) hydrolase activity has been suggested as a cause of possible adverse effects of aspartame ingestion. Twenty-five normal preschool children and 23 school-age children described by their parents as sensitive to sugar were fed diets high in sucrose, aspartame, or saccharin for three successive 3-wk periods. Blood samples were obtained at baseline (fasting) and within the last 3 d of each dietary period (postprandial). alpha-Asp-Phe concentrations were below detection limits (0.5 mumol/L) in all plasma samples and Phe and Asp concentrations remained within normal limits, alpha-Asp-Phe hydrolase activities in baseline hemolysate samples did not differ between groups. One subject had a plasma alpha-Asp-Phe hydrolase activity > 2 SD below the mean. Despite this low activity, this subject did not show consistent cognitive or behavioral anomalies that could be linked to low hydrolase activity.

Protein calculation from food diaries of adult humans underestimates values determined using a biological marker.

We evaluated the ability of a biological marker (nitrogen excretion expressed as protein) to accurately reflect the protein intake of 12 healthy subjects consuming a low protein diet (0.6 g protein/kg standard body wt). In this crossover study, protein intake was confirmed by chemically analyzing a duplicate of the constant diet each subject consumed for 3 d and by calculating protein content of self-selected diets recorded during two additional 3-d periods. Diet analysis matched excretion (difference 0.03 +/- 0.04 g protein/kg standard body wt, means +/- SEM). Self-selected intake manually calculated by subjects using educational materials matched the prescription [0.60 (0.42, 0.86) g protein/kg standard body wt, median (range)], but underestimated excretion by 0.18 +/- 0.02 g protein/kg standard body wt (means +/- SEM). Self-selected intake recalculated by the authors using a computerized database was only +0.05 (-0.08, +0.44) g protein/kg standard body wt higher than subjects' calculations, suggesting that discrepancies between databases and/or subject calculation errors only partially accounted for how greatly self-selected intake underestimated excretion. In a secondary analysis of self-selected intake, the three dietitian subjects consumed more energy and excreted less protein than nondietitians (137 +/- 4.9 vs. 94 +/- 3.5 kJ/standard body wt; 0.72 +/- 0.02 vs. 0.83 +/- 0.02 g protein/kg standard body wt), suggesting that adequate energy intake and/or additional training might improve agreement between intake and excretion. Thus, discrepancies between protein excretion and reported intake may reflect factors other than willful noncompliance.

Phenytoin-folic acid interaction.

OBJECTIVE: To review information regarding the dual and interdependent drug-nutrient interaction between phenytoin and folic acid and other literature involving phenytoin and folic acid. DATA SOURCES: Information was retrieved from a MEDLINE search of English-language literature conducted from 1983 (time of the last review) to March 1995. Search terms included folic acid, phenytoin, and folic acid deficiency. Additional references were obtained from Current Contents and from the bibliographies of the retrieved references. STUDY SELECTION: All human studies examining the effects of phenytoin on serum folate concentrations and folic acid supplementation on serum phenytoin concentrations were selected. These included studies of patients with epilepsy and healthy volunteers as well as case reports. Case reports were included because of the extensive length of time needed to study this drug interaction. DATA EXTRACTION: Data extracted included gender, dosing, serum folate concentrations if available, pharmacokinetics, and adverse events. DATA SYNTHESIS: Serum folate decreases when phenytoin therapy is initiated alone with no folate supplementation. Folic acid supplementation in folate-deficient patients with epilepsy changes the pharmacokinetics of phenytoin, usually leading to lower serum phenytoin concentrations and possible seizure breakthrough. Folate is hypothesized to be a cofactor in phenytoin metabolism and may be responsible for the "pseudo-steady-state," which is a concentration where phenytoin appears to be at steady-state, but in reality, is not. Phenytoin and folic acid therapy initiated concomitantly prevents decreased folate and phenytoin obtains steady-state concentrations sooner. CONCLUSIONS: Folic acid supplementation should be initiated each time phenytoin therapy commences because of the hypothesized cofactor mechanism, decreased adverse effects associated with folate deficiency, and better seizure control with no perturbation of phenytoin pharmacokinetics.

Folic acid improves phenytoin pharmacokinetics.

Phenytoin (PHT) therapy to control seizures decreases serum folate levels in half of epileptic patients, thus increasing the risk of folate depletion. Supplementation with folic acid prevents deficiency but also changes PHT pharmacokinetics. Kinetic monitoring of PHT when folic acid is provided as a supplement has not been reported in women of child-bearing age. This study of six fertile women examined the interdependence of PHT and folic acid in a randomized crossover study of two treatments: treatment 1 consisted of 300 mg sodium PHT per day and treatment 2 consisted of 300 mg sodium PHT plus 1 mg folic acid per day. Dietary folic acid intake was calculated daily. During treatment 1, serum folate level decreased 38.0 +/- 18.6% (mean +/- standard deviation) and serum PHT concentration was in the low therapeutic range (43.92 +/- 14.52 mumol/L). During treatment 2, serum folate level increased 26.0 +/- 33.4%, and serum PHT level (39.04 +/- 14.16 mumol/L) was similar to that in treatment 1. Only one subject attained PHT steady state during treatment 1, but four subjects achieved steady state during treatment 2. Dietary folate intakes during treatments 1 and 2 were not significantly different. This study suggests an interdependence between PHT and folic acid and supports the observation that fertile women treated with PHT require folic acid supplementation to maintain a normal serum folate level.

Altered insulin resistance is associated with increased dietary weight loss in obese children.

To determine the relationship between insulin resistance and weight loss in early obesity, we used the euglycemic, hyperinsulinemic clamp to study the effect of a 14-day weight reduction diet in 10 prepubertal and early pubertal obese children (age, 10.1 +/- 1.6 years) on insulin sensitivity. Body weight decreased from 73.7 +/- 6.0 kg to 69.1 +/- 5.8 kg (p < 0.01). Insulin sensitivity before weight reduction negatively correlated with the amount of weight loss during diet (r = -0.8, p < 0.005). Weight loss also positively correlated with height standard deviation score (r = 0.9, p < 0.005). Mean insulin sensitivity increased from 0.068 +/- 0.01 (nmol kg-1 min-1)/(pmol l-1) to 0.096 +/- 0.030 (nmol kg-1 min-1)/(pmol l-1) (p < 0.05, one-tailed test). These results indicate that weight reduction decreases insulin resistance in childhood obesity. The inverse relationship between insulin sensitivity and weight loss during calorie, restriction in these subjects suggests that insulin resistance may enhance weight loss during calorie restriction.

Is milk production impaired by dieting during lactation?

To determine the feasibility of a weight-loss program during lactation, 33 healthy, well-nourished, breast-feeding women were enrolled. Twenty-two women completed the 10-wk study, losing a mean (+/- SD) of 4.8 +/- 1.2 kg. Mean energy intake during the study was nearly 2.25 MJ (538 kcal) below the mean daily baseline intake of 9.64 +/- 2.48 MJ (2303 +/- 592 kcal). The sum of three maternal skinfold thickness, waist, and hip measurements were significantly smaller (P = 0.0001) at study completion. Mean daily milk production was 759 +/- 142 mL/d at baseline and 802 +/- 189 mL/d at week 10. The infants gained an average of 21 g/d, or 1.48 +/- 0.40 kg overall. The mean percent fat of milk at baseline and 10 wk was 4.06 +/- 2.15 and 4.00 +/- 2.56, respectively. The mean daily nitrogen content of milk at baseline and study completion was 1.82 +/- 0.32 and 1.62 +/- 27 g/L. These findings suggest that modest weight loss by healthy breast-feeding women does not adversely affect either quantity or quality of milk consumed by their infants.

Effects of diets high in sucrose or aspartame on the behavior and cognitive performance of children.

BACKGROUND: Both dietary sucrose and the sweetener aspartame have been reported to produce hyperactivity and other behavioral problems in children. METHODS: We conducted a double-blind controlled trial with two groups of children: 25 normal preschool children (3 to 5 years of age), and 23 school-age children (6 to 10 years) described by their parents as sensitive to sugar. The children and their families followed a different diet for each of three consecutive three-week periods. One diet was high in sucrose with no artificial sweeteners, another was low in sucrose and contained aspartame as a sweetener, and the third was low in sucrose and contained saccharin (placebo) as a sweetener. All the diets were essentially free of additives, artificial food coloring, and preservatives. The children's behavior and cognitive performance were evaluated weekly. RESULTS: The preschool children ingested a mean (+/- SD) of 5600 +/- 2100 mg of sucrose per kilogram of body weight per day while on the sucrose diet, 38 +/- 13 mg of aspartame per kilogram per day while on the aspartame diet, and 12 +/- 4.5 mg of saccharin per kilogram per day while on the saccharin diet. The school-age children considered to be sensitive to sugar ingested 4500 +/- 1200 mg of sucrose per kilogram, 32 +/- 8.9 mg of aspartame per kilogram, and 9.9 +/- 3.9 mg of saccharin per kilogram, respectively. For the children described as sugar-sensitive, there were no significant differences among the three diets in any of 39 behavioral and cognitive variables. For the preschool children, only 4 of the 31 measures differed significantly among the three diets, and there was no consistent pattern in the differences that were observed. CONCLUSIONS: Even when intake exceeds typical dietary levels, neither dietary sucrose nor aspartame affects children's behavior or cognitive function.

The Dietary Intervention Study in Children (DISC): dietary assessment methods for 8- to 10-year-olds.

OBJECTIVES: The dietary assessment methods used in the Dietary Intervention Study in Children (DISC) are described and the rationale, validity, and/or general usefulness of each are discussed. DESIGN: DISC is the first multicenter, randomized, clinical trial to study the feasibility and long-term efficacy, safety, and acceptability of a fat-moderately diet in 8- to 10-year-old prepubescent children with moderately elevated plasma low-density lipoprotein cholesterol (LDL-C) levels. Final data collection for the original study (DISC I) occurred December 1, 1993; continued intervention and follow-up (DISC II) will extend beyond 1997. SETTING: Six clinical centers across the country participate in DISC. SUBJECTS: Preadolescent boys and girls with fasting LDL-C levels between the 80th and 98th age-specific and sex-specific percentiles established by the Lipid Research Clinics were eligible for the study. The feasibility phase included 140 children who were then enveloped into the full-scale trial. Baseline dietary data for 652 randomized children in the full-scale trial and 6-month results for the feasibility cohort are reported. INTERVENTIONS: Dietary assessment involved several elements: (a) determining eligibility based on consumption of more than 30% of energy from total fat, (b) monitoring adherence to and adequacy of the intervention diet, (c) evaluating acceptability of the diet in the intervention group, and (d) determining appropriate foods for the intervention diet. Methods are described for each purpose. MAIN OUTCOME MEASURES: LDL-C differences between the two groups and differences in total and saturated fat intakes as calculated from three 24-hour recalls were the primary outcome measures. Six-month dietary differences in the feasibility group are reported. STATISTICAL METHODS: Baseline group means and 6-month differences in dietary intake are reported for the full-scale trial and feasibility study, respectively. RESULTS: Baseline mean intake from three dietary recalls for the intervention (n = 328) and control (n = 324) groups, respectively, were as follows: energy = 1,759 kcal and 1,728 kcal; total energy from fat = 33.3% and 34.0%; total energy from saturated fat = 12.5% and 12.7%; and total dietary cholesterol = 209 mg and 195 mg. After 6 months of intervention, percentage of energy from total fat and saturated fat was reduced by 5.1% (P = .004) and 2.9% (P < .001), respectively, in this feasibility subset (n = 73) of the intervention group. Essentially no change in these parameters occurred in the control group (n = 67), which demonstrates a measurable difference in reporting between groups. APPLICATIONS/CONCLUSIONS: Results illustrate the feasibility of implementing a variety of dietary assessment methods among preadolescent children without relying primarily on parental reports.

Prolonged maternal fluid supplementation in breast-feeding.

A randomized, crossover study design was used to evaluate the effect of prolonged maternal fluid supplementation on the milk supply of breast-feeding women. A total of 19 well-nourished women whose infants were solely breast-fed and thriving were enrolled when their infants were 90 to 120 days of age. Of this group, 15 women consumed at least a 25% increase in fluids above baseline for 7 days. Mean daily milk production was 767 +/- 178 mL for the baseline period and 744 +/- 138 mL for the increased fluid period. There was no significant change in milk production between baseline and increased fluid periods. No significant linear relationship between the percentage increase in fluid intake and percentage change in milk production was found.