1. The micro-iodimetric method has been used to study some factors affecting the concentration of lipid peroxides in the adipose tissue of vitamin E-deficient rats.

2. Cod-liver oil methyl esters (CLOME) or maize oil methyl esters (MOME) with peroxide values ranging from 3 to 330 μ-equiv./g were given by mouth to vitamin E-deficient rats deprived of food before and after the dose. Lipid peroxides did not accumulate in the adipose tissue of these rats.

3. Experiments with dietary CLOME and MOME of varying peroxide values (2–230 μ-equiv./g) showed that exogenous lipid peroxide accumulates in the adipose tissue when the rats received these lipids at 10% in the diet for 4 weeks, but not if the dietary concentration was only 4% or if the diet with 10% lipid was given for 5 days only.

4. Rats were given dietary CLOME for 4 weeks. Their adipose tissue was then found to contain about 50 μ-equiv. lipid peroxide/g. They were divided into three groups. One group was given a fat-free diet and, after 10 days, the adipose tissue concentration of lipid peroxide had decreased to about 10 μ-equiv./g. The other groups were given the fat-free basal diet supplemented with vitamin E or DPPD (N,N′-diphenyl-p-phenylenediamine). Neither supplement significantly affected the rate of disappearance of the peroxides from the adipose tissue.

5. It was shown that neither α-tocopherol nor DPPD reacted with the lipid peroxides of CLOME or MOME in vitro, at room temperature or even after 65 h at 37°.

6. It was concluded that unsaturated lipids do not become peroxidized after incorporation into the adipose tissue of vitamin E-deficient rats. Lipid peroxides taken up from the diet into the adipose tissue are not of fleeting existence, having a half-life of about 6 days. Dietary vitamin E probably prevents the accumulation of exogenous lipid peroxides in the adipose tissue by reinforcing the barrier to their absorption in the gut.

7. These studies provide further evidence that current concepts of lipid peroxidation in vitamin E-deficient animals are incorrect. In fact, vitamin E-deficient animals have low concentrations of peroxide in their adipose tissue, unless they have received large amounts of unsaturated lipid for long periods, and the role of vitamin E in controlling this concentration is not due to any effect on peroxidation in vivo.

1. Variation in endogenous nitrogen metabolism was determined by giving eleven healthy men, aged 17–22, a diet supplying daily only 6 mg N/kg body-weight. Eight subjects were given the diet for 7–10 days and three other subjects were given it for 16 days.

2. Body cell mass (BCM) was calculated from whole-body 40K in ten subjects and basal metabolism was determined in seven subjects during the ‘protein-free’ period. Urine was analysed daily for N and creatinine, and faecal N was measured in pooled samples. Plasma free amino acids, serum albumin and protein were measured in preprandial morning blood samples at the beginning and end of the study.

3. BCM did not change during the ‘protein-free’ period and accounted for 48% of the total body-weight. Basal calorie expenditure amounted to 48 ± 5 kcal/kg BCM per day.

4. Mean daily endogenous urinary N excretion in the eight subjects given the ‘protein-free’ diet for 7–10 days was 36·6 ± 3·0 mg N/kg body-weight, 79·4 ± 4·4 mg N/kg BCM and 1·6 ± 0·2 mg N/basal kcal. Endogenous faecal N excretion was 9·9 ± 1·1 mg N/kg body-weight and accounted for 20% of the total endogenous loss. Results obtained with three other subjects given the diet for 16 days were similar.

5. Plasma essential amino acids were reduced, glutamic acid, alanine and glycine increased, and the ratio of essential to non-essential amino acids decreased after 7 or 10 days of ‘protein-free’ diet.

6. The loss of endogenous N per basal kcal and of faecal N per kg body-weight was lower than the values assumed in the factorial approach to protein requirements by the FAO/WHO (1965) Expert Group on Protein Requirements.

1. Eighty weanling albino rats, five from each of sixteen litters were distributed between five dietary groups in sixteen randomized blocks. Each block was formed from within a litter and each animal in the block received a different diet.

2. The main features of the diets were: group 1, 72% sucrose; group 2, 72% uncooked wheat starch; group 3, 72% roll-dried wheat starch; group 4, 36% sucrose and 36% uncooked starch; group 5, 36% sucrose and 36% roll-dried starch.

3. The rats were killed after 20 days on the diets and assessed for dental caries. The rats consuming diets containing sucrose (groups 1, 4 and 5) had significantly more caries than animals receiving diets in which starch was the sole carbohydrate. The diet containing roll-dried wheat starch produced significantly more caries than uncooked starch. The mixture of uncooked starch and sucrose was more cariogenic than the mixture of roll-dried starch and sucrose.

1. Ten pigs which had been undernourished for a year, and weighed about 5.5 kg at that time, were rehabilitated on an excellent dict. They grew fast, but no faster per kg body-weight than normal pigs, and they stopped growing at the same chronological age. Consequently, they did not attain the same adult size as the normally reared pigs.

2. The rehabilitated animals appeared to be fatter than the control animals, but the proportions of muscle to bone in the carcasses of the males and females were within the range to be expected in normal animals of the same fat-free weight, although the castrates may have been somewhat less muscular on this basis.

3. The weights of the organs per kg of fat-free body weight were within the limits found in normally reared animals of the same fat-free weight.

1. Both male and female Cynomolgus (Macaca irus) monkeys survived for 3 years without apparent ill health when fed on diets containing groundnut meal to provide up to 0·36 μg aflatoxin B1 per g diet and thus supplying a mean daily consumption of up to 2 μg aflatoxin B1 per kg body-weight. No histological changes attributable to aflatoxicosis were discovered in any of the organs from the monkeys receiving these quantities of aflatoxin.

2. Few monkeys survived for more than a month or two when given a diet containing 1·8 μg aflatoxin B1 per g, which provided about 50 μg aflatoxin B1 per kg body-weight per day.

3. No depression in growth rate nor effect on health was noted in those monkeys which survived on diets containing 1·8 μg aflatoxin B1, nor in any of the other monkeys.

4. Histological changes were observed in the livers of all monkeys receiving the diet containing 1·8 μg aflatoxin B1 per g for more than a month or two, but no abnormalities related to aflatoxicosis could be detected in any of the other organs, except for minor changes in the kidneys of two monkeys.

5. No tumours were seen in any of the monkeys, even in those surviving for 3 years on diets providing 1·8 μg aflatoxin B1/g. Thus, no conclusions can be drawn from this work as to the carcinogenicity of aflatoxin in monkeys (still less in man), because the animals were young and little is known of the duration of exposure required to demonstrate carcinogenicity in this species.

1. The nature of the relationship between vitamins A and E has been studied in the rat and the chick.

2. Stress induced by diets rich in polyunsaturated fatty acids (PUFA) was found to have no effect on the liver vitamin A reserves of vitamin E-deficient rats given dietary vitamin A or repeated small oral doses of vitamin A.

3. Dietary PUFA did not affect the liver vitamin A reserves of young rats given necrogenic diets deficient in vitamin E and selenium, nor were these reserves affected by the onset of liver necrosis or its prevention by Se.

4. The effect of dietary PUFA on the rate of depletion of liver vitamin A reserves in weanling rats or rats depleted initially of vitamins A and E and then given a single large dose of vitamin A was studied over periods from 2 to 12½ weeks. In three experiments the dietary PUFA did not significantly accelerate vitamin A depletion. In one experiment the depletion rate was increased, but this was not reversed by dietary vitamin E and thus could not be attributed to an enhancement of peroxidation in vivo but rather to a toxic effect. The effect of vitamin E in these experiments was not consistent but, in general, it slightly decreased the rate of depletion.

5. Large doses of vitamin A did not affect the metabolism of small amounts of [14C]D-α-tocopherol in the vitamin E-deficient rat or chick, when interaction of the two vitamins in the gastro-intestinal tract was avoided.

6. Large doses of vitamin A (40000 i.u. in total) given to vitamin E-deficient chicks receiving a diet containing 1% linoleic acid (as maize oil esters) did not accelerate the onset of encephalomalacia and therefore failed to exert a pro-oxidative effect on tissue tocopherol.

7. The conclusion drawn from these experiments was that any relationship that may exist in vivo between vitamins A and E is not concerned with an effect of vitamin E in preventing oxidation of vitamin A. A critical review of the literature on the nature of the relationship in general supports this view.

1. An experiment was carried out in which protein utilization in the pregnant ewe was studied using the nitrogen balance technique.

2. Eight diets supplying four different intakes of crude protein and two different intakes of energy were each offered to eight individually penned ewes.

3. The mean crude protein intakes per day were 7·2, 5·5, 4·1 and 3·0 g/kg W0·73 (where W = body-weight) and the metabolizable energy intakes 134 and 113 kcal/kg W0·73.

4. N balances were carried out at 10–12, 14–16 and 18–20 weeks of gestation on five ewes from each treatment.

5. The apparent digestibility of both dry matter and crude protein decreased with decreasing protein intake. With the high energy intake, the apparent dry-matter digestibility was increased and the apparent digestibility of crude protein decreased. Stage of gestation had no significant effect on the apparent digestibility of either of these constituents.

6. N retention was not affected by the number of foetuses carried. With the higher energy intake and the higher protein intakes, the absolute retention of N was significantly increased at all stages of gestation. N retention increased with advancing pregnancy; the retentions at 10–12, 14–16 and 18–20 weeks of gestation being 0·086, 0·114 and 0·163 g/kg W0·73 per day respectively.

7. The efficiency of utilization of apparently digested N was calculated from the regression of retained N as a percentage of apparently digested N against apparently digested N.

8. The daily intakes of apparently digested N required for maximum efficiency were 0·551 and 0·620 g/kg W0·73 on the high and low energy intakes respectively. The daily intake for maximum efficiency decreased with advancing pregnancy, the values being 0·623, 0·587 and 0·567 g/kg W0·73 for the 10–12, 14–16 and 18–20 weeks of gestation respectively.

9. The levels of N retained at maximum efficiency were 0·235 and 0·202 g/kg W0·73 per day for the high and low energy intakes respectively. The levels of N retained increased during pregnancy from 0·170 g/kg W0·73 per day at 10–12 weeks to 0·286 g/kg W0·73 at 18–20 weeks. The requirements for zero N balance were 0·072 and 0·153 g apparently digested N/kg W0·73 per day for the high and low energy intakes respectively. The requirement for zero N balance decreased from 0·176 g/kg W0·73 per day at 10–12 weeks to 0·071 g/kg W0·73 at 18–20 weeks.

10. The results are discussed in relation to other research findings and current recommendations.

1. An experiment was conducted with 4600 children in nine schools, in which an attempt was made to persuade a greater number of children to take school milk. The proportion taking the milk before the experiment ranged from about 25 to 65%.

2. Four methods of nutrition education were used: posters, lectures and films each in two schools, and pamphlets in one school. The remaining two schools acted as controls.

3. The material was used for one term in all seven ‘experimental’ schools, and again for the following term in one of the schools receiving each of the different forms of education.

4. Although it appears that there was a small increase in the number of children that said they would take milk, there was no significant increase in the number that did in fact do so, in either the first or the first or the second term.

5. The analysis of the possible causes for this failure to increase milk consumption suggests that nutrition education does not affect dietary behaviour if the factors that limit consumption are sufficiently strong.

1. Details are given for the construction and use of an apparatus for the incubation of rumen liquor in semi-permeable sacs inside the bovine rumen. It was found practicable, using one animal, to incubate simultaneously samples of strained diluted rumen liquor in three identical vessels, each of 100–120 ml capacity, for periods of up to 23 h.

2. The optimal conditions for experiments of this type were investigated. It was shown that, under the conditions used, the pH value of the reaction mixtures varied little compared with the pH changes that occurred inside the rumen, and that the sampling technique was satisfactory.

3. The effects of the size and type of inoculum were also investigated. The microbial growth, measured by increases in turbidity and in concentration of protein, was greatest when the rumen liquor inoculum constituted about 20% of the reaction mixture and when the protozoa and large food particles were removed.

4. The apparatus was used to study microbial growth and hydrogenation of fatty acids in rumen liquor.

1. Young adult female albino rats were given 20, 40, 60, 80, and 100% raw egg white powder in their diet; controls were fed on laboratory chow. Daily clinical measurements were made for 2 weeks. The rats were then killed, and the weights and water contents of various organs were determined.

2. The experiment was repeated with groups of young male albino rats fed for 2 and 4 weeks.

3. Toxic signs caused by increasing intake of dried raw egg white powder were: decreased food intake, weight loss, soft stool, diarrhoea, glycosuria and death. Water intake and urine output rose with increasing raw egg white powder in the diet. In all groups the urine was alkaline and the urinary output of protein increased. At autopsy there was a decrease in the absolute weight and in the water content of most body organs with increasing amounts of raw egg white powder in the diet.

4. The toxicity syndrome was not prevented by a biotin supplement, but was largely prevented by heat denaturation of the egg white powder; 80% of denatured egg white was well tolerated, as was 80% of casein in the diet.

5. The syndrome was due to the direct toxic effects of large amounts of dietary raw egg white powder and not to biotin deficiency.

1. In expt 1 daily supplements of 0 or 27–28 g potassium, with 0 or 7·5 1. water, were given to each of eight fistulated wether sheep on a hay and concentrate diet in two 4 × 4 latin square experiments. Faeces were collected for the last 4 days of, and urine throughout, 10-day treatment periods.

2. Adding K to the diet decreased the urinary output of magnesium by 33% (P < 0·001) and significantly increased those of phosphorus, sodium and calcium by 98, 76 and 150%, respectively. Faecal outputs of Mg and K were increased, whereas that of P was decreased. The retentions of P and Na tended to be decreased, whereas that of K was increased (P < 0·001). Mg in serum was decreased by 0·4 mg/100 ml (P < 0·05) and K increased by 4·9 mg/100 ml (P < 0·001).

3. Increasing the water intake increased the urinary outputs of Mg, P, Na and Ca by 33, 165, 47 and 200%. The faecal output of Ca was increased and the retentions of Mg, P and Ca were decreased (P < 0·01).

4. The effects of water and K were generally independent, but interactions affected the urinary outputs of P and K and the retention of K.

5. The increases in urinary Na output were three- and eight-fold greater during the first 3 days of increased water and K intakes than during the balance study.

6. In expt 2, mineral balance studies were conducted before and after supplementing the diet with potassium acetate, using five wethers from Expt 1. K intakes were similar to those of Expt 1. The effects of potassium acetate and KCl were generally similar qualitatively but the acetate produced greater decreases in urinary Mg and faecal P outputs and greater increases in urinary Na and K outputs than KCl. K in serum was increased by 28 mg/100 ml but Mg was not affected.

7. The nature of these responses in discussed with particular reference to the aetiology of hypomagnesaemic tetany.

1. An experiment was undertaken to determine whether high rates of sweating in a tropical climate affect protein requirements by increasing the total nitrogen losses from the body.

2. Six fully acclimatized volunteers were given a diet supplying 50 g protein (= 8 g N) daily. They performed strenuous physical work of a normal nature for an average of 6½ h a day for two 5-day periods. During control periods the subjects took minimal exercise and lived in a cool environment. N balance was measured throughout.

3. Rates of sweating were measured by weighing. Whole body sweat was collected and the concentrations were measured of nitrogen, sodium and potassium. During 6½ h work approximately 3 l. of sweat were lost, containing on average 0·49 g N, 64 m-equiv. Na and 22 m-equiv. K.

4. The N concentration in sweat was 0·20 mg/g, which is lower than that found by most other workers. It is suggested that acclimatization is an important factor in reducing N loss by sweating.

5. There was a marked decrease in urinary Na excretion during sweating, which compensated fully for the loss of Na in sweat. Renal compensation for loss of K was less efficient.

6. Because the total N loss in sweat was small, it was not possible to establish with certainty whether it was compensated for by a reduced renal excretion of N. However, after the initial period the subjects were in N balance in spite of the relatively low protein intake.

7. It is concluded that there is no evidence to suggest that heavy sweating under natural conditions in a tropical climate causes a significant increase in protein requirements.

1. Food which provided from 2960 to 7880 kcal in excess of requirements was eaten by sixteen subjects, ten hospital patients and six students, in each instance for a period of 4 days.

2. The proportion of the nutrients lost in the faeces was not increased during overfeeding.

3. The metabolic rates were in no instance increased by an amount equivalent to more than 15% of the excess calories. The increase could be attributed to the specific dynamic action of the extra dietary protein.

4. The gains in weight ranged from 370 to 5460 g/4 days and the calorie equivalent of the weight gained varied from 1·1 to 10·0 kcal/g. These variations can be attributed to variations in the amount of water retained.

5. Analysis of their respiratory exchanges suggests that most subjects stored from 400 to 1500 g of carbohydrate in the tissues, possibly in the form of muscle glycogen.

1. The distribution of vitamin A esterase activity for vitamin A acetate, palmitate, and alcohol was studied in various tissues of the chick.

2. Liver and kidneys were highly active in the hydrolysis of acetate, and showed only slight activity in the hydrolysis of palmitate or in the synthesis of vitamin A esters.

3. Pancreas was highly active in both acetate and palmitate hydrolysis and in the synthesis of vitamin A esters.

4. The small intestine showed a moderate and equal activity in all three reactions.

5. Sodium taurocholate enhanced the hydrolysis of vitamin A palmitate by pancreas and small intestine. It also enhanced the hydrolysis of vitamin A acetate by pancreas, but had no effect on the hydrolysis of acetate by liver, and even inhibited this reaction in kidneys and intestine. It also inhibited the synthesis of vitamin A esters by pancreas and small intestine.

1.The oral administration of sodium molybdate caused a rapid rise of molybdenum in the milk of cows and goats fed on a low-molybdenum diet, but did not affect the xanthine oxidase activities of the milk of either species.

2.In the milks of cows not dosed with sodium molybdate, the regression of the xanthin oxidase activity (y) on the molybdenum content (x) was found to be y = 170.7x+43.86 (r = +0.9386; P < 0.0001), suggesting that all the molybdenum of such milk is bound to enzymically active xanthine oxidase.

3.The molybdenum contents of the milk of goats not does with sodium molybdate varied from animal to anumal and the xanthine oxidase activites were much lower than those of cow' milk. there was no correlation between xanthine oxidase activity and the molybdenum contend of the milks of the goats.

4. These results are discussed in relation to previous work of the authors and others.

1. Vitamin B12 nutrition was studied in normal, coprophagy-prevented and antibiotic-treated rats on Vitamin B12-deficient diets with and without a vitamin B12 supplement; the indices used were excretion of total urinary ether-soluble acid (TUESA) and methylmalonic acid, and vitamin B12 assays on the liver and intestinal tract.

2. A significant positive correlation (r = 0.61) was found between TUESA excretion and weight of rats, and a significant negative correlation (r = −0.89) between TUESA excretion and liver vitamin B12 contents.

3. Although prevention of coprophagy reduced the contents of vitamin B12 in the stomach and small intestine, no effect on vitamin B12 nutrition, as assessed by TUESA excretion and liver vitamin B12 contents, was found. Rats in which coprophagy was permitted became vitamin B12-deficient, when given a diet in which vitamin B12 was low.

4. The amounts of TUESA and methylmalonic acid excreted indicated that streptomycin and erythromycin administered orally prevented vitamin B12 deficiency in rats on a diet deficient in vitamin B12. Liver vitamin B12 contents were, however, very low in these rats. this anomaly was thought to be due to the non-specificity of the Euglena gracilis assay for vitamin B12.

5. It was concluded that, under the conditions of these experiments, coprophagy was not necessary to the vitamin B12-sparing action of antibiotics.

1. The effects have been compared of log-term administration of similar amount of ethanol given either diluted in drinking water or spaced out in the form of intoxicating doses.

2. The effect of ethanol on the development of liver lesions produced by a marginal diet was examined. The measurements of growth rate, water balance, plasma glucose and electrolytes, rate of ethanol elimination, and some behavioural tests for the detection of tolerance and possible signs of neurological disturbance were also included.

3. Isocalorically pair-fed growing male rats were subjected to three different regimens for 6 months: (A) ethanol solution as the sole drinking fluid with 2 days' intake adjusted to approximately 5 mg/g body-weight; (B) a similar quantity of ethanol give as a single intoxicating dose per os on alternate days; (C) oleic acid isocaloric with the ethanol per os on alternate days.

4. All the regimens caused fatty liver. Hepatic fibrosis, as judged macro- and micro- scopically, was equally severe after treatments A and C, but milder after treatment B.

5. Growth was retarded by intoxication, which also brought about a large increase in water consumption, without exerting other clear effects on water balance or on plasma electrolytes. The rate of ethanol elimination was increased by repeated intoxication. Behavioural tolerance of the effects of ethanol was also found in the animals subjected to intoxication.