The aim of the study was to investigate the association between pre-gestational carbohydrate quality index (CQI) and the incidence of gestational diabetes mellitus (GDM). Data from the ‘Seguimiento Universidad de Navarra’ (SUN) cohort were used, which includes 3827 women who notified at least one pregnancy between December 1999 and December 2019. We used a validated semi-quantitative 136-item FFQ to evaluate dietary exposures at baseline and at 10-year follow-up. The CQI was defined by four criteria: glycaemic index, whole-grain/total-grain carbohydrate, dietary fibre intake and solid/total carbohydrate ratio. We fitted generalised estimating equations with repeated measurements of the CQI to assess its relationship with incident GDM. A total of 6869 pregnancies and 202 new cases of incident GDM were identified. The inverse association between the global quality of carbohydrate and the development of GDM was not statistically significant: OR the highest v. the lowest CQI category: 0·67, 95 % CI (0·40, 1·10), Pfor trend = 0·10. Participants at the highest CQI category and with daily carbohydrate amounts ≥50 % of total energy intake had the lowest incidence of GDM (OR = 0·29 (95 % CI (0·09, 0·89)) compared with those with the lowest quality (lowest CQI) and quantity (≤40 %). Further studies are needed to overcome the limitations of our study. Those studies should jointly consider the quality and the quantity of dietary carbohydrates, as the quality might be of importance, especially in women with a higher intake of carbohydrates.

Barrett’s oesophagus (BE) is the precursor of oesophageal adenocarcinoma, which has become the most common type of oesophageal cancer in many Western populations. Existing evidence on diet and risk of BE predominantly comes from case–control studies, which are subject to recall bias in measurement of diet. We aimed to investigate the potential effect of diet, including macronutrients, carotenoids, food groups, specific food items, beverages and dietary scores, on risk of BE in over 20 000 participants of the Melbourne Collaborative Cohort Study. Diet at baseline (1990–1994) was measured using a food frequency questionnaire. The outcome was BE diagnosed between baseline and follow-up (2007–2010). Logistic regression models were used to estimate OR and 95 % CI for diet in relation to risk of BE. Intakes of leafy vegetables and fruit were inversely associated with risk of BE (highest v. lowest quartile: OR = 0·59; CI: 0·38, 0·94; P-trend = 0·02 and OR = 0·58; CI: 0·37, 0·93; P-trend = 0·02 respectively), as were dietary fibre and carotenoids. Stronger associations were observed for food than the nutrients found in them. Positive associations were observed for discretionary food (OR = 1·54; CI: 0·97, 2·44; P-trend = 0·04) and total fat intake (OR per 10 g/d = 1·11; CI: 1·00, 1·23), the association for fat was less robust in sensitivity analyses. No association was observed for meat, protein, dairy products or diet scores. Diet is a potential modifiable risk factor for BE. Public health and clinical guidelines that incorporate dietary recommendations could contribute to reduction in risk of BE and, thereby, oesophageal adenocarcinoma.

1. The possibility of an effect of zinc on the rate of tumour cell division, mediated through a regulation of cellular cAMP concentration, was investigated in the present study in rats.

2. Dietary Zn deficiency (< 1·5 mg Zn/kg) but not Zn excess (500 mg Zn/kg) resulted in an increased cAMP concentration in transplanted hepatoma cells. Neither treatment had any effect on the cAMP concentration in regenerating liver or normal resting liver. Both the deficient and excess Zn diets resulted in a small reduction in tumour growth (not statistically significant).

3. The results seem to indicate that the relation investigated in the present study does not apply in the cell line used.

David Southgate will always be known for his work on the composition of foods and the compilation of food tables, and for his innovation in the field of dietary carbohydrate analysis, especially dietary fibre, in which he was the natural heir to McCance and Widdowson, with whom he worked in his early years.

Differences in physical activity (PA) might lead to long-term weight control. Studies on inverse relations between PA and changes in fatness among adolescents are limited. This paper examined the effect of PA on adolescents’ changing body fatness over 5 years in Ho Chi Minh City (HCMC). Two hundred thirty-five boys and 247 girls who have had skinfold thickness measurements in the baseline survey in 2004 were selected to follow yearly. We estimated PA as the average number of accelerometers’ counts/h. Slopes of triceps, sub-scapular skinfolds and BMI were calculated and classified as increasing or stable/decreasing. To assess the effects of the low level of activity (i.e. below the median of the average number of counts) on the fat gain (i.e. increasing slopes), relative risk and 95 % CI were estimated using Poisson regression. The average number of counts/h in boys (7·8) was significantly higher than that in girls (5·0) (P < 0·001). On average, active girls still gained 0·51 mm in triceps skinfold (TSF) over 5 years, while active boys lost 0·12 mm. After controlling for baseline energy intake, baseline triceps and baseline age, inactive adolescents were 1·39 times higher than active ones to increase the slope of triceps (95 % CI 1·19, 1·63). The risk ratio was 1·62 for those with more body fat at baseline. In general, inactive students gained substantially more subcutaneous fat, especially in their TSF, than more active ones. Thus, strategies to prevent adolescent obesity in HCMC should consider the important role of PA to control this problem in adolescents effectively.

1. A low-sodium diet was given to Blackface ewes over two reproductive seasons. This diet provided a total of 3–7 mmol/d except during lactation when the intake was about 11 mmol/d. Control ewes were given the same diet supplemented with sodium chloride to provide recommended levels which were about tenfold that of the experimental diet.

2. The output of Na in urine and faeces from ewes given the low-Na diet was very low, about 3 mmol/d, from early in the experiment and continued at about this level throughout.

3. Lambs born to low-Na ewes and given a low-Na diet similar to that of their dams during lactation, grew, after weaning, more slowly than corresponding lambs from control ewes, but at 6 months of age when six from each group were killed, tissue Na contents were only slightly lower in experimental than control lambs.

4. Fluids and tissues obtained at the end of the second lactation from four ewes of each group that had suckled twin lambs, were analysed for Na and potassium. The Na concentration in saliva and rumen fluid of low-Na ewes was about half that of control ewes and there were corresponding increases in K: the differences were significant. Although Na concentrations for experimental ewes were generally lower than those for control ewes in the tissues analysed (liver, kidney, heart, brain and bone), the difference was significant only for the heart (P < 0.05). Haemoglobin and packed cell volume were significantly elevated in low-Na ewes (P < 0.01), indicating decreased body fluid volume. Enlargement of the adrenal glands in low-Na ewes (P < 0.01) and specifically in the zona glomerulosa (P < 0.001), showed the marked hormonal response to Na status of experimental ewes given a very-low-Na diet over two reproductive cycles.

1. Two groups of adult rats were placed in a metal-free environment and pair-fed with selenium-supplemented and Se-deficient diets.

2. After 5 months the animals were killed and skeletal muscle concentrations of creatine, creatine phosphate, ATP, protein and Se were determined.

3. Se deficiency was indicated by the low Se content of the skeletal muscle from the deficient animals, but no changes were found in the amounts of the other components.

4. These results suggest that Se may not be involved in creatine metabolism and that Se deficiency may not be concerned independently in the development of nutritional dystrophy, where changes are found in the levels of protein, creatine, creatine phosphate and ATP.

The primary goal of the investigation was to analyse the anti-inflammatory and antioxidant properties of Gamma-linolenic acid (GLA) on rats with indomethacin (IND)-induced gastric ulcers. Thirty rats were divided into five groups: Control, IND (50 mg/kg, p.o.), IND pretreated with GLA 100 mg/kg (p.o. for 14 d), IND pretreated with GLA 150 mg/kg (p.o. for 14 d) and IND pretreated with omeprazole (20 mg/kg, p.o. for 14 d). The stomach tissues were examined to calculate the ulcer index and pH and analyse biochemical markers (prostaglandin E2 (PGE2), cyclooxygenase 1 (COX1), TNF-1, IL-6 and intercellular adhesion molecule-1 (ICAM1)) and oxidative stress parameters (malondialdehyde: (MDA), superoxide dismutase (SOD), glutathione (GSH) and CAT (catalase)) as well as undergo histopathological assessment. GLA 100 and 150 mg/kg showed a protective effect against IND-induced gastric damage. It reduced levels of COX1, TNF-1, IL-6 and ICAM and increased PGE2 levels. GLA also normalised antioxidant function by modulating MDA, SOD, GSH and CAT. GLA intervention protects against IND-induced gastric ulcers by restoring oxidant/antioxidant balance and reducing inflammation.