Diet and Craving

Several factors may anticipate our adopted eating behaviors, including neural factors linked to our perception of energy-dense food. Current research, however, failed to explore these factors holistically, with most studies focusing on singular outcome measures and investigating the post-intervention outcomes during a single follow-up event. Giuliani et al. (2020) endeavored to elevate the currently available literature through the use of a comprehensive neurobiological behavioral change model that fastidiously investigates food consumption and food cravings at multiple time points. Using a sample of 88 individuals (community-derived, 39.17 ± 3.47 years of age, body mass index [BMI] range of 24 to 42 with an average of 31.5 ± 3.9), the authors evaluated food craving reactivity and regulation in participants with higher BMI scores while simultaneously subjecting them to a functional magnetic resonance (fMRI) scan. Across four time points (at experiment onset, 1, 3, and 6 months) the participants submitted a Food Craving Inventory (FCI) and ASA24 assessments, evaluating food cravings and consumption of both healthy and unhealthy foods (6 months n = 52 - 55 participants). Analysis of the results revealed that, contrary to a priori hypotheses that participant-reported craving and consumption of unhealthy food was linked to cerebral processes involved in observing and modulating personal cravings to unhealthy energy-dense food at baseline, the authors noted that the observed cerebral activity in the participants was linked to their reported cravings for, and the intake of, healthy food, seen during the times in which the participants were voluntarily modulating their cravings for unhealthy food. Consequently, this disproved the hypothesis that monitoring the ventromedial prefrontal cortex of the brain (vmPFC) helps anticipate behavioral patterns associated with healthy eating. However, the authors observed that the activity of the dorsolateral and ventromedial prefrontal cortices, the dorsal anterior cingulate cortex, and the inferior frontal gyrus prognosticates reductions in the craving for, and the consumption of, healthy food throughout a six-month period. [NPID: Brain activity, food consumption, food craving, food craving regulation, food cue reactivity, healthy food, unhealthy food]

This 2021 article points out that there have been mixed results on the effects of nonnutritive sweeteners (alternative to nutritive sweeteners that quench the desire for sweets while providing fewer calories) on appetite. It is unknown how sex and obesity correlate with the reward and appetitive responses to nonnutritive sweeteners (NNS). One of this study’s aims was to look at how the nervous system of healthy young adults reacts to various types of high-calorie food cues. Another objective was to examine metabolic responses and eating behaviors after the consumption of sucralose (nonnutritive sweetener) vs sucrose (nutritive sugar). The subjects taking part in this experiment underwent a functional magnetic resonance imaging task measuring blood oxygen level-dependent signal in response to visual cues. In this randomized trial, the same participants were examined during 3 separate visits. Participants arrived at each visit after fasting for 12 hours. They all received a drink containing either sucrose, sucralose, or water. Blood samples were taken at baseline and at specific time intervals following consumption of the drink. Later, each individual received a buffet meal. Compared to sucralose, the intake of sucrose was associated with increased production of circulating glucose, insulin, and glucagon-like peptide-1. People with obesity showed higher responsivity to savory cues after sucralose vs sucrose, relative to overweight and healthy weight individuals. Comparing sex, female participants had greater responses to food cues, and consumed more total calories during the buffet meal. In conclusion, the difference in neural responsivity that is elicited by sucralose (compared to sucrose) particularly affects females and obese people. [NPID: sucrose, sucralose, sweeteners, artificial sweeteners, sugars, appetite, diet, food, obese, female, snacks, unhealthy]

In this 2020 study, 229 female dependents of active duty and retired military personnel had their blood samples taken to determine cardiometabolic risk factors, were questioned on their cravings, and provided their dietary information, as well as demographics. The participants had an average BMI of 34.7 and were part of the Healthy Families Healthy Forces weight loss and maintenance study. Among individuals who reported energy intake of 2210 kilocalories and more per day, higher food craving scores were linked with a lower diet quality, more frequent consumption, longer daily eating interval, and a lower probability of following a time-restricted dietary pattern. Food cravings also positively correlated with BMI and waist circumference, but not with the measures of cardiometabolic risk such as blood pressure and HDL/LDL concentrations. This study demonstrates the high potential of targeting cravings in behavioral programs for weight management. [NPID: craving, military, craving, waist circumference, behavioral programs, behavior, weight management]

Dietary intake that is high in sugars, fat, and salt influences our perception of taste and overall dietary choices, augmenting obesity and metabolic disorders. The underlying molecular mechanisms of such phenomena remain poorly understood, thus, Vaziri et al. (2020) demonstrate in their study how a high sugar diet leads to reprogramming of the sensory neurons of Drosophila melanogaster flies through the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1), leading to a reduction in sweet sensation and the enhancement of obesity. In the authors’ experiments, animals fed high sugar diets demonstrated a binding of PRC2.1 to sweet gustatory neuron chromatin, which was subsequently rearranged to suppress a developmental transcriptional network that plays a role in the neuronal response to sweet stimuli, thereby reducing sweet sensation. Furthermore, half of these transcriptional suppressions persisted after substituting the high sugar diet for a control diet, conferring a lasting decrease in sensitivity to sweet taste. The authors conclude that their results shed light on novel epigenetic mechanisms that influence neural plasticity and dietary behaviors to upregulate the drivers for obesity, in response to dietary environmental stimuli. [NPID: Dietary behavior, sweet taste, neuronal regulation, Drosophila Melanogaster, flies, high sugar diet]

This 2019 study tested whether random access to palatable food would trigger similar addiction-like responses as observed under a fixed schedule. Providing food at a fixed time it thought to make access to food predictable, and palatable foods appear in a random manner outside the laboratory. Muñoz-Escobar et al. (2019) randomly assigned rats to one of four groups: without chocolate access (control); unrestricted access to chocolate; fixed intermittent access (CH-F); random unpredictable access (CH-R) to chocolate. Only the CH-F group was found to anticipate palatable food access, indicated by behavior and core temperature. Both groups provided with intermittent palatable food access (CH-R and CH-F) showed signs of binge eating, greater effort behavior to obtain chocolate, and high FosB/ΔFosB in corticolimbic areas. The FosB/ΔFosB ratio in all areas actually correlated with the intensity of binge eating and effort behavior. In summary, only a fixed schedule allowed rats to anticipate palatable foods, which is strongly associated with craving behaviors, while the 2 conditions involving intermittent access to palatable food stimulated addiction-like behaviors and and FosB/ΔFosB accumulation in regions of the brain linked to reward processes. [NPID: craving, palatable food, food addiction, addiction, chocolate, binge eating, reward, food reward]

This 2020 study examined the brain network arrangement of 67 older adults with obesity (65‐85 years, BMI = 35‐42 kg/m2) in 2 sets of brain regions (regions of interest [ROIs] 1 and 2) to investigate its association with the participants’ baseline measures of hedonic hunger (the Power of Food Scale) and self‐control for food intake (the Weight Efficacy Lifestyle Questionnaire). The subjects took part in a 18-month clinical trial on weight regain, from which their functional magnetic resonance imaging data at resting state and upon performing food cue tasks were obtained. During the food cue state, the Power of Food Scale (PFS) was most related to ROI 1 (the visual cortex and sensorimotor processing areas), whereas there was a link between Weight Efficacy Lifestyle Questionnaire and ROI 2 (areas of the attention network and limbic circuitry) during both the food cue and resting conditions. As well as indicating to us the connection between brain network topology and measures of hedonic hunger, Burdette et al. has exposed older adults’ confidence in resisting food consumption because of both intrapersonal and social/environmental cues. [NPID: craving, obesity, self-control, food cues, hedonic hunger, social cues, environmental cues]

Since the underlying processes behind the connection between negative mood and binge eating are not yet fully understood, this 2020 study examined the effect of mood (negative/neutral) and state of food deprivation (hunger vs. satiety) of 33 normal-weight females (mean age = 25.1 years, mean BMI = 21.6) on their level of food craving. The results indicated that in neutral mood, high calorie foods modulated craving, meaning hungry participants preferred savory foods whereas sweet foods were desired by those in the sated state. This differentiation in preference for sweet/savory taste was not observed in participants in a negative mood. Cravings were also found to be significantly higher among hungry individuals relative to those in the state of satiety. Reents et al. concludes that food craving is influenced by hunger and even more so by the person’s emotional state. These findings support etiological models of disturbed dietary behavior and is in keeping with common interventions targeting eating schedules and mood regulation. Hunger is highly relevant to the impact investigated in food-related models and should be considered by future studies. [NPID: craving, binge eating, mood, hunger, satiety, food deprivation, regulation, emotional regulation]

Since psychological distress symptoms have been widely reported during the early stages of the coronavirus disease 2019 (COVID-19) pandemic, and stress and negative affect can lead to emotional eating, Bemanian et al. (2020) examined the dietary habits, emotional eating, psychological distress symptoms, and COVID-19-related worries of 24,968 Norwegian inhabitants via electronic questionnaires. This population-based study took place in April 2020 due to the 6 weeks of interventions managing the first wave of the COVID pandemic. The data revealed the prevalence of emotional eating (54%), which was substantially more frequently reported by females. The presence of worries regarding the consequences of the pandemic was related to greater emotional eating, while the association between psychological distress and emotional eating was markedly stronger [odds ratio (OR 4.2)]. Compared to worries related to health (OR = 1.3), concern over personal economy was more strongly connected with emotional eating (OR = 1.7). The consumption of food and drinks rich in sugar was higher among those respondents with psychological distress and those feeling markedly anxious over factors related to COVID-19, compared to the overall population. [NPID: craving, insula, frontal gyrus, self-control, dorsolateral prefrontal cortex, appetite, food cues]

This 2019 review proposes fixing eating‐related psychological constructs like food addiction, disinhibition, hedonic hunger, emotional eating, and binge eating into one broad phenotype - uncontrolled eating. Vainik et al. believes these constructs have similar definitions about loss of control over consumption, and as a single phenotype researchers can review and meta-analyze evidence using results from various questionnaires. This article presents associations between uncontrolled eating, body mass index (BMI), food intake, personality traits and brain systems, and demonstrates the phenotypic and genetic link between uncontrolled eating with BMI and food intake using cross-sectional and longitudinal data. Moreover, the evidence on the association between lower cognitive control, higher negative affect, and reward sensitivity (curvilinear) with uncontrolled eating was reviewed here. Uncontrolled eating mediates all three constructs’ associations with BMI and food intake. Lastly, the following uncontrolled eating-promoting brain systems were discussed and meta-analyzed: dopamine mesolimbic circuit; frontal cognitive networks; and the hypothalamus‐pituitary‐adrenal axis amygdala and hippocampus. Vainik and colleagues have faith in using the single concept uncontrolled eating since it allows robust conclusions on the relationship between food consumption, BMI, psychological variables and brain structure and function to be made. [NPID: craving, food addiction, hedonic hunger, emotional eating, binge eating, disinhibition, personality, hypothalamus, adrenal, amygdala, hippocampus]

While cravings are associated with subsequent consumption and weight-related outcomes, Rebello & Greenway (2016) reveal that several targets for therapeutic agents have been discovered that use the food-related reward mechanism, which may help reduce the rate of obesity. As well as explaining the concepts related to appetite and reward-induced eating behavior, this review showcases the pharmacological options and food-derived components that may be utilized to address food cravings. Phentermine and liraglutide were noted as a monotherapy treatment approved for weight management, while the US Food and Drug Administration (FDA) also endorsed the use of the naltrexone–bupropion combination and lorcaserin, for weight control on a long-term basis. Furthermore, food components such as thylakoid membranes can potentially influence food cravings, while liraglutide, and phentermine alone or in combination with lorcaserin, may also be effective in targeting food cravings (suggested by preliminary studies). [NPID: craving, food reward, reward, obesity]

This 2018 review aimed at providing up-to-date evidence on interventions that alter food cravings, presenting dietary, physical activity, pharmacologic, and bariatric surgery interventions, and discussing the influence of social determinants and current controversies of food cravings. Although dietary, physical activity, pharmacologic, and bariatric surgery weight loss interventions have shown potential in reducing cravings, Myers et al. emphasizes the need for further research since differential responses in food cravings may be seen among various demographic and socioeconomic groups. It was also highlighted that reductions in food cravings are independent of energy content and occur because of reductions in the frequency of craved foods consumption. This area of research is believed to also benefit from additional relevant studies. [NPID: craving, food cravings, bariatric surgery]

This 2020 review presents the concept of craving (defined here as a strong desire to eat) from a historical, physiological, and clinical standpoint. Cue reactivity and craving may have a significant role in the obesity epidemic and the “toxic” food environment that we live in. The authors examine research on cue reactivity and cue-induced craving, their effects on eating and weight, and their underlying neural mechanisms. Sun & Kober (2020) actually worked on developing the Regulation of Craving (ROC) task, which can be adopted to determine if certain cognitive aspects cause craving for food/drugs and the mechanisms involved in its regulation. An intervention based on this ROC task, that trains individuals to utilize cognitive strategies to regulate craving, has shown promising results on subsequent food choice and caloric consumption, which was also discussed in this review. [NPID: craving, reactivity, obesity, food cues, cue-induced craving, regulation]

Since dopamine in the central nervous system is associated with reward salience and food consumption, while the peripheral dopamine has a completely different role (sympathetic stress regulation, digestion and gastrointestinal motility), Mills et al. (2020) set out to find out whether there are associations between peripheral dopamine levels, depressive symptoms and problematic eating behaviors in major depressive disorder (MDD). The MDD symptoms, problematic eating behaviours and food addiction related symptoms of the 140 participants (80 MDD patients; 60 controls) were assessed using psychometric measures of mood and appetite, while their biometrics, psychopathology and plasma dopamine levels were also compared. Sub-categories were created based on Food Addiction Scale (YFAS) criteria. Twenty-three MDD subjects (29%) met the Yale criteria for food addiction and were associated with scoring significantly greater in psychopathology for both mood and eating, when compared with control and those depressed participants who did not meet YFAS criteria. Moreover, food addiction status and sex were found to be strongly related with the plasma dopamine levels of the participants - dopamine showed positive correlations with disordered dietary behaviors among females, whereas this interaction was negative among males. This study has potentially uncovered a link between peripheral dopamine concentrations with depressogenic excess eating and weight gain. Further longitudinal exploration into endocrine dysregulation and excess eating in MDD may prove helpful for sufferers and from an intervention standpoint. [NPID: craving, reward, dopamine, stress, stress regulation, digestion, gastrointestinal motility, depression, major depressive disorder, MDD, food addiction, addiction, mood, appetite, weight gain, endocrine dysregulation]

The objective of this 2020 review was to explore the potential in adopting a low-carbohydrate ketogenic dietary approach to treat binge eating and ultraprocessed food addiction. Dalai et al. (2020) explained how a diet low in refined carbohydrates, processed sugar and higher fat content may be helpful in alleviating symptoms, by identifying the carbohydrate-insulin model of obesity which have implied that the ultraprocessed, refined or high glycaemic index carbohydrates trigger abnormal sugar levels in the blood as well as insulin spikes, leading to metabolic and neurobiological alterations, and resulting in symptoms of overeating and hunger exacerbation. Reducing or avoiding these addictive-like ultraprocessed foods and highly refined carbohydrates could be considered as a treatment approach. This review goes on to propose how these low-carbohydrate ketogenic approaches can be applied, from a theoretical and practical standpoint, for ultraprocessed food addiction and binge eating symptoms. [NPID: craving, low card, ketogenic diet, keto, binge eating, processed food, food addiction, refined carbs, refined sugar, sugar, high fat, obesity, overeating]

The aim of this 2013 study was to identify the emotional and motivational processes that reinstate food intake after high-fat meals are removed from the diet, and also to determine the associated neuroadaptations tied to neurochemical and behavioural changes underlying dopaminergic function. This animal model study on adult male C57Bl6 mice involved a 6-week diet regimen of high-fat meals (58% kcal fat) or ingredient-matched, low-fat diet (LFD; 11% kcal fat), which was either maintained at the end of the regimen or replaced with normal chow (withdrawal). Basal and stress-induced corticosterone levels, anxiety, and effort-based operant responding for sucrose and high-fat food rewards were all measured. Moreover, protein levels for tyrosine hydroxylase (TH), corticosterone releasing factor type 1 receptor (CRF-R1), brain-derived neurotrophic factor (BDNF), phospho-CREB (pCREB) and ΔFosB (truncated splice variant of FosB) in the amygdala, nucleus accumbens (NAc) and ventral tegmental area (VTA) were assessed via western immunoblotting. The results showed weight gain and signs of sucrose anhedonia, anxiety-like behaviour and hypothalamic-pituitary-adrenocortical axis (HPA) hypersensitivity to stress in the mice given a high-fat diet (HFD). Enhanced motivation for sucrose and high-fat food rewards, and elevated anxiety and basal corticosterone levels were observed following withdrawal from the HFD but not the LFD. Western immunoblotting revealed reduced CRF-R1 and increased BDNF and pCREB protein levels in the amygdala, and reduced TH and increased ΔFosB protein in NAc and VTA, following chronic high-fat feeding. Furthermore, heightened palatable food reward in mice withdrawn from HFD coincided with increased BDNF protein levels in NAc and decreased TH and pCREB expression in the amygdala. Sharma et al. (2013) concluded that anhedonia, anxiety and sensitivity to stressors develops during the course of HFD and may have a key role in the development of obesity. Other findings included raised stress responses and increased vulnerability for palatable foods after removal of HFD, and that lasting changes in dopamine and plasticity-related signals in reward circuitry may promote negative emotional states, overeating and palatable food relapse. [NPID: sugar, processed food, neuroadaptations, dopamine, corticosterone, anxiety, sucrose, BDNF, HPA, high-fat, food reward, reward, BDNF, anhedonia, stress, obesity, emotional eating, overeating]

Lennerz & Lennerz (2018) examined the literature on food addiction and the role of high-glycemic-index carbohydrates in triggering addictive symptoms in particular. The behavioral responses to certain foods were found to be similar to that seen with substances of abuse. In addition, food intake regulation and addiction relied on similar neurobiological circuits. The third piece of evidence that supported the concept of food addiction was the convergence in neurochemical- and brain activation patterns between individuals suffering from obesity/addiction. There is a wealth of similarities including the rapid shift in blood glucose and insulin levels elicited by high-glycemic-index carbohydrates, which was akin to the pharmacokinetics of addictive substances; glucose and insulin signal to the mesolimbic system to modify dopamine concentration just like drugs of abuse. There is evidence that sugar induces addiction-like craving, and self-reported problem foods are rich in high-glycemic-index carbohydrates, which makes these carbohydrates plausible triggers for food addiction. Lennerz & Lennerz (2018) presented the argument that food addiction is possibly one of the factors contributing to the diverse condition and phenotype that is obesity. [NPID: sugar, processed food, food addiction, addiction, obesity, neurobiological circuits, blood glucose, insulin, carbs, dopamine, obesity]

This 2018 systematic review examined the construct of “food addiction” in humans and animals using quantitative, peer-reviewed studies written in English. The 52 identified studies (35 articles) were qualitatively evaluated on the extent to which their findings demonstrated characteristics such as brain reward dysfunction, preoccupation, risky use, impaired control, tolerance/withdrawal, social impairment, chronicity, and relapse, in relation to food. At least one study supported each criterion, including risky use which was seen in one study. On the other hand, brain reward dysfunction and impaired control were supported by the largest number of studies (n = 21 and n = 12, respectively). Overall, food addiction was seen as a unique construct consistent with criteria for other substance use disorder diagnoses. The data appears to reinforce the idea that processed foods with added sweeteners and fats in particular possess the greatest addictive potential. Gordon et al. (2018) seem to believe that the symptoms of addiction better fit criteria for substance use disorder than behavioral addiction, although both are implicated in the process. Further research into social/role impairment, preoccupation, and risky use associated with food addiction is encouraged, as well as potential interventions of prevention and treatment. [NPID: sugar, processed food, food addiction, brain reward, control, tolerance, withdrawal, social impairment, chronicity, relapse, reward, addiction]

This 2019 study examined overweight/obese women on their neural responses to viewing images of highly processed foods, minimally processed foods, and household objects. Many of the participants (20 out of 44) met criteria for moderate-to-severe Yale Food Addiction Scale 2.0 (YFAS 2.0) food addiction. Their cues to highly processed and minimally processed foods were explored. Schulte et al. (2019) reports that in individuals with YFAS 2.0 food addiction, there was an increased response in the superior frontal gyrus for highly processed food images, and more robust, decreased activations for minimally processed food cues, whereas participants in the control group showed the opposite responses in this region. While all participants’ responses were greater for the household items than the food cues in the insula, inferior frontal gyrus, inferior parietal lobe (i.e. regions connected with interoceptive awareness and visuospatial attention). Different responses were seen between overweight/obese women with YFAS 2.0 food addiction with women who are just either overweight or obese, to highly and minimally processed food cues in a region previously associated with cue-induced craving in persons with a substance-use disorder, the study concluded. Further studies are encouraged to apply the food addiction phenotypes within overweight and obesity. [NPID: sugar, processed food, neural response, food addiction, insula, frontal gyrus, parietal lobe, obesity]

The aim of this 2013 study was to identify the emotional and motivational processes that reinstate food intake after high-fat meals are removed from the diet, and also to determine the associated neuroadaptations tied to neurochemical and behavioural changes underlying dopaminergic function. This animal model study on adult male C57Bl6 mice involved a 6-week diet regimen of high-fat meals (58% kcal fat) or ingredient-matched, low-fat diet (LFD; 11% kcal fat), which was either maintained at the end of the regimen or replaced with normal chow (withdrawal). Basal and stress-induced corticosterone levels, anxiety, and effort-based operant responding for sucrose and high-fat food rewards were all measured. Moreover, protein levels for tyrosine hydroxylase (TH), corticosterone releasing factor type 1 receptor (CRF-R1), brain-derived neurotrophic factor (BDNF), phospho-CREB (pCREB) and ΔFosB (truncated splice variant of FosB) in the amygdala, nucleus accumbens (NAc) and ventral tegmental area (VTA) were assessed via western immunoblotting. The results showed weight gain and signs of sucrose anhedonia, anxiety-like behaviour and hypothalamic-pituitary-adrenocortical axis (HPA) hypersensitivity to stress in the mice given a high-fat diet (HFD). Enhanced motivation for sucrose and high-fat food rewards, and elevated anxiety and basal corticosterone levels were observed following withdrawal from the HFD but not the LFD. Western immunoblotting revealed reduced CRF-R1 and increased BDNF and pCREB protein levels in the amygdala, and reduced TH and increased ΔFosB protein in NAc and VTA, following chronic high-fat feeding. Furthermore, heightened palatable food reward in mice withdrawn from HFD coincided with increased BDNF protein levels in NAc and decreased TH and pCREB expression in the amygdala. Sharma et al. (2013) concluded that anhedonia, anxiety and sensitivity to stressors develops during the course of HFD and may have a key role in the development of obesity. Other findings included raised stress responses and increased vulnerability for palatable foods after removal of HFD, and that lasting changes in dopamine and plasticity-related signals in reward circuitry may promote negative emotional states, overeating and palatable food relapse. [NPID: sugar, processed food, neuroplasticity, high-fat, corticosterone, anxiety, rewards, BDNF, amygdala, nucleus accumbens, ventral tegmental area, reward, HPA axis, anhedonia, anxiety, dopamine, overeating]

Wiss & Avena (2020) examined animal- and human-study models of addiction-like eating in the context of binge eating, discussed the overlapping mechanisms such as reward dysfunction, craving, impulsivity, and attentional bias presented by these studies, and explored the directionality of the binge eating cascade across different theoretical models with empirical support for multiple pathways. This chapter offers a “Diet Drives the Binge” theory of food addiction, and a “Food Environment Drives Addiction” theory of binge eating. Wiss and Avena (2020) find effective individual-level interventions to be lacking, and so discuss the current controversies surrounding food addiction, as well as show the important findings that may have public health implications. [NPID: sugar, processed food, addiction, binge eating, craving, attentional bias]

With sedentary lifestyle and many easily accessible, inexpensive palatable foods often forming the explanation for this obesity epidemic, Wiss et al. (2018) began analyzing nutrients like sugar and how they can be contributing to obesity. Sugars are often used to make foods more appealing, which could lead to habituation, and to addiction in some cases. Similar to drug addiction, the dopaminergic system is involved in the reward process associated with eating highly palatable foods. The researchers also look back at the evolutionary aspects of feeding and how they have shaped the brain to function in "survival mode", and signal to consume as much as possible. Other discussions included how other neurotransmitters, like acetylcholine, interact in the satiation processes to counteract the dopamine system, and also the important question of whether there is sufficient empirical evidence of sugar addiction. [NPID: sugar, processed food, obesity, addiction, food addiction, habituation, dopaminergic system, reward, highly palatable food, survival mode, acetylcholine, satiety]

While research on food addiction has commonly looked at binge eating as a symptom of this condition, Bonder et al. (2018) assessed the correlation between food addiction and other patterns of overeating such as compulsive grazing (a behaviour with high relevance to weight-loss surgery outcomes) among a sample of 232 adults (20-50 years old). Regression analyses were performed on participants’ answers to diet and personality questionnaires. The results showed that addictive personality traits, reward-driven eating, and compulsive grazing each contributed unique variance to the Yale Food Addiction Score (YFAS), emphasizing that similar to traditional addiction disorders such as alcoholism, binge consumption is not the only pattern of compulsive intake. [NPID: sugar, processed food, binge eating, food addiction, grazing, overeating, personality, addiction, compulsion]