Observational studies support the role of modifying lifestyle-related risk factors such as diet, physical activity and alcohol use in stroke prevention. For example, increased Na intake is associated with hypertension, and reduction in salt consumption may significantly lower blood pressure and may reduce stroke mortality. Moderately elevated homocysteine levels may be associated with stroke and are associated with deficiency of dietary intake of folate, vitamin B6 and vitamin B12. Consumption of a diet rich in fruits, vegetables, folate, K, Ca, Mg, dietary fibre, fish and milk may protect against stroke. Regular physical activity may also protect against stroke through its role in controlling various risk factors such as hypertension, diabetes mellitus and obesity. The role of fat intake as a risk factor for stroke remains uncertain, whereas the association between stroke and cholesterol has more convincingly been demonstrated by the recent intervention trials using statins. There is also evidence that a low serum albumin may be causally linked to stroke risk and outcome and that a significant number of stroke patients are undernourished on admission and their nutritional status deteriorates further whilst in hospital. Undernutrition is associated with increasing morbidity and mortality and nutritional supplements may have some beneficial effect on some outcome measures.

Data from clinical studies established that there was an inverse linear relationship between measures of postprandial blood glucose and insulin responses to an oral glucose load, consumed in a drink, and the logarithm of viscosity of the drink. These data have been re-analysed using concentration and molecular weight as the dependent variables. Molecular weight (M) of the β-glucans used was determined using high-performance size exclusion chromatography equipped with a triple detector system of right angle light scattering, viscometry and refractive index. A significant relationship between changes in peak blood glucose and a combination of logarithm of the concentration and logarithm of M was found.

Vitamin E is the main biological lipid-soluble antioxidant and plays a crucial role in the maintenance of the immune system. In the present work, twenty-one guinea-pigs (3-weeks-old) were distributed into three groups, which during 5 weeks ingested different amounts of vitamin E (/kg diet): 15 mg (low vitamin E diet), 150 mg (medium vitamin E diet; control) or 1500 mg (high vitamin E diet). The function of lymphocytes and macrophages were then studied. In macrophages obtained from the peritoneum several steps of the phagocytic process (chemotaxis, ingestion and superoxide anion production) were assayed, as well as chemotaxis and proliferation of peritoneal and spleen lymphocytes. The results indicate that with respect to the medium vitamin E diet, low ingestion of vitamin E causes a decrease in chemotaxis and production of superoxide anion by macrophages and an increase in the phagocytic capacity. With the high vitamin E diet an increase in macrophage and lymphocyte chemotaxis, superoxide anion production and lymphoproliferative capacity, as well as a decrease in phagocytosis, were observed. Therefore, diet supplementation with higher than usual levels of vitamin E appears to be beneficial for the immune system.

It was studied whether the type of bread (i.e. a low-fibre wheat–rye mixed bread and coarse or fine wholemeal rye bread) either as part of a diet or alone, had an influence on the short-chain fatty acids (SCFA) produced during in vitro fermentation. Fermentation substrates were dietary fibre residues obtained from diets and breads. In addition, it was investigated whether the faecal SCFA pattern in the inoculum donors, who ingested the experimental diets, could be predicted by in vitro fermentation. Yields of SCFA in vitro were 0·51–0·62 g/g fermented polysaccharide. In vitro, the molar ratios of butyrate were higher for the two high-fibre diets containing coarse or fine wholemeal bread than for the low fibre diet containing wheat–rye mixed bread; the difference was significant for the coarse (P < 0·01), but not for the fine bread diet (P = 0·0678). The coarse wholemeal bread alone produced a higher molar ratio of butyrate than the fine wholemeal bread (P < 0·05) and the wheat–rye mixed bread (P < 0·01). Ingestion by the inoculum donors of the diets containing wholemeal bread led to higher faecal butyrate ratios (molar ratios: coarse bread diet 19·6, fine bread diet 17·7) compared with the wheat–rye mixed bread-containing diet (14·9), but the differences between the diets were not significant. For the diets investigated, there were no significant differences between faecal and in vitro SCFA patterns.

Carbohydrate gelling agents can be regarded as being representative for the soluble and viscous fractions of dietary fibre. Their dietary concentration affects the consistency of the ingested food as well as the dilution of nutrients and energy. By feeding hydroxyethyl cellulose (HEC) differing in molecular mass, and thus in its viscosity properties, only the consistency of the diet was modified. Three HEC (of low (LV), medium (MV) and high viscosity (HV)) were employed in a 6-week feeding study with female rats to evaluate the effect of the viscosity on adaptive responses of intestinal growth variables. Each of the HEC was added in three increasing concentrations (8, 16, and 32 %, w/w) to a fibre-free control diet to yield nine test groups besides a fibre-free and an additional, fibre-rich, cereal-based control group. Except for the highest concentration of the high viscosity product (32 % HV-HEC), the dilution of the energy density of the diet was almost completely compensated by an increased food intake. With the same exception, energy utilisation was not impaired and, therefore, body-weight gains in the test groups were not significantly different from that in the control. Most other changes, e.g. increases in small intestinal length, mucosal DNA content, caecal and colonic weight, not only depended on the dietary concentration but also on the viscosity of HEC in a manner that either increasing the viscosity at a given dietary concentration or increasing the dietary concentration at a given viscosity led to the same results. These findings clearly prove the important role of the viscosity of the lumen content, as a mere physico-chemical factor, in determining adaptative growth responses in the intestinal tract of rats.

The effects of salt (NaCl) supplementation of rat diets (50 g/kg diet), with normal (200 g/kg) or high (500 g/kg) dietary casein content, were studied in 3-week-old male rats over a 3-week period. Weight gain was reduced by dietary salt but was unaffected by dietary casein. Salt-supplemented rats exhibited a two-and three-fold increase in urinary Mg and Ca excretion respectively, irrespective of dietary casein content. Dietary casein had no effect on urinary Ca or Mg. Salt reduced femoral mass but not femoral mass expressed relative to body weight, but neither variable was affected by dietary casein. Femoral Mg and P contents and concentrations were unaffected by dietary salt or casein. While femoral Ca concentration was unaffected by dietary salt, the Ca content was reduced by salt supplementation, irrespective of dietary casein content. Neither the content nor concentration of Ca in femora was affected by dietary casein. Urinary pyridinoline and deoxypyridinoline levels were increased by salt supplementation, irrespective of dietary casein content, but were unaffected by casein. Net Ca absorption was unaffected by dietary salt or casein. In conclusion, these results show that salt supplementation over the short-term increased the rate of bone resorption in rats. This was as a consequence of Na-induced calciuria. On the other hand, a high dietary protein intake had no effect on Ca metabolism, bone composition or bone resorption, nor did it augment the Na-induced calciuria or increased rate of bone resorption.

The fermentation of starch in vitro produces a higher proportion of butyrate than the fermentation of most other substrates. The α-glucosidase inhibitor acarbose increases the amount of starch entering the colon, and has been shown to increase faecal butyrate in humans. It is generally considered that colonic butyrate is quantitatively removed by the colonic mucosa and liver and does not appear in peripheral blood. However, studies in animals suggest that a small proportion of colonic butyrate reaches peripheral blood. Thus, we hypothesised that an increase in colonic butyrate production would result in a rise in serum butyrate in human subjects. To test this, subjects with impaired glucose tolerance were randomly treated in a double-blind fashion with placebo (n 11) or acarbose (n 11) (100 mg three times per day). Serum short-chain fatty acid concentrations were measured twelve times over 12 h with subjects eating a standard diet before randomization and after 4 months of therapy. At baseline, 12 h mean serum butyrate concentrations were similar in the placebo and acarbose groups (2·8 (SE 0·7) AND 3·3 (se 0·6) μm, respectively). After 4 months on placebo, mean serum butyrate (2·6 (se 0·5) μm) was no different from baseline. However, after 4 months on acarbose, serum butyrate had increased to 4·2 (se 1·0) μm, a value which differed significantly from both the baseline value in the acarbose group and the treatment value in the placebo group. We conclude that acarbose increased serum butyrate in subjects with impaired glucose tolerance. These results support the hypothesis that increased colonic butyrate production in human subjects can be detected by an increase in serum butyrate.

This study investigated how readily achievable changes to the quantity and processing of starchy foods in a typical Western diet: (1) were reflected in levels of resistant starch (RS) and NSP excreted from the small intestine; and (2) more favourable profiles of butyrate, NH3 and phenol production. Two diets, a low-starch diet (LSD) and a high-starch, low-fat diet (HSLFD) were compared. The LSD with 20 % total energy (%E) from starch was based on a ‘typical’ Australian diet, while the HSLFD (40 %E as starch) was the same Australian diet modified by an increased content of legumes, starchy foods and coarsely-ground cereals and by a reduced fat content. Four subjects with iliostomies consumed each diet for 2 d, with ileal effluent collection on the second day. On the HSLFD compared with the LSD, RS in ileal effluent increased from from 0·49 to 1·7 g/MJ per d (P < 0·005) while ileal NSP excretion increased from 2·0 to 3·3 g/MJ per d (P < 0·05). Ileal effluents obtained after each diet were incubated for 24 h in vitro with a human faecal innoculum. After fermentation, ileal effluent from the HSLFD produced more butyrate relative to other short-chain fatty acids (17·5 v. 15·8 molar %, P < 0·005) and less phenol (2·3 v. 5·7 mg/l, P < 0·05) and NH3 (20·3 v. 23·1 mmol/l, P < 0·005) than the LSD diet. The HSLFD also generated a lower pH (6·15 v. 6·27, P < 0·05). On a wt/wt basis, RS was 2·3-fold higher in the HSLFD effluent while NSP did not increase, suggesting that the change in RS largely contributed to the fermentation effects. Changes in in vitro variables when the HSLFD ileal effluent was ground before fermentation indicated the importance of physical structure in determining ileal excretion of RS. We conclude that: (1) readily achievable modifications to the amount and processing of starchy foods in an Australian diet would produce potential benefits for in vitro fermentation variables; and (2) the physical structure of grains and cereals is important in determining access by colonic bacteria to a carbohydrate substrate.

Determination of microbial degradability of N is important in formulating a sound supplementation strategy for efficient utilisation of basal as well as supplementary diet components. In vitro degradability of N (IVDN) from tannin-containing browses (Acacia cyanophylla, Acacia albida, Acioa barteri and Quercus ilex) and two herbaceous legumes (Desmodium intortum andDesmodium uncinatum) was determined using the in vitro gas-production method coupled with NH3-N measurement in the presence and absence of a tannin-binding agent (polyethylene glycol (PEG), molecular mass 6000). Addition of PEG to tannin-containing feeds significantly (P < 0·05) increased in vitro gas and short-chain fatty acid (SCFA) production, and IVDN. The use of PEG as a tannin-binding agent increased IVDN from 28 to 59, 32 to 72, 19 to 40, 32 to 73, 40 to 80, and 26 to 77 % in A. cyanophylla, A. albida, A. barteri, D. intortum,D. uncinatum and Q. ilexrespectively. There was significant correlation between total phenolic compounds (total phenol, TP; total tannin, TT) in leguminous forages and percentage increase in IVDN on addition of PEG (P < 0·05; R2 0·70 and 0·82 for TP and TT respectively). The difference in IVDN observed in the absence and presence of PEG indicates the amount of protein protected from degradation in the rumen by tannins. When measured after 24 h incubation, tannin-containing feeds incubated in absence of PEG resulted in higher microbial protein synthesis than in the presence of PEG. Addition of PEG significantly (P < 0·05) reduced the efficiency of microbial protein synthesis expressed as μmol purine/mmol SCFA.

A low (L) and high-fibre (H) diet were fed to six multiparous sows during gestation in a 2 × 2 repeated Latin square design. A single meal per day was given that provided 37·2 MJ digestible energy/d. The kinetics of heat production (HP) and its partitioning (fasting HP, activity HP, and thermic effect of feeding (TEF)) were determined. The TEF was partitioned between a dynamic component (TEFst) and a constant component (TEFlt). Digestibility of energy and nutrients was lower for the diet H. In spite of the lower metabolisable energy (ME) intake (33·9 v. 35·4 MJ/d for diets H and L respectively), HP was higher for diet H (30·5 v. 28·9 MJ/d) resulting in a lower energy retention. The estimated fasting HP was 270 kJ/kg body weight0·75 per d at day 0 of gestation and increased with advancement of pregnancy. The TEFlt was not significantly different from zero for diet L, but represented 4·1 % of ME intake for diet H. The TEFst was not affected by the diet but diet H delayed the postprandial peak of HP. Total TEF was higher for diet H than for diet L (11·7 v. 8·2 % of ME intake). The longer duration of eating with diet H was compensated for by less physical activity between meals, so that activity HP was equivalent for both diets. The activity HP represented 20 % of ME intake but was variable between sows. The ME requirements for maintenance averaged 440 kJ/kg body weight0·75per d. Feeding high-fibre diets increases HP, delays the postprandial peak of HP and maintains the basal HP at a higher level.

Many women associate one or more of their pregnancies with the development of adult obesity. Such an association has not been fully explored. This longitudinal study examines the changes in maternal anthropometric indices during pregnancy and postpartum. Seventy-seven pregnant subjects were investigated longitudinally at about 13, 25 and 36 weeks gestation, of whom forty-seven continued taking part into the postpartum period. Maternal weight, height and skinfold thickness (triceps, biceps, subscapular, suprailiac and mid thigh) were measured at each visit. Maternal fat mass was estimated from the conversion of the first four skinfold thicknesses. Maternal waist and hip circumferences were also measured at the first visit and 6 weeks and 6 months postpartum. Weight and fat gain during pregnancy (13–36 weeks gestation) was 10·9 (SD 4·7) KG AND 4·6 (sd 3·3) kg (P < 0·001) respectively. A significant increase in fat mass from 13 weeks gestation to 6-months postpartum was observed (2·6 (sd 4·5), P < 0·001). The increased weight at 6-months postpartum, however, was not statistically significant (1·1 (sd 6·0) kg, P = 0·20). Based on BMI in early pregnancy, the subjects were divided into groups of underweight, normal weight, overweight and obese. The last three groups were compared using ANOVA. The obese group showed a significant difference in the pattern of changes in the skinfold thickness, waist: hip ratio and fat mass at the postpartum period, in comparison with the other two groups. In conclusion, there is a tendency in the obese group to develop central obesity at the postpartum period.

While a wealth of data on the fatty acid composition of mature human milk has been published, limited information is available on the quantities of individual fatty acids supplied to the suckling infant with maternal milk, through the whole first year of life. Our aim was to qualitatively and quantitatively evaluate the fatty acid composition of human milk from Italian mothers, throughout extended lactation with particular emphasis on the long-chain polyunsaturated fatty acids. We have thus measured the total fat content and the concentrations of major fatty acids by quantitative GLC in pooled breast hindmilk collected from all feedings over 24 h at colostrum, 1, 3, 6, 9 and 12 months in ten mothers recruited after delivery of full-term infants. Total saturated fatty acids progressively increase and total monounsaturated progressively decrease as percentage levels, while among long-chain polyunsaturated fatty acids, percentages of arachidonic acid and docosahexaenoic acid decrease from colostrum up to the third month. Hindmilk total lipids (mg/dl) rise more than twofold up to 3 months, and then remain stable. The amounts (mg/dl) of linoleic acid and α-linolenic acid progressively increase, following the trend of total fat, while arachidonic and docosahexaenoic concentrations (mg/dl) remain stable throughout the whole nursing period. Assessment of the intakes per kg body weight shows different trends for the individual major long-chain polyunsaturated fatty acids supplied to the infant from hindmilk during exclusive breast-feeding (3 months). This information may be useful for the evaluation of infant intakes during extended lactation.

Dietary Ca and osteocalcin (OC), parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OH-D), insulin-like growth factor (IGF)-I and sex hormone binding globulin (SHBG) were assessed simultaneously to bone mineral density (BMD) in 200 adolescent girls (aged 11–15 years) and 100 young women (aged 20–23 years), selected from the lowest and highest end of the Ca intake distribution of a larger population sample. Ca intake was evaluated by food frequency questionnaires, BMD was measured by dual energy x-ray absorptiometry at ultradistal and proximal radius of non-dominant arm, bone age was estimated from x-rays of left hand and wrist according to. Surprisingly, mean Ca intakes were below the dietary reference intakes in the subgroups of girls and women with the highest measured Ca consumption. Postmenarcheal, but not premenarcheal girls showed radial densities as high as the women and in no group was BMD associated with Ca intake. In all adolescents serum PTH was negatively related to dietary Ca. In girls before menarche IGF-I was positively associated with bone age, while in the same subjects the negative relationship between SHBG and BMD pointed to the crucial role of bioavailable sex steroids on bone mass apposition in early puberty. OC levels decreased progressively with age, while serum 25-OH-D significantly increased after menarche. In conclusion, although in adolescents low Ca intake has not been shown to induce any immediate deleterious effect on radial density, the compensatory hypersecretion of PTH supports the need for an adequate Ca intake to achieve peak bone mass.

The purpose of the present work was to examine effects of the Cu–Fe interaction on intestinal β-carotene 15,15′-dioxygenase activity when a wide range of dietary Fe (deficiency to excess) was used in relation to Cu status of rats. The effect of dietary carbohydrates was also examined since they play a role in the Cu–Fe interaction in vivo. Weanling male Sprague-Dawley rats (n 72) were divided into twelve dietary groups, which were fed on either low-, normal-, or high-Fe levels (0·9, 9·0, and 90·0 mmol Fe/kg diet respectively) combined with Cu-adequate or -deficient levels (0·94 and 0·09 mmol Cu/kg diet respectively) and with starch or fructose in the diets. The data showed that both Fe concentration and β-carotene 15,15′-dioxygenase activity in small intestinal mucosa were enhanced with increasing dietary Fe and with Cu deficiency v. Cu adequacy. Dietary fructose did not aggravate the Fe-enhancement, related to Cu deficiency, in the small intestine; however, fructose increased the intestinal dioxygenase activity in rats fed on normal- or high-Fe diets when compared with starch controls. Thus, the highest intestinal dioxygenase activity associated with the lowest hepatic retinol (total) concentration was found in rats fed on the Cu-deficient, high-Fe, fructose-based diet. Finally, a positive linear relationship was found between the dioxygenase activity and Fe concentration in intestinal mucosa. In conclusion, the data indicate that β-carotene 15,15′-dioxygenase activity requires Fe as cofactor in vivoand the enzyme is modulated by the three dietary components: Cu, Fe, and fructose.

Vitamin A deficiency during pregnancy is associated with detrimental effects in the offspring. We have developed a rat model to examine specific effects of maternal vitamin A status on perinatal growth and development. A total of 54 female rats were fed a vitamin A-free (VAF), -marginal (VAM) or -sufficient (VAS) diet from weaning until mating (at 7 weeks) and throughout pregnancy. Half of the rats in each group were injected with a single large dose of vitamin A on day 10 of pregnancy. Fetal and neonatal samples were taken on day 20 of pregnancy and the day of birth respectively. Maternal plasma retinol concentrations on day 20 and at birth were 50 % and 30 % lower in the VAF and VAM when compared to the VAS group. Fetal weight and survival did not differ between groups although placental: fetal ratio was higher in the VAF group than in the VAS group (0·195 (SE 0·005) V. 0·175 (se 0·004), P < 0·05). Rats fed the VAF diet gave birth at 23·5 d, an average of 1 d later than the other groups, and had lower number of live neonates at birth. Fetal liver, heart and lung weights relative to total body weight were lower in the VAF group and had altered growth trajectories. In neonates, only the relative lung weight was reduced. In addition, an increased protein: DNA ratio indicated hypertrophy in fetal kidneys. Vitamin A injection had no additional effect on length of gestation and fetal or neonatal number. However, injection increased relative fetal organ weights in the VAF group but did not alter the effects of vitamin A deficiency in the neonate. These data suggest that chronic vitamin A deficiency during pregnancy compromises liver, heart and kidney and impairs lung growth and development during the last few days of gestation and reduces number of live neonates at birth.