The School Fruit and Vegetable Scheme (SFVS) provides children in government-run schools in England with a free piece of fruit or a vegetable each school day for the first 3 years of school. The present study examines the impact of the SFVS, in terms of its contribution towards the total daily intake of fruit and vegetables by children across England. Quantitative dietary data were collected from 2306 children in their third year of school, from 128 schools, using a 24 h food diary. The data were examined at different spatial scales, and variations in the impact of the scheme across areas with different socio-economic characteristics were analysed using a deprivation index and a geodemographic classification. The uptake of the SFVS and the total intake of fruit and vegetables by children varied across different parts of England. Participation in the SFVS was positively associated with fruit and vegetable consumption. That is, in any one area, those children who participated in the SFVS consumed more fruit and vegetables. However, children living in deprived areas still consumed less fruit and vegetables than children living in more advantaged areas: the mean daily frequency of fruit and vegetables consumed, and rates of consumption of fruit or vegetables five times or more per d, decreased as deprivation increased (r − 0·860; P = 0·001; r − 0·842; P = 0·002). So the SFVS does not eliminate the socio-economic gradient in fruit and vegetable consumption, but it does help to increase fruit and vegetable consumption in deprived (and affluent) areas.

Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71 464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1·23 (95 % CI 1·00, 1·50)) and cerebrovascular diseases (HR 0·65 (95 % CI 0·45, 0·94)); TFA from PHFO and CVD (HR 1·14 (95 % CI 1·03, 1·26)) and cerebrovascular diseases (HR 1·32 (95 % CI 1·04, 1·69)); and rTFA intake and CVD (HR 1·30 (95 % CI 1·05, 1·61)), CHD (HR 1·50 (95 % CI 1·11, 2·03)) and sudden death (HR 2·73 (95 % CI 1·19, 6·25)) in women. These associations with rTFA intake were not significant in men (Pinteraction ≥ 0·01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation.

Long-chain fatty acids have been shown to suppress appetite and reduce energy intake (EI) by stimulating the release of gastrointestinal hormones such as cholecystokinin (CCK). The effect of NEFA acyl chain length on these parameters is not comprehensively understood. An in vitro screen tested the capacity of individual NEFA (C12 to C22) to trigger CCK release. There was a gradient in CCK release with increasing chain length. DHA (C22) stimulated significantly (P < 0·01) more CCK release than all other NEFA tested. Subsequently, we conducted a randomised, controlled, crossover intervention study using healthy males (n 18). The effects of no treatment (NT) and oral doses of emulsified DHA-rich (DHA) and oleic acid (OA)-rich oils were compared using 24 h EI as the primary endpoint. Participants reported significantly (P = 0·039) lower total daily EI (29 % reduction) with DHA compared to NT. There were no differences between DHA compared to OA and OA compared to NT. There was no between-treatment difference in the time to, or EI of, the first post-intervention eating occasion. It is concluded that NEFA stimulate CCK release in a chain length-dependent manner up to C22. These effects may be extended to the in vivo setting, as a DHA-based emulsion significantly reduced short-term EI.