Search

The purpose of this current opinion paper is to describe the journey of ingested carbohydrate from ‘mouth to mitochondria’ culminating in energy production in skeletal muscles during exercise. This journey is conveniently described as primary, secondary, and tertiary events. The primary stage is detection of ingested carbohydrate by receptors in the oral cavity and on the tongue that activate reward and other centers in the brain leading to insulin secretion. After digestion, the secondary stage is the transport of monosaccharides from the small intestine into the systemic circulation. The passage of these monosaccharides is facilitated by the presence of various transport proteins. The intestinal mucosa has carbohydrate sensors that stimulate the release of two ‘incretin’ hormones (GIP and GLP-1) whose actions range from the secretion of insulin to appetite regulation. Most of the ingested carbohydrate is taken up by the liver resulting in a transient inhibition of hepatic glucose release in a dose-dependent manner. Nonetheless, the subsequent increased hepatic glucose (and lactate) output can increase exogenous carbohydrate oxidation rates by 40–50%. The recognition and successful distribution of carbohydrate to the brain and skeletal muscles to maintain carbohydrate oxidation as well as prevent hypoglycaemia underpins the mechanisms to improve exercise performance.

Liquids have been shown to have a low satiating efficiency. The may be related to the high rate of consumption for liquids which may be higher than 200 g/min. In a number of studies, we showed that the positive relationship between eating rate and energy intake is mediated by oro-sensory exposure time. Longer sensory exposure times are consistently associated with lower food intakes. This observation maybe linked to the role of cephalic phase responses to foods. Cephalic phase responses are a set of physiological responses, which are conceived to prepare the digestive system for the incoming flow of nutrients after ingestion, with the aim of maintaining homeostasis. Results from various studies suggest that cephalic phase responses are much smaller (absent) for liquids compared to solids. It is hypothesised that the absence of cephalic phase responses to liquid foods may be one of the causes why liquid energies enter the body undetected and lead to weak energy intake compensation. This idea fits with the concept of the taste system as a nutrient-sensing system that informs the brain and the gastro-intestinal system about what is coming into our body. With liquids, this system is bypassed. Slower eating may help the human body to associate the sensory signals from food with their metabolic consequences. Foods that are eaten quickly may impair this association, and may therefore lead to overconsumption of energy, and ultimately to weight gain.

Low-caloric artificial sweeteners have been around for several decades now. Still, the debate over their usefulness in decreasing energy intake is ongoing. In principle, replacing sugar-containing foods with 'light' versions will lead to decreased energy intake. However, the reality of food intake behavior is not so simple and still many people tend to consume more calories than they burn and gain weight. Thus, 'light' products are not the easy solution they seem to be. Food intake regulation takes place in the brain. There, multiple neural and hormonal signals are integrated, ultimately leading to a particular pattern of food intake. For many years, the brain has been treated as a 'black box' in food research and other behavioral research alike. In recent years, however, functional neuroimaging techniques have enabled researchers to examine, noninvasively, the effects of different food stimuli in the human brain. This review summarizes literature on the effects of caloric and low-caloric sweeteners on physiological responses and eating behavior and specifically addresses recent neuroimaging studies. Such studies, along with others, suggest that the body cannot simply be 'fooled' by providing sweet taste without calories. Prevention of excess energy intake may not only be aided by refraining from liquid calories and other energy-dense 'fast foods', but also by a consistent relation between sweetness and caloric content. More research addressing the short as well as the long term effects of the replacement of foods and drinks by (partially) artificially sweetened 'light' versions is warranted.

Low-caloric artificial sweeteners have been around for several decades now. Still, the debate over their usefulness in decreasing energy intake is ongoing. In principle, replacing sugar-containing foods with 'light' versions will lead to decreased energy intake. However, the reality of food intake behavior is not so simple and still many people tend to consume more calories than they burn and gain weight. Thus, 'light' products are not the easy solution they seem to be. Food intake regulation takes place in the brain. There, multiple neural and hormonal signals are integrated, ultimately leading to a particular pattern of food intake. For many years, the brain has been treated as a 'black box' in food research and other behavioral research alike. In recent years, however, functional neuroimaging techniques have enabled researchers to examine, noninvasively, the effects of different food stimuli in the human brain. This review summarizes literature on the effects of caloric and low-caloric sweeteners on physiological responses and eating behavior and specifically addresses recent neuroimaging studies. Such studies, along with others, suggest that the body cannot simply be 'fooled' by providing sweet taste without calories. Prevention of excess energy intake may not only be aided by refraining from liquid calories and other energy-dense 'fast foods', but also by a consistent relation between sweetness and caloric content. More research addressing the short as well as the long term effects of the replacement of foods and drinks by (partially) artificially sweetened 'light' versions is warranted.