No abstract

Both n-6 and n-3 polyunsaturated fatty acids (PUFA) are recognized as essential nutrients in the human diet, yet reliable data on population intakes are limited. The aim of the present study was to ascertain the dietary intakes and food sources of individual n-6 and n-3 PUFA in the Australian population. An existing database with fatty acid composition data on 1690 foods was updated with newly validated data on 150 foods to estimate the fatty acid content of foods recorded as eaten by 10,851 adults in the 1995 Australian National Nutrition Survey. Average daily intakes of linoleic (LA), arachidonic (AA), alpha-linolenic (LNA), eicosapentaenoic (EPA), docosapentaenoic (DPA), and docosahexaenoic (DHA) acids were 10.8, 0.052, 1.17, 0.056, 0.026, and 0.106 g, respectively, with long-chain (LC) n-3 PUFA (addition of EPA, DPA, and DHA) totaling 0.189 g; median intakes were considerably lower (9.0 g LA, 0.024 g AA, 0.95 g LNA, 0.008 g EPA, 0.006 g DPA, 0.015 g DHA, and 0.029 g LC n-3 PUFA). Fats and oils, meat and poultry, cereal-based products and cereals, vegetables, and nuts and seeds were important sources of n-6 PUFA, while cereal-based products, fats and oils, meat and poultry, cereals, milk products, and vegetable products were sources of LNA. As expected, seafood was the main source of LC n-3 PUFA, contributing 71%, while meat and eggs contributed 20 and 6%, respectively. The results indicate that the majority of Australians are failing to meet intake recommendations for LC n-3 PUFA (> 0.2 g per day) and emphasize the need for strategies to increase the availability and consumption of n-3-containing foods.

ObjectiveTo investigate whether diets differing in fat content alter the gut microbiota and faecal metabolomic profiles, and to determine their relationship with cardiometabolic risk factors in healthy adults whose diet is in a transition from a traditional low-fat diet to a diet high in fat and reduced in carbohydrate.MethodsIn a 6-month randomised controlled-feeding trial, 217 healthy young adults (aged 18–35 years; body mass index <28 kg/m2; 52% women) who completed the whole trial were included. All the foods were provided during the intervention period. The three isocaloric diets were: a lower-fat diet (fat 20% energy), a moderate-fat diet (fat 30% energy) and a higher-fat diet (fat 40% energy). The effects of the dietary interventions on the gut microbiota, faecal metabolomics and plasma inflammatory factors were investigated.ResultsThe lower-fat diet was associated with increased α-diversity assessed by the Shannon index (p=0.03), increased abundance of Blautia (p=0.007) and Faecalibacterium (p=0.04), whereas the higher-fat diet was associated with increased Alistipes (p=0.04), Bacteroides (p<0.001) and decreased Faecalibacterium (p=0.04). The concentration of total short-chain fatty acids was significantly decreased in the higher-fat diet group in comparison with the other groups (p<0.001). The cometabolites p-cresol and indole, known to be associated with host metabolic disorders, were decreased in the lower-fat diet group. In addition, the higher-fat diet was associated with faecal enrichment in arachidonic acid and the lipopolysaccharide biosynthesis pathway as well as elevated plasma proinflammatory factors after the intervention.ConclusionHigher-fat consumption by healthy young adults whose diet is in a state of nutrition transition appeared to be associated with unfavourable changes in gut microbiota, faecal metabolomic profiles and plasma proinflammatory factors, which might confer adverse consequences for long-term health outcomes.Trial registration number NCT02355795; Results.

Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.