Impaired nutritional status has been frequently reported in surveys estimating its prevalence amongst patients in hospital. While there is no doubt that protein–energy undernutrition has serious implications for health, recovery from illness or surgery and hospital costs, lack of nationally or internationally accepted cut-off points and guidelines for most nutrition-related variables make nutritional assessment difficult and proper comparisons between studies impossible. In reviewing published work in which the prevalence of undernutrition has been assessed, it can be seen that each study defined undernutrition, or nutritional risk, using different methodology. This present review aims to highlight the problems which arise when deciphering these studies, and the resulting difficulty in determining the true prevalence of undernutrition and nutritional risk, amongst both general and specific groups of hospital in-patients. It is widely agreed that routine hospital practices can further adversely affect the nutritional status of sick patients in hospital. How this occurs, and the potential effects of impaired nutritional status on clinical outcome are examined. The methods currently available to assess nutritional status are evaluated in the knowledge that such assessments are difficult in clinical practice. The review concludes by proposing that if we want the medical and nursing professions to consider the nutritional status of hospital patients seriously, definitions of undernutrition and nutritional risk, and cut-off values for the nutritional variables measured must be agreed to allow evidence-based practice. Outcome measures which allow clear comparisons between groups and treatments must be used in studies assessing the effects of nutritional interventions.

We have studied the effect of common mutations (677C → T and 1298A → C) of the methylenetetrahydrofolate reductase (MTHFR) gene in sixty-six healthy French subjects, aged 27–47 years. Serum folate, vitamin B12, and plasma total homocysteine were measured as well as the specific activity of MTHFR in lymphocytes. The frequency of subjects homozygous for the 677TT genotype was 18 %, and that of those homozygous for the 1298CC genotype was 12·5 %. The frequency of individuals heterozygous for both mutations was 23·5 %. The 1298A → C mutation was associated with decreased MTHFR specific activity in subjects with both 677CC and 677CT genotypes. This activity was 60 % for the 677CC/1298AC genotype and 52 % for the 677CC/1298CC genotype when compared with the MTHFR specific activity of the 677CC/1298AA genotype. Heterozygotes for both mutations (677CT/1298AC genotype) had 36 % of the reference specific activity. Although homocysteine levels in 677TT and 1298CC genotype subjects were higher than for other genotypes, no significant differences were observed among different genotypes. This may be due to high serum folate level in our samples, and suggests that folate therapy may be useful to prevent hyperhomocysteinaemia in homozygous mutant subjects.

Plasma triacylglycerol concentrations increase after the acute ingestion of alcohol (specifically ethanol). However, the effect of ethanol when consumed with a mixed meal has not been well studied. The objective of the present study was to determine the perturbations of lipid metabolism that occur after ingestion of ethanol in combination with a mixed meal of specific fatty acid composition. Blood samples were taken from seven healthy male subjects before and after a mixed meal, with and without ethanol. The specific fatty acid composition of the test meal allowed the fatty acids to be traced into the plasma non-esterified fatty acid pool during the postprandial period. Statistical analysis by repeated measures ANOVA showed significant effects of ethanol. For example, postprandial lipaemia was enhanced after the ethanol test meal compared with the control (P < 0·05), mainly due to increases in triacylglycerol-rich lipoproteins in the flotation range Sf 60–400 (VLDL1) (P < 0·05); those in the range Sf 20–60 (VLDL2) and also Sf > 400 (chylomicrons) were not significantly affected. The later postprandial increase in plasma non-esterified fatty acid concentrations was reduced after the ingestion of ethanol (P < 0·001), but the proportions of palmitoleic acid (a marker of fatty acid content of the test meal) and of linoleic acid (a marker of endogenous lipolysis) were not affected. The results suggest a primary effect of ethanol on the stimulation of secretion of large VLDL particles, which then compete for clearance with chylomicrons by lipoprotein lipase. The results do not support an effect of ethanol on the release of non-esterified fatty acid into the plasma. The suppression of plasma non-esterified fatty acid concentrations during the postprandial period may contribute towards the beneficial effects of moderate ethanol consumption.

This present study investigated the effect of a 17-week intervention programme with nutrient-dense foods (enriched with vitamins and minerals at 25–100 % of the Dutch recommended dietary allowance) and/or physical exercise in 159 frail elderly subjects (forty-six men, 113 women, mean age 78·7 (SD 5·6) years). Subjects were randomized into four groups: (1) control, (2) nutrition intervention, (3) exercise or (4) both nutrition intervention and exercise. Main outcome variables were sensory perception (smell test and questionnaire), appetite (questionnaire), energy intake (3 d food record) and body weight (on a weighing scale and with dual energy X-ray absorptiometry measurements). At baseline, moderate but significant correlations were found between appetite and energy intake (r 0·30, P < 0·0001), between smell test and smell perception assessed by questionnaire (r 0·40, P < 0·0001) and between lean body weight and energy intake (r 0·50, P < 0·0001). Results after 17-weeks intervention revealed neither change in smell test scores (P = 0·19) nor in appetite (P = 0·17). A slight positive effect of exercise compared with non-exercising groups on energy intake (difference 0·5 MJ, P = 0·05) was shown next to a preserving effect of exercise on lean body mass (+0·08 kg) compared with a decrease (-0·4 kg) in non-exercisers (P < 0·02). The correlation between the change in lean body mass and change in energy intake was 0·18 (P = 0·05). In conclusion, an interesting preserving effect on lean body mass in frail elderly subjects due to 17 weeks of exercise was shown. Since a decline in lean body mass was observed in the non-exercisers, effects may be attributable to change in activity pattern. Changes in lean mass were also slightly, but significantly, correlated with changes in energy intake. In turn, energy intake was not related to a change in reported appetite or sensory perception. Nutrient-dense foods were not able to improve any of the outcome variables in this study.

This present case report describes two siblings with severe type V hyperlipoproteinaemia, diagnosed very early in life and due to the combination of the common apolipoprotein (Apo) E2 allele and a rare mutant variant of ApoE, ApoE3 (Arg 136 → Ser). Phenotyping of ApoE falsely identified E2/E2 phenotype. The presence of mutated ApoE was suspected on an unusual restriction polymorphism of a Hha 1 restriction site and confirmed by sequence analysis of the cloned polymerase chain reaction fragment of exon 4 and familial segregation study. The severity of the hypertriacylglycerolaemia was modulated by the lipid content of the diet. A low-fat diet enriched in medium-chain triacylglycerol (TAG) decreased but did not normalize plasma TAG levels in both affected patients of the pedigree. A standardized lipid-enriched test meal showed a marked impairment of TAG-rich lipoprotein (TRL) clearance, especially the exogeneous TRL bearing ApoB-48 which still represented 79 % of total TRL 7 h after the fat load. Finally, differences between the male and female siblings with the existence of a consanguine relationship in their parents suggested the involvement of other genetic factors in modulating the severity of phenotypic expression. This observation reinforces the usefulness of genotyping of ApoE for the characterization of genetic hypertriacylglycerolaemia and selection of the appropriate diet and treatment.

There is evidence that food consistency may influence postprandial physiological responses. Recently we found that homogenization of a vegetable-rich meal significantly delayed the gastric emptying rate and was more satiating than the same meal in solid–liquid form. In this present study we investigated whether homogenization also influences endocrine and metabolic responses to the meal. Eight healthy men, aged 21–28 (mean 24·5) years, were given the meal (cooked vegetables 250 g, cheese 35 g, croutons 50 g and olive oil 25 g, with water 300 ml; total energy 2·6 MJ) in both solid–liquid (SM) and homogenized (HM) form, in random order, at 1-week intervals. Variables assayed were plasma glucose, insulin and glucose-dependent insulinotropic peptide (GIP) levels for 2 h and diet-induced thermogenesis (DIT) for 5 h. Plasma glucose pattern was similar after both meals. However, HM induced significantly greater insulin, GIP and DIT responses than SM. Mean integrated areas under the curves (AUC) were 1·7 (SEM 0·38) V. 1·2 (sem 0·33) U/l per 120 min (P = 0·005) for insulin, 19·9 (sem 2·44) v. 16 (sem 1·92) nmol/l per 120 min (P = 0·042) for GIP, and 237·7 (sem 16·32) v. 126·4 (sem 23·48) kJ/300 min (P = 0·0029) for DIT respectively. Differences between GIP-AUC after HM and SM correlated significantly with differences between insulin-AUC after HM and SM (r2 0·62, P = 0·021). These findings demonstrate that homogenization of a meal results in a coordinated series of changes of physiological gastroentero–pancreatic functions and confirm that the physical state of the meal plays an important role in modulating endocrine and metabolic responses to food.

Randomized controlled trials of the effects of the dietary supplement Efacal® (Scotia Pharmaceuticals Plc, Guildford, Surrey, UK) v. Ca only on total body bone mineral density (BMD) and markers of bone turnover were conducted in healthy pre- and postmenopausal women separately. Total daily dose for 12 months for the Efacal® groups was: Ca 1·0 g, evening primrose oil 4·0 g and marine fish oil 440 mg; and for the control groups was: Ca 1·0 g. Reported compliance was better than 90 % in both age groups. For the forty-three premenopausal women (age range 25–40 years), initial mean total body BMD values were similar for Efacal® and control groups and both groups showed highly significant mean increases of about 1 %; however, there were no significant between-group differences for the changes in BMD or markers of bone turnover. For the forty-two postmenopausal women (age range 50–65 years), initial mean total body BMD values were again well-matched across treatment groups. Both Efacal® and control groups showed highly significant decreases in total body BMD of about 1 %, but again there were no significant between-group differences in total body BMD or markers of bone turnover. Possible confounding variables such as initial total body BMD were explored but had no effect on the outcome in either age group. Nail quality improved in both age groups and in both Efacal® and control groups. Again, there was no significant difference between treatment groups. No evidence was found to support a beneficial effect of Efacal® on BMD in these women.

Pigs (n 144, 30 kg liveweight) were allocated to one of three diets differing in the level of whole linseed (Linum usitatissimum, also known as flaxseed). The diets contained 0, 50 and 100 g/kg for diets L0, L50 and L100 respectively, while containing a constant oil content (60 g/kg). Pigs were slaughtered at a liveweight of 77–87 kg. With the exception of a slight difference in feed intake, there was no effect of diet on production characteristics or carcass traits. Levels of α-linolenic acid were increased in all tissues studied as the amount of linseed in the diet increased. In the plasma, m. longissimus thoracis, liver and kidney eicosapentaenoic acid concentration increased markedly. Docosapentaenoic acid concentration increased in the muscle, liver and kidney, whereas in the plasma higher levels of docosahexaenoic acid were observed. None of the longer-chain fatty acids (C20 or longer) were detected in the subcutaneous fat. The changes in fatty acid composition resulted in marked changes to the n-6 : n-3 and arachidonic : eicosapentaenoic acid ratios. Feeding whole linseed had no negative effect on the oxidative stability of the meat. Sensory panel results showed no significant differences by diet except for a reduction in abnormal odour (odour perceived by panellists to be abnormal in pigmeat) in the L50 diet and a reduction in the skatole odour (odour of 3-methylindole) in the pigs fed on diet L100. It is concluded that increasing the linseed content of pig diets up to 100 g/kg has no adverse effect on the carcass or meat quality whilst enhancing the levels of n-3 fatty acids which have a potentially positive health effect in man.

The plasma glucose–insulin relationships and thyroid status were investigated in two lines of adult cockerels divergently selected for high (R+) or low (R-) residual food consumption (RFC). For a given body weight, R+ birds had a 74 % higher food intake than R- birds. Plasma glucose concentrations were significantly lower in the R+ line compared with the R- when fasted, whereas R+ birds exhibited a significantly lower plasma insulin concentration than R- birds either in fed or fasted state. After an overnight fast, R+ birds also exhibited a higher sensitivity to exogenous insulin in view of its more pronounced hypoglycaemic effect. After an oral glucose load, the glucose disposal of R+ cockerels was faster despite lower glucose-induced plasma insulin concentration. Whilst plasma triacylglycerol concentrations were lower in the R+ line when fed, plasma non-esterified fatty acid concentrations were higher in fasted R+ than R- cockerels (684 v. 522 μmol/l). Higher plasma triiodothyronine concentrations were observed in fed R+ compared with R- birds (3·0 v. 2·1 nmol/l respectively). The higher plasma concentrations of triiodothyronine associated with lower concentrations of insulin could account for the leanness and the elevated diet-induced thermogenesis previously observed in the R+ line.

Two rapeseed (Brassica napus) meals, RM1 and RM2, with two levels of glucosinolates (GLS; 5 and 41 μmol/g DM respectively) were incorporated at the levels of 300 and 500 g/kg of the diets of juvenile rainbow trout (Oncorhynchus mykiss) in replacement of fish meal, and compared with a fish-meal-based diet. A decrease in the digestibility of the DM, protein, gross energy and P was observed with high-rapeseed meal (RM) incorporation. In trout fed on RM-based diets, growth performance was reduced even after only 3 weeks of feeding. Feed efficiency was adversely affected by RM and GLS intake. Protein and energy retention coefficients were significantly lower in fish fed on the diet containing the higher level of GLS. P retention was significantly lower with all the RM-based diets than with the fish-meal diet. Irrespective of the degree of growth inhibition, fish fed on RM-based diets exhibited similar typical features of hypothyroid condition due to GLS intake, expressed by lower plasma levels of triiodothyronine and especially thyroxine and a hyperactivity of the thyroid follicles. This hypothyroidal condition led to a strong adjustment of the deiodinase activities in the liver, the kidney and the brain. A significant increase of the outer ring deiodinase activities (deiodinases type I and II respectively) and a decrease of the inner ring deiodinase activity (deiodinase type III) were observed. It is concluded that the observed growth depression could be attributed to the concomitant presence of GLS, depressing the thyroid function, and of other antinutritional factors affecting digestibility and the metabolic utilization of dietary nutrients and energy.

The purpose of this study was to differentiate between the effects of the amount and the type of dietary lipids on the expression of the retinoic acid receptor (RAR), but also the peroxisome proliferator-activated receptor (PPAR) and the receptor of the 9-cis retinoic acid (retinoid X receptor (RXR)) in rat liver. Six groups of eight rats (5-weeks old) were fed during 4 weeks on the following diets: control 50 g vegetable oil/kg, high-fat diet 250 g vegetable oil/kg. These oils were either coconut oil (rich in saturated fatty acids) or olive oil (rich in monounsaturated fatty acids) or safflower oil (rich in polyunsaturated fatty acids, mainly as n-6). The three high-fat diets induced a significant decrease of the maximal binding capacity of RAR and of the abundance of RARβ mRNA. Simultaneously, an increased expression of PPARα mRNA was observed while no significant difference on abundance of RXRα mRNA was observed. The mechanisms involved are probably multiple, but one hypothesis is that a modification of the equilibrium between the nuclear receptors, resulting from an increased expression of PPAR, induces a decreased expression of RAR in rat liver.

The effect of the level or source of dietary protein or protein-derived peptides on Ca absorption is not well understood. We determined, therefore, the influence of habitual dietary casein level, meal casein and meal casein phosphopeptide (CPP) on Ca absorption in the rat. True fractional Ca absorption was investigated in male 7-week-old rats, Wistar strain, in three separate studies using a faecal 47Sc : 47Ca ratio method. In studies A and C, rats (n 8 per group) were fed on a purified diet containing 200 g casein/kg for 2 weeks. Rats were then given a 47Ca-labelled meal (10 g) containing (per kg) either 0, 100, 200, or 300 g casein (study A) or 0, 100, 200, 350 or 500 g CPP (study C). In study B, rats (n 24 per group) were fed on a purified diet containing (per kg) either 200, 350 or 500 g casein for 2 weeks. Each group was then further randomized into three groups (n 8 per group) and given a 47Ca-labelled meal (10 g of the same diet) containing (per kg) either 200, 350 or 500 g casein. Ca absorption from a meal was unaffected by increasing meal casein concentration from 0 to 300 g/kg (study A), but was increased with a meal casein content of 500 g/kg (study B). Fractional Ca absorption decreased with increasing usual dietary casein intake in the range 200–500 g/kg (study B), suggesting intestinal adaptation. Ca absorption was unaffected by inclusion of 100 g CPP/kg in a single meal but was significantly (P < 0·001) reduced by 200, 350 and 500 g CPP/kg meal, with no evident dose-relationship. Thus, while Ca absorption was enhanced by high-casein meals, the mechanism remains unclear.