The goal of this experiment was to measure the effect of rate of eating on the size of a binge meal among patients with BN and controls. We were able to manipulate rate of eating in the laboratory successfully in both groups. The principal finding of the study was that ingestion rate affected binge size only in the normal control subjects, not in subjects with BN. The patients with BN did not need to eat quickly in order to binge, and reducing their rate of eating failed to influence binge size. However, manipulating rates of consumption did affect meal size for control subjects. Both the demonstration of an effect of rate of eating on meal size in controls and the lack of such an effect in patients with BN are of interest.
Although several previous feeding laboratory studies have demonstrated that obese individuals eat more rapidly than normal weight individuals [10
], previous studies have not directly manipulated eating rate. The amount of food eaten in a meal depends on a number of changes that occur over time following the beginning of the meal, including gastric distension, passage of food into the small intestine, and the subsequent release of various satiety-mediating peptides. In theory, more rapid eating may allow the consumption of a greater amount of food prior to the development of physiological inhibitory signals that contribute to termination of the meal and thus determine its size. The current study did not measure any of these physiological signals; thus, we were unable to determine the relationship between food ingestion and the time course of post-ingestive signals related to meal termination. However, there is considerable evidence that controls of eating that operate in normal subjects are attenuated or delayed in individuals with BN, possibly rendering them less responsive to the signals that would limit eating at a slower rate [11
The lack of an effect of rate of consumption on meal size in patients with BN, in contrast with the observed effect in normal controls, suggests that the large size of binge meals in BN is not attributable simply to a rapid eating rate during a binge meal. Slowing the rate of eating of individuals with BN during a binge meal did not significantly decrease meal size. Conversely, increasing the rate of consumption of normal controls, while it does increase the amount consumed, did not immediately lead to the consumption of meals of comparable size to those of patients with BN. Taken together, these findings suggest that the signals, or responses to the signals, that lead to meal termination in a binge meal in BN patients may differ from those in normal subjects. For example there is evidence that the release of CCK, an important satiety signal, is diminished in patients with BN [11
]. It is additionally possible that individuals with BN continue eating after meal-terminating signals reach values that terminate meals in controls, or that they are eating to achieve a different end point, such as the ability to readily induce vomiting. In fact, in a single case study, Azrin et al. [15
] found that the instruction to eat at a faster rate was associated with increased desire to vomit in a patient with BN. In our study, subjects were queried in a postmeal checklist about several sensations they may have had during the meal, including whether they felt like vomiting. All of our patients with BN reported feeling like vomiting, and did vomit after meals delivered at slow and fast rates, while none of the controls reported feeling like vomiting or vomiting.
It is important to note that the meal instruction, while the same for both groups, may have had a different meaning for the two groups. By definition, patients with BN had experience with recurrent binge eating while controls did not. Therefore, in the BN group, the instruction to “binge eat” may have prompted a well-practiced behavior that was not sensitive to manipulation of rate of eating. It is possible that in other circumstances, for example, in the absence of an instruction to binge eat, manipulation of rate of eating would have a greater impact on amount consumed in individuals with BN.
An unexpected finding of the study was that, despite the use of an adaptation meal, subjects overall ate 89.5 g more in the second than the first laboratory meal, giving rise to a rate by order interaction. The trial effect (rate × order interaction) was not significantly different in the patients with BN and controls. In subjects assigned to the slow-fast sequence this order effect augmented the effect of the rate instruction, while in subjects assigned to the fast-slow sequence, the rate and order effects negated each other. While our prior studies [16
] have demonstrated that laboratory meal intake stabilizes after an adaptation meal, we did not instruct subjects to binge eat in those studies. We do not know how many adaptation meals are required for laboratory binge meal intake to stabilize, and it may be well for future investigations to note this caveat.
Some caveats are in order. Although laboratory studies presumably reflect the same physiological controls that would operate in any environment, they may not replicate all the controls of eating in an individual’s usual environment, particularly cognitive and social controls. Our study was also limited to the consumption of a single food given at two predetermined rates accompanied by the instruction to binge eat. Whether similar results would be observed under other experimental conditions, such as faster or slower rates, with solid or even other liquid foods, without an explicit instruction to binge eat, or with manipulation of participants’ emotional states via mood induction is unknown. Finally, since subjects were not instructed to eat either faster or slower, but simply to eat to keep the level in the cup constant, these results do not directly address the clinical impression that telling patients to eat more slowly helps them reduce intake.
A series of studies by Spiegel [17
] examining the effect of bite size and ingestion rate on food intake on lean and obese subjects, found that ingestion rate did not determine meal size in lean or obese groups. While the current study also failed to demonstrate a relationship between experimentally controlled eating rate and binge meal size in patients with BN, our study did find an effect of eating rate on intake in control subjects. Rapid eating remains a salient feature of binge eating in BN, but this study suggests rapid eating may not be an essential element of binge eating in BN. Our results do not, however, imply that rate of eating plays no role in binge eating, nor that interventions focusing on modifying the rate of eating would necessarily be ineffective. Further laboratory studies using different instruction, e.g. an instruction to eat rapidly or slowly, rather than to binge eat or refrain from binge eating, may further elucidate the relationship among rate of eating, meal size and desire to vomit in individuals with eating disorders.