The stable isotope-labeled [1,1,2,3,3-2H5]glycerol analyzed by negative-ion chemical ionization (NCI) mass spectrometry has been proven a valid tracer for studying glycerol kinetics in humans. Because of its high technical complexity, NCI mass spectrometry is available to only a few laboratories. Thus, the aim of our study was to create an alternative method for measuring [1,1,2,3,3-2H5]glycerol enrichment in plasma with a new derivative and positive-ion chemical ionization (PCI) mass spectrometry. It could be demonstrated that the trisacetyl[1,1,2,3,3-2H5]glycerol derivative was able to produce a fragment at m/z = 164 with sufficient intensity. Application of [1,1,2,3,3-2H5]glycerol in seven healthy volunteers resulted in reproducible measurements of basal glycerol turnover rates. The mean glycerol flux rate of 3.02 +/- 0.37 mumol.kg-1 body wt.min-1 after an overnight fast was similar to values reported from studies with comparable protocols. Physiological changes of lipolysis rates after 48 h of fasting followed by infusion of 4 mg.kg-1 body wt.min-1 glucose could also be adequately studied in one subject. Fast-induced elevated glycerol turnover at 7.56 mumol.kg-1 body wt.min-1, was substantially suppressed to 1.13 mumol.kg-1 body wt.min-1, when glucose was administered. The easily performed trisacetyl[1,1,2,3,3-2H5]glycerol derivative analyzed by PCI mass spectrometry is suitable for studying glycerol kinetics in humans.
Colon cancer is an exceptionally aggressive disease, and the use of natural or synthetic substances to prevent or decrease cancer risk without adverse effects remains a major challenge. In this study, the mechanistic basis for the chemopreventive effect of resveratrol (Res) on 1,2-dimethylhydrazine-induced colon carcinogenesis in an rat model was evaluated.
Rats were randomized into six groups. Group 1 were control rats, group 2 were control rats that received Res (8mg/kg of body weight orally every day), and rats in groups 3-6 were treated once per week with 1,2-dimethylhydrazine (20mg/kg of body weight, subcutaenously, 15 times). In addition, groups 4-6 received Res (as in group 2) in three dietary regimens: initiation, postinitiation, and entire period. All rats were sacrificed after 30 wk and the degree of inflammation, cell proliferation, apoptosis, and mucosal integrity was evaluated.
Res supplementation during the entire period significantly amended the expression of inflammatory, cell proliferative, and apoptotic biomarkers such as cyclo-oxygenase-2, ornithine decarboxylase, caspase-3, and heat shock proteins 70 and 27. Moreover, supplementing Res for the entire study period modulated the colonic mucosal protein mucin 1 and 2 expression.
The results clearly indicate that chronic Res supplementation inhibited the colon cancer development through modulating the early and late events of carcinogenesis and helped to maintain the colonic mucosal integrity. Thus our study demonstrates that the chemopreventive efficacy of Res could be attributed to its action on multiple direct targets of carcinogenesis.
We assessed the ability of novel lipid structures including medium-chain triacylglycerols (MCTs) and 1,3-diacylglycerol (DG) oil to lower postprandial triacylglycerol (TG) elevation and increase hepatic fat oxidation when substituted for dietary TG, which may be useful in the prevention and treatment of obesity and other related metabolic conditions, such as dyslipidemias.
This double-blind, randomized, crossover trial evaluated the effects of an oral fat load containing DG or MCTs compared with equivalent intakes of long-chain triacylglycerols (LCTs) on the postprandial metabolic responses of insulin-resistant men and women (n = 36). Each subject consumed a single oral fat load on each test day. The fat loads were delivered in milkshakes that contained 30 g of one of the three test oils.
The postprandial TG incremental area under the curve after MCT was 73% lower, and that for DG was 22% lower, compared with the response after LCT oil. The incremental area under the curve values for chylomicron TG were reduced versus LCT by 89% and 28%, respectively, in the MCT and DG conditions. Compared with the LCT treatment, beta-hydroxybutyrate concentration was increased after MCT oil, but not after DG.
These results indicate that dietary DG decreased postprandial triglyceridemia compared with LCT, but to a lesser extent than MCT.
The protective effects of D-glucaro 1,4-lactone (1,4-GL) against oxidative/nitrative protein damage (determined by parameters such as levels of protein carbonyl groups and nitrotyrosine residues) to human plasma treated with peroxynitrite (ONOO-) or hydroperoxide (H2O2) were studied in vitro. We also investigated the effects of 1,4-GL on the level of total free thiol groups and low-molecular-weight thiols (glutathione and homocysteine) in plasma treated with ONOO- (0.1 mM).
Levels of carbonyl groups and nitrotyrosine residues in human plasma proteins were measured by ELISA and a competition ELISA, respectively. High-performance liquid chromatography (HPLC) was used to analyze free thiols from plasma.
Exposure of plasma to ONOO- (0.1 mM) resulted in an increase of the level of carbonyl groups and nitrotyrosine residues in plasma proteins and in a distinct decrease in total thiols and low-molecular-weight thiols (glutathione and homocysteine) measured by high-performance liquid chromatography. In the presence of 1,4-GL (0.4-6.4 mM), a distinct decrease in carbonyl group formation and tyrosine nitration in plasma proteins and changes in plasma thiols caused by 0.1 mM of peroxynitrite were observed. Moreover, 1,4-GL inhibited plasma protein oxidation induced by H2O2 (2 mM).
The obtained results indicate that in vitro 1,4-GL has inhibitory effects on ONOO-- or hydroperoxide-mediated oxidative stress in human plasma and changes plasma redox thiol status. The mechanism of the antioxidative action of 1,4-GL present in plasma is not known yet.
Anorexia is a major clinical problem in large number of patients with advanced cancer disease. Serotonergic mechanisms are assumed to play a role in the process of feeding behavior during normal and pathologic circumstances, which may also involve cancer anorexia according to previous experimental and clinical studies.
In the present study, we evaluated the effect of the tricyclic antidepressants desipramine (7.5 mg x kg(-1) x d(-1), intraperitoneal) and imipramine (2 to 5 mg. kg(-1) x d(-1), intraperitoneal) the serotonin synthesis inhibitor para-chlorophenylalanine (300 mg x kg(-1) x d(-1), intraperitoneal), the serotonin receptor 5-HT(2C) antagonist cyproheptadine (5 mg x kg(-1) x d(-1), intraperitoneal) and the selective serotonin reuptake inhibitor citalopram (20 mg x kg(-1) x d(-1), intraperitoneal) on anorexia in MCG-101 tumor-bearing mice, a model with significant anorexia and cachexia sensitive to cyclooxygenase inhibition. Also, MCG 101-bearing mice develop well-recognized alterations in brain tryptophan/serotonin metabolism as increased Trp, 5-HPT, and 5-HIAA during tumor progression.
Daily provision of desipramine, imipramine, para-chloropheylalanine, cyproheptadine, and citalopram at doses that cause behavioral and metabolic alterations in normal mice did not alter food intake or body weight in tumor-bearing and healthy control mice. Also, the treatments did not decrease elevated plasma concentrations of interleukin-6 and prostaglandin E(2) in the tumor-bearing mice.
Thus, our results do not support previous observations that serotonin metabolism itself is a major factor behind anorexia in tumor-bearing animals in general. Rather, other mechanisms, such as eicosanoid and nitric oxide-dependent pathways, seem to be more important for induction of anorexia along tumor progression in the present model.
An increased glucose requirement by many solid tumors produces an increased metabolic demand on the liver, resulting in an increased energy expenditure. In addition, several cytokines and tumor catabolic products have been suggested as being responsible for the depletion of adipose tissue and skeletal-muscle mass in cachexia. A sulphated glycoprotein of molecular mass 24 kDa, produced by cachexia-inducing tumors and present in the urine of cancer patients actively losing weight, has been shown to be capable of inducing direct muscle catabolism in vitro and a state of cachexia in vivo, with specific loss of the non-fat carcass mass. In vitro studies have shown the bioactivity of this proteolysis-inducing factor to be attenuated by the polyunsaturated fatty acid, eicosapentaenoic acid. Preliminary clinical studies have shown that eicosapentaenoic acid stabilizes body weight and protein and fat reserves in patients with pancreatic carcinoma. Further trials are required to confirm the efficacy of eicosapentaenoic acid and to determine the anticachectic activity in other types of cancer.
Insulin resistance in diabetes mellitus type 2 (DM2) can result from membrane lipid alterations. Blacks are at a higher risk of developing DM2; therefore, we investigated whether membrane lipid differences exist between blacks and whites and if differences contribute to impaired insulin binding in diabetes.
Subjects were recruited from four groups: white control (n = 10), black control (n = 10), white diabetic (n = 5), and black diabetic (n = 10). Diabetic subjects who had DM2 with insulin resistance on insulin monotherapy were matched by age and sex. The following determinations were made: fasting serum glucose, fasting serum insulin, plasma lipid profile, red blood cell (RBC) membrane lipids and cholesterol, and RBC insulin binding.
The membrane lipid analysis showed racial differences in phosphatidyl ethanolamine (PE) and phosphatidyl choline (PC). The plasma membrane of whites showed higher PE and lower PC levels than that in blacks. The RBC rheologic (PE/phosphatidyl serine) properties (deformability) were lower in diabetics and black subjects. The saturated nature of RBC ([sphingomyelin + PC)/(PE + phosphatidyl serine]) was the lowest in white control subjects (P < 0.056).
The combination of increased saturated/polyunsaturated fatty acids, increased saturated nature, and increased cholesterol/phospholipid can contribute to decreased membrane fluidity, resulting in insulin resistance. Also, decreased RBC deformability can make oxygen delivery through the capillaries difficult, create tissue hypoxia, and contribute to some of the known complications of diabetes. Membrane lipid alteration may be one of the reasons for a higher incidence of diabetes among blacks.
We investigated the effect of conjugated linoleic acid (CLA) on energy metabolism in Otsuka Long-Evans Tokushima Fatty (OLETF) rats.
In experiment 1, male OLETF rats were fed either control diet, 10% safflower oil or CLA diet, 9% safflower oil plus 1% CLA for 4 wk. In experiment 2, male OLETF rats were fed either 9c,11t-CLA diet, 9% safflower oil plus 1% 9c,11t-CLA-rich oil or 10t,12c-CLA diet, 9% safflower oil plus 1% 10t,12c-CLA-rich oil for 10 d.
In experiment 1, after 4 wk of feeding, serum and hepatic triacylglycerol concentrations in the CLA group were decreased significantly as compared with the control group. The CLA diet increased oxygen consumption and energy expenditure as compared with the control diet in OLETF rats. In experiment 2, a significant reduction of serum and hepatic triacylglycerol concentrations was seen in the 10t,12c-CLA group as opposed to the 9c,11t-CLA group. Oxygen consumption and energy expenditure were significantly higher in the 10t,12c-CLA group than in the 9c,11t-CLA group.
These results demonstrated that the hypolipidemic effect and the enhancement of energy metabolism by CLA can be attributed to the effect of the 10t,12c-CLA isomer.
To investigate whether the preoperative nutritional state influences the postoperative inflammatory reaction and immunity, we grouped patients whose postoperative nutritional support was performed by total parenteral nutrition into the good nutritional state group (group I) and the latent protein-calorie malnutrition suggested group (group II) based on the preoperative rapid turnover protein (RTP). Nutritional markers markedly decreased after surgery and recovered almost to preoperative levels on postoperative day (POD-) 7 in groups I and II. Nutritional markers on POD-7 in group II were significantly lower than those in group I (RTP, P < 0.001; albumin, P < 0.05). After surgery, levels of interleukin-6 (IL-6), C-reactive protein (CRP), and polymorphonuclear (PMN-) elastase were higher in group II than in group I (P < 0.01). In groups I and II, IL-6 and interleukin-8 (IL-8) rose before the remarkable elevation of CRP and PMN-elastase. In group I, all the nutritional markers showed a negative correlation with CRP and PMN-elastase. Further, a positive correlation was observed between IL-6 and CRP and between IL-8 and PMN-elastase. In conclusion, evaluation of the preoperative nutritional state appears to be very important for the prediction of postoperative complication.
Malnutrition has been associated with immunosuppression, reduced host defenses, and increased incidence of infections and mortality. Improvement of nutritional status through various nutritional support regimens may restore immunocompetence and consequently reduce the rate and severity of infections in hospitalized patients. However, several investigators, exploring the effect of total parenteral nutrition (TPN) on the immune system, have suggested that TPN may adversely affect immune function. During the past 20 yr special interest was given to the possible immunosuppressive effect of parenteral fat emulsions and conflicting reports have been published. This review focuses on the consequences of TPN on immune response and investigates whether there might be a link between the nutrients, the immune system, and possibly the central nervous system, which also seems to affect immune response.
Cancer cachexia is associated with impaired nutritional status and systemic inflammation. The goal of this study was to evaluate the nutritional status and resting energy expenditure (REE) changes in patients with newly detected esophageal cancer, and the influence of weight loss on REE.
Fifty-six patients and 30 healthy controls were prospectively enrolled, and patients were further divided into weight-stable (WS) and weight-loss (WL) subgroups. Body composition, measured REE (mREE), and the ratio of mREE to predicted REE (pREE) by Harris-Benedict formula were assessed. Blood levels of hemoglobin, albumin, prealbumin, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-6 were measured in patients.
Cancer patients had lower body mass index (BMI) and percentage of fat mass, but higher mREE and percentage of mREE/pREE compared with healthy controls (P < 0.05). WS (n = 32) and WL patients (n = 24) had similar BMI and body composition indices, but the latter had obviously higher mREE, mREE per kilogram body weight (mREE/BW), percentage of mREE/pREE, hs-CRP and IL-6 levels, and lower albumin and prealbumin levels. Percentage of weight loss was positively correlated with REE/BW, hs-CRP, and IL-6 level (r = 0.238, P = 0.044; r = 0.446, P = 0.01; r = 0.196, P = 0.047, respectively).
Impaired nutrition status, elevated energy expenditure, and higher inflammation status tend to be apparent in weight-losing patients with newly diagnosed esophageal cancer, which suggested that early recognition of body weight change and routine nutritional risk screening followed by adequate nutrition intervention should be applied in these patients.
Weight loss and muscle wasting adversely affect morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). Maintenance systemic glucocorticosteroids, prescribed in a substantial number of patients, further contribute to muscle weakness. We investigated the efficacy of oral nutritional supplementation therapy in depleted patients with COPD.
The therapy consisted of daily two to three oral liquid nutritional supplements (mean +/- standard deviation: 2812 +/- 523 kJ/24 h) incorporated into an 8-wk inpatient pulmonary rehabilitation program in 64 (49 men) depleted patients with COPD. Endpoints were body weight, fat-free mass by bioelectrical impedance analysis, respiratory and peripheral muscle function (maximal inspiratory mouth pressure and handgrip strength, respectively), exercise performance (incremental bicycle ergometry), and disease-specific health status by St. George's Respiratory Questionnaire. Forty-eight percent of the patients were treated with low-dose oral glucocorticosteroids as maintenance medication (dose equivalent to 7.6 +/- 2.5 mg of methylprednisolone per day).
Increases in body weight (2.1 +/- 2.1 kg, P < 0.001) and fat-free mass (1.1 +/- 2.0 kg, P < 0.001) were seen. Further, maximal inspiratory mouth pressure (4 +/- 10 cm of H(2)O, P = 0.001), handgrip strength (1.2 +/- 3.1 kg, P = 0.004), and peak workload (7 +/- 11 W, P = 0.001) significantly improved. Clinically significant improvements in the items symptoms (9 +/- 16 points, P < 0.001) and impact (4 +/- 15 points, P = 0.043) of St. George's Respiratory Questionnaire were achieved. Oral glucocorticosteroid treatment significantly impaired the response to nutritional supplementation therapy with respect to maximal inspiratory mouth pressure, peak workload, and St. George's Respiratory Questionnaire symptom score.
Nutritional supplementation therapy implemented in a pulmonary rehabilitation program was effective in depleted patients with COPD. However, oral glucocorticosteroid treatment attenuated the anabolic response to nutritional supplementation.
The prognosis in ovarian cancer patients remains poor, and there is a need to identify patients who are less likely to respond to treatment. In a prospective study of patients with ovarian carcinoma treated by a standard protocol, variables such as age, tumor type, International Federation of Gynecology and Obstetrics stage, histologic grade, results from flow cytometry, receptors for estrogen (ER) and progesterone (PR), and serum CA 125 were correlated to relapse and survival. Univariate analysis revealed that stage, histologic grade, DNA ploidy, ER, PR, and CA 125 were of significant association to survival, but only stage, DNA ploidy, PR, and CA 125 were found to be of significant value to relapse. Multivariate analysis identified DNA ploidy as an independent prognostic variable for both relapse and survival.
The aim of this study was to examine food patterns of Australian children ages 9 to 13 y in relation to ω-3 long-chain polyunsaturated fatty acid (ω-3 LCPUFA) intake.
Secondary analysis was conducted on nationally representative food data of 1110 Australian children ages 9 to 13 y (525 boys and 585 girls) that was obtained using two 24-h recalls. Principle component factor analysis was used to identify food patterns. Discriminant function analysis was used to identify the relationship between the food patterns and total ω-3 LCPUFA intake.
Four major food patterns emerged for each sex. For boys these were labeled: "snack foods," "soft drinks," "vegetables," and "pork and meat chops, steak, and mince." For girls they were labeled: "vegetables," "take-away," "tea, coffee, iced coffee drinks" and "canned meals and soup." Fish consumption bought from take-away outlets was more frequently consumed in the "soft drink" (r = 0.577) and take-away (r = 0.485) food pattern in boys and girls, respectively. In contrast, fish prepared at home was more often consumed in "vegetables" in both boys (r = 0.018) and girls (r = 0.106), as well as in the "pork and meat chops, steak and mince" food pattern in boys (r = 0.060). There was a trend that in boys, the "vegetables" group discriminated children who consumed ω-3 LCPUFA levels similar to adequate intakes (AI) (P = 0.067), whereas in girls, the take-away food pattern discriminated for being a fish consumer (P = 0.060).
Dietary patterns associated with a high consumption of vegetables and "take-aways" food that include meat and fish are likely to positively influence dietary ω-3 LCPUFA intake in Australian children.
When naturally (13)C-enriched carbohydrate is used to label hepatic glycogen, (13)C-liver glycogen oxidation can be monitored subsequently by measuring the (13)C enrichment of breath CO(2) during a sedentary fast. In our previous breath test studies, we used a 1-d labeling protocol to enrich liver glycogen. Others found that after 3 d of labeling the liver glycogen (13)C enrichment is identical to the dietary carbohydrate (13)C enrichment.
We compared a diet protocol in which naturally (13)C-enriched carbohydrate was given for 3 d before the breath test with our previously applied 1-d labeling design. The (13)CO(2) breath test was combined with indirect calorimetry. The results were compared with those from our previous studies. In addition, we compared liver glycogen oxidation rates with those from our present technique and different techniques as used in other published studies.
Six healthy volunteers were included in this study. The (13)C enrichment of breath CO(2) at plateau excretion level did not differ after 1 or 3 d on a labeling diet. However, the end of plateau time tended to be later after the 3-d diet, 14.3 h versus 12.5 to 13.5 h postprandially in the 1-d labeling studies. Also, the return to baseline time was later in the 3-d study, at 25.8 h versus 19.0 to 23.2 h postprandially after 1 d of labeling. The liver glycogen oxidation rate was similar in both techniques until 17 h postprandially. After this time the 3-d labeling protocol showed a higher level of liver glycogen oxidation.
The results indicated that the labeling of liver glycogen is slightly less complete after 1 d on a (13)C-enriched diet as compared with 3-d labeling. Our (13)C breath test results compared rather well with studies from the literature using the (13)C-NMR technique, the D(2)O technique, or the (13)CO(2) breath method to measure liver glycogen oxidation.
The aim of this study was to estimate the concentration of cholecalciferol and 13-cis-retinoic acid (RA) in the plasma and pleural fluid of patients with tuberculosis (TB) against controls.
Plasma levels of cholecalciferol and 13-cis-RA were measured in 22 patients with TB and healthy controls and their pleural fluids levels were measured in 6 TB patients and diseased controls by established high-performance liquid chromatography-based procedure.
Cholecalciferol levels in plasma and pleural fluid of patients with TB and healthy controls were 67.45 (10.71) nmol/L and 21.40 (8.58) nmol/L compared with 117.43 (18.40) nmol/L (P < 0.001) and 94.73 (33.34) nmol/L (P = 0.0049), respectively. 13-cis-RA level in the plasma of patients with TB and healthy controls were 1.51 (0.72) nmol/L and 6.67 (0.81) nmol/L (P < 0.001), respectively. 13-cis-RA was not detectable in pleural fluid. The levels of both the agents were lower in patients with TB than in controls.
It was observed that in patients with TB there is a combined deficiency of cholecalciferol and 13-cis-RA compared with healthy volunteers. Because cholecalciferol and 13-cis-RA are in equilibrium with active ingredients of vitamins A and D, we feel that there is a combined deficiency of these vitamins in patients with TB. There is an evidence that concomitant vitamin A and D supplementation can kill intracellular Mycobacterium tuberculosis in vitro. Therefore, the observations made in this study can pave the path for a trial of combined supplementation of available formulations of vitamin A and D (cholecalciferol and 13-cis-RA) for novel anti-tubercular drug therapy. Because such an approach is host-based it has potential to treat even multidrug-resistant and extensively drug-resistant forms of TB.
The main objective was to evaluate a patient's immunologic and nutritional status as a prognostic indicator of morbidity and mortality in patients with gastric cancer. A prospective clinical study carried out at the National Cancer Institute in Bogotá, Colombia. Our study group consisted of 40 patients with a diagnosis of gastric adenocarcinoma that was treated surgically. Blood samples were taken before and 5 d after surgery; mononuclear cell typing was done by flow cytometry allowing a bicolor analysis. Nutritional evaluation was obtained through measurement of albumin levels, average weight loss, and nutritional risk index (NRI). Half of the malignancies were localized to the middle and lower third of the stomach: stage I, 17.55%; stage II, 10%; stage III, 55%; and stage IV, 17.5%. Twenty subtotal gastrectomies, 11 total gastrectomies, 7 gastrojejunostomies, and 2 esophagogastrectomies with D1 and D2-D3 lymph node resection were performed. A postoperative morbidity of 22.5% and a mortality of 7.5% were observed. A preoperative cellular immunosuppression was identified, with a helper lymphocyte (CD4) to suppressor/cytotoxic lymphocyte (CD8) ratio of 1.38 normal value (NV > 1.5), which increased according to the stage of the disease. Patients who died presented with a significantly greater preoperative cellular immunosuppression than those who survived (P = 0.05). Postoperative mortality correlated significantly with hypoalbuminemia (P = 0.008). In those who died, weight loss was greater than in those who survived (P = 0.06). Patients with severe malnutrition had greater postoperative mortality according to the NRI. Severe preoperative cellular immunosuppression (CD4/CD8 < 1), hypoalbuminemia, weight loss, and severe NRI have a positive predictive value for mortality in patients with gastric cancer.
This study assessed the noninvasive 13C-acetate breath test (13C-ABT) as a reliable and reproducible method to evaluate gastric emptying in infants
Gastric emptying was measured simultaneously by scintigraphy and 13C-ABT in 11 infants with clinical symptoms of gastroesophageal reflux to validate the method compared with the gold standard. Gastric emptying was also measured with 13C-ABT in a separate group of 14 healthy infants on 2 consecutive days to evaluate reproducibility of the method. Half-emptying times obtained with scintigraphy and 13C-ABT were correlated with Pearson's analysis. The variability of the half-emptying times obtained on 2 consecutive days was analyzed with paired t test and by the coefficient of variation as proposed by Bland and Altman.
The mean emptying times obtained with scintigraphy and 13C-ABT were not different (89 +/- 27 min and 70 +/- 39 min, respectively, P = 0.22). Both methods correlated significantly (r = 0.75, P < 0.05). Half-emptying times measured on 2 consecutive days with 13C-ABT were 69 +/- 31 min and 68 +/- 30 min, respectively (mean difference = 1.4 +/- 12.4 min, P = 0.67). Intraindividual coefficient of variation was 6.3%.
This study supports the 13C-ABT method as a useful tool to evaluate gastric emptying of liquids in healthy infants and in infants with gastroesophageal reflux in the field of research and in clinical evaluations.
There is still some concern about the safety of early enteral nutrition (EN) to patients with recent anastomoses. A pilot trial was carried out on a prospective basis to evaluate the tolerance and clinical outcome of 56 patients who received early EN following gastrointestinal (GI) surgery. A continuous infusion of an elemental, peptide-based diet was administered using a nasointestinal feeding tube placed beyond the pylorus by the operating surgeon. Tube feeds were started at 6.07 +/- 4.99 h after surgery and advanced as tolerated to a rate of 60 mL/h on the third postoperative day. Patients received the diet either proximal or distal (in the case of gastrectomies) to their recent anastomosis. Forty-six patients met the inclusion criteria and were included in the analysis. EN was well tolerated with a low incidence of side effects (19.5%), nausea and vomiting being the most frequent. Oral feeding was started 2.89 +/- 1.28 d after surgery. There was one case of small bowel suture leakage, but no relationship to the tube feeding was established. Early EN appears to be a useful and safe therapeutic alternative for the postoperative management of patients undergoing GI surgery. It may contribute to faster recovery of bowel function and lead to a shorter hospital stay. Careful selection of patients is necessary in order to obtain the greatest benefit of early enteral feeding in this patient population.
A diet containing naturally 13C-enriched carbohydrate combined with a 13CO2 breath-test analysis can be used to monitor liver glycogen oxidation in persons used to a diet low in 13C, e.g., the Western European diet. In this study, we evaluated this test principle further by changing the way we label the glycogen pool. The 13C enrichment of exhaled CO2 was studied in two groups, one in Europe and one in Africa. The European group (n = 12) was accustomed to a diet low in 13C, and they went on a 13C-enriched study diet to identify liver glycogen. The African group (n = 6) was accustomed to a diet naturally high in 13C, and they went on a diet low in 13C. The basal 13C abundance in exhaled CO2 was higher in the African group (1.0879 At%; atmospheric 1.1 atom percent) than in the European group (1.0821 At%). During the study period, the parameters for liver glycogen oxidation--the 13CO2 enrichment plateau, the plateau duration, and the return to baseline time--did not differ between groups. The abundance of 13CO2 in exhaled CO2 over time in the two groups was similar but inverse. This study confirms the use of a 13CO2 breath test to monitor liver glycogen oxidation and demonstrates how to use such a test in persons accustomed to a diet high in 13C.
The non-invasive (13)C-octanoic acid breath test ((13)C-OABT) has recently been used to monitor gastric emptying. We evaluated (13)C-OABT as a method for assessing gastric emptying in relation to the amount of milk ingested in preterm neonates during their first days of life.
The (13)C-OABT was performed in 16 stable preterm neonates born between weeks 31 and 37 of gestation (mean +/- standard deviation: 34.0 +/- 1.5 wk). Birth weight was 1400 to 2680 g (2076 +/- 350 g); four newborns were small for gestational age. The newborns underwent (13)C-OABT three times according to the amount of (13)C-primed breast milk being fed to them (<7 mL/kg, 7-13 mL/kg, and 10-19 mL/kg per dose). (13)C-primed breast milk (the test meal) was prepared by adding (13)C-octanoic acid to pasteurized breast milk to achieve a concentration of 1 microL of (13)C-octanoic acid/mL of milk. Exhaled air samples were taken through an original nasal mask. Amounts of (13)C and (12)C in the exhaled air samples were measured by mass spectrometry. Results were expressed as delta over baseline and related to the international standard of Pee Dee Belemnite Limestone. To assess the half-life of elimination (t(1/2)E), we modeled the process of elimination with the incomplete gamma-function, which has a convenient form for the empiric plotting of breath test data. We estimated the parameters of the function, f(x) = A x(b) e(-cx), by using the moment method. The curves were determined by the t(1/2)E of (13)CO(2) and characterized by the shape of the elimination curve. The half-time of gastric emptying (t(1/2)GE) was calculated as t(1/2)E reduced by the mean metabolic half-time of octanoic acid.
Forty-eight (13)C-OABT results from 16 premature newborns were analyzed. The mean and median of t(1/2)GE calculated from all three tests were 50.3 (+/-29.9) and 43.7 min, respectively. The t(1/2)GE did not change significantly (P = 0.6811) with the administered dose of (13)C-primed breast milk in the stomach. The coefficient of variation among the studied infants was 4.0% to 33.6% (mean, 11.5%). In 12 infants, the characteristic type of elimination curve was the same for all three tests.
In the first hours of gastric feeding, neither the age of the neonate nor the amount of administered (13)C-primed breast milk had any effect on t(1/2)GE. The gastric emptying rate and the evacuation curve shape for individual neonates were similar and independent of milk amount.
In a series of studies on histaminergic functions in the hypothalamus, probes to manipulate activities of histaminergic neuron systems were applied to assess its physiologic and pathophysiologic implications using non-obese normal and Zucker obese rats, an animal model of genetic obesity. Food intake is suppressed by either activation of H1-receptor or inhibition of the H3-receptor in the ventromedial hypothalamus (VMH) or the paraventricular nucleus, each of which is involved in satiety regulation. Histamine neurons in the mesencephalic trigeminal sensory nucleus modulate masticatory functions, particularly eating speed through the mesencephalic trigeminal motor nucleus, and activation of the histamine neurons in the VMH suppress intake volume of feeding at meals. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, activates neuronal histamine in the hypothalamus. Such low energy intake in turn accelerates glycogenolysis in the astrocytes to prevent the brain from energy deficit. Thus, both mastication and low energy intake act as afferent signals for activation of histaminergic nerve systems in the hypothalamus and result in enhancement of satiation. There is a rationale for efficacy of a very-low-calorie conventional Japanese diet as a therapeutic tool for weight reduction. Feeding circadian rhythm is modulated by manipulation of hypothalamic histamine neurons. Hypothalamic histamine neurons are activated by an increase in ambient temperature. Hypothalamic neuronal histamine controls adaptive behavior including a decrease in food intake and ambulation, and an increase in water intake to maintain body temperature to be normally constant. In addition, interleukin-1 beta, an endogenous pyrogen, enhanced turnover of neuronal histamine through prostaglandin E2 in the brain. Taken together, the histamine neuron system in the hypothalamus is essential for maintenance of thermoregulation through the direct and indirect control of adaptive behavior. Behavioral and metabolic abnormalities of obese Zucker rats including hyperphagia, disruption of feeding circadian rhythm, hyperlipidemia, hyperinsulinemia, and disturbance of thermoregulation are essentially derived from a defect in hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the hypothalamus in normal rats mimic those of obese Zuckers. Grafting the lean Zucker fetal hypothalamus into the obese Zucker pups attenuates those abnormalities. These findings indicate that histamine nerve systems in the brain play a crucial role in maintaining homeostatic energy balance.
Obesity has now developed into a world-wide epidemic and is associated with large economic costs and prevalent diseases, particularly with central body fat distribution. Insulin resistance almost invariably occurs, and might be a major trigger for disease-generating mechanisms either directly or via generation of other disease precursors ("risk factors"). The hypothalamo-pituitary-adrenal (HPA) axis seems to be hypersensitive in abdominal obesity, a statement supported by increased responses to challenges from the adrenals to central regulatory centers. Furthermore, the feedback control by central glucocorticoid receptors, probably a secondary, functional consequence of an elevated HPA axis activity, because the receptor gene appears normal. Secretion of sex steroid and growth hormones is diminished, which might be consequence of elevated HPA axis activity. Hyperandrogenicity in women is probably of adrenal origin and another consequence of the sensitivity of the HPA axis. The endocrine abnormalities thus are periodically elevated cortisol and androgen (women) concentrations, as well as low secretions of gender-specific steroid and growth hormones. Since elevated cortisol, and low sex-steroid and growth hormone secretions, probably direct storage fat to visceral depots, the multiple endocrine abnormalities probably cause enlargement of these depots. Furthermore, these hormonal abnormalities most likely at least contribute to the creation of insulin resistance with additional effects of elevated fatty acids from central fat depots, which are sensitive to lipid mobilization agents. This chain of events indicates the central role of the hypersensitive HPA axis. Known causes of sensitization of this axis have been identified in subjects with abdominal obesity, including depression, anxiety, alcohol, and smoking. A common cause of HPA axis activation is perceived stress, with a depressive, defeatist, or "helplessness" reaction. In subjects with abdominal preponderance of body fat stores a number of psychosocial and socioeconomics handicaps have been identified, hypothetically predisposing to such reactions. In a primate model (monkeys), mild psychosocial stress is followed by identical psychological, endocrine, anthropometric, and metabolic abnormalities as in humans with abdominal preponderance of body fat stores, including early signs of diabetes and cardiovascular disease. These findings strongly support the interpretation that a stress reaction activating the HPA axis is involved also in the human syndrome. Interventions with normalization of the endocrine perturbations are followed by clear improvements of the multiple abnormalities in both clinical, experimental, cellular and molecular studies, suggesting that the pathogenesis of abdominal preponderance of body fat and its endocrine, anthropometric and metabolic abnormalities are indeed consequences of the endocrine abnormalities identified.
An abundant amino acid in the human body, glutamine (Gln) has many important metabolic roles that may protect or promote tissue integrity and enhance the immune system. Low plasma and tissue levels of Gln in the critically ill suggest that demand may exceed endogenous supply. A relative deficiency of Gln in such patients could compromise recovery and result in prolonged illness and an increase in late mortality. This study examines this hypothesis. Using a prospective, block-randomized, double-blind treatment study design, we tested whether a Gln-containing parenteral nutrition (PN) compared with an isonitrogenous, isoenergetic control feed would influence outcome, with the endpoints of morbidity, mortality, and cost at 6 mo postintervention. In one general intensive care unit (ICU), to ensure consistency of management policies, 84 critically ill adult patients, with Acute Physiological and Chronic Health Evaluation II score > 10, requiring nutritional support received PN only if enteral nutrition was contraindicated or unsuccessful. Survival at 6 mo was significantly improved in those receiving Gln PN (24/42 versus 14/42; P = 0.049). Significantly more deaths occurred in patients requiring control PN for > 10 d (P = 0.03). The excess control deaths occurred later and those patients had had a significantly longer postintervention stay (P = 0.012) and use of ICU. In the Gln recipients, the total ICU and hospital cost per survivor was reduced by 50%. In critically ill ICU patients unable to receive enteral nutrition, a Gln-containing PN solution improves survival at 6 mo and reduces the hospital costs per survivor.
The association of birthweight with length at 12 mo and with height at different ages was assessed in a sample of 260 healthy adolescents (130 boys and 130 girls). The longitudinal study included measures on body weight and height at 4, 6, 12, and 14 yr of age. Birthweight is highly correlated with stature at 14 years, particularly in male adolescents. Longitudinal principal components analysis (LPCA) showed that it is also correlated with the growing process. There is also strong evidence that birthweight can be a good predictor of the onset of the pubertal maturation process.
Cardiovascular diseases and cancers constitute major public health problems in all industrialized countries, where they are the main causes of premature mortality. There is a large body of evidence suggesting that free-radical production can directly or indirectly play a major role in cellular processes implicated in atherosclerosis and carcinogenesis. Here we present mechanistic data and results of epidemiologic studies on the relationship between antioxidant vitamin intake or biochemical status and the risk of cancer and cardiovascular diseases. Most epidemiologic data obtained on this topic were based on an observational approach, i.e., ecologic, case-control, or prospective studies. All these studies indicate that a high dietary intake or high blood concentrations of antioxidant vitamins are associated with a reduced risk of cardiovascular diseases and cancer at several common sites. Although the results of these studies are convergent, they merely suggest a relationship at the population and individual level but do not affirm a causality link. Only intervention studies (randomized trials), by specifically changing antioxidant vitamin intake, can provide conclusive answers. The apparent discrepancies between the results of four recently published trials may be explained by the type of population (general or high-risk subjects), the differing doses of supplementation (nutritional levels or higher), the number of antioxidants tested (one, two, or more), and the type of administration (alone or in balanced association). It thus appears that a low risk of pathologies may be related to multiple nutrients consumed at nutritional doses and in combination. Optimal effects may be expected with a combination of nutrients at levels similar to those found in a healthy diet. A single antioxidant vitamin given at high doses in subjects with high risk of pathologies (smokers, asbestos-exposed subjects) may not have substantial benefits and could even have negative consequences.
The relevance of the association of the body mass index (BMI) at 1,4,6, and 12 years of age with the growing process and its capacity for predicting height at age 14 was investigated in a sample of 354 adolescents (182 boys and 172 girls). Regression analysis showed that body bulk at various ages, as expressed by the BMI is closely related with the height attained at age 14, and longitudinal principal components analysis suggested that it is also associated with the whole growing process. The way in which BMI affects height could be related with the stage of sexual development, which seems to play an intermediate role in the pathway linking body bulk and height.
Glutamine has traditionally been thought of as a nonessential amino acid, but laboratory and clinical data suggests that it may be essential during certain inflammatory conditions, such as infection and injury. Glutamine is a necessary nutrient for cell proliferation, serves as a specific fuel for inflammatory cells and enterocytes, and, when present in appropriate concentrations, enhances cell function. During inflammatory states, glutamine consumption may outstrip endogenous production and a relative glutamine deficiency state may exist. Animal and clinical studies suggest that improved outcome may be possible by providing the appropriate dose of this nutrient by the appropriate route to achieve adequate tissue concentrations. Such an approach prevents patients from being exposed to some of the inadequacies of present day conventional nutrition. The overall benefit of providing an appropriate glutamine-supplemented diet to all metabolically compromised patients arises from the multiple anabolic and host protective effects of this amino acid, of which immunomodulation is only one important facet of glutamine's essential nature.
Nutritional support is important in critically ill patients, with variable energy and nitrogen requirements (e.g., sepsis, trauma, postsurgical state) in this population. This study investigates how age, severity of illness, and mechanical ventilation are related to resting energy expenditure (REE) and nitrogen balance. Nineteen critically ill children (mean age, 8 +/- 6 [SD] y and range 0.4-17.0 y) receiving total parenteral nutrition (TPN) were enrolled. We used indirect calorimetry to measure REE. Expected energy requirements (EER) were obtained from Talbot tables. Pediatric Risk of Mortality (PRISM) and Therapeutic Intervention Scoring System (TISS) score were calculated. Total urinary nitrogen was measured using the Kjeldahl method. PRISM and TISS scores were 9 +/- 5 and 31 +/- 6 points, respectively. REE was 62 +/- 25 kcal.kg-1.d-1, EER was 42 +/- 11 kcal.kg-1. d-1, and caloric intake was 49 +/- 22 kcal.kg-1.d-1. Nitrogen intake was 279 +/- 125 mg.kg-1.d-1, total urinary nitrogen was 324 +/- 133 mg.kg-1.d-1, and nitrogen balance was -120 +/- 153 mg.kg-1.d-1. The protein requirement in this population was approximately 2.8 g.kg-1.d-1. These critically ill children were hypermetabolic, with REE 48% higher (20 kcal.kg-1.d-1) than expected. Nitrogen balance significantly correlated with caloric and protein intake, urinary nitrogen, and age, but not with severity of illness scores or ventilatory parameters.
A study of the metabolism of ascorbic-1-14C acid in experimental human scurvy was conducted with the following results: 1) Labeling the body ascorbic acid pool during the depletion phase resulted in no detectable urinary excretion of 14C labeled reduced ascorbic acid or dehydroascorbic acid. 2) Urinary excretion of 14C by all subjects occurred as a first order process during the depletion phase. The urinary 14C excretion curves of the four subjects did not differ from the average man by more than ± 3%, despite marked differences in body weight and age. 3) First symptoms of mild scurvy appeared in the subjects when their body ascorbic acid pool had been reduced to approximately 300 mg. 4) Once the body pool of ascorbic acid was repleted to a level of 1.5 g, urinary loss of reduced ascorbic acid occurred. 5) The rate of repletion of ascorbic acid was found to be a zero-order process and proportional to the level of daily ascorbic acid intake. 6) When the subjects were fed a high intake of ascorbic acid, only a limited quantity of the ingested vitamin was equilibrated with the 14C labeled ascorbate pool. 7) All of the radioactivity excreted during the depletion phase was in the form of stable organic material that did not behave as ascorbic acid. This organic material was separated into four unknown compounds. 8) The daily intake of 6.5 mg/day of ascorbic acid was sufficient to alleviate and cure the clinical signs of scurvy in one man.
It is fascinating to reflect that tea, the world's most widely consumed beverage next to water, began in Chinese antiquity not as a beverage but as a medicine. Several millennia later, modern scientific research is confirming that such ancient intuition has relevance to contemporary health concerns including cancer, heart disease, and antibiotic-resistant bacteria. The timeliness of this message as the 20th century concludes could not be better. The importance of a balanced diet has been recognized and studied throughout this century. The concept that we are what we eat has become a part of popular culture. If tea's health message, which future scientific research will continue to articulate, is creatively presented and embraces the romantic image that tea affords the industry, there is every reason to expect a rebirth and reinvigoration of this ancient beverage as a new millennium commences.
Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in ∼25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the β-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration.Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulinstimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one. However, even if insulin resistance and hyperinsulinemia are not involved in the etiology of hypertension, it is likely that the increased risk of coronary artery disease (CAD) in patients with hypertension and the fact that this risk if not reduced with antihypertensive treatment are due to the clustering of risk factors for CAD, in addition to high blood pressure, associated with insulin resistance. These include hyperinsulinemia, IGT, increased plasma triglyceride concentration, and decreased high-density lipoprotein cholesterol concentration, all of which are associated with increased risk for CAD. It is likely that the same risk factors play a significant role in the genesis of CAD in the population as a whole. Based on these considerations the possibility is raised that resistance to insulin-stimulated glucose uptake and hyperinsulinemia are involved in the etiology and clinical course of three major related diseases— NIDDM, hypertension, and CAD.
It has been proposed that the increase in amino acid flux and derived protein synthesis rates observed in weight-losing cancer patients may contribute to an ongoing negative energy balance. The mediators and tissues responsible for such apparent increased protein synthesis have not been clearly identified. The aim of this study was to examine the relationship between protein synthetic rates in whole-body, skeletal muscle, and circulating cortisol concentrations in healthy subjects (n = 6) and cancer patients with evidence of an inflammatory response (n = 6). Protein synthetic rates were measured with a primed continuous 20-h infusion of [15N]glycine. Skeletal muscle was biopsied at laparotomy. Serum cortisol, resting energy expenditure, plasma proteins, nitrogen metabolites in urine, and skeletal muscle free amino acids were also measured. Derived whole-body and skeletal muscle protein synthetic rates in the cancer group were increased significantly (by 70 and 93%, respectively, p < 0.05). Circulating concentrations of cortisol, fibrinogen, and C-reactive protein were also significantly increased in the cancer group and indicated the presence of an inflammatory response. However, there was no significant increase in resting energy expenditure. Mechanisms by which apparent increases in whole-body and skeletal protein synthesis do not result in an increase in resting energy expenditure are discussed. We conclude that glycine utilization is increased in cancer patients but that rates of protein synthesis derived from [15N]glycine kinetics may not be valid in such patients.
In five male cirrhotic patients (Child A) and in four age- and sex-matched healthy control subjects, whole-body protein turnover was measured using a single oral dose of 15N-glycine as a tracer and urinary ammonia as end product. Subjects were studied in the fasting and feeding state, with different levels of protein and energy intake. The patients were underweight and presented lower plasma transthyretin and retinol-binding protein levels. When compared with controls, the kinetic studies showed patients to be hypometabolic in the fasting (D0) state and with the control diet [D1 = (0.85 g of protein/ 154 kJ) x kg-1.day-1]. However, when corrected by body weight, the kinetic differences between groups disappeared, whereas the N-retention in the feeding state showed better results for the patients due mainly to their efficient breakdown decrease. When fed high-level protein or energy diets [D1 = (0.9 g protein/195 kJ) and D3 = (1.56 g protein/158 kJ) x kg-1.day-1], the patients showed D0 = D1 = D2 < D3 for N-flux and (D0 = D1) < D3 (D2 is intermediary) for protein synthesis. Thus, the present data suggest that the remaining mass of the undernourished mild cirrhotic patients has fairly good protein synthesis activity and also that protein, rather than energy intake, would be the limiting factor for increasing their whole-body protein synthesis.
Drugs to treat obesity can be divided into three groups: those that reduce food intake; those that alter metabolism; and those that increase thermogenesis. Monoamines acting on noradrenergic receptors, serotonin receptors, dopamine receptors, and histamine receptors can reduce food intake. A number of peptides also affect food intake. The noradrenergic drugs phentermine, diethylpropion, mazindol, benzphetamine, and phendimetrazine are approved only for short-term use. Sibutramine, a norepinephrine-serotonin reuptake inhibitor, is approved for long-term use. Orlistat inhibits pancreatic lipase and can block 30% of the triacylglycerol hydrolysis in subjects eating a 30% fat diet. The only thermogenic drug combination that has been tested is ephedrine and caffeine, but this treatment has not been approved by regulatory agencies. In clinical trials other drugs that may modulate peptide-feeding systems are being developed.
We previously reported that higher circulating concentrations of folate are independently associated with a lower likelihood of becoming positive for high-risk human papillomaviruses (HR-HPVs) and of having a persistent HR-HPV infection and a greater likelihood of becoming HR-HPV negative (Cancer Res 2004;64:8788-93). In the present study conducted in the same study population, we tested whether circulating folate concentrations modify the risk of cervical intraepithelial neoplasia (CIN) > or =2 associated with specific types of HR-HPV.
Multiple logistic regression models were used to assess associations (odds ratio with 95% confidence intervals) across HR-HPV, folate, and rigorously reviewed cervical histology of each subject.
HPV-16-positive women with low red blood cell folate were significantly more likely to be diagnosed with CIN > or =2 than were HPV-16-negative women with higher red blood cell folate (odds ratio 9, 95% confidence interval 3.3-24.8).
To our knowledge, this is the first study reporting an independent association of folate with risk of having CIN > or =2 in a population tested extensively for HR-HPV and CIN that also adequately controlled for several other micronutrients and known risk factors for CIN. Our findings suggest that improving the folate status in HR-HPV-infected women may reduce the risk of CIN and thus the risk of cervical cancer. Folate supplementation should be tested as a means of reducing the risk of developing CIN > or =2 in women exposed to HR-HPV, especially HPV-16.
Oral habituation is a relatively long-lasting decrease in oral responsiveness that results from the repeated presentation of a single stimulus. The purpose of this study was to evaluate the degree of habituation to sweet-tasting foods and to determine whether there are differences in the rate of habituation between African Americans and European Americans. These two groups were compared because the prevalence of obesity and obesity-related disorders such as diabetes and hypertension is significantly higher among African Americans than among European Americans. Nine different commercial foods and beverages that differed in sweetness intensity and caloric density served as stimuli. Subjects tasted and rated each food once per minute for a 30-min period on scales related to desire for another taste of the same sample and desire for a different taste. The stimuli and portion size for each of the 30 samples were two candy bars (Ultra Slim-Fast Cocoa Almond Crunch Bar, 1/16 of a bar; Natural Nectar Peanut Butter Granola Bar, 1/16 of a bar), three beverages (Nestea Lemon Flavored Instant Tea with NutraSweet, 5 mL; Welch's Grape Juice, 5 mL; Pink Swimmingo Kool-Aid, 5 mL), two gelatin desserts (Cherry Flavored Jell-O Gelatin, 5 g; Cherry Flavored Jell-O Gelatin with NutraSweet, 5 g), one enteral nutrition drink (Vanilla Ensure Plus, 5 mL), and one pudding (Ultra Slim-Fast Chocolate Pudding, 5 g). Subjects consumed the entire portion of each sample. Habituation occurred for seven of the nine foods as judged by a decrease in the desire for another taste of the same food. The degree of habituation for European Americans and African Americans was similar except for the sweetest food (Cherry Flavored Jell-O Gelatin with NutraSweet), for which African Americans showed no habituation. The degree of habituation in both groups was unrelated to caloric density. Overall, young African Americans had a significantly greater desire for another taste of the same food than did young European Americans for seven of the nine foods, and this desire was strongly correlated with the sweetness intensity for young African Americans but not for young European Americans. Furthermore, young African Americans had a greater desire than young European Americans for a different taste for seven of nine foods. The greater desire for intense sweet tastes may be a factor in the elevated incidence of obesity and diabetes in African Americans. In addition, young African Americans had greater perceived stress in this study than did young European Americans. If African Americans use sweet taste to compensate for feelings of stress, this compensation may also contribute to weight gain.
Malnutrition is an important predictor of morbidity and mortality. In the non-elderly, a subjective global assessment (SGA) has been developed. It has a high inter-rater agreement, correlates with other measures of nutritional status, and predicts subsequent morbidity. The purpose of this study was to determine the validity and reproducibility of the SGA in a group of patients older than 70 y of age. Consecutive patients from four geriatric/rehabilitation units were considered for the study. Each patient underwent independent nutritional assessments by a geriatrician and senior medical resident. At the completion of the assessment, skinfold caliper measurements were obtained and the patient reclassified according to the results, which were then compared with objective measures of nutritional status. Six-month follow-up was obtained on all patients. The agreement between the two clinicians was 0.48 +/- 0.17 (unweighted kappa), which represents moderate agreement and is less than the reported agreement in nonelderly subjects. Skin calipers improved the agreement between clinicians but did not improve the correlation with other nutritional markers or prediction of morbidity and mortality. There was a correlation between a patient's severely malnourished state and mortality. In addition, patients with a body mass index (BMI) of <75% or >150% age/sex standardized norms had an increased mortality. The SGA is a reproducible and valid tool for determining nutritional status in the elderly. The reproducibility is less than in the nonelderly, which may relate to changes in body composition or ability to obtain an accurate nutritional history.
We recently identified an inverse relation between systolic blood pressure (SBP) and serum 16α-hydroxyestrone, a metabolite of 17β-estradiol, in postmenopausal women. Formation of 16α-hydroxyestrone is catalyzed primarily by CYP1A2, a cytochrome P450 enzyme. The objective of this study was to evaluate the relations between known modifiers of CYP1A2 activity and serum 16α-hydroxyestrone in postmenopausal women. We hypothesized that fruits, vegetables, and grains, which contain more soluble fiber (a known inducer of CYP1A2) as a proportion of total fiber, would be more positively associated with serum 16α-hydroxyestrone than legumes, which contain less soluble fiber as a proportion of total fiber.
Serum from a population-based sample of 42 postmenopausal women 55 to 69 y of age living in Cook County, Illinois, was assayed for 16α-hydroxyestrone using mass spectrometry. Ordinal logistic regression was used to evaluate the cross-sectional relation between dietary fiber and serum 16α-hydroxyestrone after adjusting for multiple covariates.
Compared with dietary fiber from legumes, dietary fiber from fruits and vegetables was associated with a greater log odds (B=0.201, P=0.036) of having higher serum concentrations of 16α-hydroxyestrone. The log odds of having higher serum concentrations of 16α-hydroxyestrone was also lower in African-American women (B=-2.300, P=0.030) compared with white women.
These results are consistent with previous studies demonstrating a negative relation between SBP and dietary fruits and vegetables and a positive relation between African-American race and SBP. Further research is needed regarding dietary factors that may influence the serum concentration of 16α-hydroxyestrone.