Vitamin B6 is a water-soluble vitamin, and is readily metabolized and excreted, so it has generally been assumed to have negligible toxicity, although at very high levels of intake it can cause peripheral nerve damage. Nutritional deficiency disease is extremely rare, although a significant proportion of the population shows biochemical evidence of inadequate status, despite apparently adequate levels of intake. The vitamin has been used to treat a wide variety of conditions, which may or may not be related to inadequate intake. In some conditions use of vitamin B6 supplements has been purely empirical; in other conditions there is a reasonable physiological or metabolic mechanism to explain why supplements of the vitamin many times greater than average requirements may have therapeutic uses. However, even in such conditions there is little evidence of efficacy from properly conducted controlled trials.

The effects of physical exercise on the lipid profile in mitochondrial membranes of liver and skeletal muscle were examined in rats fed with virgin olive oil or sunflower oil. Thirty male Wistar rats, 21 d old, were randomly assigned to four groups according to fat ingestion and physical activity over an 8-week period. For each type of oil, one group acted as a control group while rats from the other were trained to run for 40 min daily on a horizontal treadmill, at a speed of 35 m/min. The results show that diet affected the fatty acid profile of the mitochondrial membranes from skeletal muscle and liver. Physical exercise also modified the fatty acid profile of the mitochondrial membranes. Total monounsaturated fatty acids decreased (P < 0.001) in liver mitochondria of exercised animals. Total polyunsaturated fatty acids in mitochondrial membranes of liver increased (P < 0.005) after exercise but those in mitochondrial membranes of skeletal muscle decreased (P < 0.05). These changes due to the exercise may arise via several mechanisms, e.g. fluidity regulation; changes in the eicosanoid metabolism; differences in the availability or oxidation rate of the different fatty acids.

Present literature indicates that whereas an acute fat intake of 5 g does not elicit a postprandial triacylglycerolaemic response, 20 g of fat does. Since 67 % of fat intake occasions involve fat doses of less than 20 g, the present study examined the effect of a relatively low-fat (LF) meal (0·2 g/kg body weight; mean 14 g) on postprandial triacylglycerol (TAG) metabolism, compared with a high-fat (HF) meal (0·6 g/kg body weight; mean 43 g), a fat dose which is more typical of laboratory studies. Plasma- and chylomicron-TAG concentrations increased significantly (P ≤ 0·001) following both meals, and the increase was significantly (P ≤ 0·02) greater after the HF meal. The postprandial areas under the curves and maximal postprandial TAG concentrations for plasma- and chylomicron-TAG were significantly higher following the HF meal (P ≤ 0·05). Postprandial plasma insulin and gastric inhibitory polypeptide concentrations increased significantly (P ≤ 0·001) after each meal, but there was no difference between the two meals. These data show that modest amounts of fat in a meal will elicit a measurable postprandial TAG response. Since postprandial lipaemia affects the composition and concentration of the TAG- and cholesterol-rich lipoproteins, controlling dietary TAG supply may influence the metabolic fate of these lipoproteins.

The purpose of the present study was to evaluate the capacity of the‘Determine Your Nutritional Health’ Checklist (NSI Checklist) and the ‘Mini Nutritional Assessment’ (MNA) methods to predict nutrition-related health problems. Data were from the Danish part of the ‘Survey in Europe of Nutrition in the Elderly, a Concerted Action’ (SENECA) baseline survey from 1988, and the follow-up study from 1993. Based on the baseline survey thirty-nine (19.3 %) of the subjects were classified at high nutritional risk, 103 (51 %) were considered at moderate nutritional risk and sixty (29.7 %) were within the ‘good’ range according to the criteria in the NSI Checklist. With the MNA, 171 subjects were classified according to their nutritional risk into a well-nourished group, comprising 78.4 %, and a group who were at risk of undernutrition, comprising 21·6 % at baseline. A total of 115 subjects participated in the follow-up study. The mortality rate and the prevalence of various morbidity indicators were compared between the different risk groups. The analysis showed that subjects with a high MNA score (≥ 24) had significantly lower mortality (rate ratio estimate: 0.35; 95 % Cl 0.18, 0.66) compared with subjects with a low MNA score (≤ 23.5). In contrast, the NSI Checklist score was not a significant predictor of mortality (rate ratio estimate: 1.45; 95 % Cl 0.78, 2.71). The sixteen Danes judged to be at high nutritional risk by the NSI Checklist in 1988, had more acute diseases (P < 0.001) than the rest of the participants, between 1988 and 1993. No significant differences were found in the participation rates, hospitalization rates, physician visits, need of help or weight loss between the groups. The thirteen Danes judged to be at risk of undernutrition in 1988 by the MNA, had a lower participation rate (P < 0.01) and higher occurrence of acute disease (P < 0.05), need of help (P < 0.05), and weight loss (P < 0.001) than the well-nourished group, between 1988 and 1993. No significant differences were found in hospitalization rates and physician visits between the two groups. In conclusion, the results indicate that modified versions of the NSI Checklist and the MNA are capable of identifying a group of 70–75-year-old subjects with increased risk of certain nutrition-related health problems. Further, an MNA score ≤ 23.5 predicts mortality in a Danish population.

The gastrointestinal handling and metabolic disposal of [1-13C]palmitic acid, [1-13C]stearic acid and [1-13C]oleic acid administered within a lipid–casein–glucose–sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the 13C label in stool and label excreted on breath as 13CO2. The greatest excretion of 13C label in stool was in the stearic acid trial (9.2 % of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1.2 % of administered dose) or oleic acid (1.9 % of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13C]palmitic acid in the palmitic acid trial and [13C]oleic acid in the oleic acid trial). In contrast, only 87 % of the label in the stool in the stearic acid trial was identified as [13C]stearic acid, the remainder was identified as [13C]palmitic acid which may reflect chain shortening of [1-13C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of 13C label on breath over the initial 9 h of the study period (oleic acid = palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as 13CO2 was similar in all three trials (approximately 25 % of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion.

Observational studies primarily based on diet questionnaires or food records have reported that vegetarians can have a very low I intake. However, analytically ascertained data on the possible degree of I deficiency with this form of diet is lacking. Six healthy adult volunteers participated in the present controlled experimental diet study carried out in four separate 5 d diet periods. The study diets, normal, protein-rich, lactovegetarian, and repeat of the initial normal diet, were almost isoenergetic and contained no fish, sea food, iodized salt or processed foods fortified with I. During the last 48 h of each diet period two 24 h urine samples were obtained from each subject. I analyses were performed in the urine samples and in representative samples taken from all ingested diets. Urinary I excretion was significantly lower with the lactovegetarian diet (36·6 (sd 8·8) μg/d) than with the normal and the protein-rich diets (50·2 (sd 14·0) and 61·0 (sd 8·0) μg/d respectively). Accordingly, a markedly reduced I intake was confirmed analytically for the lactovegetarian diet (15·6 μg/d v. 35·2 and 44·5 μg/d respectively). Our results provide experimental confirmation of literature findings indicating that I supply is higher with non-vegetarian than with vegetarian diets. Specifically, the extremely low intake and urinary output of I as analytically determined for one exemplary vegetarian diet, demonstrate that dietary I may be limiting when strict forms of vegetarian dietary practices (no iodized salt, no I supplements) are followed. The present study is, therefore, the first diet-experiment-based pointer to the potential danger of I deficiency disorders due to strict forms of vegetarian nutrition, especially when fruits and vegetables grown in soils with low I levels are ingested.

The extent and duration of postprandial lipaemia have been linked to risk of CHD but the influence of dietary variables on, and the relative contributions of, exogenous (chylomicron) and endogenous (VLDL) triacylglycerols to the total lipaemic response have not been comprehensively evaluated. In the present study the triacylglycerol, apolipoprotein (apo) B-48 and retinyl ester (RE) responses to three test meals of varying monounsaturated (MUFA) and saturated fatty acid (SFA) content were measured in the triacylglycerol-rich lipoprotein (TRL) fraction of plasma (ρ = 1·006 g/ml) for 9 h after meal consumption. Fifteen healthy normolipidaemic young men consumed, on separate occasions, three test meals which were identical apart from their MUFA and SFA contents. Expressed as a percentage of total energy the MUFA/SFA contents of the meals were: (1) 12 %/17 %; (2) 17 %/12 % and (3) 24 %/5 %. The contribution of the intestinally-derived lipoproteins (chylomicrons) to the lipaemic response was investigated by determining the time to reach peak concentration and the total and incremental areas under the time response curves (AUC and incremental AUC) for RE, apoB-48 and triacylglycerol in the TRL fraction. No significant differences in these measurements were observed for the three meals. However, visual comparison of the postprandial responses to the three meals suggested that as meal MUFA content increased there was a tendency for the triacylglycerol, apoB-48 and RE responses to become biphasic as opposed to the typical monophasic response seen with the 12 % MUFA/17 % SFA meal. Comparison of the apoB-48 and RE responses for the three test meals confirmed other workers’ findings of delayed entry of RE relative to apoB-48 in TRL. The value of the two markers in investigating dietary fat absorption and metabolism is discussed.

The influence of sodium fumarate on rumen fermentation was investigated in vitro using batch and semi-continuous cultures of mixed rumen micro-organisms taken from three sheep receiving a basal diet of hay, barley, molasses, fish meal and a mineral–vitamin supplement (500, 299·5, 100, 91 and 9·5 g/kg DM respectively). Batch cultures consisted of 10 ml strained rumen fluid in 40 ml anaerobic buffer containing 200 mg of the same feed given to the sheep. Sodium fumarate was added to achieve a final concentration of 0, 5 or 10 mmol/l, as a result of the addition of 0, 250 or 500 μmol, equivalent to 0, 200 and 400 g/kg feed. CH4 production at 24 h (360 μmol in the control cultures) fell (P < 0·05) by 18 and 22 μmol respectively (SED 7·5). Total gas production was increased by the addition of fumarate without significant accumulation of H2. Substantial increases in acetate production (92 and 194 μmol; SED 26·7, P < 0·01) were accompanied by increases in propionate formation (212 and 396 μmol; SED 13·0, P < 0·001). Longer-term effects of fumarate supplementation on ruminal fermentation and CH4 production were investigated using the rumen simulation technique (Rusitec). Eight vessels were given 20 g basal diet/d, and half of them received a supplement of fumarate (disodium salt) over a period of 19 d. The response to the daily addition of 6·25 mmol sodium fumarate was a decrease in CH4 production of 1·2 mmol (SED 0·39, P < 0·05), equivalent to the consumption of 4·8 mmol H2, and an increase in propionate production of 4·9 mmol (from 10·4 to 15·3 (SED 1·05) mmol/d, P < 0·01). The inhibition of CH4 production did not decline during the period of time that fumarate was added to the vessels. Thus, the decrease in CH4 corresponded well to the fraction of the fumarate that was converted to propionate. Fumarate had no significant (P > 0·05) effect on total bacterial numbers or on the number of methanogenic archaea, but numbers of cellulolytic bacteria were increased (8·8 v. 23·9 (SED 2·49) × 105 per ml, P < 0·01). Fumarate also increased DM digestibility of the basal diet after 48 h incubation (0·476 v. 0·508 (SED 0·0123), P < 0·05). Thus, it was concluded that sodium fumarate may be a useful dietary additive for ruminants, because it diverts some H2 from CH4 production and because it is able to stimulate proliferation of cellulolytic bacteria and digestion of fibre.

Both experimental and clinical studies have indicated that a novel source of dietary fibre, produced from rhubarb (Rheum rhaponticum) stalks, is potentially hypolipidaemic. The present study, using C57BL/6J mice, was undertaken to examine if this fibre source affects cholesterol degradation. Mice were maintained on semi-purified diets containing 50 g rhubarb fibre or cellulose/kg with or without 5 g cholesterol/kg for 4 weeks. In cholesterol-supplemented mice, rhubarb fibre caused significant lowering of plasma cholesterol (-13 %) and the hepatic concentrations of total cholesterol (-34 %) and cholesteryl esters (-34 %). In parallel to the reduction of hepatic cholesteryl ester content, animals fed on rhubarb fibre had significantly lower activity of acyl CoA: cholesterol acyltransferase (EC 2.3.1.26) than the mice maintained on a diet containing cellulose and cholesterol. Rhubarb-fibre feeding accelerated the faecal bile-acid loss and diminished the gall-bladder bile-acid pool in both the normal and the cholesterol-fed mice. The increase in the bile-acid excretion was positively correlated with an increased activity as well as mRNA abundance of cholesterol 7α-hydroxylase (EC 1.14.13.17). The increased excretion of bile acids and induction of cholesterol 7α-hydroxylase activity may account for the hypocholesterolaemic effect of rhubarb fibre.

Food restriction during pregnancy in rats induces intrauterine growth retardation with consequences persisting into adulthood. In the present study we have investigated the hypothesis that malnutrition in pregnant rats may lead to altered cardiovascular function in adult female offspring. Perinatal growth retardation was induced by a 50 % reduction of normal dietary intake in rats during the second half of pregnancy. Systolic and diastolic blood pressure values and heart rate were recorded in conscious female offspring (100 d old) using a femoral artery probe. No significant differences in heart rate, or in systolic and diastolic blood pressures were recorded between control offspring and offspring of nutritionally deprived rats. In order to ascertain whether cardiovascular variables in the offspring were influenced by lactation, subgroups of offspring from food-restricted dams were fostered with lactating dams fed on a normal diet. Blood pressure and heart rate were also found to be normal in these offspring. The rise in blood pressure associated with NO inhibition was similar in all groups. Isolated resistance artery function was assessed in vitro in offspring (100–120 d old) of a second group of semi-starved dams. Small mesenteric arteries from these animals showed reduced endothelium-dependent relaxation (to acetylcholine and bradykinin), but enhanced sensitivity to exogenous NO (sodium nitroprusside). We conclude that food restriction during the second half of pregnancy and/or lactation does not induce hypertension in adult offspring, but may effect subtle changes in vascular function.