It has been demonstrated that self-reported eating at a fast speed leads to weight gain [1
], increases risk of type 2 diabetes [3
], obesity [6
], and metabolic syndrome [8
] in epidemiological and cohort studies. Eating fast encourages higher energy intake by increasing food stimuli, hunger, and the desire to eat [11
]. However, in epidemiological and retrospective reports, eating speed was entirely assessed by self-reported questionnaire, which might lead to report bias and eating speed might lack objectivity, leaving the effect of eating speed on glycemic response unclear. Additionally, an interventional study of the effect of eating speed on glycemic response has not been investigated. Therefore, the rate of eating speed should be evaluated objectively by an interventional randomized control study.
The aim of this study was to evaluate the acute effect of different eating speeds on glycemic parameters in young healthy women with a flash glucose monitoring system (FGM, FreeStyle Libre Pro, Abbott Japan, Tokyo, Japan). FGM is a new technology among continuous glucose monitoring systems that does not require regular capillary glucose sampling by finger prick (self-monitored blood glucose, SMBG) like traditional continuous glucose monitoring (CGM). The FGM sensor stores interstitial fluid glucose levels every 15 min for 14 days and was reported to be accurate and effectively replaced SMBG [14
To the best of our knowledge, this is the first interventional study to investigate the association between eating speed and glycemic parameters by FGM. The results of this study suggest the possibility that fast eating induces higher postprandial glucose concentrations and higher daily glycemic excursions in young healthy women. Numerous studies reported that fast eating was associated with increased body weight and overeating [1
], elevated blood pressure and fasting plasma glucose concentration [8
], increased insulin resistance [4
], and increased the risk of impaired glucose tolerance and type 2 diabetes [3
]. It has also been pointed out the association between fast eating and lipid abnormality, such as elevated plasma triglyceride and reduced plasma HDL concentration [10
]. However, it is important to mention that the extent of eating speed in these previous reports was assessed subjectively, such as using questionnaires answered by participants themselves, which might yield bias in evaluating the effect of eating speed on physiological parameters. The interventional method used in the present study is expected to evaluate objectively the effect of eating speed on glycemic parameters.
On the other hand, several reasons may be that eating slowly may exert its beneficial effect by enhancing diet-induced thermogenesis (DIT), increasing serum adiponectin concentration, and suppressing endotoxin and non-esterified fatty acid, as reported previously [22
]. It has been reported that interleukin-1β and interleukin-6, which are both involved in insulin resistance, are decreased in individuals with slow eating [23
], indicating the link between eating speed and glycemic parameters observed in the present study. Moreover, eating slowly may influence gastrointestinal satiety hormones, such as ghrelin and peptide tyrosine-tyrosine (PYY) which control appetite and influence food consumption, suggesting that modifiable eating behaviors actually regulate the hormonal response to food [25
]. In contrast, Shah M et al. reported that eating speed could not be explained by the changes in meal-related hormones. In their study, eating breakfast slowly (30 min) and quickly (10 min) did not affect postprandial gut hormone responses such as ghrelin, glucagon-like-peptide-1 (GLP-1), PYY, nor hunger and daily food consumption [26
]. In the present study, IAUC for glucose of breakfast and lunch demonstrated no difference, possibly because the secretion of the incretin hormones might not be affected by eating speed in the daytime. Additionally, another possible reason was that the energy ratio of dinner was large (40%) compared to that of breakfast (25%) and of lunch (35%). We employed this energy ratio to design the three test meals according to the general meal plans of Japanese dietary habits. However, as there are controversial reports in association with gastrointestinal hormones and eating speed, the mechanisms underlying the association with eating speed and metabolic responses needs to be verified in further studies.
The strength of our study is that this is the first randomized controlled cross-over interventional study to explore the association between eating speed and the glycemic responses in healthy Japanese women. Postprandial hyperglycemia and higher MAGE are associated with increased risk of type 2 diabetes and cardiovascular diseases in people with and without diabetes [27
]. It is reported that the large blood glucose fluctuation not only increases tumor necrosis factor-α, interleukin-6 [30
], and platelet aggregability [31
], but also decreases endothelium dependent vasodilation [32
] even before the onset of diabetes. Therefore, decreasing postprandial glucose concentrations and MAGE may reduce the risks of developing impaired glucose tolerance, type 2 diabetes, and cardiovascular diseases in people without diabetes.
Some limitations to the present study should be mentioned. First, the present study is an acute interventional study, therefore, it is unable to translate all these effects on glycemic responses to long-term benefits. Second, the participants of this study consisted only of young healthy Japanese women who experience a diet and lifestyle specific to Japan. Therefore, we should be cautious to apply our results to individuals with other gender, race, genetic backgrounds, and lifestyle, and individuals with diabetes. For the third, because how the metabolism is regulated by eating speed is not fully understood, the role of insulin, incretin hormones, cytokines, and endogenous glucose production on significance of eating speed is still unclear. Fourth, the eating protocol between fast eating (eating sequentially) and slow eating (eating at once as a mixture) in this study was not exactly the same, leaving possibility that the difference in the eating protocol contributed to the results. As the fifth limitation, psychological conditions such as satiety may have influenced the glycemic responses, but we did not measure the extent of satiety between the study days of fast and slow eating. It has been reported that eating fast tended to increase the amount of food intake by suppressing satiety [11
]. Since there was no difference in the amount of food taken between study days of fast and slow eating in our study, how and/or whether satiety influenced the glycemic parameters observed in our study is left unanswered. The sixth limitation was the possibility that participants might not have followed strictly the study protocol. Although, we had thoroughly and repeatedly explained and instructed the protocol prior to and during the study period to maintain high adherence. Therefore, further study needs to explore the comparison between fast eating and slow eating on glycemic responses when meals were consumed in the same manner, with the meal sequence of vegetable, main dish, and rice/bread.
The disadvantage of eating fast shown in this study brings the possibility of raising the risk of type 2 diabetes and obesity in healthy young individuals. Eating slowly is potentially advantageous to public health, because the modification of eating speed could be cost effective for promoting management of body weight and glycemic control [33
]. Dietary education on the benefit of eating slow could be a simple way to reduce excess food intake, since eating fast leads to higher energy intake but lower satiety [11
]. One practical approach that can be done for promoting slow eating behavior is to try eating slowly at lunch breaks in schools or workplaces. However, in future studies, additional investigations are required to explain the mechanisms under these effects and the long-term effects of eating speed on metabolic control in individuals with and without diabetes.