1. Nitrogen balance, weight loss and resting metabolic rate were measured in thirty-eight obese inpatients on 3.4 MJ (800 kcal)/d diets over 3 weeks.

2. All subjects were fed on 13% protein-energy in three rneals/d for the first week.

3. In weeks 2 or 3, using a cross-over design, ten subjects were fed on 15 or 10% protein-energy as three meals/d; fourteen subjects were fed on five or one meal/d with 13%protein energy; and fourteen subjects were fed on 15% protein-energy as five meals/d or 10% protein-energy as one meal/d.

4. N loss was least on the high-protein week and frequent-meal week: the largest difference was found when these effects were combined (P < 0.001).

5. When protein-energy was held constant at 13% N loss decreased significantly (P < 0.01) between week 2 and 3, but when the protein-energy was manipulated there was no significant N conservation in the third week. This suggests that the protein:energy value is more important than meal frequency in the preservation of lean tissue.

6. Weight loss was also least on the ‘high-protein’ week and ‘frequent-meal’ week, but this result reached significance only when the effects were combined (P < 0.05).

7. Resting metabolic rate decreased with time but was not significantly altered by the dietary regimens.

8. Therefore, during the first 3 weeks at an intake of 3.4 MJ/d, a diet with a high-protein concentration, fed as frequent small meals, is associated with better preservation of lean tissue than an isoenergetic diet with lower-protein concentration fed as fewer meals. There was no evidence that meal frequency or protein concentration affect the rate of fat loss.

1. Review of the evidence of the Irish Nutrition Survey concerning a marked rise in the incidence of rickets in Dublin in 1942 concludes that a rise in the extraction rate of the national flour from 70 to 100% was principally responsible.

2. This rise and subsequent decrease in incidence as the extraction rate of flour was reduced is not explained by changes in the proportion of children protected by vitamin D supplements or by small changes in dietary vitamin D intake.

3. The evidence suggests that nutritional rickets in man cannot be explained on the basis of deficient vitamin D intake alone, whether derived from diet or U.V. radiation.

1. The dietary intakes of sixty-three adults, randomly-selected from the electoral role of a large village near Cambridge, have been measured using the weighed-intake technique for 7 d.

2. Mean (±sD) daily intakes (g) for men and women respectively were: energy (MJ) 10.0±2.4, 8.2±2.1; fat 104±27,90±21; protein 77±20,67± 16; carbohydrate 285±81,229±74; sucrose 91±47, 57±33.

3. When interviewed at the end of the study 40% of subjects said they were watching their weight.

4. Women ate less food over all than men, and proportionately less potato and bread, and used only one-third as much sugar in drinks, probably in an attempt to control their weight. Men took considerably more alcohol than the women. In the age-group 20–39 years alcohol provided 9% (1.0 MJ/d) of the total energy intake in the men.

5. Wide variation in the intake of nutrients was observed amongst the individuals. For vitamin C and fibre intake this was partly explained by seasonal variation but for most nutrients total energy intake and food choice were the main determinants. The range. of intakes of nutrients such as fat was similar in these individuals to that seen amongst countries internationally. It is suggested that if differences in nutrient intake amongst the various populations of the world can be associated with disease risk, then the same interpretation should be possible in individuals.

1. Acute riboflavin deficiency was produced in weanling rats by feeding a deficient diet and using tailcups to prevent refection. Animals were killed at weekly interval for 7 weeks, by the end of which they had become severely deficient, and mortality was high.

2. Growth of the deficient animals virtually ceased in the early stages of deficiency; food intake was severely and progressively depressed. Liver: body-weight increased markedly; packed cell volume fell at a late stage only. Pathological signs accumulated throughout the deficiency but were not closely related to the biochemical changes within the deficient group.

3. The activation coefficient (stimulated: basal activity; AC) of glutathione oxidoreductase (EC 1.6.4.2; glutathione reductase; GR) in erythrocytes rose to a mean value of 3–8 after 3 weeks, and subsequently remained almost constant: this change was not seen in pair-fed or ud lib.-fed controls. Both deficient and pair-fed animals exhibited a twofold reduction in FAD-stimulated erythrocyteGR activity at an early stage. In liver, both deficient and pair-fed groups showed a major progressive fall in FAD-stimulated GR activity, but only the deficient group showed an increase in AC, which occurred towards the later stages of the experiment. In skin, too, the deficient group showed an increase in AC during the terminal stages.

4. Hepatic, intestinal and brain succinate: (acceptor) oxidoreductase (EC 1.3.99,1; succinate dehydrogenase) activity fell relatively early during deficiency; in liver and intestine this was at least partly shared by the pair-fed group, and therefore attributable to inanition. Changes in hepatic NADH:(acceptor) oxidoreductase (EC I.6.99.3; NADH dehydrogenase) activity appeared to be entidy attributable to inanition.

5. An early reduction was observed in hepatic ATP: riboflavin 5-phosphotransferase (EC 2.7.1.26; flavo- kinase) activity in the deficient group, values falling by nearly half within 1 week, and then remaining almost constant. Similar but smaller changes were seen in renal flavokinase activity. Hepatic ATP: FMN adenylyltrans- ferase (EC 2.7.7.2; FAD pyrophosphorylase) was unchanged until the third week, at which point it rose sharply to a new plateau in the deficient group; in kidney it did not respond. These changes were not observed in pair-fed or ad-lib.-fed controls.

6. Hepatic flavin levels fell dramatically during the first 2 weeks of deficiency, FAD being conserved at the expense of FMN. Smaller changes were observed in kidney.

7. Of the processes which are affected by riboflavin deficiency, AC of erythrocyte GR (EGRAC) responds earlier, more dramatically and more specifically than most others, with the possible exception of hepatic flavin levels and flavokinase. Potentially, it is therefore a good index of over-all body riboflavin status, but in acute deficiency the rate of response of many variables is not related to the final extent of response; consequently the correlation between EGRAC and other riboflavin-sensitive processes is less satisfactory than it would be in an equilibrium situation.

1. Chronic marginal riboflavin deficiency was induced in groups of weanling rats by feeding a deficient diet supplemented with 0, 0·5, 1·0 and 1·5 mg riboflavin/kg diet. Ad lib.- and pair-fed controls received 3·0 and 15 mg riboflavin/kg diet respectively.

2. Serial measurement of erythrocyte NAD(P)H2 glutathione oxidoreductase (glutathione reductase; EC 1.6.4.2) and its activation coefficient revealed that after 12 weeks a steady-state of deficiency had been reached following initial fluctuations in status; the animals were then killed, and their tissues analysed.

3. Food intake, growth rate and the appearance of pathological signs were directly proportional to riboflavin content; however relative liver weight was increased above control levels only in the most-severelydeficient group, and anaemia was not detected in any group.

4. The activation coefficient of glutathione reductase in erythrocytes and liver was closely related to dietary riboflavin content; that of skin responded maximally even in the least-severelydepleted animals.

5. Hepatic and renal flavin contents were directly proportional to dietary riboflavin, FAD being conserved at the expense of ribotlavin and FMN. ATP: riboflavin 5-phosphotransferase (flavokinase; EC 2.7.1.26) activity was reduced, even in the least-severely deficient animals; ATP: FMN adenylyltransferase (FAD pyrophosphory1ase; EC 2.7.7.2) was increased in liver, but only in the most-severely-deficient animals.

6. Hepatic succinate: (acceptor) oxidoreductase (succinate dehydrogenase; EC 1. 3.99.1) activity fell sharply between 1·5 and 0·5 mg riboflavin/kg diet, producing an S-shaped dose-response curve; it showed smaller or less specific changes in other tissues such as brain, skin and intestine. NADH: (acceptor) oxidoreductase (NADH dehydrogenase; EC 1.6.99.3) activity declined in liver and intestine, but not in skin or brain.

7. Theactivation coefficient of glutathione reductase was correlated strongly with nearly all the riboflavin-sensitive variables measured, once equilibrium had been reached in this chronic deficiency model, and it was particularly strongly correlated with hepatic and renal FAD levels. Under equilibrium conditions, therefore, it appears to represent a good index of the extent of riboflavin deficiency, and significant changes in flavin levels and enzymes in the internal organs were detected even under conditions of marginal deficiency, associated with relatively small increases in the activation coefficient.

1. Thirty Mossi male farmers from Upper-Volta were investigated, twenty-three in the dry season (March-April) and sixteen in the rainy season (July-August), eight of them being studied twice. A 48 htime-and-motion study was carried out and the daily energy expenditure was computed.

2. The mean height was 1.70 m and the mean weight 58.5 kg. The average percentage of body fat calculated from skinfold thickness was 10.

3. During the dry season the subjects could be classified as very moderately active with an energy output of 10.1 MJ (2410 kcal)/d. By contrast, with an energy expenditure of 14.4 MJ (3460 kcal)/d, they were considered as exceptionally active in July-August when performing the agricultural work.

4. In this study we measured the intensity of physical work in a society where human labour is still the main tool of production. The determination of seasonal variations in energy expenditure may be useful to assess the nutritional requirements in arid zones of West Africa.

1. Bowel transit time has been investigated in vegetarians and non-vegetarians and related to dietary fibre intake and the presence of diverticular disease.

2. Vegetarians who have less diverticular disease than non-vegetarians have more rapid transit times.

3. Subjects with total dietary fibre intake of more than 30 g/d all had transit times of less than 75 h whereas 38% of those eating less had transit times exceeding 75 h and varying up to 124 h.

4. Individuals with diverticular disease were found to have faster transit times than those without the disease.

5. The colon may respond to a fibre-depleted diet either by becoming hyperactive and prone to diverticular disease or by becoming hypoactive leading to constipation.

1. Dietary fibre has a water holding capacity (WHC) and this is a function of the fibre source and method of measurement. Water can be associated with fibre either as trapped water or bound water. This makes it difficult to predict the ability of fibre to influence stool weight in humans.

2. Examination of various fibre concentrates for chemical composition, as neutral detergent fibre (NDF), acid detergent fibre (ADF) and lignin; structure, by scanning electron microscopy; WHC, by centrifugation, suggests that WHC is more a function of fibre structure than chemical composition. Cereal fibre and vegetable fibre have a different chemical composition and are structurally very distinct. Structure is also dependent on the method of fibre preparation.

3. Measurement of WHC by centrifugation gives an estimate of the water which can be bound and also trapped by the fibre. The amount of trapped water will depend on the structure of the fibre whereas bound water will depend on the chemical composition.

1. Previous measurements of energy intake on sledging journeys in Antarctica have given a mean intake of 14.2 MJ (Acheson, 1974; Campbell, 1975), markedly lower than values reported earlier (see Edholm & Goldsmith, 1966). The technique used (individual weighed-diet survey) was more detailed and could be assumed to be more accurate than most of the earlier work where intakes had been largely inferred from the known energy content of food boxes. In the present study an individual weighed-diet survey was carried out on male subjects during a summer manhauling journey on the east coast of Greenland.

2. Mean daily energy intake of six subjects over 33 d travelling was 16.5 MJ. Mean weight loss was 2.3 kg, probably accounted for entirely by fat loss. Weight loss occurred despite the presence of excess food. Mean daily energy intake rose gradually but persistently over the 5 weeks of the journey despite a constant level of activity and to 20.1 MJ during the 4 d rest at the end of the journey.

3. Intakes were thus higher than those found in the earlier Antarctic studies (Acheson, 1974; Campbell, 1975) but not as high as intakes reported previously (see Edholm & Goldsmith, 1966). The fact that weight loss occurred despite the presence of excess food was ascribed to the monotonous nature of the diet. The fact that energy intake rose persistently over the 5-week study period may imply that a new state of balance of intake and expenditure was reached.

1. Eighteen male sledge dogs were weighed immediately on removal from their sheltered winter quarters at Halley Bay, Antarctica (75° 31′s, 26° 42′W) and weekly thereafter for 14 weeks. The first 2 weeks they were tethered and inactive and the following 12 weeks travelled an average of 10.9 km/d fully laden. Daily energy intake during winter and while tethered averaged 18–25 MJ/d and while travelling 13.9 MJ/0d.

2. Mean weight loss during the 2 weeks of inactivity was 2.3 kg despite an energy intake almost twice the recommended requirement. During the 12 weeks travelling energy intake decreased to 13.9 MJ/d but the weight loss stopped. Weather conditions at this time were becoming progressively milder.

3. The evidence suggests that sledge dogs are capable of high levels of cold-induced and possibly diet-induced thermogenesis and that these factors, particularly the former should be taken into account when designing dog rations and feeding schedules.

1. An experiment is reported in which copper, as cupric oxide, was fed to two breeds of laying hen for 336 d at levels equivalent to 150, 300, 450, 600 and 750 mg added Cu/kg diet. The results obtained were compared with those found using similar diets to which the Cu was added as CuSO4. 5H2O.

2. Addition of the CuO had no effect on food intake, food conversion efficiency, body-weight or egg production. The CuSO4 addition caused the quadratic response of food intake and the adverse effects on food intake, egg production and body-weight noted in previous experiments.

3. The CuO had no effect on liver, kidney, ovary, oviduct or gizzard weight per unit body-weight while the CuSO4 decreased these with the exception of gizzard weight which was significantly increased.

4. CuO addition did not affect liver Cu concentration but CuSO4 caused a subtantial increase of liver Cu especially at the 750 mg Cu/kg level of addition.

5. CuO addition had no effect on liver lipid concentration but this was depressed at the highest level of CuSO4 addition. Effects on individual fatty acids are presented but no specific conclusions have been reached.

1. The influence of ammonia concentration on the distribution of nitrogen derived from opaque-2 maize uniformly-labelled with 15N has been investigated during short-term in vitro incubation of bovine rumen contents.

2. Less 15N derived from maize was found in the non-protein-N (NPN) fraction during incubation without added NH3 than with added NH3, due entirely to differences in the amount of N derived from maize in the NH3 fraction.

3. From calculations based on the transfer of N derived from maize to the NPN pool and to a bacterial fraction, it was concluded that degradation of maize protein was not influenced by NH3 concentration within the examined limits.

4. The decrease in relative amount of N derived from maize in the NH3 fraction at low concentrations of NH3, together with evidence for an increased fractional turnover rate of NH3-N suggests that a deficient supply of NH3 is compensated for by increased catabolism of nitrogenous compounds derived from the rumen micro-organisms.

1. Six adult Friesian cows were given 75Se as either 75SeO32− or 75SeO42− intravenously. Five of the cows had cannulas in an hepatic vein, the portal vein and one carotid artery to enable the uptake of 75Se by the liver to be measured. Radioactive balance studies were carried out on two of the cows given 75SeO32− and two given 75SeO42−. A seventh cow was given an oral dose of 75Se-labelled barley and the excretion of 75Se in faeces, urine and milk was measured for 14 d.

2. After the injection of 75SeO32− plasma 75Se concentration decreased during the first 30 min with a mean half-life (t½) of 15.6 min. From 30 to 60 min after dosing the concentration of radioactivity increased to reach approximately 50% of the level present 2 min after dosing. Following the injection of 75SeO42− the 75Se was cleared with a mean t½ of 28.5 min during the first 30 min and plasma radioactivity increased only slightly during the next 30 min.

3. During the phase of rapid clearance of 75Se after the injection of 75SeO32− the hepatic venous 75Se concentration was approximately 5% lower than portal veous 75Se concentration. During the period when plasma 75Se activity was increasing the activity in hepatic venous plasma was 3% greater than portal activity. Of the 75Se cleared from plasma after injecting 75SeO32− 40% was calculated to be removed by the liver.

4. After intravenous dosing with 75SeO32− or 75SeO42− approximately 9.5 and 17.0% respectively of the dose injected was excreted in faeces and 10% in urine within 14 d. Almost three times as much 75Se was excreted in urine and 3.5 times as much in faeces during the first 24 h after dosing with 75SeO42− as after 75SeO32−.

1. Levels of zinc in liver and plasma of the Zn-depleted rats fluctuated with the feeding cycle and were significantly higher at the bottom than at the top of the cycle. As Zn deficiency became more severe fluctuations in plasma Zn diminished. Concentrations of Zn in liver, in contrast to levels in plasma and femur, were not markedly lowered by day 15.

2. In contrast to udlib.-fed (AL) and overnight-fasted (OF) controls, some pair-fed (PF) controls had elevated levels of Zn in liver and plasma.

3. Intakes of water and food were sigdicantly correlated in Zn-deficient rats. Packed cell volumes were significantly higher for Zn-depleted than for AL and PF rats.

4. Food intakes and plasma glucose concentrations were related in AL, OF and PF control rats but not in Zn-deficient rats.

5. At day 15 of Zn deficiency the order of total plasma amino acid concentrations in the groups of rats was AL > Zn-deficient > OF > PF. Many of the differences between the AL and OF groups for individual plasma amino acids also appeared in the Zn-deficient group at the top and bottom of the feeding cycle. Differences in individual amino acid conmntrations at the top and bottom of the feeding cycle tended to be opposite in the PF and the Zn-ddicient group. Levels of tyrosine and tryptophan in plasma were correlated (P ≶ 0.05) with the cyclic feeding pattern of the Zn-deficient group; however, the ratios tryptophan or tyrosine: sum of other large neutral amino acids did not correlate significantly with the eating habits of Zndeficient rats.

1. Rainbow trout (Salmo gairdneri) of mean initial weight 35 g were given one of five experimental diets for 20 weeks. The diets contained (g/kg dry diet) 15 calcium, 10 phosphorus and graded levels of magnesium from 0.04 (diet no. 1) to 1.0 (diet no. 5). In a second experiment rainbow trout of mean initial weight 16 g were given one of six experimental diets for 20 weeks. The diets contained (g/kg dry diet): Ca (40), P (30) and levels of Mg from 0.06 (diet no. 6) to 2.0 (diet no. 11).

2. In both experiments weight gains were lowest in those trout given diets containing the basal levels of Mg (diet no. 1 and diet no. 6) but increased with increasing dietary Mg concentration. In neither experiment was there any further increase in weight gain once the Mg concentration reached 0.25–0.5 g/kg dry diet; weight gain reached a plateau at this dietary Mg level.

3. The following trends occurred in serum electrolyte concentrations as dietary Mg increased. Mg increased in both experiments, in Expt 2 it reached a maximum of 1 mmol/l when the diet containted 0.5 g Mg/kg and did not increase further; sodium was positively correlated in both experiments; potassium decreased and in Expt 2 reached a plateau minimum of 1.7 mmol/l at a dietary Mg concentration of 0.5 g/kg; Ca and P altered little in either experiment.

4. In both experiments renal Ca concentrations were greatly increased in trout given diets lacking supplementary Mg; they fell to low levels (3–5 mmol/kg) when diets conained 0.15 g Mg/kg or more. Renal K and P concentrations were negatively correlated with dietary Mg in Expt 2; other electrolytes measured were not altered in concentration by the treatments used.

5. Extracellular fluid volume (ECFV) of muscle was negatively correlated with dietary Mg. In Expt 2 it reached a minimal or normal value at 0.5 g Mg/kg diet and did not decease further. Muscle Mg concentration increased with diet Mg in both experiments and muscle K concentration was also correlated with diet Mg in Expt 2. These changes were related to the shift in muscle water. In Expt 1, P concentration was decreased with increasing diet Mg but in Expt 2 its concentration increased, these changes may have been connected with the three-fold difference in dietary P in the two experiments.

6. By contrast with skeletal muscle, Mg levels in cardiac muscle increased at low dietary Mg intakes.

7. Concentrations of electrolytes in liver did not alter with dietary treatments used.

8. The results show that Mg requirement of rainbow trout is met by a diet containing 0.5 g Mg/kg diet.

1. Changes in the concentrations of the minor constituents of goat's milk were observed during 48 h starvation and on refeeding.

2. The concentrations of hexose phosphate and UDP-hexoses increased during starvation and decreased on refeeding.

3. The concentrations of phosphoenolpyruvate and glycerate 3-phosphate decreased during starvation and increased on refeeding.

4. Isocitrate: 2-oxoglutarate increased during starvation and decreased on refeeding.

5. Changes in the minor constituents of milk can be explained in terms of the metabolic changes occurring in the mammary gland during starvation. It is proposed that changes in the concentrations of these metabolites in milk reflect changes in their concentrations in the cytosol or Golgi vesicles of the mammary gland.

1. A method for gas-liquid chromatographic analysis of the dimethyl esters of a homologous series of diabolic acids is described.

2. Only when combined with low-resolution mass spectrometry could the method be used to show unequivocally the existence of diabolic acids in natural products.

3. Diabolic acids occurred naturally in rumen and faecal lipids of all ruminants examined but could not be detected in a number of ruminant tissue samples.

4. Infused 14C-labelled (C16:0)2 diabolic acid was poorly absorbed by both simple-stomached and ruminant animals. Oxidation was more extensive in the ruminant, but there was no evidence of deposition of diabolic acid in the tissues of either animal.

1. The digestibilities of microbial and food proteins in the small intestine were studied in three sheep fitted with re-entrant cannulas in the proximal duodenum and terminal ileum.

2. The quantities of microbial and food proteins at the small intestine were varied by infusion of a microbial isolate or by dietary manipulation and the balance of amino acids along the small intestine was determined.

3. A mean value of 0.69 for the apparent digestibility and 0.86 for the true digestibility of total amino acids was obtained.

4. From the composition of digesta at the duodenum the daily flows of microbial and food proteins were estimated. Their true digestibilities in the small intestine were calculated by regression and found to be: microbial protein 0.87 and food protein 0.82. The mean endogenous loss of amino acids secreted into the small intestine was estimated to be 13.3 g/d.