Sweets and the brain — why do we crave more after eating sugar?

Aim of the study: Sugar addiction, characterized by excessive cravings for high-sugar foods, poses a significant health challenge in modern society. The parallels between sugar and drug addiction have attracted attention, prompting extensive research on the neurological mechanisms involved.

Results: High-sugar consumption activates the brain's reward circuits-a positive reinforcement mechanism-including the dopamine and endorphin systems, which are associated with satisfaction and pleasure. Chronic exposure to high-sugar foods may alter these systems, leading to heightened cravings and a dependence on sugar. Appetite is regulated by complex neural pathways, including those in the prefrontal cortex, amygdala, and hypothalamus. Therefore, dysfunction of these areas may lead to excessive sugar intake and impulsivity. Sugar addiction also negatively affects physical health, with high-sugar intake strongly associated with obesity, diabetes, cardiovascular diseases, and other health problems. Sugar addiction can lead to weight gain and metabolic disorders, which in turn increase the risk of developing these diseases. Pharmacological and psychological interventions are the primary treatment for sugar addiction.

Aim of the study: To review research that tests the validity of the analogy between addictive drugs, like cocaine, and hyperpalatable foods, notably those high in added sugar (i.e., sucrose).

Results: Available evidence in humans shows that sugar and sweetness can induce reward and craving that are comparable in magnitude to those induced by addictive drugs. Although this evidence is limited by the inherent difficulty of comparing different types of rewards and psychological experiences in humans, it is nevertheless supported by recent experimental research on sugar and sweet reward in laboratory rats. Overall, this research has revealed that sugar and sweet reward can not only substitute to addictive drugs, like cocaine, but can even be more rewarding and attractive. At the neurobiological level, the neural substrates of sugar and sweet reward appear to be more robust than those of cocaine (i.e., more resistant to functional failures), possibly reflecting past selective evolutionary pressures for seeking and taking foods high in sugar and calories.

Aim of the study: In animal studies, sugar has been found to produce more symptoms than is required to be considered an addictive substance. Animal data has shown significant overlap between the consumption of added sugars and drug-like effects, including bingeing, craving, tolerance, withdrawal, cross-sensitisation, cross-tolerance, cross-dependence, reward and opioid effects.

Results: In animal studies, sugar has been found to produce more symptoms than is required to be considered an addictive substance. Animal data has shown significant overlap between the consumption of added sugars and drug-like effects, including bingeing, craving, tolerance, withdrawal, cross-sensitisation, cross-tolerance, cross-dependence, reward and opioid effects. Sugar addiction seems to be dependence to the natural endogenous opioids that get released upon sugar intake. In both animals and humans, the evidence in the literature shows substantial parallels and overlap between drugs of abuse and sugar, from the standpoint of brain neurochemistry as well as behaviour.

Aim of the study: [Avena, N.M., Rada, P., Hoebel B.G., 2007. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake.

Results: These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs. Neural adaptations include changes in dopamine and opioid receptor binding, enkephalin mRNA expression and dopamine and acetylcholine release in the nucleus accumbens. The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent. This may translate to some human conditions as suggested by the literature on eating disorders and obesity.

Aim of the study: Treatment success in obesity remains low, and recently food addiction has been delineated as an underlying etiologic factor with therapeutic relevance. Specifically, current treatment focuses on reduced food intake and increase of physical activity, whereas interventions for addiction encompass behavioral therapy, abstinence, and environmental interventions such as taxation, restrictions on advertising, and regulation of school menus.

Aim of the study: The consumption of sugar-sweetened beverages (SSBs) is associated with weight gain in both children and adults. In addition to environmental factors, such as food availability, psychological variables, including mood states, also impact intake. In the current study, we focus on momentary associations between feelings of loneliness and craving for SSBs among adolescents and explore the moderating role of family functioning.

Results: Results suggest that loneliness in adolescents was associated with a small increase in craving for SSBs. Importantly, the relationship held after controlling for negative emotions, suggesting the unique role of loneliness. However, positive family functioning did not mitigate the relations between loneliness and craving for SSBs. Loneliness uniquely contributes to cravings for SSBs. At the same time, family functioning did not buffer the influence of loneliness on cravings for SSBs among adolescents.

Aim of the study: The aim of the present study was to assess the anthropometric measures, food intake and food cravings during the menstrual cycle of undergraduate students of the faculty of nutrition.

Results: The desire for foods rich in sugar, salt, and fat, such as chocolate, pastries, snacks and desserts were higher (p < 0.05) during the premenstrual period, although it did not reflect neither a higher energy intake nor an alteration in the distribution of macronutrients. A higher intake of carbohydrates, proteins, fibers, and calcium was observed during the LP; however, without statistical difference between the groups. There were no differences either in the intake of any food group or in the anthropometric measurements (p > 0.05). Food cravings of nutrition students differed between the phases of the menstrual cycle; however, with no difference in food intake and in anthropometric measures.

Aim of the study: Background/Objectives: Food cravings are common with high-palatability foods that are high in sugar and/or fat. Food cues can strongly induce food craving, and heightened food cue reactivity is associated with eating disorders and obesity.

Results: Mouth rinse induced a stable increase in food craving, which reached a maximum after food cues. Interstitial glucose levels over the after-trial periods (incremental area under the curve, iAUC) were significantly higher for the rinse trial day than for the ingestion trial day, which may suggest higher carbohydrate/sugar intake after the rinse trial, while craving levels were associated with iAUC in the rinse trial. Conclusions: Outcomes indicate that taste/flavour in connection with food cues may generate an error signal experienced as food craving, whereas receipt of sugars, with concomitant physiological responses, reduces the signal and diminishes food craving. These results highlight the importance of sensory-metabolic mismatch in the food craving experience.

Aim of the study: As a disease of energy dysregulation, obesity involves metabolic, hormonal, and neural factors, the interconnection of which is referred to as the "gut-brain axis." This review aimed to provide an overview of the clinical evidence of physiological and objective or subjective changes in eating behavior with gut hormone analogs and NB-ER, as well as a mechanistic rationale for the combined use of these medications to target multiple pathways along the gut-brain axis, particularly for patients who have not achieved their health goals with a single medication.

Results: Peripheral hormones such as glucagon-like peptide-1 (GLP-1) are released in response to food consumption. Peripheral signals are integrated in the hypothalamus and hindbrain to promote energy homeostasis. These brain regions also interact with other systems such as the mesolimbic dopamine system, which promotes food intake for its rewarding properties. Thus, medical interventions for obesity, such as pharmacotherapy and bariatric surgery, aim to regulate various components of this gut hormone-hedonic brain axis. Gut hormone analog medications such as liraglutide, semaglutide, and tirzepatide target the GLP-1 receptor, with tirzepatide also targeting the glucose-dependent insulinotropic polypeptide receptor. These gut hormone analog medications primarily exert their effects on the hypothalamus and brainstem to reduce energy intake. Evidence on their effects on the reward system and reward-based eating is inconsistent.

Aim of the study: Using ecological momentary assessment (EMA), we tested whether momentary palatable food availability and appetitive drive predict adolescents' palatable food/drink intake and dysregulated eating and whether trait hedonic hunger moderates these momentary links. Adolescents aged 13-17 (N = 74) completed a 10-day smartphone EMA protocol with three to seven semi-randomly delivered surveys daily and event reports of eating episodes.

Results: Within-person increases in food availability prospectively predicted higher odds of sweet food intake at the subsequent eating episode, and between-person food availability was associated with higher odds of salty/fried foods intake. Appetitive drive was inversely associated with sweet food intake. Trait hedonic hunger strengthened the positive association between appetitive drive and subsequent salty/fried food intake and LOCE. Findings emphasize the need to consider both momentary contexts and trait-level factors when designing strategies to support healthy eating among adolescents.