The relationship between dietary fat intake, impulsive choice, and metabolic health

Abstract

Unhealthful foods are convenient, ubiquitous, and inexpensive. Overconsumption of unhealthful foods can result in disease states such as obesity and Type 2 diabetes. In addition to the physiological consequences of unhealthful foods, research in rats has shown that diets high in processed fat and sugar induce impulsive choice behavior. Research in humans has demonstrated a link between metabolic health and impulsive choice, but most investigations have not included diet. We investigated how dietary fat intake interacts with body fat percentage, fasting glucose, insulin response, and systemic inflammation levels to predict impulsive choices in humans. Participants were split into either Control (<35% calories from fat) or High-Fat (≥40% calories from fat) groups based on self-reported dietary intake, completed an impulsive choice task, and underwent testing to determine their body fat, glucose, insulin response, and inflammation levels. High-fat diets were not predictive of impulsive choices, but added sugar was predictive. Body fat percentage was associated with impulsive choices only in the group who reported consuming high-fat diets. In addition, fasting glucose was associated with impulsive choices in the control group. Therefore, metabolic health and dietary fat intake interacted to predict impulsive choices. These findings indicate that knowledge of dietary patterns coupled with metabolic health markers may help us better understand impulsive choices, thereby improving our ability to target individuals who could benefit from interventions to reduce impulsive choice behavior, with the goal of promoting more self-controlled food choices.

Keywords: Body fat percentage; Diet; Glucose; Impulsive choice; Inflammation; Insulin response.

Figure 1.. Procedure.

Overview of the procedure and timeline. ASA24 = 24 h dietary recall; DXA = Dual-energy X-ray Absorptiometry.

Figure 2.. Dietary effects in humans.

Mean proportion of larger-later (LL) choices for each group as a function of delay (A) and magnitude (B) ratio in humans. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model. There were no group difference in intercept or slope for delay (A) or magnitude (B) ratio.

Figure 3.

Mean proportion of larger-later (LL) choices as a function of percentage of calories consumed from sugar and delay (A) and magnitude (B) ratio in humans. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model. There was a significant interaction between percentage of calories from added sugar and delay ratio, such that delay sensitivity increased from lower to higher amounts of added sugar. People who consume more added sugar had a greater preference for the larger magnitude when the magnitudes were maximally different. Magnitude sensitivity increased as percentage of calories from added sugar went from lower to higher amounts of sugar.

Figure 4.. Body fat percentage and choice in humans.

Mean proportion of larger-later (LL) choices for each group as a function of body fat percentage and delay (A) and magnitude (B) ratio in humans. Sensitivity to delay or magnitude did not change significantly from lower to higher body fat percentages for the control group. However, sensitivity to delay and magnitude increased from lower to higher body fat percentages for the high-fat group. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control; PBF = percent body fat. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model.

Figure 5.. Fasting glucose and choice in humans.

Mean proportion of larger-later (LL) choices for each group as a function of fasting glucose and delay (A) and magnitude (B) ratio in humans. Sensitivity to delay and magnitude increased from lower to higher fasting glucose levels for the control group. However, sensitivity to delay and magnitude did not change significantly from lower to higher fasting glucose levels for the high-fat group. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control; FG = fasting glucose. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model.

Figure 6.. Insulin sensitivity and choice in humans.

Mean proportion of larger-later (LL) choices for each group as a function of insulin sensitivity and delay (A) and magnitude (B) ratio in humans. Insulin sensitivity did not interact with diet to predict delay sensitivity or magnitude sensitivity. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control; SI = insulin sensitivity. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model.

Figure 7.. Insulin secretion and choice in humans.

Mean proportion of larger-later (LL) choices for each group as a function of insulin secretion and delay (A) and magnitude (B) ratio in humans. Insulin secretion interacted with diet to predict delay sensitivity. However, post-hoc comparisons were unable to localize the source of the effect. Insulin secretion did not interact with diet to predict magnitude sensitivity. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control; invsqrtPCGR = insulin secretion-inverse square root transformed. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model.

Figure 8.. Inflammation and choice in humans.

Mean proportion of larger-later (LL) choices for each group as a function of inflammation and delay (A) and magnitude (B) ratio in humans. Inflammation did not interact with diet to predict delay or magnitude sensitivity. The delay and magnitude ratios were the SS / LL delay or magnitude, respectively. Smaller ratios indicate a larger difference in the delays or magnitudes. HF = high-fat; C = control; IL6 = inflammation. Error bars (+/− SEM) were computed with respect to the estimated marginal means of the fitted generalized linear mixed-effects model.