OBJECTIVE: To investigate the degree of bias in under-reporting of food intake in obese and non-obese subjects, hypothesising that under-reporting may be selective for either macronutrient content (carbohydrate (CHO), fat, protein, alcohol), speci®c food types or eating occasions (meals, snacks). DESIGN: Thirty-three women (18 obese, 15 non-obese) were recruited to a long-stay metabolic facility for 24 h. Ad libitum food intake was covertly measured throughout the study and a reported food intake completed at the end of 24 h. RESULTS: Reported total daily energy intake was signi®cantly lower than measured intake. Whilst meals were accurately reported, energy from snack foods eaten between meals was signi®cantly under-reported. (P`0.001) Reported total carbohydrate and added sugar intakes were signi®cantly lower than measured, whilst reported protein and fat intakes were not signi®cantly different from measured. Reported alcohol intake was also considerably lower than measured, but high variability prevented signi®cance. CONCLUSIONS: In both obese and non-obese women the major cause of under-reporting, as assessed by covert study design in subjects restricted within a metabolic facility, is the failure to report between-meal snack foods. There is some evidence for increased under-reporting in high CHO, but no evidence of a bias in under-reporting towards high fat or high protein foods.

Murine gammaherpesvirus-68 (MHV-68

OBJECTIVE: The effect of two low-fat treatments on ad libitum energy intake (EI) was investigated in ®ve lean men living within a metabolic facility. DESIGN: Diet was controlled over two consecutive periods of 12 d when either, i) all foods eaten or ii) only a single (lunch) meal, was manipulated to increase the fat content from 20, 40 to 60% of energy, and ad libitum EI measured. RESULTS: All foods: EI increased from 8.6 (2.9 s.d.) ± 14.8 (3.1 s.d.) MJad and energy density (ED) from 4.1 (0.8 s.d.) ± 7.7 (1.6 s.d.) kJag as fat content increased from 20 ± 60% (P`0.0001). There was no decrease in weight of food eaten across diets (P b 0.05) and hence no energy compensation. Lunch meal: EI (20%:13.1 MJad, 40%:13.8 MJad, 60%:14.8 MJad) and ED (6.03 kJag, 5.89 kJag, 6.41 kJag) increased but not signi®cantly across treatments (P b 0.05). There was partial energy compensation on the low-fat 20% diet (due in part to compensatory increase in fat intake), but no compensation for the high-fat 60% diet. CONCLUSIONS: Changes in total dietary fat and ED result in concomitant changes in EI; low fat diets reducing EI. However, the dietary strategy of intermittent use of low-and high-fat items fail to signi®cantly alter ED, and hence EI, in free-feeding lean men. Whilst there is a trend towards reduction in intake, manipulation of the fat content of a single meal may not be suf®cient to induce signi®cant long-term weight loss.

Background: Studies in lean men show poor regulation of energy (EB) and fat balance (FB) during manipulation of dietary ratios of fat to carbohydrate. High-fat (HF), high-energy diets cause hyperphagia and a positive EB and FB. Objective: The protocol was designed to measure substrate flux and EB in obese women taking dexfenfluramine (DF) or placebo (PL) during an HF (50% of energy) or low-fat (25% of energy; LF) diet. We hypothesized that alterations in dietary fat would not be regulated and would lead to a positive EB and FB. Design: The study was double-blind, randomized, and placebocontrolled, with 4 treatments (LF/DF, HF/DF, LF/PL, and HF/PL) and a crossover. Five days of continuous, whole-body calorimetry measurements were made in 6 subjects after 8 d of home DF/PL treatment. Macronutrient balance and EB were measured within the chamber as the cumulative difference between ad libitum intake and oxidation. Conclusions: EB and FB are poorly regulated with HF, energydense diets in obese women, which leads to fat deposition and weight gain.