Did fat intake in the United States really decline between 1989-1991 and 1994-1996?

The objectives of this study were to determine changes in fat and energy intakes in the United States between 1989-1991 and 1994-1996, and to examine the implications of expressing fat intake in grams vs as a percent of total energy intake. The source of data was the Continuing Survey of Food Intake by Individuals. The results suggest that intake of energy rose between the 2 time periods, primarily due to higher carbohydrate intake. There was also a modest increase in fat intake. However fat intake, as a percent of total energy, declined. The higher energy intakes were primarily from beverages, especially soft drinks, food mixtures, grain snacks, and pastries. The primary sources of higher fat intakes were meat mixtures, vegetables, and some categories of the grain group. Similar trends in the Food Supply Series suggested that the changes observed were not entirely due to changes in survey methodology. Because the increase in fat intake was masked by the increase in energy intake, we conclude that assessing trends in fat intake as a percent of energy consumption can be misleading, unless information on total energy and fat intake, in grams, is also provided. These preliminary findings should be interpreted cautiously until they are confirmed by formal secular trend analyses.

Differential modulation of Toll-like receptors by fatty acids: preferential inhibition by n-3 polyunsaturated fatty acids.

Human subjects consuming fish oil showed a significant suppression of cyclooxygenase-2 (COX-2) expression in blood monocytes when stimulated in vitro with lipopolysaccharide (LPS), an agonist for Toll-like receptor 4 (TLR4). Results with a murine monocytic cell line (RAW 264.7) stably transfected with COX-2 promoter reporter gene also demonstrated that LPS-induced COX-2 expression was preferentially inhibited by docosahexaenoic acid (DHA, C22:6n-3) and eicosapentaenoic acid (EPA, C20:5n-3), the major n-3 polyunsaturated fatty acids (PUFAs) present in fish oil. Additionally, DHA and EPA significantly suppressed COX-2 expression induced by a synthetic lipopeptide, a TLR2 agonist. These results correlated with the preferential suppression of LPS- or lipopeptide-induced NF kappa B activation by DHA and EPA. The target of inhibition by DHA is TLR itself or its associated molecules, but not downstream signaling components. In contrast, COX-2 expression by TLR2 or TRL4 agonist was potentiated by lauric acid, a saturated fatty acid. These results demonstrate that inhibition of COX-2 expression by n-3 PUFAs is mediated through the modulation of TLR-mediated signaling pathways. Thus, the beneficial or detrimental effects of different types of dietary fatty acids on the risk of the development of many chronic inflammatory diseases may be in part mediated through the modulation of TLRs.