Few trials have evaluated the metabolic effects and health outcomes of lowering dietary n-6 PUFA. The objectives of the present paper were (1) to report the methods employed to lower dietary n-6 PUFA, while either increasing or maintaining n-3 PUFA intake and (2) to validate our methods with 24 h recalls and erythrocyte fatty acid analyses. A total of sixty-seven subjects were randomised to either (1) an average-n-3 PUFA, low-n-6 PUFA (L6) intervention designed to lower linoleic acid (LA; ≤ 2·5 % of energy (en%)) and arachidonic acid ( ≤ 60 mg/d), while maintaining an average US intake of n-3 PUFA or (2) a high-n-3 PUFA, low-n-6 PUFA (H3-L6) intervention designed to lower n-6 LA, while increasing the n-3 PUFA α-linolenic acid (ALA; ≥ 1·5 en%) and EPA+DHA ( ≥ 1000 mg/d). Pre- and intra-intervention nutrient intakes were estimated with six 24 h dietary recalls per subject. Both groups achieved the targeted reductions in dietary LA to ≤ 2·5 en% (median LA 2·45 (2·1, 3·1); P< 0·001). Intakes of n-3 PUFA did not change for the L6 group. Target increases in n-3 ALA (median 1·6 en%, (1·3, 2·0), P< 0·001) and EPA+DHA (1482 mg, (374, 2558), P< 0·001) were achieved in the H3-L6 group. Dietary changes were validated by corresponding changes in erythrocyte n-6 and n-3 fatty acid composition. Dietary LA can be lowered to ≤ 2·5 en%, with or without concurrent increases in dietary n-3 PUFA, in an outpatient clinical trial setting using this integrated diet method.

A mathematical model is described for estimating changes in plasma 25-hydroxyvitamin D (25(OH)D) levels throughout the year as a consequence of varying the oral intake of vitamin D and the behaviour outdoors of white British adults resident in different regions of the UK. The model yields seasonal and geographical patterns of 25(OH)D concentrations that agree closely with observational studies. Use of the model allows estimates to be easily made of the sun exposure and oral intake necessary to avoid vitamin D deficiency in defined proportions of the population, as well as strategies that would lead to vitamin D sufficiency throughout the year. The analysis demonstrates that addressing concerns about insufficient vitamin D levels, especially during the winter, may be achieved by modifying oral vitamin D intake over the winter, increasing summer sun exposure or a combination of both.

Previous research suggests that increasing beverage protein content enhances subsequent satiety, but whether this effect is entirely attributable to post-ingestive effects of protein or is partly caused by the distinct sensory characteristics imparted by the presence of protein remains unclear. To try and discriminate nutritive from sensory effects of added protein, we contrasted effects of three higher-energy (about 1·2 MJ) and one lower-energy (LE: 0·35 MJ) drink preloads on subsequent appetite and lunch intake. Two higher-energy drinks had 44 % of energy from protein, one with the sensory characteristics of a juice drink (HP − , low-sensory protein) and the second a thicker and creamier (HP+, high-sensory protein) drink. The high-carbohydrate preload (HC+, high-sensory carbohydrate) was matched for thickness and creaminess to the HP+ drink. Participants (healthy male volunteers, n 26) consumed significantly less at lunch after the HP+(566 g) and HC+(572 g) than after HP −  (623 g) and LE (668 g) drinks, although the compensation for drink energy accounted for only 50 % of extra energy at best. Appetite ratings indicated that participants felt significantly less hungry and more full immediately before lunch in HP+ and HC+ groups compared with LE, with HP −  being intermediate. The finding that protein generated stronger satiety in the context of a thicker creamier drink (HP+ but not HP − ) and that an isoenergetic carbohydrate drink (HC+), matched in thickness and creaminess to the HP+ drink, generated the same pattern of satiety as HP+, both suggest an important role for these sensory cues in the development of protein-based satiety.