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Psychology & addition eating behaviour

New evidence linking obesity and food addiction.
Cope E, Gould E (2017). Biological Psychiatry, 81:734-736.

‘Evidence is accumulating that brain reward circuits also regulate food consumption. Highly palatable foods, such as processed foods that are rich in sugar and fat, are associated with increased eating. The phrase “food addiction” was first used in a scientific publication in the 1950s. Since then, human… neuroimaging studies have demonstrated that obese individuals have similar over-activation in brain reward circuits as those observed in people with drug addiction. The findings of Brown et al (2017) provide compelling evidence that diet-induced obesity leads to so-called food addiction.’

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Addiction-like synaptic impairments in diet-induced obesity.
Brown RM et al (2017). Biological Psychiatry, 81(9):797-806.

‘We found that propensity to develop DIO [diet-induced obesity] is linked to deficits in the ability to induce long-term depression in the nucleus accumbens, as well as increased potentiation at these synapses… Consistent with these impairments, we observed addictive-like behavior in DIO-prone rats, including 1) heightened motivation for palatable food; 2) excessive intake; and 3) increased food seeking when food was unavailable. Our results show overlap between the propensity for DIO and the synaptic changes associated with facets of addictive behavior, supporting partial coincident neurological underpinnings for compulsive overeating and drug addiction.’

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Understanding and addressing food addiction: a science-based approach to policy practice and research.
The National Center on Addiction and Substance Abuse (2016).

‘The construct of food addiction has been defined as a clinically significant physical and psychological dependence on high fat, high sugar, and highly palatable foods. It is not a recognized disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the primary resource for diagnostic criteria standards for a range of psychiatric and behavioral disorders. However, many studies that have examined the construct have utilized the Yale Food Addiction Scale (YFAS), a validated and reliable instrument based primarily on the diagnostic criteria for substance dependence in the DSM-IV-TR, which measures behavioral indicators of addictive eating. Although we do not generally think of food as an addictive drug, one way that food addiction has been conceptualized places the emphasis on the addictive qualities of certain ingredients found in most highly palatable and calorie-dense foods – sugar, fat and salt. These food ingredients, like psychoactive substances: stimulate the reward and motivation-oriented regions of the brain during consumption or in the presence of related environmental cues, promote craving, reinforce continued consumption/use and tolerance, and elicit withdrawal symptoms when consumption/use is cut back or eliminated.’

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A commentary on the ‘eating addiction’ versus ‘food addiction’ perspectives on addictive-like food consumption.
Schulte EM, Potenza MN, Gearhardt AN (2016). Appetite,1-7. (Article in press.)

‘Overall, the current state of the literature suggests that the substance-based food-addiction perspective, rather than eating as a behavioral addiction, most appropriately reflects the interaction between an individual’s propensity for addiction, behavioral patterns of engagement that elevate addictive potential, and the possible role of high-fat, high-sugar foods to trigger and perpetuate the addictive-like phenotype.’

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Food addiction as a new piece of the obesity framework.
Lerma-Cabrera JM, Carvajal F, Lopez-Legarrea P (2016). Nutrition Journal, 15:5.

‘Basic research using animal and humans models has shown that certain foods, mainly highly palatable foods, have addictive properties. In addition, exposure to food and drugs of abuse have shown similar responses in the dopaminergic and opioid systems… The prevalence of food addiction was positively related to measures of adiposity (e.g. body fat, BMI). These data suggest that food addiction is likely an important factor in the development of human obesity and that it is associated with the severity of obesity from normal to obese individuals. In fact, obese people showing a worse weight loss response to treatment and greater weight gain after undergoing bariatric surgery obtain higher YFAS [Yale Food Addiction Scale] scores. Thus, weight-loss treatments should consider the role of food addiction as a psychological factor underlying difficult weight management situations.’

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Current considerations regarding food addiction.
Schulte EM, Joyner MA, Potenza MN, Grilo CM, Gearhardt AN (2015). Current Psychiatry Reports, 17:19.

‘Critiques of “food addiction” that emphasize descriptive differences between addictive-like eating and the consumption of intoxicating or illegal drugs may be repeating mistakes that delayed the identification of tobacco as an addictive substance… Although food is necessary for survival, the highly processed foods associated with addictive-like eating may provide little health benefit.’

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A substance called food: long-term psychodynamic group treatment for compulsive overeating.
Schwartz C et al (2015). International Journal of Group Psychotherapy, 65:3,386-409.

This paper describes a psychodynamically-oriented approach to treating compulsive overeating as an addiction. ‘Common to all addictions is a compulsion to consume a substance or engage in a behavior, a preoccupation with using behavior and rituals, and a lifestyle marked by an inability to manage the behavior and its harmful consequences. The approach represents a shift away from primarily medical models of intervention to integrated models focusing on the psychological underpinnings of obesity. Central to the recovery process is an understanding that the compulsive overeater cannot recover alone. Groups are pivotal in healing shame associated with addiction and underlying trauma. Members are more likely to reveal disease behaviors when they hear others’ accounts. Furthermore, members often challenge one another to face difficult truths. Long-term psychodynamic group psychotherapy is recommended as a primary treatment.’

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Mindfulness-based interventions for obesity-related eating behaviours: a literature review.
O’Reilly GA, Cook L, Spruiit-Metz D, Black DS (2014). Obesity Reviews, 15(6):453-61.

Mindfulness-based interventions (MBIs) targeting eating behaviours have gained popularity in recent years. A literature review was conducted to determine the effectiveness of MBIs for treating obesity-related eating behaviours. Interventions used a variety of approaches to implement mindfulness training, including combined mindfulness and cognitive behavioural therapies, mindfulness-based stress reduction, acceptance-based therapies, mindful eating programmes, and combinations of mindfulness exercises. Eighteen (86%) of the reviewed studies reported improvements in the targeted eating behaviours. The results of this first review on the topic support the efficacy of MBIs for changing obesity-related eating behaviours, specifically binge eating, emotional eating and external eating.

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Is food addiction a valid phenomenon through the lens of the DSM-5?
Pai N, Vella SL, Richardson K (2014). Australian and New Zealand Journal of Psychiatry, 48(3):216-218.

DSM-5 [Diagnostic and Statistical Manual of Mental Disorders] introduced the first non-substance related addictive disorder, namely Gambling Disorder, as well as including Internet Gaming Disorder as a condition warranting further study. The inclusion of these non-substance related, behavioural or process addictions is noteworthy in the context of food addiction. Readers of the DSM-5…may be left wondering why food addiction was excluded based upon the rationale for the inclusion of Gambling Disorder… specifically that gambling activates the same reward and motivation pathways as drugs of abuse. There is copious research indicating the neurological overlap that exists between drugs of abuse and the ingestion of hyperpalatable food stuffs, both in the animal model and human research. There is compelling evidence for the notion of food addiction as a “true” addiction [and] with the change away from considering withdrawal and tolerance as essential features of dependence, food – akin to substances of abuse – now meets the ideology of addiction.’

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Obesity and addiction: neurobiological overlaps.
Volkow ND, Wang GJ, Tomasi D, Baler RD (2013). Obesity Reviews, 14:2-18.

‘Drug addiction and obesity appear to share several properties. Both can be defined as disorders in which the saliency of a specific type of reward (food or drug) becomes exaggerated relative to, and at the expense of other rewards. Both drugs and food have powerful reinforcing effects, which are in part mediated by abrupt dopamine increases in the brain reward centres. The abrupt dopamine increases, in vulnerable individuals, can override the brain’s homeostatic control mechanisms. Brain imaging studies are beginning to uncover common features between these two conditions and delineate some of the overlapping brain circuits whose dysfunctions may underlie the observed deficits. The combined results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, self-control, stress reactivity and interoceptive awareness.’

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Food Addiction: Its Prevalence and Significant Association with Obesity in the General Population.
Pedram P et al (2013). PLoS ONE, 8(9): e74832.

This study assessed (1) the prevalence of food addiction in a sample of 652 adults recruited from the general population in Newfoundland, (2) if clinical-symptom counts of food addiction were significantly correlated with body composition measurements, (3) if food addicts were significantly more obese than controls, (4) if macronutrient intakes are associated with food addiction. ‘The prevalence of food addiction was 5.4% (6.7% in females, 3.0% in males) and increased with obesity status. Clinical-symptom counts of food addiction were positively correlated with all body composition measurements across the entire sample (p<0.001). Obesity measurements were significantly higher in food addicts than controls; food addicts were 11.7kg heavier, 4.6 BMI units higher, had 8.2% more body fat and 8.5% more trunk fat. Furthermore, food addicts consumed more calories from fat and protein compared with controls. Results demonstrated that food addiction contributes to severity of obesity and body composition measurements from normal weight to obese individuals in the general population.’

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American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V).
May 2013, pp.350-352, Arlington VA.

The DSM-V now acknowledges food addiction as part of binge-eating disorder. It also now recognises behavioural addiction – this change, according to the American Psychiatric Association, reflecting ‘the increasing and consistent evidence that some behaviours, such as gambling, activate the brain reward system with effects similar to those of drugs of abuse…’ Currently, the only disorder featured in this new category is pathological gambling, but it is suggested that other behavioural disorders will be added in due course, pending further research.

Behavioural addiction consists of a compulsion to repeatedly engage in an action until it causes negative consequences to the person’s physical, mental, social, and/or financial wellbeing, and behaviour persisting in spite of these consequences can be taken as a sign of addiction.

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Evidence that ‘food addiction’ is a valid phenotype of obesity.
Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, Kennedy JL (2011). Appetite, 57:711-717.

‘Using a sample of obese adults and a case-control methodology, we focused assessment on three domains relevant to the characterization of conventional substance-dependence disorders: clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance. Results were strongly supportive of the food addiction (FA) construct. Those who met the diagnostic criteria for FA had a significantly greater co-morbidity with Binge Eating Disorder, depression and attention-deficit/ hyperactivity disorder compared to their age- and weight-equivalent counterparts. Those with FA were also more impulsive and displayed greater emotional reactivity than obese controls. They also displayed greater food cravings and the tendency to “self-soothe” with food.’

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Adding cognitive behavioural treatment to either low-carbohydrate or low-fat diets: differential short-term results.
Rodriguez-Hernandez et al (2009). British Journal of Nutrition, 102(12):1847-53.

‘The present results showed that adding CBT to either the low-fat or low-carbohydrate diet produced significantly greater short-term weight loss in obese women compared with diet alone. These finding support the efficacy of CBT in breaking previous dietary patterns and in developing healthier attitudes that reinforce a healthier lifestyle.’

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Does cognitive behavioral therapy change the brain? A systematic review of neuroimaging in anxiety disorders.
Porto PR et al (2009). Journal of Neuropsychiatry and Clinical Neurosciences, spring 21(2):114-125.

‘Cognitive-behavioral therapy modified the neural circuits involved in the regulation of negative emotions and fear extinction in judged treatment responders… Despite methodological limitations, neuroimaging studies revealed that CBT was able to change dysfunctions of the nervous system.’

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Psychological interventions for overweight or obesity.
Shaw K, O’Rourke P, Del Mar C, Kenardy J (2005). Cochrane Database Systematic Review, April, 18(2):CD003818.

‘People who are overweight or obese benefit from psychological interventions, particularly behavioural and cognitive-behavioural strategies, to enhance weight reduction. They are predominantly useful when combined with dietary and exercise strategies. The bulk of the evidence supports the use of behavioural and cognitive-behavioural strategies.’

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‘Change the mind and you change the brain’: effects of cognitive-behavioral therapy on the neural correlates of spider phobia.
Paquette V et al (2003). NeuroImage, 18(2):401-409.

‘These findings suggest that a psychotherapeutic approach, such as CBT, has the potential to modify the dysfunctional neural circuitry associated with anxiety disorders. They further indicate that the changes made at the mind level, within a psychotherapeutic context, are able to functionally “rewire” the brain.’

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Social and psychological effects of weight loss.
Foster GD, Wadden TA. 2002. In: Fairburn CG, Brownell KD (editors). Eating disorders and obesity: A comprehensive handbook. New York: Guilford. pp 500-504.
Psychological consequences of obesity and weight loss.
Wadden TA, Womble LG, Stunkard AJ, Anderson DA. 2002. In: Wadden TA, Stunkard AJ (editors). Handbook of obesity treatment. New York: Guilford. pp 144-169.

Medically orientated weight-loss programmes involving behavioural interventions, CBT and group support are typically associated with improvements in mood.

Treatment of obesity by moderate and severe calorific restriction: results of clinical research trials.
Wadden TA (1993). Annals of Internal Medicine, 119:688-693.

Combined with the use of a VLCD, CBT has been shown to produce significant weight loss.

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