1 INTRODUCTION

Compulsion is often regarded as a key feature of addictions and obsessive-compulsive disorders (OCD).¹ One of the leading drug addiction theories describes addictive behaviour as a transition from voluntary goal-directed, recreational drug use to compulsive drug-seeking habits that result from prefrontal cortical to striatal control over drug-seeking as well as a progression from the ventral to the dorsal striatum.^{2, 3} Thus, an individual may compulsively seek drugs – that is, persist in seeking drugs despite the negative consequences of doing so – when executive control over this maladaptive behaviour is diminished and when the neural systems that underlie habitual behaviour dominate goal-directed behavioural systems.⁴ In other words, habits and the ventral to dorsal striatal shift are the building blocks of compulsive drug-seeking behaviour.

Here, we argue that this theory may adequately characterize drug-seeking behaviour in certain animal studies but does not adequately describe human addictive behaviour. In particular, we argue that, in humans, obsessive and compulsive behaviours, as observed in the OCD spectrum, differ significantly from addictive behaviour, and that a shift from goal-directed towards habitual behaviour does not necessarily lead to compulsive behaviour.

2 HUMAN OBSESSIVE-COMPULSIVE DISORDERS (OCD) DIFFER SIGNIFICANTLY FROM ADDICTIONS

Although symptoms of OCD have been compared with obsessive craving and ruminating about drug consumption as well as compulsive drug taking in spite of adverse consequences, compulsive behaviour in OCD has a different meaning than in addictions. In OCD, obsessive thoughts usually trigger compulsive behaviour which in turn helps to dispel the thoughts and reduce distress, whereas in addictions compulsive behaviour is defined as the maladaptive persistence of responding despite adverse consequences.

The first indication that obsessions and compulsions in OCD differ substantially from addictive behaviour is based on clinical observation. Thus, individuals with both OCD and addiction disorders can clearly distinguish between such symptoms and are able to describe substantial differences in their respective experiences. For example, a patient suffering from OCD, alcohol dependence and pathological gambling described that with OCD, he always had to perform certain rituals in order to cope with his aversive obsessions. Interruption of ritualistic behaviour or postponement of its initiation was so highly aversive that it was only possible for short moments of time. His experience was quite different with respect to alcohol craving, which was elicited unexpectedly by alcohol-associated cues, and differed from his craving for gambling, which usually occurred at 6 p.m., when he was previously able to engage in online gambling.⁵ Furthermore, obsessions usually focus on aversive thought content, for example being somewhat impure or soiled, or on highly aversive, aggressive thoughts directed against other human beings including children.⁶ Ritualistic behaviour often aims at compensating for the negative, evil thoughts, which are experienced as inadequate and highly threatening by the afflicted individual.^{6, 7} Craving for alcohol or other drugs of abuse, on the other hand, represents craving for a certain reward, which is at least in the initial stages of drug dependence associated with a positive mood state⁸ but at a more severe stage, craving can be also induced by a negative state such as conditioned drug withdrawal or stress.⁹

3 NEURAL CORRELATES OF OCD DIFFER SIGNIFICANTLY FROM ADDICTIONS

A second substantial difference between OCD and addictive behaviour is in their neurobiological correlates: in the frontal cortex, which has a key role in goal-directed behaviour, increased glucose utilization was found in patients with OCD.^{10, 11} Accordingly, successful treatment with antidepressants or behaviour therapy was associated with a significant decrease in glucose utilization in the orbitofrontal cortex.^10-12 This is in contrast to neurobiological correlates of individuals with drug addiction: glucose utilization in the frontal cortex was repeatedly reported to be reduced.^{13, 14}

For example, Volkow and co-workers¹³ found a reduction of whole brain glucose metabolism during rest in heavy drinkers, and Adams and colleagues¹⁵ an association between low glucose utilization in the medial prefrontal cortex and increased errors in the Wisconsin Card Sorting Test that assesses executive functions. Furthermore, alterations in dopamine neurotransmission as evinced by a reduction of dopamine D2 receptor availability in the striatum were associated with low levels of orbitofrontal glucose utilization in individuals with methamphetamine abuse.¹⁴ Finally, in addictive behaviours, low availability of dopamine D2 receptors following immediate detoxification has repeatedly been described in the striatum,^{16, 17} while in the OCD spectrum, increased D2 receptor availability was associated with motor tic manifestation.¹⁸ Finally, in OCD, more complex obsessive and compulsive symptoms were associated with serotonergic alterations in the brainstem,¹⁹ an alteration that is not regularly seen in individuals with addictive behaviour.²⁰

Despite these dissimilarities between OCD and addictions on the behavioural and neural level, some studies suggest that there are similarities between the obsessive-compulsive spectrum and addictive behaviour, particularly a general reduction in goal-directed behaviour and a shift towards habitual behaviour.^{2, 3} However, a reduction in goal-directed behaviour may occur due to different neural processes: it may e.g. result from the neurotoxic effects of alcohol or other drugs on the frontal cortex or be related to an overactivation of frontal cortical-striatal circuits in OCD.^{10, 21, 22} These different effects may lead to a shift towards habitual behaviour in addictions as well as in OCD. However, habits should not necessarily be considered as building blocks for compulsive behaviour unless they occur in spite of immediate aversive consequences, which is usually not the case in addiction. This will be discussed in the following.

4 A SHIFT FROM GOAL-DIRECTED TOWARDS HABITUAL BEHAVIOUR DOES NOT NECESSARILY LEAD TO COMPULSIVE BEHAVIOUR

A significant contribution of habitual behaviour in human drug addiction^{6, 23, 24} is disputed by the group of Lee Hogarth, who showed that, in some but not all studies, goal-directed behaviour is preserved, as e.g. indicated by intact effects of the devaluation of outcomes among human persons with drug addiction.^{25, 26} Furthermore, Hogarth argues that effects of drug cues do not correlate with addiction severity, as shown e.g. in the lack of significant differences in drug cue effects between addicted and non-addicted persons.²⁷ Hogarth's approach refers to the so-called dual systems theory, which suggests that habitual decision-making relies on a neural system that is completely independent of the brain system underlying goal-directed decision.^{10, 22} However, there is a relevant overlap in the neural correlates of brain areas that underlie goal-directed and habitual decision as shown by anatomical and functional studies in humans and non-human primates,²⁸ arguing against a strict dichotomy between these brain networks and their behavioural correlates. Furthermore, the dual systems approach does not adequately reflect complex differences in ventral striatal shell and core and their respective effects on stimulus-drug associations on the one hand and sensitization towards drug effects on the other as evidenced in animal experiments.²⁹ Regarding effects of drug-related stimuli in humans, we and others observed significant associations between Pavlovian conditioned non-drug and drug cues on unrelated instrumental behaviour in so-called Pavlovian-to-Instrumental Transfer tasks as well as cue-induced brain activation^{30, 31} on the one hand, and addiction severity as indicated by the prospective relapse risk on the other.^31-33 Confirming the relevance of human abilities to reflect on ongoing behaviour, drug cues tended to promote behavioural withdrawal (and not approach) in patients with alcohol dependence who managed to abstain after detoxification, while this was not the case in subsequent relapsers or controls.³⁴

Altogether, we suggest that habit formation plays a significant role in drug addiction, as long as habitual behaviour is regarded as dimensionally but not categorically different from goal-directed decision-making and modifiable by human cognition. It was indeed shown that an increase in habitual behaviour is associated with the severity of drug use, in this case, relapse after detoxification, but only if it is accompanied by high alcohol expectations.³⁵ These findings suggest that Pavlovian cues and a shift from goal-directed towards habitual behaviour may contribute to automatic drug intake as suggested by Tiffany and Carter.³⁶ However, humans appear to be able to reflect upon their behaviour and are usually able to change it, also evidenced by the 10 to 20% of alcohol-dependent patients who manage to kick the habit without professional help by achieving abstinence or extensively reducing drug intake.^37-40

This is certainly not the case in animal experiments where animals are defined as habitual by reward devaluation testing; they are simply not able to kick the habit by intrinsic motivation. But do laboratory animals such as mice or rats that show a specific task behaviour show also compulsive behaviour? This is usually tested by punishment; i.e., if an animal goes for a conditioned reward (in this case the drug cue) despite the fact that it receives a foot-shock it is considered as compulsive. However, drug taking in spite of aversive consequences can also occur without previous habit formation in rodents.⁴¹ Moreover, does this definition of compulsion as maladaptive persistence of responding despite adverse consequences also hold true for the human condition?

We argue that this is not the case in human addiction. In fact, aversive outcomes of repeated drug intake often take months or years to manifest. This is not only true for somatic illnesses, such as liver cirrhosis, neurotoxicity or cancer following long-term alcohol intake,^{42, 43} but also for negative consequences in the form of social problems associated with repeated drug intake, even more so because such consequences vary widely depending on whether a certain drug can be legally consumed, as is the case in certain countries.⁴⁴ In the case of illegal drug consumption, immediate negative consequences may occur, for example when an individual gets arrested while trying to acquire an illegal drug. However, such socially variant conditions depend on national legislation and are not characteristics of the individual with an addictive behaviour.

Since the legality of a drug differs widely not only between nations but also in the history of societies (alcohol prohibition in the United States of America being a prominent example), the sociocultural framework of drug intake is hardly comparable across and within different countries.⁴⁵ Accordingly, the replacement of the well-defined concept of dependence⁴⁶ by a dimensional approach, as defined in the DSM-5, which includes social problems, may lead to inconsistent classification, as some sociocultural settings may only occur in some countries.^47-49

In summary, even if an individual is severely dependent negative consequences including life-threatening somatic diseases may usually not occur immediately following repeated drug intake.⁴³ This punishment discounting, which is scarcely studied in humans, differs substantially from immediate punishment in animal experiments focusing mainly on drug-seeking seeking behaviour.⁴ Additionally, in most animal experiments animals are in isolation, which is unusual for rodents and may influence motivation for drug taking.^{50, 51} In some animal experiments, environmental enrichment reduced the acquisition of drug seeking and facilitated drug abstinence.^{52, 53} Animal experiments thus often differ substantially from human studies with respect to social settings as well as very basic settings such as the delay between drug taking and punishment, which limits the comparability to humans. Therefore, the concept that habits and the ventral to dorsal striatal shift are the building blocks of compulsive drug-seeking behaviour and that compulsion is the maladaptive persistence of responding despite adverse consequences in humans should be critically addressed and potentially revised.

5 CONCLUSIONS

Our considerations do not neglect that individuals with addictions may have habitual behaviour and that it can be very difficult to kick the habit of drug intake. However, we hypothesize that such habits should not be described as a compulsion that is carried out irrespective of immediate aversive consequences under all circumstances. Individuals with drug addiction are neither automatons that carry out habitual behaviour without cognitive control nor are they just individuals with bad choices. Repeated drug consumption has profound impacts on motivationally and cognitively relevant neurocircuits and may bias an individual towards repeated drug intake.⁶ Compared to other human behaviours, such as trained movements in sports, it can be extremely difficult to change habitual behaviour. This is particularly true when drug addiction is accompanied by a lack of alternative rewards that are at least in the long run healthier for the individual. Accordingly, social deprivation and poverty, which may limit access to alternative rewards, should regularly be considered in human studies. Altogether, we feel that compulsive behaviour as defined primarily from the perspective of animal experimentation falls short of the clinical phenomena and their neurobiological correlates.

Summary

Compulsion is a defining characteristic of addiction and obsessive-compulsive disorder (OCD). A prominent theory posits that addiction involves a shift from voluntary drug use to compulsive drug-seeking, driven by a change in brain control from the prefrontal cortex to the striatum. This theory, however, may not fully capture the complexities of human addictive behavior. Significant differences exist between human OCD and addiction, challenging the direct application of animal models to human conditions.

Human Obsessive-Compulsive Disorders (OCD) Differ Significantly From Addictions

While OCD symptoms share some superficial similarities with addiction (e.g., obsessive craving, compulsive drug use despite negative consequences), crucial distinctions exist. In OCD, compulsive behaviors are triggered by obsessive thoughts, serving to alleviate distress. Addiction, conversely, is characterized by persistent maladaptive behavior despite negative consequences. Clinical observations reveal that individuals with both OCD and addiction readily differentiate their experiences. Obsessions often involve aversive thoughts, whereas drug craving reflects a desire for reward, initially positive but later potentially driven by negative states like withdrawal or stress.

Neural Correlates of OCD Differ Significantly From Addictions

Neurobiological differences further distinguish OCD and addiction. OCD is associated with increased glucose utilization in the frontal cortex, while addiction shows reduced frontal cortex activity. Successful OCD treatment often correlates with decreased orbitofrontal glucose utilization, contrasting with findings in addiction where reduced frontal glucose utilization and altered dopamine neurotransmission are frequently observed. These neurobiological distinctions highlight fundamental differences in the underlying neural mechanisms. While both conditions may involve a reduction in goal-directed behavior and a shift toward habitual behavior, the neural pathways driving these changes appear distinct.

A Shift From Goal-Directed Towards Habitual Behaviour Does Not Necessarily Lead to Compulsive Behaviour

The role of habitual behavior in human addiction remains debated. Some research suggests preserved goal-directed behavior in addiction, challenging the notion of a complete shift to habitual responding. While habitual behavior might contribute to automatic drug intake, human capacity for self-reflection and behavioral modification complicates the straightforward application of animal models. Studies show correlations between habitual behavior and addiction severity, but these correlations are nuanced and context-dependent, highlighting the importance of cognitive and motivational factors.

Conclusions

Habitual behavior is likely significant in addiction, but it should not be equated with compulsion in all cases. Individuals with addiction are not simply driven by automatic habits; the impact of repeated drug use on neurocircuits significantly influences motivation and cognition, making habit modification challenging. Social and economic factors further complicate the situation, highlighting the limitations of animal models in fully capturing the complexity of human addiction. Compulsion, as defined largely through animal studies, may not fully capture the clinical reality of human addictive behavior.

Summary

Compulsive behavior is a hallmark of addiction and obsessive-compulsive disorder (OCD). A prevalent theory posits that addiction stems from a shift in brain control from the prefrontal cortex to the striatum, leading to habitual drug-seeking despite negative consequences. This paper challenges this theory's applicability to human addiction, arguing that human OCD and addiction differ significantly in both behavioral and neural aspects.

Human Obsessive-Compulsive Disorders (OCD) Differ Significantly from Addictions

While OCD symptoms share superficial similarities with addiction (e.g., obsessive craving, compulsive behavior despite negative consequences), the underlying mechanisms differ. In OCD, obsessions trigger compulsions to alleviate distress; in addiction, compulsive behavior persists despite known negative consequences. Clinical observations reveal distinct subjective experiences between OCD and addiction symptoms in individuals with both conditions. Obsessions typically involve aversive thoughts (e.g., contamination, aggression), while drug craving seeks reward or relief from negative states.

Neural Correlates of OCD Differ Significantly from Addictions

Neurobiological differences further distinguish OCD and addiction. OCD is associated with increased frontal cortex activity, while addiction shows reduced activity in this region. Studies reveal decreased glucose metabolism in the frontal cortex of individuals with drug addiction, contrasting with increased utilization in OCD patients. Dopamine receptor availability also differs: reduced D2 receptor availability in the striatum is linked to addiction, whereas increased availability is associated with motor tics in OCD. Serotonergic alterations in the brainstem, more prevalent in OCD, are less common in addiction.

A Shift from Goal-Directed Towards Habitual Behavior Does Not Necessarily Lead to Compulsive Behavior

While both OCD and addiction may involve a shift from goal-directed to habitual behavior, the underlying neural mechanisms differ. In addiction, this shift might result from neurotoxic drug effects or overactivation of cortico-striatal circuits, unlike the distinct processes in OCD. The dual-systems theory, suggesting independent neural systems for habitual and goal-directed behavior, is challenged by evidence of neural overlap. Studies show correlations between drug cues, behavioral responses, and addiction severity, highlighting the role of Pavlovian conditioning and the capacity for cognitive control in humans.

Conclusions

Habitual behavior significantly contributes to addiction, but this does not equate to compulsion in all instances. Humans possess cognitive control enabling behavior modification; addiction severity correlates with habitual behavior but depends on factors such as drug expectations and social contexts. The animal model, with its focus on immediate aversive consequences, may not fully capture the complexities of human addiction, where delayed negative consequences and individual differences in cognitive control play crucial roles. A more nuanced understanding is needed, acknowledging both the impact of habitual behaviors and the capacity for human agency.

Summary

Addiction and obsessive-compulsive disorder (OCD) share the characteristic of compulsion, but significant differences exist. A prominent theory posits that addiction involves a shift from voluntary drug use to compulsive drug-seeking driven by changes in brain activity. This theory, while possibly accurate for some animal studies, doesn't fully capture human addiction.

Human OCD Differs Significantly From Addictions

While OCD symptoms may resemble addiction (e.g., obsessive craving, compulsive drug use despite negative consequences), their underlying mechanisms differ. In OCD, obsessions trigger compulsions to alleviate distress; in addiction, compulsion is characterized by persistent drug-seeking despite negative outcomes. Clinical observations show individuals with both OCD and addiction can differentiate between their experiences. Obsessions often involve aversive thoughts, unlike the reward-seeking nature of drug cravings.

Neural Correlates of OCD Differ Significantly From Addictions

Neurobiological differences further distinguish OCD and addiction. OCD is associated with increased brain activity (glucose utilization) in the frontal cortex, a key region for goal-directed behavior, while addiction often shows reduced activity in this area. Differences also exist in dopamine receptor activity and serotonergic function in the brainstem. While both conditions may involve reduced goal-directed behavior and a shift toward habitual behavior, the underlying neural processes differ.

A Shift From Goal-Directed Towards Habitual Behavior Does Not Necessarily Lead to Compulsive Behavior

The role of habit formation in human addiction is debated. Some studies suggest that goal-directed behavior remains intact in some individuals with addiction. The "dual systems theory," which posits separate neural systems for habitual and goal-directed behavior, is challenged by evidence of overlap in these brain networks. Research shows associations between drug cues, brain activation, and addiction severity, indicating a complex interplay of factors. Humans retain cognitive control; successful abstinence demonstrates the ability to override habitual behaviors.

Conclusions

Habitual behavior is significant in addiction, but it shouldn't be equated with compulsion irrespective of consequences. Addicts aren't automatons; their behavior is influenced by neurocircuit changes impacting motivation and cognition. Changing these habits is challenging, especially without access to alternative rewards. Social factors like poverty and deprivation should be considered. The animal model of compulsion, based on immediate punishment, may not fully reflect the human experience, particularly due to the delayed and varied nature of negative consequences in human addiction.

Summary

People with addiction often do things over and over, even if those things are bad for them. This is similar to how people with OCD have unwanted thoughts and feel compelled to do certain things. But there are important differences.

Human OCD and Addiction Are Different

OCD and addiction are different. People with both can tell the difference between their experiences. In OCD, unwanted thoughts cause someone to do something to make the thoughts go away. In addiction, someone keeps doing something harmful even though they know it's bad.

The Brain Works Differently in OCD and Addiction

Scientists can see differences in the brains of people with OCD and addiction. People with OCD have more activity in certain parts of their brains that help with decision-making. People with addiction have less activity in those areas. They also have different levels of certain brain chemicals.

Habits Don't Always Mean Compulsion

Having a habit doesn't automatically mean someone is compulsive. Some people with addiction still make choices. It's hard to change habits, especially when there aren't better things to do. Experiments with animals can’t fully explain what happens in humans.

Thinking About Addiction

People with addictions might have habits, and it's very hard to stop. But it's not always because they don't care about the consequences. Addiction changes how their brain works, making it harder to resist. We need to think about addiction in a way that recognizes the role of habits and brain changes, but also recognizes that people can still control their actions, and that social and economic factors play a part.