The nutritional status of 201 hospitalized stroke patients was assessed from anthropometric, haematological and biochemical data in an observational prospective study. On admission, sixty-two (31%) stroke patients had BMI < 20, ninety-nine (49%) had a triceps skinfolds thickness below the 25th centile, twenty-five (12%) had a mid-arm circumference below the 25th centile and thirty-eight (19%) had a serum albumin concentration below 35 g/1. Baseline nutritional status was worse among those who later died or remained in hospital compared with those discharged and most patients who remained in hospital showed marked and significant deterioration in all measures of nutritional status within 4 weeks of hospitalization. After adjusting for age, stroke severity and co-morbidity, low serum albumin concentrations of these patients in hospital were a strong and independent predictor of death following acute stroke (odds ratio 1.13 (95% CI 1.01−1.27) for 1 g/1 lower serum albumin concentration).

Longitudinal studies suggest that women who already have a high BMI are at greater risk of maternal obesity than their lighter counterparts. The aim of the present study was to investigate this possibility by examining the relationship between reproductive history and maternal BMI in a community of 627 women from South Africa with a high prevalence of obesity. Standardized questionnaires were used to obtain detailed sociodemographic and behavioural information, while maternal weight and height were both measured at the time of the interview. Analysis of covariance (ANCOVA) showed that maternal age (r2 0·015, P = 0·001), smoking status (r2 0·012, P = 0·036), and social support (r2 0·011, P = 0·006) were all independently associated with maternal BMI. If overweight women were at increased risk of maternal obesity, then the positive relationship between reproductive history and maternal BMI should be enhanced in this relatively obese community, yet the ANCOVA models showed no independent association between gravidity and maternal BMI after controlling for the effects of confounding factors. Although previous longitudinal studies have found a positive association between prepregnant weight and long-term weight gain, this relationship might arise because overweight women gain more weight over a fixed period of time than normal weight women, and therefore they may appear to be at greater risk of pregnancy-related weight gains. Overweight women are at greater risk of weight gain generally, but there is little unequivocal evidence to suggest that they are at any increased risk of maternal obesity, when compared with women of lower BMI.

Faecal bulk, pH, water content, the concentrations of neutral sterols and bile acids and dietary intakes were measured in twenty-two Indian vegetarian, twenty-two white omnivorous and eighteen white vegetarian premenopausal women. Faecal bulk and water content were greater and pH lower in the Indian vegetarians. Total faecal animal sterol and coprostanol concentrations expressed on a dry-weight basis were lower in the vegetarians compared with the omnivores. The faecal sterol concentrations were correlated with dietary cholesterol intake. Primary bile acids were detected in six Indian vegetarians, two white vegetarians and two white omnivores; secondary bile acids were detected in all the white omnivore and vegetarian subjects but not in two of the Indian vegetarians. Total faecal free bile acid and conjugated bile acid concentrations were lower in the white vegetarians compared with the omnivores. Faecal lithocholic acid concentrations were lower in both Indian and white vegetarians. The lithocholic: deoxycholic acid ratio and coprostanol: total animal sterols ratio were significantly lower in the Indian vegetarians compared with the omnivores. Both ratios were positively correlated with faecal pH. Stepwise multiple regression analyses were undertaken in order to identify which nutrients influenced faecal pH, lithocholic and deoxycholic acid concentrations. The intakes of starch and dietary fibre were negatively associated with faecal concentrations of lithocholic and deoxycholic acid. Starch intake alone was negatively associated with faecal pH. The results of this study confirm that diets high in dietary fibre decrease faecal bile acid concentrations and suggest that the complex carbohydrates present in Indian vegetarian diets influence faecal pH and inhibit the degradation of faecal steroids.

The aim of the present study was to investigate the relationship of Ca intake and serum Ca levels during the third trimester of pregnancy with levels of the same mineral in transition milk (days 13−14 of lactation) and mature milk (day 40 of lactation). The study subjects were a group of fifty-seven healthy, lactating mothers aged between 18 and 35 years (mean 27 (SD 3·7) years) whose pregnancies and labour were attended by the Department of Obstetrics and Gynaecology of Cuenca INSALUD Hospital, Spain. Ca intake during the third trimester was determined by recording the consumption of foods over a 5 d period and by registering Ca provided by dietary supplements. The same method was used to investigate the intake of protein, vitamin D, fibre and Fe, nutrients that could affect the use of dietary Ca. Ca levels in maternal serum during this stage of pregnancy, during lactation and in transition and mature milk samples, were determined using 2-cresolphthalein complexone. During pregnancy 70·2% of subjects showed Ca intakes below 1100mg/d (75th percentile). The consumption of Ca supplements was very small and hardly modified the mean quantity supplied by the diet. Subjects with an intake < 1100mg/d showed no fall in Ca levels in serum, either during pregnancy or lactation, nor were decreased levels found in transition milk. However, these subjects showed lower Ca levels in mature milk (5·95 (SD 1·56) mmol/1) than did subjects with greater Ca intakes (6·82 (SD 1·31) mmol/1). This may suggest that breast-fed babies of mothers with lower Ca intakes during pregnancy also receive less Ca.

A total of sixty-five observations on heat production during fasting and physical activity were obtained in four groups of pigs differing in breed and/or castration (Meishan (MC) and Large White (LWC) castrates and Large White (LWM) and Piétrain (PM) males) with body weight (BW) ranging between 25 and 60 kg. Pigs were fed ad libitum before fasting. Heat production was measured using indirect calorimetry. Fasting heat production (FHP) was proportional to the body weight raised to the power 0.55, but with group-specific proportionality parameters (810, 1200, 1220 and 1120kJ/kg BW0.55 per d for MC, LWC, LWM and PM respectively). Group effects could be removed by expressing FHP as a function of muscle, viscera and fat: FHP (kJ/d) = 457(muscle)0.81 + 1969(viscera)0.81 - 644(fat)0.81. It is hypothesized that different breeds with equal muscle and visceral mass, can have different FHP. The negative coefficient for fat would then be the result of a low FHP rather than a cause of it. Because a large part of the variation in tissue composition between groups was due to MC group, a separate equation for the lean groups was established. For lean pigs, FHP could be expressed as a function of muscle and viscera alone: FHP (kJ/d) = 508(muscle)0.66 + 2011(viscera)0.66. Both type of pig and BW affected the number of bouts of physical activities (i.e. standing or sitting) per day, the duration of activity and the total cost of activity. Energetic cost of activity was proportional to the muscle mass raised to the power 0.91 (FHPactivity (kJ/h activity) = 21.0(muscle)0.91). Physical activity represented less than 10% of the total heat production in fasting growing pigs housed alone in metabolic cages and kept in a quiet environment.

Differences between the fermentation characteristics of cell contents (CC) and protease-treated cell walls (CW) of young leaves of Italian ryegrass (Lolium multiflorum Lam.) cultivar Multimo (tetraploid), were studied in vitro. Gas and volatile fatty acid (VFA) production rates were measured at regular intervals, as was the degradability of organic matter (OM) of CW. The measured VFA were used to predict the gas production and fermentable OM using stoichiometric calculations. For CW the volume and kinetics of measured gas production were the same as those predicted from the VFA formed. In contrast, the measured gas production for CC was consistently less than predicted, indicating that the stoichiometric equations were not valid for rapidly fermenting substrates. For both CC and CW, the relative rate of acetic acid production levelled off more slowly than for other VFA, resulting in an increasing gas yield (in ml/g fermentable OM) after 12 (CW)-24 (CC)h incubation. Consequently, the fermentation of OM was not linearly related to gas production kinetics. For CW, the kinetics of decline of degradable OM and fermentable OM were the same, after correction for a constant ‘lost fraction’ of degradable OM of 205 g/kg OM. This work indicates the value of detailed studies of fermentation processes to evaluate herbage quality. In particular, the role of CC and the difference between degradation and fermentation require further attention.

We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) received 37·5 μg cholecalciferol/d for 14 d and were subsequently studied for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14−17) and at the end of the study (days 98−101). During treatment, plasma cholecalciferol increased rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1 - 2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1·4, 22·5, 97·5 and 80·9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a ‘buffer to functional vitamin D status’ by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.

To evaluate the extent to which daily oral Fe supplements may block Fe absorption from a subsequent dose, we compared effects of oral and intraperitoneal (i.p.) Fe supplementation on Fe status in anaemic rats (haemoglobin (Hb) 90 g/l). A ligated duodenal loop technique was used to assess the effects of the Fe supplements administered either orally or i.p. at different frequencies on Fe absorption from a subsequent test dose. Anaemic Sprague–Dawley rats were assigned to seven groups of eight rats each and received either oral or i.p. Fe supplements for 3 d as follows: (1) 4 mg oral supplement daily (three doses in 3 d); (2) 4 mg oral supplement once (one dose on day 1, low-Fe dose on days 2 and 3); (3) 12mg oral supplement once (one dose on day 1, low-Fe dose on days 2 and 3); (4) 3.2 mg i.p. supplement daily (three doses in 3d); (5) 3.2 mg i.p. supplement once (one dose on day 1); (6) 9.6 mg i.p. supplement once (one dose on day 1); (7) low-Fe diet (control). The effectiveness of the supplements in treating Fe deficiency on each of the two test-factors, i.e. route of administration and frequency of dose, was assessed by determining Hb-Fe gain and liver-Fe stores after the 3 d test period. Oral supplementation was as effective as i.p. in improving the Fe status of the anaemic animals. However, a 15 min absorption of a radio-Fe test dose from a ligated loop in i.p.-supplemented groups was significantly higher (11.68 (sd 1.70) %, 17.49 (sd 4.59) %, 16.71 (sd 3.39) %) than in orally supplemented groups (3.24 (sd 1.35) %, 2.45 (sd 1.05) %, 1.80 (sd 0.35) %) despite equal body Fe stores. No significant difference in intestinal Fe absorption efficiency was detected within the oral groups but those supplemented only once were more effective than or as effective as the group receiving daily supplements for 3d in improving Fe status as indicated by Hb-regeneration efficiency. We conclude that there is a mucosal block with the administration of oral Fe supplements but the extent of this blocking effect during oral Fe supplementation is not as dramatic as currently thought in the context of the poor efficacy of daily Fe supplementation programmes.

Stable isotope breath tests offer a safe, repeatable non-invasive method of measuring fat digestion. They involve the ingestion of a substrate labelled with 13C followed by serial measurements of the 13C: 12C ratio in expired CO2, from which the percentage of the 13C dose recovered (PDR) can be calculated. However PDR depends on the CO2-production rate. Our aim was to compare results obtained using directly measured CO2-production rates with those calculated from two predicted values. Twelve normal healthy children and twenty-four children with cystic fibrosis (CF) (without or with the normal dose of enzyme supplementation) were studied with 1,3-distearyl, 2[carboxyl[13C]octanoyl glycerol. The volume of CO2 produced (litres/min) was measured at rest for 30 min approximately 3 h after substrate ingestion, and the results were converted to mmol/min. For each subject the expected BMR was calculated from the equation of Schofield (1985), based on sex, age, weight and height, and from these values, CO2-production rate was derived. Surface area was calculated and an estimated value of 5 mmol/m2 per min (Shreeve et al. 1970) was used. Using these three CO2-production rates, three different PDR were calculated and compared. In healthy children there was a close concordance between measured and predicted CO2-production rates, but children with CF had a mean measured CO2-production rate 39% higher than normal children. This use of normal data for predicted CO2-production rates in children with CF underestimates cumulative PDR. If direct measurements of CO2-production rate are not available or impossible to perform the Vco2 obtained from the BMR calculated using the equations of Schofield (1985) or Shreeve et al. (1970) can be used in normal children. However, if accurate results for PDR are to be obtained, CO2-production rates should be measured when performing breath tests in conditions where energy expenditure and/or CO2-production rate are not expected to be normal.