Once an individual has lost control over drug or non-drug (e.g., gambling) use, rising negative consequences do not necessarily lead to any adjustment in their maladaptive choices and actions (1). Reasons for the transition from controlled use to addiction are numerous and include individual vulnerabilities in attention, reward, emotion, decision-making, self-regulation, pain, and stress [for a review, see Ref. (2)]. Additional reasons include the neurotoxic and neuroadaptive effects of drugs and withdrawal on the central nervous system [e.g., Ref. (3)].

Historically, the research on addiction has attracted studies that focus on only one neural system at a time. For instance, during the 1980s, the research focused on the role of the striatum and mesolimbic dopamine system, as well as the amygdala, in drug reward [e.g., see Ref. (4) for a review]. During the 1990s, the prefrontal cortex attracted most of the research on addiction, and its role in various mechanisms of decision-making and impulse control. More recently, there has been a rising interest in the role of the insular cortex in addiction [e.g., Ref. (4, 5)]. In an attempt to unify the concept of addiction that integrates both experimental and clinical perspectives, we present here the triadic neurocognitive model of addiction, which takes into account all the neural systems that have been implicated historically in the neurobiology of addiction, including “willpower,” the ability to self-control, and the capacity to choose according to long-term, rather than short-term, outcomes [see also (6)]. We argue that in addiction to drugs (e.g., cocaine) and non-drugs (e.g., gambling), the weakened “willpower” associated with most addictive behaviors is the product of an abnormal functioning in the interaction between three key neural and cognitive systems: (a) an amygdala-striatum dependent neural system, which promotes automatic cognitions and habitual actions; we have referred to this neural system as the “impulsive” system, and it becomes hyperactive in states of addiction; and (b) a prefrontal cortex dependent neural system, which is important for decision-making, forecasting the future consequences of a behavior, and inhibitory control and self-awareness; we have referred to this neural system as the “reflective” system, and it may become hypoactive in states of addiction; and (c) the insular cortex, which plays a key role in modulating the dynamics between the “impulsive” and “reflective” systems. More specifically, the (anterior) insula is important for translating bottom-up, interoceptive signals into subjective experiences (e.g., craving), which in turn potentiates the activity of the impulsive system, and/or weakens or hijacks the goal-driven cognitive resources needed for the normal operation of the reflective system. At the cognitive level, the characteristics of the impulsive and reflective neural systems mirror those from the dual-processing accounts; one is fast, automatic, and unconscious and the other is slow, deliberative, and conscious (7–9). Automatic or poorly controllable processes include what has been addressed in the literature as biased attention processing toward addiction-related cues (e.g., a bottle of beer, a slot machine, a syringe), implicit memory associations (e.g., alcohol-pleasant associations), and approach/avoidance responses to addiction-related cues (10). However, habits and impulsive behaviors can be brought under control by controlled processes related to goal-directed actions, at least to some extent. These automatic processes can be modified through the engagement of self-regulation processes. In case of addictive behaviors, a number of executive functions either cool (e.g., working memory) or hot (e.g., redirecting attention from addiction- to non-addiction-related cues, inhibiting addiction-related pre-potent responses) are viewed as compromised and unable to exert an effective control of behaviors elicited by automatic processes [e.g., Ref. (11)].

While this dual-process model may explain many aspects of complex decision-making, self-control, and “willpower” to resist the temptation of addictive stimuli, we argue that the model is not sufficient to explain all aspects of addictive behaviors, especially those related to deprivation from the reward stimulus or withdrawal, stress, anxiety, and other homeostatic disturbances. For example, while an individual with alcoholism may manage to exert self-control over his or impulse to have a drink for a period of time, the mere sight of a bottle, or experiencing a stressful situation, can throw this control completely out of balance, and the old automatic and habit systems take over. We argue that this drastic weakening of control systems brought about by changes in the internal body state of the organism play a key role in modulating the strengths of impulsive and reflective systems, and incorporating this influential role of internal states is not part of the dual-process models. For this reason, we propose a key role for a third neural system, namely the insula [e.g., see its role in nicotine dependence, (12)]. The insula is viewed as a “gate” system involved in the way a person feels at a particular point in time, which responds to homeostatic perturbations (13), and in turn modulates the interaction between these two systems, i.e., the impulsive and reflective systems (4, 5, 14). Specifically, engagement of the insula exacerbates activity of the impulsive system and hijack activity of the reflective system; thus creating a severe imbalance between the two. At the neuroanatomic level, strong afferent projections connect the insula to the ventral striatum (15). In addition, insular hyperactivity during addiction-related cue exposure may result in compromising self-control efficiency. In light of well-documented links between stressor exposure and addiction-related experiences (e.g., relapse), stressor exposure modulate cue reactivity to drug cues [for a review, see Ref. (16)] and thus may dramatically impact the balance between the impulsive and reflective systems. Besides, the imbalance found in individuals struggling with their compulsive behaviors often accompanies blunted sensitivity to non-drug rewards (17); thus making addiction-related activities highly attractive.

Finally, in this article, we will elaborate on clinical model-based interventions targeting implicit processes, interoceptive processing, and supervisory functioning aimed at helping individuals become less governed by immediate situations and automatic pre-potent responses, and more influenced by systems involved in the pursuit of future valued goals. We argue that this pathway may restore some kind of “free will,” thus making the initiation and the maintenance of a change process of addictive behaviors more likely and more effective.

Over the course of the development of an addiction, related behaviors become progressively controlled by addiction-associated information that have acquired, through Pavlovian and instrumental learning mechanisms, the property to automatically elicit substance-related (or gambling) actions (18, 19). In this section, we describe some neural and cognitive properties of what we have called “impulsive system,” and focus on some of its properties that are associated with addictive behaviors.

These fast and poorly deliberated responses triggered by competent cues present in the environment (e.g., the view of a bottle of beer by a drinker) depend on basal ganglia neural circuits (20). Critically, the amygdala-striatal (dopamine dependent) neural system is a key structure for the incentive motivational effects of a variety of non-natural rewards (e.g., psychoactive drugs) and natural rewards (e.g., food) (21). This stimulus bound rigid and automatic-habit decision-making system requires little mental elaboration (22), and it is modified by drugs, alcohol, and gambling through changes in the phasic characteristics of dopamine activity in reward signaling, and the tonic function of dopamine levels in permitting and facilitating a large variety of motor and cognitive functions (23, 24). Increased mesolimbic dopamine activity, stimulated by drugs of abuse, reinforces the repetition of behaviors, influencing learning and attentional processes, and the strengthening of associations of reinforcing effects (10, 25, 26). Through intensive practice and operant conditioning processes, instrumental performance (e.g., a rat pressing a lever to receive cocaine) could easily switch from goal-directed action-outcome associations, which requires a representation of the outcome as a goal, to actions more independent of the current value of the goal (27); thus characterizing a state of compulsivity (28). The transition between goal-directed and compulsive behaviors was associated with specific aspects of synaptic structural plasticity in both dorsal (29–31) and ventral striatal regions (31). This transition process is accelerated by the sensitization of dopaminergic systems (32). At the cognitive processing level, the impulsive system processes information automatically/implicitly, which describes a number of properties such as goal independence, absence of intentionality, uncontrollability, lack of awareness of one or more aspects of the process (e.g., stimuli, origins, attributes, behavioral effects), efficiency (effectiveness under processing load), and operation even under time constraints (33).

A vast literature has investigated the relationship between automatic/implicit processes and behaviors and reached the conclusion that those processes could modify action in the absence of any decision (34). For instance, in experiments investigating priming effects, participants who were primed with words such as “wrinkles” or “gray” walked more slowly when leaving the experiment (35). In this case, one could expect that conscious deliberation be not impacted by this experimental condition; thus highlighting a direct implicit cognition/action pathway. In other cases, viewing a beer advertisement in the television may result in making the decision to go to the fridge and grasping a beer, it seems reasonable to posit that some automatic processes resulted in biasing the decision possibly through the signaling of the immediate rewarding aspects of the experience (e.g., pleasant taste of the beer), sometimes at the detriment of differed consequences (e.g., fatigue). In line with this idea, is the experiment showing that altering the effort required to reach foods by manipulating their proximity can increase the selection of easier-to-reach food options (36). With respect to drug use and gambling, addiction-related cues are progressively flagged as salient and grab the addicts’ attention (i.e., attentional bias) (37). The attentional processing of such stimuli trigger implicit “wanting” and generate automatic approach behaviors (10).

Addicts exhibit a modified attentional processing for addiction-relevant stimuli (25). These attentional biases occur at both early and later levels of attentional processing, that is, at both automatic, and at more conscious and deliberate, levels (37). Indeed, early level of attentional processing (e.g., attentional encoding; initial orientation of attention) depends primarily on automatic-habit processes (38, 39), whereas later attentional processes (i.e., maintenance of attention; disengagement of attention) involve higher level of conscious control processes (39). Attentional bias at the level of attentional encoding has been studied with the attentional blink (AB) paradigm (40). The AB phenomenon refers to the observation that the second of two-masked targets (T1 and T2), which appears in a rapid serial visual presentation (RSVP) stream of distracters, is usually poorly identified when it is presented within a short time interval after T1 [e.g., within a several 100 ms; (40)]. Using this task, recent studies [e.g., Ref. (41, 42)] have shown that, in addicts, addiction-related words were less affected by interference of other RSVP items within a short time interval after T1, as compared with neutral words. These results suggest that individuals suffering from addiction are more likely to identify addiction-related words than neutral words under conditions of limited attentional resources, which is consistent with an enhanced attentional bias for addiction cues at the encoding level. Attentional bias at the engagement and the maintenance/disengagement levels of attention has been highlighted through the monitoring of eye-movements during performance of attentional tasks [for a review, see Ref. (37)]. For instance, using a change detection task, Brevers et al. (43) showed that, compared with their controls, problem gamblers were faster to detect gambling-related than neutral-related stimulus change. In addition, these investigators observed that problem gamblers directed their first eye-movements (i.e., attentional engagement) more frequently toward gambling-related than toward neutral stimuli, exhibited more gaze fixation counts (i.e., attentional maintenance) on gambling stimuli and spent more time looking (i.e., attentional maintenance) at gambling-related than neutral stimuli.

Implicit addiction-related association refers to spontaneous associations between addiction-related cues and affective, arousal, motivational representation in memory. This association tends to reveal automatic, impulsive cognitive-motivational mental processes, which are sparsely independent of, or not available to, conscious awareness (10). In other words, implicit association could be defined as an introspectively unidentified (or inaccurately identified) trace of past experience that mediate feeling, thought, or action (44). The Implicit Association Task [IAT; Ref. (45)] is a paradigm commonly used to assess implicit association. In a typical IAT, stimuli belonging to one of four possible categories are presented one by one on a computer screen. On each trial, participants categorize as fast as they can the presented stimulus by pressing one of two keys. The assumption underlying the IAT effect is that two concepts that are more closely related in memory should facilitate responses (faster responses and less errors) when they share the same response key, and impair responses when they do not share the same response key. Hence, they should be faster in the first categorization than in the second. For instance, when classifying names of alcohol or soft drinks (i.e., target stimuli), and positive or negative words (i.e., attribute stimuli), people who hold stronger alcohol-positive affect associations than soft drink positive affect associations should be faster when alcohol and positive words are assigned to one key, and soft drinks and negative words to the second key, when compared to the condition in which soft drinks and positive words are assigned to one key, and alcohol and negative words to the other. Using this task, researches have shown that appetitive associations (i.e., positive, arousal) predict alcohol and substance use (46). For instance, Thush and Wiers (47) observed that positive affect and arousal associations predict the level of drinking in adolescents for the following year.

In addition to attentional bias and implicit association, prominent addiction models posit that automatically activated approach/avoidance tendencies play a critical role in addition. Indeed, the repetition of addiction-related behaviors elicits automatic approach tendencies toward addiction-related cues (10). Several paradigms have been developed to assess this action tendency. Consider, for example, the stimulus-response compatibility task (48), in which participants are instructed, in one block, to move a manikin (i.e., a little man) as fast as they can toward substance-related pictures, and away from neutral pictures (approach substance block). In another block, the task is to move the manikin away from the substance-related pictures and toward neutral pictures (avoid substance block). Through this task, substance abusers (alcohol, cigarettes, marijuana) exhibited relatively fast approach movements toward substance cues (48–50). Hence, by highlighting that addiction-related cues automatically trigger a corresponding impulse, which consists of a behavioral schema to approach it (10), these studies provide strong evidence for the presence of automatic incentive habits in gambling addiction. However, it is important to realize that these tendencies are likely to be highly malleable and context-dependent. For instance, unlike controls, abstaining alcohol-dependent patients revealed a relative avoidance bias rather than relative approach bias and moreover, relapse rates were found to increase as the relative tendency to avoid alcohol increased (51).

Altogether, these cognitive aspects are consistent with the incentive-sensitization theory (19, 52), which suggests that, through repetition of rewarding appetitive experiences, the degree to which addiction-related objects are “wanted,” desired, and their effect anticipated, increases disproportionately when compared with the degree to which they are “liked” (i.e., the actual mood change), and this dissociation may progressively increase with the development of addiction. In addition to the increased salience attributed to cues that predict drug reward, addiction is characterized by relatively reduced sensitivity to natural rewards (17, 53), as seen for instance in cocaine abusers for whom non-addiction rewards generate below normal mesocorticolimbic neural activations as compared to monetary reward (54). Also, while occasional smokers show greater neural responses to money than cigarettes, dependent smokers react equally across conditions (55). We should note here that money reward may be exchanged for smoking or drugs or any other addictive stimulus. For this reason monetary reward seems to exert strong neural responses. Most importantly, addictive stimuli acquire a strong incentive motivational salience (e.g., Robinson and Berridge), which renders it highly more preferable to any other type of reward (except money). This increased reward salience is also evident in animal paradigms. While novelty serves as a strong reward stimulus in animals, those animals that become exposed to drugs begin to prefer the choice of the drug instead of the novelty (56), and even instead of maternal behavior (57), or food (58).

While the habit (or impulsive) system, which is key to generating at least the “wanting” component to seek reward, may explain one important aspect of the behaviors associated with approach behaviors, it is clear that it does not explain how one does control his or her behavior. This function refers to the action of what we called the “reflective system,” which is necessary to control these more basic impulses, particularly when the behavior may not be optimal or advantageous, or is perceived as the incorrect thing to do; and it disallows a more flexible pursuit of long-term goals (17). In this section, we review some evidence showing that addicted individuals have abnormalities in this system and have difficulties in exercising willpower to resist the habits and temptations associated with their compulsive actions.

Self-control can be estimated through the capacity to inhibit pre-potent motor responses. This process refers to the ability to deliberately suppress dominant, automatic responses that are no longer relevant or required. This type of inhibitory control can be indexed by the stop-signal [e.g., Ref. (59)] and go/no-go tasks [e.g., Ref. (60)], which require the subject to withhold simple motor responses when a stop-signal occurs (stop-signal task), or when a no-go stimulus is presented (go/no-go task). Impaired response inhibition performance has been previously highlighted in addicts by using the stop-signal task (i.e., prolonged latency of motor response inhibition), and the go/no-go paradigm (i.e., more errors of commission: subject had to withhold a response but pressed a button instead) [for a review of response inhibition impairment in gambling, opiate, and alcohol addiction, see respectively (17, 61, 62)]. Moreover, results from several brain imaging studies showed that, in drug addicts (63, 64), impaired performance on response inhibition tasks is associated with a hypoactivation in the anterior cingulate cortex, implicated in mechanisms of error detection, and conflict monitoring. Several studies also reported intact response inhibition in addicts [e.g., Ref. (65, 66)]. Nevertheless, this absence of behavioral difference is not necessarily indicative of intact response inhibition processes. For instance, van Holst et al. (67) observed increased dorsolateral and anterior cingulate cortex activity in pathological gamblers who exhibited a similar behavioral performance as their controls on motor response inhibition. In other words, a more effortful strategy (i.e., higher brain activation) was undertaken in pathological gamblers to perform at a similar level as their controls (67). Importantly, disruption in response inhibition processes could lead to abnormal salience attribution directed at addiction-related cues in addicts. In other words, a dysfunction of the inhibitory control system could further exacerbate automatic impulsive processes. For instance, implicit memory associations are a strong predictor of alcohol use in young adults with poor ability of motor response inhibition (68). Moreover, several studies showed that response inhibition deficits affecting drug and gambling addicted persons (69) are thought to accelerate the course of addiction by compromising abstinence from cocaine (70), gambling (71), nicotine (72), alcohol (73), aggravating problem gambling (74), and by increasing attrition from treatment (75).

The action of the “reflective” system is also crucial for choosing according to long-term, rather than short-term, outcomes (6). This function is mediated by paralimbic, medial orbitofrontal, and ventromedial prefrontal structures involved in triggering somatic states from memories, knowledge, and cognition, which allow activation of numerous affective/emotional (somatic) responses that conflict with each other; the end result is that an overall positive or negative signal emerges (76). The impact of somatic responses in addiction has been initially demonstrated in clinical research with patient populations with damage in frontal lobe regions as well as imaging studies that delineate the likely neural basis of each of these functions (76–78). After damage to the ventromedial region of the prefrontal cortex, previously well-adapted individuals become unable to observe social conventions and decide advantageously on personal matters (79). The nature of these deficits revealed that the vmPFC region serves as a link between (a) a certain category of event based on memory records in high order association cortices to (b) effector structures that produce an emotional response (77). Damage to the systems that impact emotion and/or memory compromise the ability to make advantageous decisions (79). The Iowa Gambling Task [IGT; (80)], which was initially developed to investigate the decision-making defects of neurological patients in real-life has been shown to tap into aspects of decision-making that are influenced by affect and emotion (77). This task has been regarded as the most widely used and ecologically valid measure of decision making in this clinical population. One of the reasons for this ecological validity is that performing advantageously on this task requires, as in real-life, dealing with uncertainty in a context of punishment and reward, with some choices being advantageous in the short-term (high reward), but disadvantageous in the long run (higher punishment); other choices are less attractive in the short-term (low reward), but advantageous in the long run (lower punishment). Hence, the key feature of this task is that participants have to forgo short-term benefits for long-term benefits, a process that is presumably severely hampered in drug and gambling addicts (1). Accordingly, performance on the IGT has been shown to be a sensitive measure of impaired decision-making in a diversity of neurological and psychiatric conditions (6). For instance, patients with frontal lesions [e.g., Ref. (80–82)], individuals suffering from substance [e.g., Ref. (83–87)] or non-substance addiction [e.g., Ref. (88, 89)] have demonstrated a preference for short-term gains despite larger net losses while performing the IGT.

In sum, disrupted function of the “reflective” prefrontal cortex could lead to impaired response inhibition and abnormal salience attribution toward high-short-term rewards in addictive individuals. This provides one explanation of addicts’ inability to resist substance (or addiction-related behavior) seeking and taking at the expense of non-addiction-related activities.

The central message of this article is that the two systems described so far are influenced by interoceptive processes (e.g., drug cravings) (see Figure 1).

At the heart of this phenomenon is the insula in which activation in craving paradigms is a reliable observation (5, 90). However, before discussing further about the specific role of the insula, one should keep in mind that the insula does not work in isolation in the brain, and that in the case of a craving for a certain drug, other regions are activated in cue-reactivity and drug-craving paradigms [for a review, see, Ref. (90)]. These data are in line with the proposal of the present article, which suggests that the insula is connected to brain-related impulsive (amygdalar striatal complex) and reflective (prefrontal cortex) systems; and it modulates their impact on decision and action (4).

The insular cortex has recently emerged as a key neural structure that plays a key role in the formation of interoceptive representation, which is crucial for subjective emotional feelings (5, 13, 91). Interoception refers to the practice of receiving, processing and integrating body-relevant signals with external stimuli of affect on-going motivated behavior (13). According to the notion of embodiment, high-level cognitive and affective processing is grounded in the organism’s sensory and motor experiences (92). Moreover, it has recently been argued that the insular cortex may contribute to the onset and maintenance of addiction by translating interoceptive signals into what one subjectively experiences as a feeling of desire, anticipation, or urge leading to approach behaviors (5, 14, 93). Indeed, highly embodied experience may overwhelm the cognitive control system by providing a highly emotional experience. But also, low levels of embodied experience may not engage the cognitive control system to adjust on-going behavior, which may result, for instance, in high risk-taking (14).

Imaging studies show activity within the insula correlating with the subjects’ rating of urge for cigarettes, cocaine, alcohol, and heroin (5, 13, 93). In addition, insula activation was closely associated with higher levels of nicotine dependence (94) and both attentional bias and the risk of relapse (95). Indeed, smokers at risk for relapse showed more insula activation while processing smoking-related words (95). In individuals with dependence to cocaine, hyperactivity to drug-specific stimuli contrasts with abnormally low activity when self-regulation processes are engaged [e.g., inhibition; (96)].

Other evidence supporting the important role of the insula in addiction processes arise from human brain lesion studies. Strokes that damage the insular cortex tend to literally wipe out the urge to smoke in some individuals previously addicted to cigarette smoking (12). In this study, smokers with brain damage involving the insula were more likely to quit smoking easily and immediately, without relapse and without a persistent urge to smoke (12). These results support a novel conceptualization of one of the mechanisms by which the insula participates in maintaining addiction.

The insular cortex (and most likely the anterior insula) responds to interoceptive signals (due to homeostatic imbalance, deprivation state, stress, sleep deprivation, etc.). Besides the translation of these interoceptive signals into what may become subjectively experienced as a feeling of “urge” or “craving,” we hypothesize that the insular cortex activity increases the drive and motivation to smoke (or take drugs or to gamble) (a) by sensitizing or exacerbating the activity of the habit/impulsive system; and (b) by subverting attention, reasoning, planning, and decision-making processes to formulate plans for action to seek and procure cigarettes or drugs (97). Put differently, these interoceptive representations have the capacity to “hijack” the cognitive resources necessary for exerting inhibitory control to resist the temptation to smoke or use drugs by disabling (or “hijacking”) activity of the prefrontal (control/reflective) system.

Stress could be a critical candidate for understanding the impact of abnormal level of proprioception on impulsive and reflective systems (98, 99). Indeed, whereas at low to moderate levels of stress, the reflective system’s activity may be enhanced, abnormally high levels of stress tend to attenuate activity within the reflective system (99). This may be applied to alcohol use by successfully inducing drug craving in the laboratory through the generation of stress (e.g., 5-min individualized guided imagery exposure of each participants’ own recent stressful scenarios) (100). Research has emphasized the existing association between exposure to stress, abnormal persistent level of changes in the body state (heart rate, salivary cortisol levels), persistent craving, and use of compulsive individuals’ preferred drug [for a review, see Ref. (101)]. Interestingly, alcoholics’ prefrontal and striatal-limbic regions (including the insula) are hyper-responsive to neutral-relaxing condition, making activation pattern between neutral relaxed and stressful cues indistinguishable (102). This result suggests a dysregulated response to stress that induces craving and increases the risk of relapse in alcoholics (101).

Based upon the model proposed in this article, a number of clinical and cognitive interventions are thought to improve treatment outcomes of addictive behaviors. These interventions generally aim at targeting one subsystem at a time from the triadic neural system model of willpower presented in this article. One strategy may be fooling the impulsive system by desensitizing automatic attention toward addiction cues, positive implicit memory associations with addiction cues, and approach tendencies toward addictive object. Boosting self-regulation control along with boosting metacognition and self-awareness of the cognitive limitation, and reducing interoceptive signaling of homeostatic disturbances are also key strategies to alter addiction-related choices and actions. Applications of some of these strategies are already taking place, such as boosting the capacity of the reflective system through physical exercise and mindfulness, through which researchers aim to modulate how an individual processes and integrates afferent sensing from the inside of the body (14). Although interesting, we argue that clinical interventions rooted in the qualitative description of abnormal interactions between the three above mentioned systems could lead to more robust and significant changes. Importantly, our defended clinical approach considers the necessity to adapt clinical strategies to every addicted individual. Indeed, there is evidence showing that these participants are highly heterogeneous with respect to cognitive and brain determinants of their addictive behaviors [for pathological gamblers, see Ref. (143); for polysubstance abusers, see Ref. (144)]. For instance, the principle of equifinality (a give end state – e.g., compulsive drug use – can be reached by many potential pathways) is particularly clear in case of impulsivity, a concept that encompasses a number of aspects including impulsive, reflective and proprioceptive determinants (14, 145).

The discovery of the insula as a important brain structure specifically in smoking addiction does not undermine the seminal work generated to date on the roles of other components of the neural circuitry implicated in addiction, and impulse control disorders in general, especially the mesolimbic dopamine system (incentive habit system), and the prefrontal cortex (executive control system). Addressing the role of the insula only complements this prior work, leading researchers to investigate how inter-connected activities between the prefrontal cortex, the striatum-amygdala system and the striatum accounts for distinct dimensions of clinical phenomenology of addictive behaviors. At the cognitive and behavioral level, various aspects of sensitized automatic stimulus-driven processing associated with poor self-control capacities elevate the likelihood that a state of addiction be perpetuated, particularly in the context of stress and of addiction-cue exposure.

With respect to clinical interventions, our recommendation is to adapt treatments to each individual’s triadic system configuration by adopting a multidimensional approach, focusing on the interactions between automatic, intentional, and proprioceptive cognitive processes involved in the risk of developing an addictive behavior (in vulnerable populations), in the maintenance of such behaviors (in addicted people) or in the risk of relapse (in patients). While neuropsychological testing has advanced tremendously with respect to brain areas such as the prefrontal cortex (or measuring executive functions), there is still a great lag in neuropsychological evaluation of those state-dependent systems (such as the insula). Measuring strengths or weaknesses in these systems could be the next great advancement in neuropsychological evaluation.

This effort will undoubtedly allow the discovery of novel therapeutic approaches for treating several impulse control disorders, including breaking the cycle of addiction.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.