Introduction: Binge eating is a behavior described as excessive eating which is not driven by hunger or metabolic need. This excessive eating pattern is associated with weight gain and obesity. Being overweight or obese is a risk factor for insulin resistance and metabolic syndrome. Individuals whom binge eat tend to eat until they are uncomfortably full, resulting in an increase in energy consumption and positive energy balance. This positive energy balance results in weight gain. Binge eating is associated with many stressors, including inter-personal and work-related stress. The metabolic consequences of binge eating are relatively unknown. Binge eating is associated with the excessive consumption of palatable foods, which are generally high in fat and/or sugar. Diets high in saturated fats are associated with insulin resistance. Therefore, the goal of this study was to assess the metabolic response to a single day of binge eating, consisting of a high-fat, SFA-rich food intake in non-obese healthy individuals.
Subject Description: Fifteen healthy individuals were recruited for the study. The subjects were physically active, which was defined as exercising at least three times per week for more than 30 minutes at a time. Inclusion criteria included non-smoker, free from cardiovascular and metabolic disease, not taking medication, and stable weight for the past 6 months.
Methods: An initial assessment was performed to determine baseline anthropometrics including height, weight, and body mass index. These measurements were used to estimate resting energy expenditure (REE) using the calculations by Miffin. Standard correction for physical activity level was applied at 1.6 times REE for females and 1.7 REE for males to estimate total daily energy requirements. An oral glucose tolerance test (OGTT) was also performed as a baseline. Food intake was tracked over a period of 6 days. On the 7th day the subjects consumed the experimental diet. The experimental diet consisted of a high fat (68% total energy) and excess energy (+78% kJ). All foods were purchased and prepared by the research team. The subjects were required to consume all food provided and to avoid additional food/beverages. On day 8, a second OGTT was performed. Testing on day 0 and 8 was performed following a 10 h fast. Blood samples were obtained via the antecubital vein. Subjects consumed a 25% glucose solution (75 g glucose) and blood was drawn at time intervals of 0, 15, 30, 45, 60, and 120 min post ingestion. Plasma sample was analyzed via spectrophotometric assay for glucose and triglyceride concentrations. Serum insulin was determined using enzyme-linked immune-sorbent assay (ELISA). Insulin sensitivity was determined using the Matsuda insulin sensitivity index (ISI).
Overall, the methods for this study are relatively straight-forward given this is a pilot study. The authors adequately explained the details about conducting the experiment. One thing to note was the failure to justify sample size. The authors made no mention of basing their research on prior studies or using theoretical samples to predict a sample size which could detect a certain level of significance. The authors did mention using a t-test to calculate significance, which is standard for a small sample (<30). Inclusion of a either a control group or use of a cross-over design would have really strengthened this study. Another potential group could have been a high glycemic, sugary diet. This would help determine the effects of binge eating on sugary sweets. As mentioned previously, I prefer research articles to report both tests of statistical significance and magnitude. This gives the reader a better picture of the impact of the results and allows for greater interruption. As a final point, a table with food selection should have been provided. It leaves the reader wondering what foods the researchers decided to select.
Results: The estimated energy requirement for the group was 14,028 ± 433 kJ. The energy consumption during the experiment was 24,949 ± 797 * kJ, which was statistically significant (p<0.05). Macronutrient consumption during the experiment was as follows: carbohydrate (g) 192 ± 6, protein (g) 278 ± 8, and fat (g) 449 ± 15. Fatty acid composition was further broken down (%): saturated fat 42 ± 0.6, monounsaturated fat 40 ± 0.4, and polyunsaturated fat 10 ± 0.2. Fifteen insulin-sensitive (5.0 +/- 0.5 ISI) individuals (13 male, 2 female) with a mean BMI of 26.4 ± 1.1 kg/m2 were included. An average increase of 0.85 ± 0.20 kg was found post binge eating (p = 0.001). Whole body insulin sensitivity was reduced by 28% (p = 0.001). No changes in fasting insulin or TG were noted. Fasting plasma non-essential fatty acid levels were significantly decreased (p = 0.009). Postprandial plasma glucose concentrations increased 17.1% after binge eating (p<0.001). Postprandial serum insulin concentrations increased 16.4% after binge eating (p=0.007).
The results of this study were reported in a clear and concise manner. Accompanying graphs were provided to allow quick interpretation of the results by the reader. As pointed out above, the subjects of this study were not obese, but would be considered overweight. The description of the subjects as healthy is misleading to the reader. It is possible that these overweight individuals will respond differently to a binge eating regime than leaner subjects. Also, the subjects were heavily male (n=13) as compared to female (n=2). This limits the application of the results to a general population considering the limited sample size and limited number of female participants. Another interesting detail of this study was the high protein intake. The protein intake for the experimental day was much higher than the carbohydrate intake. An increase in carbohydrate intake may exacerbate glucose concentrations to an even greater extent.
Discussion: The findings of this study indicate a one day binge eating diet consisting of high amounts of fat results in impaired whole-body insulin sensitivity. The authors suggest brief periods of excessive consumption of foods typical of a Western diet may lead to metabolic syndrome. The experimental diet did not allow the results to be attributed solely to high fat intake, excess energy, or both. Therefore, the results of this study must be interrupted with caution. Another finding of this study was one day of excessive consumption results in a significant increase in postprandial glucose. The current study design did not allow for analysis of why this increase occurred. Studies in type 2 diabetics demonstrate alterations in regulatory factors. Future research will need to further examine these factors in response to binge dieting. The current study demonstrated a lack of change in triglyceride levels in response to binge eating. This is consistent with other short-term overfeeding research has observed a reduction in insulin sensitivity without an increase in triglyceride levels. Although this study demonstrated significant increase in postprandial glucose, levels returned well below levels considered for glucose impairment 2 hours post. Overall, this pilot study set the stage for a future, larger, randomized control trial which can further examine binge eating on glucose sensitivity. Future research will strive to examine what causes these changes in insulin sensitivity.
Conclusion/Limitations: In conclusion, a single day of binge eating on a high fat, excessive energy diet results in impaired glucose sensitivity in relatively healthy adults. Limitations of this study include a small and mainly male sample, lack of control, lack of power analysis, and failure to acknowledge the subjects were overweight. The use of two different sections to provide the subject characteristics forces the reader to bounce around the article in order to understand the sample population. Strengths of the study include a clear description of the study protocol and methods along with a concise description of the results.
Parry, S., Woods, R., Hodson, L., & Hulston, C. (2017). A Single Day of Excessive Dietary Fat Intake Reduces Whole-Body Insulin Sensitivity: The Metabolic Consequence of Binge Eating. Nutrients, 9(8), 818. doi:10.3390/nu9080818
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