Background: Plant sterols reduce cholesterol absorption, which leads to a decrease in plasma and LDL-cholesterol concentrations. Plant sterols also lower plasma concentrations of carotenoids and α-tocopherol, but the mechanism of action is not yet understood. Objectives: The aims of this clinical study were to determine whether plant sterols affect the bioavailability of β-carotene and α-tocopherol in normocholesterolemic men and to compare the effects of plant sterol esters and plant free sterols on cholesterol absorption. Design: Twenty-six normocholesterolemic men completed the double-blind, randomized, crossover study. Subjects consumed daily, for 1 wk, each of the following 3 supplements: a low-fat milk-based beverage alone (control) or the same beverage supplemented with 2.2 g plant sterol equivalents provided as either free sterols or sterol esters. During this 1-wk supplementation period, subjects consumed a standardized diet. Results: Both of the milks enriched with plant sterols induced a similar (60%) decrease in cholesterol absorption. Plant free sterols and plant sterol esters reduced the bioavailability of β-carotene by ≈50% and that of α-tocopherol by ≈20%. The reduction in β-carotene bioavailability was significantly less with plant free sterols than with plant sterol esters. At the limit of significance (P = 0.054) in the area under the curve, the reduction in α-tocopherol bioavailability was also less with plant free sterols than with plant sterol esters. Conclusions: Both plant sterols reduced β-carotene and α-tocopherol bioavailability and cholesterol absorption in normocholesterolemic men. However, plant sterol esters reduced the bioavailability of β-carotene and α-tocopherol more than did plant free sterols.

1. The present experiments were designed to elucidate the reasons for the fall in central body temperature during hypoglycaemia. 2. The first experiment was carried out at a room temperature of 25 °C on 11 male subjects. Hypoglycaemia was induced by infusion of insulin. Heat production (calculated from respiratory gas exchange) rose from a baseline of 5.10 ± 0.13 kJ/min (mean ± sem) to a peak of 6.25 ± 0.21 kJ/min (P < 0.001), but core temperature fell concurrently by 0.51 ± 0.08°C and skin temperature fell by 1.1 ± 0.2°C. The net heat loss was due to peripheral vasodilatation and sweating. 3. To determine the effect of insulin-induced hypoglycaemia on thermoregulation in a cool environment, the experiment was repeated at a room temperature of 18–19°C on five of the subjects who had air blown over them until shivering was sustained. During this time heat production rose to 10.13 ± 1.67 kJ/min, but core temperature remained constant. Shivering stopped as plasma glucose fell below 2.5 mmol/l during insulin infusion and the subjects said they no longer felt cold. 4. During hypoglycaemia in the cold peripheral vasodilatation and sweating occurred, skin temperature fell by up to 0.8°C and core temperature fell below 35°C, so subjects had to be rewarmed. 5. Recovery of plasma glucose after hypoglycaemia in the cold was impaired at low body temperatures, but shivering was restored within seconds when glucose was given intravenously.

In twenty-eight healthy subjects, ten men and eighteen women, with a range in body mass index (BMI) of 17.9–31.6 kg/m² and an age range 20–60 years, body composition was estimated by dual-energy X-ray absorptiometry (DEXA), skinfold anthropometry (SFA) and bioelectrical impedance analysis (BIA) of the ‘whole body’and body segments. In thirteen subjects muscle mass was also estimated by 24 h urinary creatinine excretion. The relationship between fat-free mass (FFM) determined by DEXA and the impedance index of each body segment (calculated as Iength²/impedance (Z)) was analysed. The strongest correlation was between FFM (DEXA) and height²/‘whole-body’Z (Z_w) (r 0.97 for the combined sexes, standard error of estimate (SEE) 2.72 kg). Separate prediction equations were found to be necessary for males and females when estimating FFM from BIA measurement of the arm (for men, r 0.93, SEE 1.98 kg; for women, r 0.75, SEE 2.87 kg). Muscle mass derived from 24 h creatinine excretion showed weak correlation with FFM (DEXA) (r 0.57, P = 0.03) and no correlation with FFM (SFA). FFM (SFA) correlated well with both FFM (DEXA) (r 0.96, SEE = 3.12 kg) and with height²/Z_w (r 0.92, SEE 4.52 kg). Measurement of the impedance of the arm offers a simple method of assessing the composition of the whole body in normal individuals, and it appears comparable with other methods of assessment.

Most babies treated with dexamethasone for bronchopulmonary dysplasia exhibit an appreciable rise in the blood urea concentration, from a mean of 2.3 mmol/l before steroid to a mean of 7.1 mmol/l after. In order to discover whether this was primarily the result of increased protein catabolism, nitrogen balance studies before and after the start of dexamethasone were performed and a mean deficit in nitrogen retention of 158 mg/kg/24 hours was found. Similarly the urinary 3-methylhistidine (3MH):creatinine ratio before and after the commencement of dexamethasone treatment in a group of preterm babies was measured. It was found that there was a substantial increase in 3MH excretion after dexamethasone: from a mean 3MH:creatinine ratio of 46 in the week before steroids to a mean ratio of 77 in the week after. As 3MH emanates almost exclusively from the breakdown of actin in skeletal muscle cell, this finding implies the loss of muscle tissue. It was also found that the babies were in less positive nitrogen balance after dexamethasone, to a degree which is significant relative to their protein reserves. The long term consequences of a period of increased catabolism are not yet known but the authors suggest caution in the use of dexamethasone, at least in babies with milder degrees of bronchopulmonary dysplasia in whom the ratio of benefit to risk may be less favourable.

Dietary guidelines indicate that complex carbohydrates should provide around half of the calories in a balanced diet, while sugars (i.e., simple carbohydrates) should be limited to no more than 5–10% of total energy intake. To achieve this public health goal a collective effort from different entities including governments, food & beverage industries and consumers is required. Some food companies have committed to continually reduce sugars in their products. Different solutions can be used to replace sugars in food products but it is important to ensure that these solutions are more healthful than the sugars they replace. The objectives of this paper are, (1) to identify carbohydrates and carbohydrates sources to promote and those to limit for dietary intake and food product development, based on current knowledge about the impact of carbohydrates on the development of dental caries, obesity and cardio-metabolic disorders (2) to evaluate the impact of food processing on the quality of carbohydrates and (3) to highlight the challenges of developing healthier products due to the limitations and gaps in food regulations, science & technology and consumer education.