Observations
Weight gain has been linked to a preference for both sweet and/or high-fat foods [
114,
115], which may partly explain why obese people regain body weight frequently after ‘dieting’ [
116,
117]. The common view summarised earlier by Pangborn and Simone is: “In the mind of a normal person, sugar and sweets are ‘fattening’ and most overweight people have a ‘sweet tooth’” [
118]. Hedonism associated with palatable foods is considered a significant factor which increases the prevalence of obesity. A motivational factor that is referred to as ‘hedonic hunger’ [
119] may be a trigger for overeating [
120].
Patients after RYGB tend to increase the intake of fruit and vegetables as well as low-fat food [
121,
122]. The dumping syndrome was thought to induce these changes in food preference [
123], as initially it was considered as a useful characteristic of the RYGB to ‘teach’ patients to avoid calorie-dense foods and thus consume fewer calories [
124]. However, patients after RYGB appear to make healthier food choices and adopt a more balanced diet (even when they do not experience dumping) [
121,
125] and have considerable reduction in energy intake (EI) and energy density. A comparison on food groups was done for a group of patients after RYGB and total number of servings from fat, grains and sweetened beverages was reduced and remained reduced in the longer term. However, meats, dairy products, fruits and sweets were reduced in the short term, but then returned to baseline by 12 months [
22]. When energy intake was reduced to 1300 kcal, 60 and 25 % of patients ,respectively, were consuming less than one serving per day from both fruits and vegetables. Whole grains intake increased from 25 to 40 % within the first 3 months, but then returned to baseline at 12 months [
22]. The association between reduced diet energy density and weight loss is controversial as some studies describe no association [
126], while others show that shifts in food preferences are partially responsible for the decreased calorie intake and weight loss after RYGB [
127].
RYGB in humans appears to alter taste through unconditional and conditional mechanisms [
24,
128‐
130] leading to the concept of ‘behaviour surgery’ [
123]. In 1987, Sugerman et al. reported that ‘sweet-eaters’ did particularly well after RYGB [
131,
132]. Some of the initial findings were confounded by intolerance to sweets related to symptoms of the dumping syndrome [
38,
131‐
133]. Conditioned taste aversion may thus be a factor in some patients. These initial assumptions resulted in many clinicians thinking that the RYGB works by ‘punishing’ the ‘poor behaviours’ of obese patients. The notion that RYGB becomes an external enforcer that goes against the free will of the patient has led to some authors questioning the morality of RYGB as a tool that changes patients’ behaviour against patients’ natural wishes [
134]. This misconception may have reduced the wider acceptance of RYGB as a valid physiological treatment for the pathology that results in obesity. Classical
conditioned food aversion is, however, an unlikely explanation as most patients with severe dumping still report that they like the taste of sweet foods, but that they have learned to consume only small quantities that do not cause negative visceral symptoms or consume sweets at night before bedtime, suggesting a
conditioned food avoidance to be a more likely explanation. Distinguishing between the terms is important because avoidance implies that the palatability of sweet or fat did not change when small quantities are consumed, but that the subject ‘learns’ to stop consuming the food sooner (earlier avoidance) because large quantities may have negative visceral consequences [
135‐
137].
RYGB could be exerting its effects on food selection and preference through any one of the taste function domains important in normal physiology such as sensory-discriminative (stimulus identification), hedonic (ingestive motivation) and physiological (digestive preparation) [
138,
139]. Affective responses to taste stimuli, which can be considered an example of ingestive motivation, can be both conditioned and unconditioned. It remains controversial which of these three domains are involved and what their interactions are to determine food preferences after RYGB surgery. For example, RYGB could have effects directly on the central gustatory pathways related with feeding and reward through gut hormonal mediators. Alternatively, changes in the sensory signals could alter the intensity or the quality of tastants, but also lead to an unconditioned change in palatability. If RYGB causes visceral malaise after ingestion of fat, then it is possible that the palatability of fat could alter through a process of learning (conditioned response) [
140].
Although there are suggestions in animal models that the hedonic properties of sweet and fat stimuli may change after RYGB [
23,
140‐
144], less work has been done in humans. Miras et al. using the progressive ratio task showed that RYGB resulted in the selective decrease of the reward value of a sweet and fat tastant, but not vegetables [
145]. Further support comes from studies of brain reward cognitive systems linked to eating behaviour as studied by functional MRI (fMRI), where brain hedonic responses to calorie-dense food are lower after RYGB compared to patients who have lost similar amounts of weight after adjustable gastric banding [
128].