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The aim of this study was to test the hypothesis that a high consumption of sugars promotes obesity in children and has adverse effects on diet composition. Children aged between 11 and 12 years (76 boys and 67 girls) completed a 7-day weighed and recorded inventory of all food and drinks consumed. Energy and nutrient intakes were calculated using standard food composition tables, and heights and weights were measured. We found that: (i) sugars did not contribute disproportionately to high energy intakes; (ii) body mass index (kg/m2) was unrelated to total energy intake, but fell as the proportion of energy derived from sugars rose–this trend was statistically significant in boys (P

The response to the covert removal of around 500 kcal/d from the food of 10 healthy free-living male volunteers was measured over 10 days. A similar amount of energy was added to the food of four subjects. Normal food and drink was available ad libitum, and adjustments in food energy were made by the interchange of sugar and artificial sweeteners. Compensation for the theoretical energy deficit or surplus was incomplete, averaging around 50%. This, however, was very variable, some subjects achieving more than 90% recovery, whereas others failed completely to adjust energy intake within this timespan. It is concluded that the regulation of energy balance in the lean is a long-term phenomenon, conditioned by large day-to-day fluctuations in energy intake. The removal of sugar from the food raised the energy density of the diet. The substitution of artificial sweeteners for sugar caused an increase of 11% in total fat intake. The restoration of sugar had an opposite effect. This inverse relationship between dietary sugar and fat poses problems for those seeking to lose weight, and for the lean attempting to follow current guidelines for a ‘healthier’ diet without incurring weight loss.

The alleged beneficial properties of barley in the treatment of diabetes were investigated. Rates of growth, water and food (digestible energy) intakes, and blood glucose concentrations were measured before and after the induction of diabetes in rats fed diets containing either barley or wheat. No differences were found in healthy animals, but in the diabetic state the blood glucose concentration, water consumption and weight loss was significantly lower in the rats fed barley. It is suggested that a factor other than the fibre content of the cereals may be responsible for the difference in response.

A high sodium intake, to which bread makes a major contribution, and a low potassium intake are believed to be important factors in the promotion of cardiovascular disease. Our aims was to determine to what extent salts of potassium could substitute sodium chloride and potassium-rich soya flour could replace wheat flour without detrimental effect on acceptability, and to measure the bioavailability of a potassium salt added to bread. A single-blind organoleptic evaluation was carried out on eight different potassium-enriched breads by 41 panellists. Thereafter, six volunteers consumed standard or potassium-chloride-fortified bread in an 11-day single-blind cross-over feeding trial to determine the bioavailability of the supplemental potassium. Two breads in which 30% of the sodium was replaced by potassium salts, and bread in which 10% of wheat flour was replaced with soy flour, had acceptability scores similar to the standard bread. In the metabolic study a supplement of 22 mmol/day potassium chloride incorporated into the bread was found to be wholly bioavailable. A substantial reduction in sodium and an increase in potassium intake could be achieved by substituting potassium salts for sodium chloride in bread.

Blood pressure (BP) shows a continuous relationship with the risk of CVD. There is substantial evidence that dietary potassium exerts an anti-pressor effect. Most clinical trials have used KCl. However, the chloride ion may have a pressor effect and in foods potassium is associated with organic anions. In a double-blind randomized placebo-controlled trial we explored the effect on BP of two salts of potassium, KCl and potassium citrate (K-cit), in predominantly young healthy normotensive volunteers. The primary outcome was the change in mean arterial pressure as measured in a clinic setting. After 6 weeks of supplementation, compared with the placebo group (n31), 30 mmol K-cit/d (n28) changed mean arterial pressure by − 5·22 mmHg (95 % CI − 8·85, − 4·53) which did not differ significantly from that induced by KCl (n26), − 4·70 mmHg ( − 6·56, − 2·84). The changes in systolic and diastolic BP were − 6·69 (95 % CI − 8·85, − 4·43) and − 4·26 (95 % CI − 6·31, − 2·21) mmHg with K-cit and − 5·24 (95 % CI − 7·43, − 3·06) and − 4·30 (95 % CI − 6·39, − 2·20) mmHg with KCl, and did not differ significantly between the two treatments. Changes in BP were not related to baseline urinary electrolytes. A greater treatment-related effect was observed in those with higher systolic BP. Increasing dietary potassium could therefore have a significant impact on the progressive rise in BP in the entire population.

Epidemiological and clinical trials suggest an inverse relationship between dietary K intake and blood pressure (BP). Most trials however have been of short duration, the dose of K was high, and the results have been conflicting. The aim of the present study was to evaluate the effect on BP of a low-dose supplementation (24 mmol/d) for an extended period. A double-blind placebo-controlled trial was conducted on fifty-nine volunteers, randomly assigned to receive 24 mmol slow-release KC1/d (n 30) or a placebo (n 29). Measures of BP, anthropometric characteristics and urine analysis for electrolytes were recorded during a 1-week baseline period. Supplementation was for 6 weeks during which BP and changes in weight were assessed and a second 24h urine collection made. The primary outcome was the change in mean arterial pressure (MAP); systolic BP(SBP) and diastolic BP(DBP) were secondary outcomes. After 6 weeks of supplementation MAP was reduced by 7·01 (95% CI −9·12, −4·89; PPPP

In adult diabetic rats, a diet containing barley had a modulating effect on the symptoms of diabetes (blood glucose concentration and water consumption) when compared with a starch or sucrose-based diet. It was postulated that the beneficial effect of barley might be explained by its very high content of chromium (5.69 micrograms/g). Supplementation of the sucrose-based diet with an amount of trivalent inorganic chromium calculated to be equivalent to the available chromium in the barley-based diet abolished the differences in response to the diabetic state.

Children (227), aged 7–12 years, weighed and recorded all food and drink consumed for seven consecutive days. Each child completed tests of verbal and non-verbal intelligence, and was then randomly allocated to one of two groups after matching for age, sex, IQ and height. In a double-blind trial lasting for 28 d, one group received a vitamin-mineral supplement daily and the other group a placebo. On re-testing, there were no significant differences in performance between the two groups. Furthermore, there were no consistent correlations between test scores and micronutrient intakes based on the weighed records. Thus, we found no evidence that learning ability in a cross-section of British schoolchildren was limited by the quality of their diets.

1. The activities of two hepatic enzymes that participate in the regulation of amino acid oxidation and urea synthesis were measured in lactating rats (day 15 of lactation) and virgin controls. The enzymes were alanine aminotransferase (EC2. 6. 1.2) and argininosuccinate synthase (EC6. 3. 4.5). Carcasses of the dams were also analysed.2. Changes in the activities of both enzymes in dams fedad lib. on a diet containing an excess of protein indicated that amino acid oxidation was depressed. In dams restricted in protein to the level of intake of their controls but allowed to satisfy their needs for energy, enzyme activities were significantly reduced. In these animals lean tissue catabolism supplemented the dietary protein supply.3. This adjustment in protein metabolism which effectively spares protein for milk-protein synthesis could be explained either by a reduction in the availability of substrate in the liver, or by the intervention of an anabolic hormone secreted in lactation.

Rats treated with prolactin showed a rise in food consumption and an increased deposition of both lean tissue and fat. Rats pair-fed with untreated controls showed an increase in lean tissue, and a reduction in the activities of two key enzymes that control amino acid oxidation and urea synthesis in the liver. This adjustment in protein metabolism may regulate the amino acid supply in relation to the needs for milk protein synthesis during lactation.

Concern for the growth and development of poor inner-city children prompted an investigation of the relationship of growth to diet, health and sociological background. Between 1973 and 1976, 1000 households in poor areas of London were screened for at-risk children between the ages of one and 12 years. Two hundred and thirty-one children from 112 families qualified for the survey. Of the white children, 21 per cent fell below the 10th percentile for height. The mean energy intake of the shortest children was 72 per cent of the RDI. Half the families spent 4.80 pounds or less per person per week on food, and 33 per cent of the children fell below the 10th percentile for height. A remedial feeding programme may be of benefit to these and similar children.

The influence of diet on the course and outcome of pregnancy was studied in the rat. The protein value of the diet fed during pregnancy had no effect on the number and composition of the fetuses, and a slight effect only on individual fetal weight. On a diet providing 5.9 per cent of the total calories as wholly-utilizable protein (NDpCal per cent 5.9) there occurred a significant loss of protein from the maternal carcass accompanied by a rise in body fat. The liver was enlarged, and its content of protein, ribonucleic acid, phospholipid and neutral fat was increased. On diets of NDpCal per cent 10.0 and 13.0, the carcass showed no net gain or loss of protein, but fat reserves were greatly augmented. The changes in liver size and composition were more marked. Analyses suggested that the fat deposited in the liver during pregnancy was not derived from the diet, nor was it mobilized from fat depots, but was synthesized, under the influence of a placental factor, from carbohydrate or protein. During the first 14 days of pregnancy, a reserve of protein and fat was laid down in the mother's tissues. Over the last 7 days, carcass protein was catabolized. A scheme for the endocrine control of protein metabolism in pregnancy is postulated. It accounts for the inability of the rat to store protein in late pregnancy, and provides a physiologic mechanism whereby the fetus is protected from the injurious effect of an inadequate maternal diet. Evidence was obtained against the concept of calcium storage during pregnancy.

One of the earliest reports of the relationship between obesity and reproduction was a study of the circumstances under which 40 women became overweight as a result of pregnancy. No consistent pattern emerged from this study. Excessive gain in weight was recognised in some women during pregnancy, in others only some time after delivery. Furthermore, the response to successive pregnancies was varied, but all the patients had continued to gain weight over the years, and for this reason had sought medical advice. In this selected sample, abnormalities of pregnancy were common, with a high incidence of stillbirths and neonatal mortality.