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We assessed evidence for changes in efficacy of food-based interventions aimed at reducing appetite or energy intake (EI), and whether this could be used to provide guidance on trial design. A systematic search identified randomized controlled trials testing sustained efficacy of diets, foods, supplements or food ingredients on appetite and/or EI. Trials had to include sufficient exposure duration (≥3 days) with appetite and/or EI measured after both acute and repeated exposures. Twenty-six trials met the inclusion criteria and reported data allowing for assessment of the acute and chronic effects of interventions. Most (21/26) measured appetite outcomes and over half (14/26) had objective measures of EI. A significant acute effect of the intervention was retained in 10 of 12 trials for appetite outcomes, and six of nine studies for EI. Initial effects were most likely retained where these were more robust and studies adequately powered. Where the initial, acute effect was not statistically significant, a significant effect was later observed in only two of nine studies for appetite and none of five studies for EI. Maintenance of intervention effects on appetite or EI needs to be confirmed but seems likely where acute effects are robust and replicable in adequately powered studies.

A trained panel performed sensory assessments of intensity of taste and viscosity of 50% oil-in-water and water-in-oil emulsions prepared with varied concentrations of sucrose, NaCl, or citric acid. No main effects of emulsion type occurred for taste intensity or slope of the tastant concentration – intensity relationships. NaCl and citric acid increased perceived viscosity of both emulsion types, and these effects were most pronounced in oil-in-water emulsions. The results are hypothesized as related to functions of saliva and breakdown of emulsion structure in the mouth.

Two-hundred and ninety-three UK consumers completed a questionnaire eliciting estimates of fat content (as a percentage of energy) of 24 common foods, along with information on respondents' nutrition training, perceived knowledge and use of nutrition information, age, sex, height, weight, and eating restraint. The relative positioning of foods with regard to fat content was generally correct; however, there was a consistent tendency to overestimate the fat content of foods low in fat and to underestimate those high in fat. Estimates of fat content were characterized by wide deviations from true values, and were particularly poor for several specific foods. Females and respondents with formal (but not informal) nutrition training were more accurate overall, but still made large errors in estimate for certain food items. The results indicate that many consumers are likely to have substantial misconceptions regarding the relative proportion of energy derived from fat in many common foods.

A questionnaire on attitudes and beliefs regarding low fat diets was mailed to 2000 consumers throughout the United Kingdom. Information was also obtained about present fat intake by means of a food frequency questionnaire. A total of 665 (33%) questionnaires were returned of which 390 (20%) were completed correctly and used in the present analysis. Respondents were divided into tertiles for percentage energy from fat, allowing classification into low, medium and high fat intake groups, and no consistent differences emerged in the attitudes and beliefs of respondents. The majority of people were familiar with current guidelines concerning reduction of fat intake and accepted the putative health benefits of adopting lower fat diets. Regardless of actual fat intake, the majority of people felt that their diet was healthy and was not high in fat, and indicated that they had already reduced their fat intake. A major barrier to reducing fat intake in the UK may therefore be associated with a general failure to recognize what comprises effective dietary change.

The possibility of replacing fats in foods through the use of alternative ingredients has generated substantial interest among food industry and nutrition professionals as well as among the lay public and news media. However, even in academic circles, there is a tendency to consider "fat substitutes" as a homogeneous group, when they are not, and also to make unproven assumptions regarding their likely efficacy in reducing fat intake and aiding in maintenance of appropriate energy balance. Governmental and industrial bodies have tended to place much greater emphasis on the potential risks of these materials than on their possible benefits. A reasoned consideration of the nutritional implications of fat substitutes examines what these materials are, how they might be used, and how they might affect eating behavior and nutritional status in the general population. The existing literature suggests that although the risks of existing and proposed fat substitutes are probably limited, their nutritional benefits are largely unproven.

Histological changes in the aorta were used as criteria to assess the effect of treadmill exercise on the development of atherosclerosis in rats consuming a moderately hyperlipemic diet. While grossly visible atherosclerotic plaques were absent, microscopic examination of sections of the abdominal aorta were distinctly different between exercised and sedentary rats. Aortas of sedentary rats fed a diet containing lard and cholesterol had a high degree of plaque development, fat accumulation, mineralization, erosion and necrosis. Aortas of exercised rats fed the same diet had considerably less atherogenic involvement. Both hyperlipemic groups had greater plaque formation than sedentary rats fed a normolipemic diet. In addition, there were marked differences in plasma lipids; exercise ameliorated the diet-induced changes in plasmatic atherogenic lipids. Our results indicate that exercise retards the development of atherosclerosis in rats fed a hyperlipemic diet.

Hypothyroid rats fed an atherogenic diet (A) for 3 weeks developed a marked hyperlipidemia characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) cholesterol. Cholesterol concentrations of adipose tissue, liver, carcass and soleus muscle were significantly increased in rats fed the A diet versus rats fed a control diet (C). After 5 months on the A diet, cholesterol concentrations of adipose tissue, carcass and soleus muscle were not different from those measured in rats fed the A diet for 3 weeks; however, liver cholesterol concentration was 20-fold higher. To study the mechanisms by which the A diet increased adipocyte cholesterol content, in vitro binding studies were conducted with normal (N) and cholesterol enriched (CH) 125I-labeled VLDL. The inability of unlabeled N and CH VLDL to displace 125I-labeled VLDL supports the concept that VLDL was not specifically bound by rat adipocytes. The observation that adipocyte and other tissue cholesterol levels were similar at 3 weeks and 5 months suggests regulation of tissue cholesterol concentrations. The mechanism of regulation of adipocyte cholesterol was not related to VLDL binding or differential binding rates between N and CH VLDL.

Exercise generally has been found to produce beneficial effects on plasma lipid and lipoprotein profiles, but the mechanisms involved and possible dietary interactions have not been well defined. Weanling male Fischer 344 rats were assigned to three groups: normocholesterolemic diet sedentary (NS), hypercholesterolemic diet sedentary (HS), and hypercholesterolemic diet exercised (HE). Exercise consisted of treadmill running at 1.2 to 1.4 km/h at a 9% grade, six days weekly, for a 10-week experimental period. Lipoproteins from plasma and from a recirculating in situ liver perfusion system were then isolated and analyzed. The values of several parameters for HE tended to fall intermediate between HS and NS. Final total plasma cholesterol and liver cholesterol concentrations were significantly different among all three groups (HS greater than HE greater than NS). Plasma HDL-cholesterol and phospholipids and perfusate HDL-cholesterol production rate per gram liver were all significantly lower in HS v NS, with HE lying in between. Plasma HDL protein was lower in HS than in both other groups. Plasma total triglyceride levels were significantly lowered by exercise, but neither plasma nor perfusate VLDL triglyceride levels differed significantly among the three groups. Food intakes of HE and HS rats were similar, but HE rats had significantly lower final body weights. The results suggest that (1) exercise may ameliorate many of the changes in lipoprotein and cholesterol metabolism induced by a diet containing lard and cholesterol, and (2) some of these changes may be mediated by changes in hepatic lipoprotein production.

Obesity in humans is associated with decreased plasma levels of high density lipoprotein (HDL), but the mechanisms effecting this relationship have not been established. Four treatment groups were used to develop a range of moderate adiposity: rat pups were raised in litters of 4 or 14 and fed from weaning diets of 6 or 24% fat (wt/wt) for 15-17 wk. Lipoproteins from plasma and from a recirculating in situ liver perfusion system were then separated and analyzed, lipoprotein lipase (LPL) activity was assayed in samples of adipose tissue and skeletal muscle and body composition and cholesterol concentrations of various tissues were determined. There was little effect of the diet or litter size treatments on plasma lipids or lipoprotein profiles. Compared to the marked changes in lipid and lipoprotein metabolism that have been observed in severely obese animal models, there was generally little effect of the treatments used to produce this model of moderate diet-induced adiposity. Adiposity was unrelated to plasma total cholesterol and triglycerides. While fatness was positively, although weakly, correlated with plasma levels of several HDL components, including HDL cholesterol, there were no consistent treatment effects on these measures. Plasma HDL levels and adiposity were unrelated to hepatic HDL production or tissue LPL activities. A review of the literature suggests that differences in plasma HDL responses to adiposity in humans and in experimental animals may be due to inherent species differences in lipoprotein metabolism.