Decision Making Deficits

Decision Making Difficulties in Gambling and Eating Disorders




Following on from yesterday’s blog Can decision-making research provide a better understanding of chemical and behavioral addictions  today the second part of this blog which addresses decision making deficits in behavioral addictions of gambling and eating disorders.

The main findings of this review were that several cognitive distortions are found in pathological gambling that seems to harness the brain reward system that has evolved to face situations related to skill, not random chance.  Abnormalities in risk assessment and impulsivity are found in variety of eating disorders, in particularly related to eating behavior. Corresponding findings in eating disorder patients include abnormalities in the limbic system, i.e. orbitofrontal cortex (OFC), striatum and insula. 

Tomorrow we conclude our blog trilogy by looking at internet and sexual addictions.


Pathological Gambling

Pathological gambling is defined as a compelling urge to gamble and inappropriate, persistent, and maladaptive gambling behaviors that have repercussions on family, personal and professional life [72]. Harmful effects of excessive gambling are usually debt, illegal activity and interpersonal conflicts. Gambling can be motivated by financial reasons, as well as cognitive and emotional factors. It is fueled by positive reinforcement as evidenced by physiological arousal including increase in heart rate and cortisol levels [73, 74].

Pathological gambling shares several features with drug addiction. Several studies targeting decision making in pathological gamblers demonstrated profound deficits in decision making. In a set of studies comparing pathological gambling with patients with alcohol dependence, patients with Tourette syndrome and healthy controls, the first two groups showed impaired performance in the Iowa Gambling Task, the Card Playing Task and Go/No-Go discrimination task, as well as in inhibition, time estimation, cognitive flexibility and planning tasks compared to healthy controls [75, 76].

Furthermore, differential performance in the Iowa Gambling Task in pathological gamblers was associated with lower psychophysiological responses to disadvantageous choices and wins, suggestive impaired risk assessment and reward sensitivity [77]. Furthermore, disinhibition and impaired decision-making were predictive of relapse in pathological gamblers [78].

As very aptly reviewed by Clark, gambling is associated with monoamine dysfunction, impulsive and risky decision making [79]. Additionally, significant cognitive distortions occur in gamblers such as ‘illusion of control’, ‘near miss effect’, ‘loss chasing’ and exaggerated temporal discounting. ‘Illusion of personal control’ refers to the gambler’s belief that his/her level of involvement in arranging the gamble will change the outcome, despite being a game of chance (lucky ticket number or throwing dice in a particular fashion).

A false sense of control over future outcomes is associated with altered VMPFC – dorsal ACC circuitry [80]. The ‘near miss effect’ occurs when an unsuccessful gamble that was close to a win is interpreted by a gambler as evidence of mastering the game. A telling contribution from neuroimaging shows that while playing a slot machine task, winning was associated with increased activation in the ventral striatum, medial PFC, anterior insula, thalamus and midbrain.

However, near misses were associated with activation in the ventral striatum and anterior insula [81]. In both ‘illusion of control’ and ‘near miss effect’ gamblers confuse a game of chance (determined by random probabilities) with a game of skill [82, 83]. Continuing gambling to recover losses is known as loss chasing and is found in recreational and pathological gamblers. This behavior is strongly associated with impaired control over gambling impulse and is thought to be critical in the development of pathological gambling [84].

In a gambling task, healthy subjects were given the choice of ‘double or nothing’ versus accepting their losses and quitting. The former decision was associated with increased neural activity in the VMPFC and subgenual ACC, whereas quitting was associated with increased activation in the insula, dorsal ACC and posterior cingulate [85].

Additional evidence that gambling is associated with dysfunction in the frontostriatal valuation circuit was seen in reduced activation of the VMPFC and striatum in response to wins in games of chance in gamblers compared to healthy controls [86]. Additionally, viewing gambling scenarios was associated with distinct activation in frontal and limbic regions in pathological gambling men [87]. Overall, neuroimaging data suggest that gambling games harness a brain reward system that has evolved to face situations related to skill-oriented behaviors, not random chance situations. This context leads to cognitive errors about response feedback and illusion of control of future random outcomes.

Eating Disorders

Anorexia nervosa is characterized by severe emaciation, amenorrhea and hyperactivity in > 80% of patients [88]. It has the highest psychiatric mortality in young women and current available treatments are mostly unsatisfactory. Several animal models demonstrated alteration of dopamine, acetylcholine and opioid systems in reward-related brain areas related to binge eating, bulimia nervosa and anorexia nervosa [89].

Despite an unknown pathophysiology, there is mounting evidence of alterations in dopamine and reward systems. Cerebrospinal fluid dopamine metabolites concentrations are decreased in anorexic patients, even after symptom recovery [90]. Anorexia has also been associated with D2 receptor gene polymorphisms [91]. Patients recovered from anorexia nervosa had increased binding of D2/D3 receptors in the anteroventral striatum [92].

In a simple monetary reward task, women recovered from restricting-type anorexia nervosa showed altered patterns of response in the ventral and dorsal striatum to positive and negative feedback [93].

There is evidence that anorexia nervosa involves not only quantitative but also qualitative alterations in the reward system. This is illustrated by differential ventral striatum activation when anorexic women were presented with underweight female images rather than normal weight or overweight images [94]. Although less severe, bulimia nervosa and binge-eating disorder (BED) are more prevalent comparatively to anorexia nervosa.

The lifetime prevalence estimates of anorexia nervosa, bulimia nervosa, and binge-eating disorder are 0.3%, 0.9% and 1.6%, respectively [95]. BED patients scored significantly higher on apathy, disinhibition and executive dysfunction compared with non-Eating Disorder patients [96]. Women with BED display decision-making deficit on the Iowa Gambling Task [97]; risky behavior and impaired capacity to advantageously utilize feedback processing on Game of Dice Task [98].

Adults with BED were highly impulsive, especially in context of negative affect [99]. Obese binge eating women displayed greater motor impulsivity than obese controls [100]. Adults with BED comparatively to simply obese individuals experience more often a sense of loss of control which may represent a silent feature of binging episodes [101].

As in drug addiction, deficits in temporal discounting are found in obese individuals [102-105]. It has been proposed that a disequilibrium between food reinforcing value and temporal discounting might be central to understand excessive calorie intake and obesity [104]. Recently neuroimaging studies support the idea that food may elicit responses in reward-related/decision-making brain regions that mimic those of addictive substances and promise to uncover the neural substrate of food addiction (for review see [106]).

Gearhardt and colleagues [107] demonstrated that food addiction scores correlated with greater activation in the ACC, VMPFC, and amygdala in response to anticipated receipt of food. Participants with higher versus lower food addiction scores showed greater activation in the DLPFC and the caudate in response to anticipated receipt of food but less activation in the lateral OFC in response to receipt of food.

Using fMRI, Stice and colleagues [108], showed that highrisk obesity youth had greater activation in the caudate, parietal operculum and frontal operculum in response to food intake, and in the caudate, putamen, insula, thalamus and VMPFC in response to monetary reward. Individuals with BED demonstrated a different pattern of brain activation comparatively to individuals with bulimia nervosa while viewing food pictures: the BED patients reported enhanced reward sensitivity and showed stronger VMPFC responses, when the bulimic patients displayed greater arousal, ACC activation, and insula activation [109].

Patients with BED and BN have greater volumes of the VMPFC comparatively to healthy controls, whereas BN patients display increased ventral striatum volume [110]. Individuals with Prader-Willi syndrome (an extreme model of genetic obesity) show hyperactivation in subcortical reward circuitry and hypoactivation in cortical inhibitory regions after eating [111].


Above data demonstrate that similar pattern of activation are implicated in addictive-like eating behavior and substance dependence.



  1. Engel, A., & Cáceda, R. (2015). Can Decision Making Research Provide a Better Understanding of Chemical and Behavioral Addictions?. Current drug abuse reviews, 8(2), 75-85.


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