We previously developed a malnutrition risk index, the Elderly Nutritional Index for Geriatric Malnutrition Assessment (ENIGMA) with good predictive accuracy for mortality risk in an original population cohort (SLAS1). Herein, we further evaluate the concurrent and predictive validity of the ENIGMA construct in an external validation cohort (SLAS-2) of 2824 community-dwelling older adults aged 55+ years. They were assessed on the ENIGMA index, Mini Nutritional Assessment-Short Form (MNA-SF) and the Geriatric Nutritional Risk Index (GNRI), known correlates of malnutrition, and baseline and follow-up functional dependency and 10-year mortality risk. Higher ENIGMA risk categories were significantly associated (P < 0·001) with lower education, living alone, smoking, low physical activity, BMI < 18·5 kg/m2, poorer muscle strength and functional mobility, exhaustion, physical frailty, homocysteine, glomerular filtration rate, Hb, red and white blood cell counts, platelets, systemic inflammation indexes, metabolic syndrome, CVD, cognitive impairment and depressive symptoms (Geriatric Depression Scale ≥ 5). ENIGMA scores showed statistically significant (P < 0·001) correlations but low-to-moderate concordance with MNA-SF (r = 0·148, agreement = 45·9 %, kappa = 0·085) and GNRI scores (r = 0·156, agreement = 45·8 %, kappa = 0·096). Controlling for known correlates of malnutrition, only high-risk ENIGMA among the indexes significantly predicted baseline functional dependency (OR = 1·64, 95 % CI 1·01, 2·65) and mortality (hazard ratio = 1·65 (95 % CI 1·04, 2·62). ENIGMA marginally out-performed MNA-SF and GNRI in predicting baseline functional dependency (AUC: 0·625 v. 0·584 v. 0·526), follow-up functional dependency (AUC: 0·594 v. 0·525 v. 0·479) and 10-year mortality risk (AUC: 0·641 v. 0·596 v. 0·595). The concurrent and predictive validity of the ENIGMA construct is replicated in an external evaluation study of community-dwelling older persons.

Postprandial hypotension may be influenced by the digestion of fat. The aim of the present study was to evaluate the hypothesis that products of fat digestion mediate the hypotensive response to fat. In part A of the study, nine healthy older subjects were studied on three separate occasions in randomised order. Blood pressure, heart rate (HR), plasma TAG and gastric emptying were measured following the ingestion of equivolaemic drinks: (1) 300 ml of high-fat drink (88 % fat); (2) fat drink mixed with 120 mg orlistat (lipase inhibitor); (3) water (control). In part B of the study, ten healthy older subjects were studied on two separate occasions. Blood pressure, HR, plasma TAG and superior mesenteric artery flow were measured during 90 min intraduodenal infusions of 10 % intralipid (2·7 ml/min), with and without 120 mg orlistat. Oral fat ingestion was associated with decreases in systolic and diastolic blood pressures (both P = 0·0001) that were greater when orlistat was co-administered (both P < 0·05), and an increase in HR (P = 0·0001) that was inhibited by orlistat co-administration (P < 0·03). Gastric emptying was slowed by oral fat digestion, and orlistat administration inhibited this slowing (P < 0·04). Intraduodenal fat infusion was not associated with changes in blood pressure but increased HR (P < 0·0001), an effect attenuated by orlistat (P < 0·05). In conclusion, orlistat potentiates the hypotensive response to oral fat in older adults, possibly as a result of faster gastric emptying of fat. The results do not support a role for fat digestion in lowering blood pressure.

Protein degradation rates were assessed by the excretion of Nt-methylhistidine (NtMH) in four strains of mature chickens, two White Leghorns and two broilers (dwarf and normal), fed on diets containing two levels of dietary protein. Over 0.9 of labelled NtMH was recovered within 7 d of injection from three White Leghorn, three dwarf and three normal broiler males. Protein degradation, measured by NtMH output, was related to adult body-weight by the power 0.71 and strain intercepts were significantly different. Strain differences disappeared when the rate of output of NtMH per unit lean was evaluated. The rate of output of NtMH per unit muscle was higher in birds fed on a low-protein diet of 100 g crude protein (nitrogen x 6.25; CP)/kg compared with males fed on 150 g CP/kg. It was concluded that the lower rate of protein degradation in broiler compared with layer strains at young ages is related to increased adult body-weight in agreement with well-established biological principles.

From the observation that fasting heat production includes the cost of body protein resynthesis and the evidence that protein resynthesis is included in the regression estimate of protein retention efficiency it is conjectured that the estimate of maintenance from fasting heat production must be conceptually equal to the regression intercept estimate of maintenance plus the cost of body protein resynthesis. Experimental evidence for comparable situations shows an approximate observational equality in agreement with the conjectured conceptual equality. This approximate equality implies that the theoretical (stiochiometric) efficiency of protein synthesis should be used in conjunction with the estimate of maintenance from fasting heat production for the prediction of growth energy requirements. The approximate maintenance equalities suggest furthermore approximate equality of theoretical fat synthesis efficiency and regression fat retention efficiency. This conjecture is also supported by experimental evidence. Some practical nutrition and pig breeding implications of the foregoing conclusions are indicated.

There is a growing awareness that the gut microbiota and an appropriately functioning immune system play an important role in maintaining human health. Recent population statistics have highlighted some worrying trends, specifically that there is a growing burden of immunological disease in Western populations, that Western populations are ageing, and that obesity, with its strong inflammatory component, is reaching epidemic proportions.

Individual differences in sleep patterns of children may have developmental origins. In the present study, two factors known to influence behavioural development, monoamine oxidase A (MAOA) genotype and prenatal Fe-deficient (ID) diet, were examined for their influences on sleep patterns in juvenile rhesus monkeys. Sleep patterns were assessed based on a threshold for inactivity as recorded by activity monitors. Pregnant monkeys were fed diets containing either 100 parts per million (ppm) Fe (Fe sufficient, IS) or 10 ppm Fe (ID). At 3–4 months of age, male offspring were genotyped for polymorphisms of the MAOA gene that lead to high or low transcription. At 1 and 2 years of age, sleep patterns were assessed. Several parameters of sleep architecture changed with age. At 1 year of age, monkeys with the low-MAOA genotype demonstrated a trend towards more sleep episodes at night compared with those with the high-MAOA genotype. When monkeys reached 2 years of age, prenatal ID reversed this trend; ID in the low-MAOA group resulted in sleep fragmentation, more awakenings at night and more sleep episodes during the day when compared with prenatal IS in this genotype. The ability to consolidate sleep during the dark cycle was disrupted by prenatal ID, specifically in monkeys with the low-MAOA genotype.

1. The metabolic responses to daily treatment with 1 μg cyanocobalamin were studied in sixteen patients with megaloblastic anaemia due to cobalamin deficiency.

2. The fall in serum iron was sluggish in most patients. The pattern of reticulocyte responses varied widely, the most common being a plateau with suboptimal maximal value.

3. Urinary propionic acid excretion before treatment was normal in two out of six patients. A transient rise during treatment was observed in two patients, possibly owing to demands on coenzyme stores. The fall in urinary propionic acid excretion during treatment was slow.

4. Serum vitamin B12 levels rose during treatment. In two patients an abrupt rise was found, possibly owing to release of stored cobalamin into the circulation.

Only one previous study has examined the association between coffee consumption and risk of acute pancreatitis, and it found a reduced risk for alcohol-related episodes among high consumers of coffee. Therefore, we examined (1) the association between coffee consumption and risk of non-gallstone-related acute pancreatitis and (2) whether this association was modified by alcohol intake. Data were obtained from two prospective cohorts, the Cohort of Swedish Men and the Swedish Mammography Cohort, including 76 731 men and women (born 1914–1952). Coffee consumption was assessed at baseline with a FFQ, and the cohorts were followed up between 1998 and 2012 via linkage to national health registries. Hazard ratios were estimated using Cox models, with adjustment for potential confounding factors. During 1 035 881 person-years of total follow-up, 383 cases (246 in men and 137 in women) of incident non-gallstone-related acute pancreatitis were identified. Overall, and irrespective of whether a categorical or a continuous exposure model was used, we observed no association between coffee consumption and risk of non-gallstone-related acute pancreatitis (e.g. the multivariable-adjusted hazard ratio for each 1 cup/d increase in coffee consumption was 0·97; 95 % CI 0·92, 1·03). There was no evidence of effect modification by alcohol intake (Pinteraction=0·77). In conclusion, coffee consumption was not associated with risk of non-gallstone-related acute pancreatitis in this large prospective cohort study. Because of the limited number of epidemiological studies and their conflicting results, further research is needed to elucidate this potential association.

1. Serum prolactin (PRL) levels, both basal and post-suckling peak, were estimated in fifty-seven lactating women.

2. Basal PRL levels were significantly higher in all lactating women irrespective of the duration of lactation as compared to the levels in non-pregnant, non-lactating women.

3. There was a significant positive correlation (r 0·69, P < 0·001) between the basal PRL levels and the post-suckling peak values.

4. After 8 months of lactation, peak post-suckling, PRL levels were not significantly different from basal values.

5. Basal PRL levels were significantly lower (P < 0·05) in mothers whose infants were being supplemented.

6. PRL levels were not related to the mother's nutritional status as determined by body-weight.

7. The findings suggest that high PRL levels during lactation prolong the duration of lactional amenorrhoea and hence the relative infertility.

1. The relationship of vitamin A and carotenoids with encephalomalacia was examined in chick-raising farms and under laboratory conditions. 2. In encephalomalacic chicks on the farms a significant decrease in liver carotenoid content was demonstrated. In the diseased chicks the carotenoid contentwas below 0.30 mg/100 g liver, as against the normal values of 0.40–1.0 mg/ 100 g. 3. Under experimental conditions incidence of encephalomalacia could be decreased by oral treatment with the synthetic carotenoid ethyl β-apo-8'-carotenoate. This implies that deficiency in carotenoid is not merely a concomitant sign of encephalomalacia, but has also a causative role, as sufficient carotenoid reserves confer a certain protection against the disease. 4. The pathogenetic role of carotenoid metabolism in encephalomalacia was supported by certain observations. Factors inhibiting the accumulation of ethyl β-apo-8'-carotenoate in the liver predispose chicks to the disease. In chicks 4–5 weeks old in addition to those with vitamin A reserves higher than 800 i.u./g liver, the accumulation of carotenoids in the liver was about 10% of that measured in chicks more than 7 weeks old, or in those with vitamin A reserves not higher than from 100 to 200 i.u./g. In fact, encephalomalacia occurs mainly among chicks 3–5 weeks old. Also, reserves of vitamin A exceeding 800 i.u./g liver were found to predispose chickens to encephalomalacia.

The present study investigated the effect of the acute-phase ‘injury’ response, induced by subcutaneous injection of turpentine, on the hydration and protein content of organs and tissues of normally nourished rats receiving a diet containing 200g protein/kg, and of protein-malnourished rats receiving a diet containing 30 g protein/kg. The measurements were carried out 48 h after turpentine injection, and were compared with both saline-injected animals, and pair-fed control animals. Circulating α2-macroglobulin was also measured as an index of the acute-phase-protein response. In normally nourished rats turpentine injection caused a significant increase in the mean masses of the liver, kidney and lung (7–35% compared with saline-injected animals, and 20–44% compared with pair-fed controls), and a small reduction in the mass of extra-abdominal and extrathoracic tissues (‘carcass’). In general the protein content of tissues changed in a similar way (for liver, kidney and lung a 16–33% increase compared with saline-injected animals, and 32–49% compared with pair-fed controls). Protein deficiency produced a significant attenuation in the response to turpentine. The change in the mass and protein content of several tissues was reduced (for lung, liver and kidney, the increase in protein content was only 5–15%), and the effects on anorexia (1 v. 41% reduction infood intake) and the α2,-macroglobulin response (1·28 v. 4·28 g/l; P< 0·001) were also reduced. It is concluded that the injury response spares most central thoracic and abdominal organs, but this effect as well as the anorexia and acute-phase-protein response to injury are attenuated by protein deficiency.

1. The effectiveness of supplementing a vitamin E-deficient basal diet with levels from 0 to 20 ppm of selenium as sodium selenite, alone and in combination with graded levels of L-cystine, sodium sulphate, L-serine and vitamine E, has been studied in chicks from 1 day of age to 4 weeks. Supplementation with Se at levels up to 1 ppm had maximum beneficial effects on growth and prevention of muscular dystrophy. Levels of Se above 1 ppm were progressively less effective, and, in chicks given supplements of 20 ppm Se, growth and muscular dystrophy were depressed to that found with chicks given the basal diet.

2. Supplementation with L-cystine (0.08% and 0.16%) in combination with Se up to 1 ppm was beneficial, but this effect was progressively suppressed as the amount of Se was increased beyond this level. Supplementation with sodium sulphate (0.08% and 0.16%) or L-serine (0.08% and 0.16%) instead of L-cystine had no influence on the effectiveness of Se at any level of the latter tested.

3. The effectiveness of dietary D-α-tocopheryl acetate, up to 20 mg/kg, for growth and in the prevention of muscular dystrophy was improved by Se at levels up to 1 ppm. Its effectiveness was then progressively reduced as the amount of Se was increased above 1 ppm.

4. It appears that Se at low levels spares L-cystine and vitamin E in the chick, whereas at high levels it increases their requirement for growth and prevention of muscular dystrophy.

1. The effects of bucket- v. teat-feeding and warm- v. cold-milk feeding on the flow of duodenal digesta and the concurrent pancreatic secretion were studied in two experiments in preruminant Ayrshire calves (28–43 d of age), fitted with duodenal re-entrant and pancreatic sac cannulas.

2. As measured by the time interval taken for total recovery of the polyethylene glycol fed in the milk, the whey fluids had a more rapid passage through the abomasum when the calves were given warm milk by teat rather than by bucket (Expts 1 and 2). The duodenal digesta contained less sodium ions and more ‘Cl-Na+’ when the calves were fed by teat even though the volumes of milk drunk and duodenal flow were similar. It was concluded that more abomasal acid was secreted when calves were fed by teat.

3. When the calves were fed by teat rather than by bucket, the protein-nitrogen : N (PN : N) in the duodenal digesta was lower, especially during the first 6 h after feeding and there was a tendency for more pancreatic proteases to be secreted.

4. In Expt 1, when the calves were given warm milk the total flow of N and lipid in the duodenal digesta was 22 and 19% greater than that ingested. This was considered to be due to the coagulum from the penultimate meal plus the experimental meal passing more readily through the duodenum when sampling and to endogenous secretion of N and lipid.

5. When four Ayrshire calves were bucket-fed cold, rather than warm milk there was a reduced secretion of abomasal and pancreatic fluids and abomasal acid. There were no differences in the time interval required for the whey fluids to leave the abomasum or the PN : N value.

6. There was a positive correlation between the total duodenal flow of non-whey fluids and the pancreatic secretion regardless of the method of feeding.

7. The completeness of digestion and susceptibility of calves to diarrhoea when fed by teat and bucket is discussed.

1. In two experiments, involving 110 chicks up to 5 weeks of age, retention of an oral dose of 54Mn was always low; less than 5%.

2. There were no significant differences in retention by hybrid broiler cocks, hybrid layer cocks, and hybrid layer pullets, nor was retention affected by the period of fasting, i.e. 1 ½ or 24 h, before dosing.

3. Two-weeks-old birds retained 58% more radioactive manganese than 5-week-old birds, and retention in birds killed 24 h after the dose was only 64% of that in birds killed 4 h after the dose.

4. With the addition to a fixed dose of 54Mn of increasing quantities of non-radioactive Mn retention decreased only from 2.52% with no Mn added to 1.02% with 5000 μg Mn added, representing a very large increase in total retention of Mn.