E O Smith
Baylor College of Medicine
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Featured researches published by E O Smith.
The American Journal of Clinical Nutrition | 1998
William W. Wong; E O Smith; Janice E. Stuff; David L. Hachey; William C. Heird; H J Pownell
Cardiovascular heart disease is a major health problem in the United States. Elevated blood cholesterol has been shown to significantly increase the risk of cardiovascular heart disease. The National Cholesterol Educational Program (NCEP) Step I diet, which restricts fat and cholesterol intakes, is usually recommended as the initial treatment to lower blood cholesterol. Soy protein has been shown to be hypocholesterolemic, particularly in hypercholesterolemic subjects. However, the hypocholesterolemic effect of soy protein in subjects with a blood total cholesterol concentration <5.17 mmol/L is not clear. To determine whether soy protein could enhance the hypocholesterolemic effect of the NCEP Step I diet, 13 normocholesterolemic and 13 hypercholesterolemic men aged 20-50 y were enrolled in a randomized, 2-part, crossover study. Subjects were fed either an NCEP Step I soy-protein diet or an NCEP Step I animal protein diet for 5 wk. After a washout period of 10-15 wk, the subjects were fed the alternate diet for 5 wk. The hypocholesterolemic effect of soy protein was found to be independent of age, body weight, pretreatment plasma lipid concentrations, and sequence of dietary treatment. Regardless of plasma lipid status, the soy-protein diet was associated with a statistically significant decrease in the plasma concentrations of LDL cholesterol (P = 0.029) as well as the in the ratio of plasma LDL cholesterol to HDL cholesterol (P = 0.005). Our results indicate that soy protein enhances the hypocholesterolemic effect of the NCEP Step I diet in both normocholesterolemic and hypercholesterolemic men.
Journal of Pediatric Gastroenterology and Nutrition | 2009
Claudia C. Robayo-Torres; Antone R. Opekun; Roberto Quezada-Calvillo; Xavier Villa; E O Smith; Marilyn Navarrete; Susan S. Baker; Buford L. Nichols
Background: Congenital sucrase-isomaltase deficiency (CSID) is characterized by absence or deficiency of the mucosal sucrase-isomaltase enzyme. Specific diagnosis requires upper gastrointestinal biopsy with evidence of low to absent sucrase enzyme activity and normal histology. The hydrogen breath test (BT) is useful, but is not specific for confirmation of CSID. We investigated a more specific 13C-sucrose labeled BT. Objectives: Determine whether CSID can be detected with the 13C-sucrose BT without duodenal biopsy sucrase assay, and if the 13C-sucrose BT can document restoration of sucrose digestion by CSID patients after oral supplementation with sacrosidase (Sucraid). Methods: Ten CSID patients were diagnosed by low biopsy sucrase activity. Ten controls were children who underwent endoscopy and biopsy because of dyspepsia or chronic diarrhea with normal mucosal enzymes activity and histology. Uniformly labeled 13C-glucose and 13C-sucrose loads were orally administered. 13CO2 breath enrichments were assayed using an infrared spectrophotometer. In CSID patients, the 13C-sucrose load was repeated adding Sucraid. Sucrose digestion and oxidation were calculated as a mean percent coefficient of glucose oxidation averaged between 30 and 90 minutes. Results: Classification of patients by 13C-sucrose BT percent coefficient of glucose oxidation agreed with biopsy sucrase activity. The breath test also documented the return to normal of sucrose digestion and oxidation after supplementation of CSID patients with Sucraid. Conclusions: 13C-sucrose BT is an accurate and specific noninvasive confirmatory test for CSID and for enzyme replacement management.
The American Journal of Clinical Nutrition | 1995
Nancy F. Butte; Jon K. Moon; William W. Wong; Judy M. Hopkinson; E O Smith
To investigate how age and body composition affect energy requirements, the sedentary daily expenditure (SDE) and basal metabolic rate (BMR) of 101 infants, 82 girls, and 27 adults were measured. Energy expenditure was scaled for differences in body size to test the effects of age and body fatness. A power function was superior to linear models. For all subjects, WT0.63 (where WT is weight) or FFM0.63 (where FFM is fat-free mass) explained 94% of the variability in BMR, and WT0.70 or FFM0.70 explained 97% of the variability in SDE. The effects of height and fat mass (kg or % body wt) on BMR and SDE scaled for weight or fat-free mass were age dependent. Best-fitted exponents relating BMR or SDE to body size differed between children (0.40-0.52) and infants (1.04-1.30) (P = 0.001). Human energy requirements from infancy to adulthood appear to be a power, not a linear, function of body weight and composition.
Journal of The American College of Nutrition | 1991
Nancy F. Butte; William W. Wong; Cutberto Garza; Janice E. Stuff; E O Smith; Peter D. Klein; Buford L. Nichols
Current recommendations for energy intake are reviewed in light of emerging data on energy intakes of breast-fed infants and on total daily energy expenditure of infants. For determination of energy requirements, the historical approach based on observed intakes of healthy infants is compared with a newly proposed approach based on energy expenditure and deposition. A data set of exclusively breast-fed infants is used to illustrate the circuity of either approach. Energy intake, expenditure, and stores must be evaluated in an assessment of dietary adequacy. Ultimately, energy requirements of infants should reflect growth rate, body composition, and level of physical activity conducive to optimal health and neurobehavioral development.
Meat Science | 2004
Kerri B. Harris; Wilson G. Pond; Harry J. Mersmann; E O Smith; H.R. Cross; J.W. Savell
At approximately 8 weeks of age, four-way cross (Chester White×Landrace×Large White×Yorkshire) pigs (n=24) were selected based on genetically high (H) or low (L) serum cholesterol levels-12 from each genetic group-to determine the relationship between genetics, fat source, and sex class on plasma cholesterol, growth, carcass characteristics, and cholesterol and lipid content of muscle and adipose tissues. Boars and gilts, six each from the two genetic groups, were assigned randomly to one of three dietary treatments for 46 days. A standard grower diet was modified to include beef tallow (T), corn oil (CR) or coconut oil (CC), and the pigs were given ad libitum access to feed. Cholesterol was added to each diet to ensure the diets contained the same amount of cholesterol. Except for the plasma lipids, there were no differences between boars and gilts at the initial evaluation or at the end of the treatment; therefore, sex means were pooled for statistical analyses. Body weight was unaffected by diet on days 18, 29 or 46. Blood samples were taken on days 1, 29, and 46 via the anterior vena cava. Plasma total cholesterol (TC) and low density lipoprotein cholesterol (LDL) concentrations were greater in the H than L groups (overall TC in H and L pigs=150 and 124 mg/dl, respectively, and LDL in H and L pigs=105 and 76 mg/dl, respectively). Pigs fed diets containing saturated fats had greater TC and LDL than pigs fed unsaturated fats (TC=165, 149, and 126 mg/dl for T, CC, and CR diets, respectively, and LDL=108, 88, and 77 mg/dl for T, CC, and CR diets, respectively). There were significant time×gene×sex interactions for both TC and LDL yielding subtle differences in the response of the sexes from the two genetic groups over time. Pigs were slaughtered on day 46, and carcass data were collected. There were no differences in fat at the first rib, 10th rib, last rib, or last lumbar vertebra, but differences (P <0.05) were found between genetic groups for M. longissimus thoracis et lumborum (LTL) muscle area (H=21.0±0.8 cm(2), L=18.1±1.0 cm(2)) and USDA muscle score (H=2.1±0.1, L=1.7±0.1). There were no genetic or diet effects for cholesterol content of pre-rigor or post-rigor LTL muscle. Neither genetics nor dietary treatment affected the cholesterol content of the adipose tissue. There were no differences in fat percentage between genetic groups for muscle or adipose tissue. There were differences (P <0.05) in total lipid content among the dietary treatments for the pre-rigor (T=6.0±0.6%, CC=4.3±0.3%, CN=3.9±0.5%) and post-rigor (T=6.4±0.9%, CC=4.1±0.3%, CN=5.0±0.4%) LTL. Cholesterol accretion in muscle and adipose tissues of growing pigs was not influenced by source of fat in the diet or by their genetic propensity for high or low plasma cholesterol.
Journal of Pediatric Gastroenterology and Nutrition | 1986
Corinne M. Montandon; Wills C; Cutberto Garza; E O Smith; Buford L. Nichols
Summary: This study was designed to estimate energy intake in exclusively formula-fed infants. Formula intake of twenty-four 1− and 4-month-old infants was studied for 5 consecutive days; six boys and six girls were in each age group. Intake was estimated by laboratory-determined weights of formula consumed, spilled, and regurgitated. Two additional methods were used to estimate intake in the first nine infants during the 1st day of observation: test-weighing the infant at each feeding and mothers weighing of formula consumed, regurgitated, and spilled at each feeding. No consistent differences were detected among methods, but test-weighing appeared to have the greatest feed-to-feed variability. Intake was estimated to be 747 ± 100 g or 125.5 ± 17 kcal/kg, and 958 ± 131 g or 94.0 ± 13 kcal/kg for 1− and 4-month-old infants, respectively. The day-to-day variability (expressed as the coefficient of variation) was 13 and 15% (CV, g/kg) for 1− and 4-month-old infants, respectively. Between-infant variability of intake was ∼8% (CV, g/kg) for both age groups. Energy intakes of 1-month-old formula-fed infants were similar to published values of breast-fed infants of similar age, but the energy intakes of 4-month-old formula-fed infants were significantly higher than values published for 4-month-old breast-fed infants.
The American Journal of Clinical Nutrition | 1984
Nancy F. Butte; Cutberto Garza; Janice E. Stuff; E O Smith; Buford L. Nichols
The American Journal of Clinical Nutrition | 1988
William W. Wong; W. J. Cochran; William J. Klish; E O Smith; Lee Ls; Peter D. Klein
The American Journal of Clinical Nutrition | 1983
Janice E. Stuff; Cutberto Garza; E O Smith; Buford L. Nichols; Corinne M. Montandon
The American Journal of Clinical Nutrition | 1998
Jorge A. Coss-Bu; Larry S. Jefferson; David Walding; Yadin David; E O Smith; William J. Klish