Eating disorders, obesity and addiction.
TL;DR: Evidence from laboratory feeding studies, epidemiology, genetic and familial research, psychopathological mechanisms, and treatment outcome research on cognitive behaviour therapy (CBT) is inconsistent with the clinical validity or utility of the addiction model of eating disorders.
Abstract: An addiction model of both eating disorders and obesity has received increasing attention in the popular and scientific literature. The addiction is viewed as a brain disease that must be directly targeted if treatment is to succeed. Evidence from laboratory feeding studies, epidemiology, genetic and familial research, psychopathological mechanisms, and treatment outcome research on cognitive behaviour therapy (CBT) is inconsistent with the clinical validity or utility of the addiction model of eating disorders. Neurobiological research has shown commonalities in brain reward processes between obesity and substance abuse disorders. Yet emphasis on apparent similarities overlooks important differences between obesity and drug addiction. Interest in obesity as a brain disease should not detract from a public health focus on the ‘toxic food environment’ that is arguably responsible for the obesity epidemic and related nutrition-based chronic disease. Copyright © 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
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TL;DR: The present findings suggest that food cue reactivity, cue‐induced craving and tonic craving systematically and prospectively predict food‐related outcomes.
Abstract: According to learning-based models of behavior, food cue reactivity and craving are conditioned responses that lead to increased eating and subsequent weight gain. However, evidence supporting this relationship has been mixed. We conducted a quantitative meta-analysis to assess the predictive effects of food cue reactivity and craving on eating and weight-related outcomes. Across 69 reported statistics from 45 published reports representing 3,292 participants, we found an overall medium effect of food cue reactivity and craving on outcomes (r = 0.33, p < 0.001; approximately 11% of variance), suggesting that cue exposure and the experience of craving significantly influence and contribute to eating behavior and weight gain. Follow-up tests revealed a medium effect size for the effect of both tonic and cue-induced craving on eating behavior (r = 0.33). We did not find significant differences in effect sizes based on body mass index, age, or dietary restraint. However, we did find that visual food cues (e.g. pictures and videos) were associated with a similar effect size to real food exposure and a stronger effect size than olfactory cues. Overall, the present findings suggest that food cue reactivity, cue-induced craving and tonic craving systematically and prospectively predict food-related outcomes. These results have theoretical, methodological, public health and clinical implications.
473 citations
TL;DR: It is argued that the evidence for food addiction in humans is actually rather limited and, in addition, there are fundamental theoretical difficulties that require consideration.
Abstract: In this paper, we consider the concept of food addiction from a clinical and neuroscientific perspective. Food addiction has an established and growing currency in the context of models of overeating and obesity, and its acceptance shapes debate and research. However, we argue that the evidence for its existence in humans is actually rather limited and, in addition, there are fundamental theoretical difficulties that require consideration.
We therefore review food addiction as a phenotypic description, one that is based on overlap between certain eating behaviours and substance dependence. To begin, we consider limitations in the general application of this concept to obesity. We share the widely held view that such a broad perspective is not sustainable and consider a more focused view: that it underlies particular eating patterns, notably binge eating. However, even with this more specific focus, there are still problems. Validation of food addiction at the neurobiological level is absolutely critical, but there are inconsistencies in the evidence from humans suggesting that caution should be exercised in accepting food addiction as a valid concept. We argue the current evidence is preliminary and suggest directions for future work that may provide more useful tests of the concept.
289 citations
Cites background from "Eating disorders, obesity and addic..."
...The implications of the addiction model for treatment of obesity and BED are discussed elegantly, and in detail, by Wilson, particularly with regards to psychological treatment (5)....
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...We and others have previously examined the neuroscientific (4), behavioural and clinical evidence (5,6) for the addiction model....
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TL;DR: This Review synthesized the existing information on select biological mechanisms associated with reward-related food intake, dealing primarily with consumption of highly palatable foods, to explain aberrant eating patterns, and provide insight into the current rates of overweight and obesity.
Abstract: With rising rates of obesity, research continues to explore the contributions of homeostatic and hedonic mechanisms related to eating behaviour. In this Review, we synthesize the existing information on select biological mechanisms associated with reward-related food intake, dealing primarily with consumption of highly palatable foods. In addition to their established functions in normal feeding, three primary peripheral hormones (leptin, ghrelin and insulin) play important parts in food reward. Studies in laboratory animals and humans also show relationships between hyperphagia or obesity and neural pathways involved in reward. These findings have prompted questions regarding the possibility of addictive-like aspects in food consumption. Further exploration of this topic may help to explain aberrant eating patterns, such as binge eating, and provide insight into the current rates of overweight and obesity.
215 citations
TL;DR: If and how the new SUD criteria for substance dependence may be translated to overeating will impact future research on food addiction, and if “diagnosing” food addiction should also be adapted by considering all of the new symptoms.
Abstract: The idea that specific kind of foods may have an addiction potential and that some forms of overeating may represent an addicted behavior has been discussed for decades. In recent years, the interest in food addiction is growing and research on this topic lead to more precise definitions and assessment methods. For example, the Yale Food Addiction Scale has been developed for the measurement of addiction-like eating behavior based on the diagnostic criteria for substance dependence of the fourth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). In 2013, diagnostic criteria for substance abuse and-dependence were merged, thereby increasing the number of symptoms for substance use disorders (SUDs) in the DSM-5. Moreover, gambling disorder is now included along SUDs as a behavioral addiction. Although a plethora of review articles exist that discuss the applicability of the DSM-IV substance dependence criteria to eating behavior, the transferability of the newly added criteria to eating is unknown. Thus, the current article discusses if and how these new criteria may be translated to overeating. Furthermore, it is examined if the new SUD criteria will impact future research on food addiction, for example, if "diagnosing" food addiction should also be adapted by considering all of the new symptoms. Given the critical response to the revisions in DSM-5, we also discuss if the recent approach of Research Domain Criteria can be helpful in evaluating the concept of food addiction.
204 citations
TL;DR: Stop signals appear a promising tool for chronic dieters to control behavior to palatable foods, and the merits and potential applications of this tool for facilitating dieting behavior are discussed.
198 citations
Cites background from "Eating disorders, obesity and addic..."
...Considering that palatable foods are abundant in the environment (Hill & Peters, 1998; Stroebe, 2008; Wilson, 2010), an intervention that directly modifies impulses toward palatable foods may thus provide a promising route to improve self-control among chronic dieters in daily life (e....
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...Consensus is growing that such an environment renders it very hard to regulate consumption of these foods, even when people are dieting and motivated to restrain themselves (e.g., Hill & Peters, 1998; Stroebe, 2008; Wilson, 2010)....
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...Considering that palatable foods are abundant in the environment (Hill & Peters, 1998; Stroebe, 2008; Wilson, 2010), an intervention that directly modifies impulses toward palatable foods may thus provide a promising route to improve self-control among chronic dieters in daily life (e.g., Hofmann…...
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References
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TL;DR: An issue concerning the criteria for tic disorders is highlighted, and how this might affect classification of dyskinesias in psychotic spectrum disorders.
Abstract: Given the recent attention to movement abnormalities in psychosis spectrum disorders (e.g., prodromal/high-risk syndromes, schizophrenia) (Mittal et al., 2008; Pappa and Dazzan, 2009), and an ongoing discussion pertaining to revisions of the Diagnostic and Statistical Manuel of Mental Disorders (DSM) for the upcoming 5th edition, we would like to take this opportunity to highlight an issue concerning the criteria for tic disorders, and how this might affect classification of dyskinesias in psychotic spectrum disorders.
Rapid, non-rhythmic, abnormal movements can appear in psychosis spectrum disorders, as well as in a host of commonly co-occurring conditions, including Tourette’s Syndrome and Transient Tic Disorder (Kerbeshian et al., 2009). Confusion can arise when it becomes necessary to determine whether an observed movement (e.g., a sudden head jerk) represents a spontaneous dyskinesia (i.e., spontaneous transient chorea, athetosis, dystonia, ballismus involving muscle groups of the arms, legs, trunk, face, and/or neck) or a tic (i.e., stereotypic or patterned movements defined by the relationship to voluntary movement, acute and chronic time course, and sensory urges). Indeed, dyskinetic movements such as dystonia (i.e., sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions) closely resemble tics in a patterned appearance, and may only be visually discernable by attending to timing differences (Gilbert, 2006).
When turning to the current DSM-IV TR for clarification, the description reads: “Tic Disorders must be distinguished from other types of abnormal movements that may accompany general medical conditions (e.g., Huntington’s disease, stroke, Lesch-Nyhan syndrome, Wilson’s disease, Sydenham’s chorea, multiple sclerosis, postviral encephalitis, head injury) and from abnormal movements that are due to the direct effects of a substance (e.g., a neuroleptic medication)”. However, as it is written, it is unclear if psychosis falls under one such exclusionary medical disorder. The “direct effects of a substance” criteria, referencing neuroleptic medications, further contributes to the uncertainty around this issue. As a result, ruling-out or differentiating tics in psychosis spectrum disorders is at best, a murky endeavor.
Historically, the advent of antipsychotic medication in the 1950s has contributed to the confusion about movement signs in psychiatric populations. Because neuroleptic medications produce characteristic movement disorder in some patients (i.e. extrapyramidal side effects), drug-induced movement disturbances have been the focus of research attention in psychotic disorders. However, accumulating data have documented that spontaneous dyskinesias, including choreoathetodic movements, can occur in medication naive adults with schizophrenia spectrum disorders (Pappa and Dazzan, 2009), as well as healthy first-degree relatives of chronically ill schizophrenia patients (McCreadie et al., 2003). Taken together, this suggests that movement abnormalities may reflect pathogenic processes underlying some psychotic disorders (Mittal et al., 2008; Pappa and Dazzan, 2009).
More specifically, because spontaneous hyperkinetic movements are believed to reflect abnormal striatal dopamine activity (DeLong and Wichmann, 2007), and dysfunction in this same circuit is also proposed to contribute to psychosis, it is possible that spontaneous dyskinesias serve as an outward manifestation of circuit dysfunction underlying some schizophrenia-spectrum symptoms (Walker, 1994). Further, because these movements precede the clinical onset of psychotic symptoms, sometimes occurring in early childhood (Walker, 1994), and may steadily increase during adolescence among populations at high-risk for schizophrenia (Mittal et al., 2008), observable dyskinesias could reflect a susceptibility that later interacts with environmental and neurodevelopmental factors, in the genesis of psychosis.
In adolescents who meet criteria for a prodromal syndrome (i.e., the period preceding formal onset of psychotic disorders characterized by subtle attenuated positive symptoms coupled with a decline in functioning), there is sometimes a history of childhood conditions which are also characterized by suppressible tics or tic like movements (Niendam et al., 2009). On the other hand, differentiating between tics and dyskinesias has also complicated research on childhood disorders such as Tourette syndrome (Kompoliti and Goetz, 1998; Gilbert, 2006).
We propose consideration of more explicit and operationalized criteria for differentiating tics and dyskinesias, based on empirically derived understanding of neural mechanisms. Further, revisions of the DSM should allow for the possibility that movement abnormalities might reflect neuropathologic processes underlying the etiology of psychosis for a subgroup of patients. Psychotic disorders might also be included among the medical disorders that are considered a rule-out for tics.
Related to this, the reliability of movement assessment needs to be improved, and this may require more training for mental health professionals in movement symptoms. Although standardized assessment of movement and neurological abnormalities is common in research settings, it has been proposed that an examination of neuromotor signs should figure in the assessment of any patient, and be as much a part of the patient assessment as the mental state examination (Picchioni and Dazzan, 2009).
To this end it is important for researchers and clinicians to be aware of differentiating characteristics for these two classes of abnormal movement. For example, tics tend to be more complex than myoclonic twitches, and less flowing than choreoathetodic movements (Kompoliti and Goetz, 1998). Patients with tics often describe a sensory premonition or urge to perform a tic, and the ability to postpone tics at the cost of rising inner tension (Gilbert, 2006). For example, one study showed that patients with tic disorders could accurately distinguish tics from other movement abnormalities based on the subjective experience of some voluntary control of tics (Lang, 1991). Another differentiating factor derives from the relationship of the movement in question to other voluntary movements. Tics in one body area rarely occur during purposeful and voluntary movements in that same body area whereas dyskinesia are often exacerbated by voluntary movement (Gilbert, 2006). Finally, it is noteworthy that tics wax and wane in frequency and intensity and migrate in location over time, often becoming more complex and peaking between the ages of 9 and 14 years (Gilbert, 2006). In the case of dyskinesias among youth at-risk for psychosis, there is evidence that the movements tend to increase in severity and frequency as the individual approaches the mean age of conversion to schizophrenia spectrum disorders (Mittal et al., 2008).
As revisions to the DSM are currently underway in preparation for the new edition (DSM V), we encourage greater attention to the important, though often subtle, distinctions among subtypes of movement abnormalities and their association with psychiatric syndromes.
67,017 citations
TL;DR: The weight of epidemiologic and experimental evidence indicates that a greater consumption of SSBs is associated with weight gain and obesity, and sufficient evidence exists for public health strategies to discourage consumption of sugary drinks as part of a healthy lifestyle.
2,559 citations
TL;DR: During follow-up after DPP, incidences in the former placebo and metformin groups fell to equal those in theFormer lifestyle group, but the cumulative incidence of diabetes remained lowest in the lifestyle group.
2,539 citations
TL;DR: Dopamine modulates motivation and reward circuits and hence dopamine deficiency in obese individuals may perpetuate pathological eating as a means to compensate for decreased activation of these circuits.
1,743 citations
"Eating disorders, obesity and addic..." refers background in this paper
...For example, Wang et al. (2001) suggested that ‘strategies aimed at improving dopamine function may be beneficial in the treatment of obesity’ (p. 357)....
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Book•
21 Apr 2008TL;DR: Fairburn, Cooper, Shafran, Bohn, Hawker, Fairburn, Inpatient, Day Patient and Two Forms of Outpatient CBT-E: An Overview.
Abstract: Introduction. Fairburn, This Book and How to Use It. Fairburn, Eating Disorders: The Transdiagnostic View and the Cognitive Behavioral Theory. Fairburn, Cooper, Shafran, Enhanced Cognitive Behavior Therapy for Eating Disorders (CBT-E): An Overview. Fairburn, Cooper, Waller, The Patients: Their Assessment, Preparation for Treatment and Medical Management. Fairburn, Cooper, Shafran, Bohn, Hawker, Murphy, Straebler, Enhanced Cognitive Behavior Therapy for Eating Disorders: The Core Protocol. Starting Well. Achieving Early Change. Taking Stock and Designing the Rest of Treatment. Shape Concern. Shape Checking. Feeling Fat and Mindsets. Dietary Restraint, Dietary Rules and Controlling Eating. Events, Moods and Eating. Underweight and Under-eating. Ending Well. Adaptations of CBT-E. Fairburn, Cooper, Shafran, Bohn, Hawker, Clinical Perfectionism, Core Low Self-esteem and Interpersonal Problems. Cooper, Stewart, CBT-E and the Younger Patient. Grave, Bohn, Hawker, Fairburn, Inpatient, Day Patient and Two Forms of Outpatient CBT-E. Fairburn, Cooper, Waller, 'Complex Cases' and Comorbidity. Postscript. Fairburn, Looking Forward. Appendices. Fairburn, Cooper, O'Connor, Appendix A: Eating Disorder Examination (16.0D). Fairburn, Beglin, Appendix B: Eating Disorder Examination Questionnaire (EDE-Q6.0). Bohn, Fairburn, Appendix C: Clinical Impairment Assessment Questionnaire (CIA 3.0).
1,603 citations
"Eating disorders, obesity and addic..." refers background in this paper
...…Ltd and Eating Disorders Association. commitment to developing a pattern of regular eating designed to replace dysfunctional dietary restraint, the component of the treatment that likely mediates reduction of binge eating (Fairburn, 2008; Shah, Passi, Bryson, & Agras, 2005; Wilson et al., 2002)....
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...In turn, evidence-based CBT predicts that the abstinence model of addiction is ineffective at best and potentially hazardous at worst because it encourages dietary restriction that is known to cause or maintain BN (Fairburn, 2008)....
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...Disorders Rev. 18 (2010) 341–351 2010 John Wiley & Sons, Ltd and tenance of BN this overvaluation of body weight or shape drives the dysfunctional dieting that leads to binge eating (Fairburn, 2008)....
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...A defining feature of manual-based CBT (Fairburn, 2008) is the early...
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...A defining feature of manual-based CBT (Fairburn, 2008) is the early 341–351 2010 John Wiley & Sons, Ltd and Eating Disorders Association. commitment to developing a pattern of regular eating designed to replace dysfunctional dietary restraint, the component of the treatment that likely mediates…...
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