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Circadian and diurnal rhythms affect food intake, and earlier research has suggested that meal sizes increase, whereas the after-meal intervals and satiety ratios decrease over the day. We hypothesized that the time of day of food intake would be related to total intake such that intake early in the day would tend to reduce overall intake, whereas intake later in the day would tend to increase intake over the entire day. The intakes of 375 male and 492 female free-living individuals, previously obtained via 7-d diet diaries, were reanalyzed. The total and meal intakes of food energy, the amounts of the macronutrients ingested and the density of intake occurring during five 4-h periods (0600-0959, 1000-1359, 1400-1759, 1800-2159 and 2200-0159 h) were identified and related to overall and meal intakes during the entire day. The proportion of intake in the morning was negatively correlated with overall intake (r=-0.13, P<0.01), whereas the proportion ingested late in the evening was positively correlated with overall intake (r=0.14, P<0.01). The energy densities of intake during all periods of the day were positively related to overall intake (range, r=0.13-0.23, P<0.01). The results suggest that low energy density intake during any portion of the day can reduce overall intake, that intake in the morning is particularly satiating and can reduce the total amount ingested for the day, and that intake in the late night lacks satiating value and can result in greater overall daily intake.

The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the ‘obesity epidemic’ – the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models – the general intake model and the dual intervention point model – that address this issue and might offer better ways to understand how body fatness is controlled.

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