Diet composition and energy intake in humans

Abstract

Absolute energy from fats and carbohydrates and the proportion of carbohydrates in the food supply have increased over 50 years. Dietary energy density (ED) is primarily decreased by the water and increased by the fat content of foods. Protein, carbohydrates and fat exert different effects on satiety or energy intake (EI) in the order protein > carbohydrates > fat. When the ED of different foods is equalized the differences between fat and carbohydrates are modest. Covertly increasing dietary ED with fat, carbohydrate or mixed macronutrients elevates EI, producing weight gain and vice versa. In more naturalistic situations where learning cues are intact, there appears to be greater compensation for the different ED of foods. There is considerable individual variability in response. Macronutrient-specific negative feedback models of EI regulation have limited capacity to explain how availability of cheap, highly palatable, readily assimilated, energy-dense foods lead to obesity in modern environments. Neuropsychological constructs including food reward (liking, wanting and learning), reactive and reflective decision making, in the context of asymmetric energy balance regulation, give more comprehensive explanations of how environmental superabundance of foods containing mixtures of readily assimilated fats and carbohydrates and caloric beverages elevate EI through combined hedonic, affective, cognitive and physiological mechanisms. This article is part of a discussion meeting issue ‘Causes of obesity: theories, conjectures and evidence (Part II)’.

Impaired metabolic flexibility to fasting is associated with increased ad libitum energy intake in healthy adults

“…Given the small size of glycogen reserves relative to its turnover and the physiological importance of maintaining minimum blood glucose concentrations, there may be evolutionary adaptations to maintain glycogen levels through feedback signals to the brain driving hunger to increase ad libitum food and carbohydrate intake [36]. The evolution of these signals may be driven by the “selfish brain,” which is reliant on glucose as substrate and accounts for about one‐half of glucose utilization in the entire body [39]; however, reviews of more recent studies that investigated the depletion of glycogen stores and its effects on subsequent intake could not find such an effect [40]. It may be important to note, however, that the method by which glycogen depletion was achieved in these studies was not fasting but rather low carbohydrate overfeeding that was paired with exercise [40].…”

“…The evolution of these signals may be driven by the “selfish brain,” which is reliant on glucose as substrate and accounts for about one‐half of glucose utilization in the entire body [39]; however, reviews of more recent studies that investigated the depletion of glycogen stores and its effects on subsequent intake could not find such an effect [40]. It may be important to note, however, that the method by which glycogen depletion was achieved in these studies was not fasting but rather low carbohydrate overfeeding that was paired with exercise [40]. The reported effects of low carbohydrate feeding [41] and exercise [42] on appetite may confound their effects on glycogen‐mediated appetite regulation.…”

Breaking down silos: the multifaceted nature of obesity and the future of weight management

“…Specifically, research highlights the neural basis for sugar and fat preference that can drive consumption, craving, and appetite. Exposure to high fat and sugar diets can influence food reward mediated by central dopamine signalling, and promote overeating and weight gain [13]. Importantly, however, cultural, marketing and other stealth strategies (e.g.…”

“…interaction between biology and environment), possibly because largescale observational studies or interventions with repeated measures of the genetic/biological factors, environmental exposure and weight change are sparse. Interactions between the environment and individual-level contributors, such as the influence of various diets on physiology of body weight, are under continuous investigation [11,13,89,90]. However, waiting to understand the precise mechanisms by which dietary profiles increase body weight (e.g.…”

“…However, waiting to understand the precise mechanisms by which dietary profiles increase body weight (e.g. diets high in ultra-processed foods) may not be necessary to inform prudent interventions [9,11,13,89,90]. Investigation of the social and demographic factors explaining between-person differences in body weight and weight gain at a population-level is needed.…”