Our daily lives involve high levels of repetition of activities within similar contexts. We buy the same foods from the same grocery store, cook with the same spices, and typically sit at the same place at the dinner table. However, when questioned about these routine activities, most of us barely remember the details of our actions. Habits are automatically triggered behaviours in which we engage without conscious awareness or deliberate control. Although habits help us to operate efficiently, breaking them requires great effort. We have developed a 27-item questionnaire to measure individual differences in habitual responding in everyday life. The Creature of Habit Scale (COHS) incorporates two aspects of the general concept of habits, namely routine behaviour and automatic responses. Both aspects of habitual behaviour were weakly correlated with underlying anxiety levels, but showed a more substantial difference in relation to goal-oriented motivation. We also observed that experiences of adversity during childhood increased self-reported automaticity, and this effect was further amplified in participants who also reported exposure to stimulant drugs. The COHS is a valid and reliable self-report measure of habits, which may prove useful in a number of contexts where discerning individuals' propensity for habit is beneficial.

BACKGROUND: The balance between goal-directed behavior and habits has been hypothesized to be biased toward the latter in individuals with cocaine use disorder (CUD), suggesting possible neurochemical changes in the putamen, which may contribute to their compulsive behavior. METHODS: We assessed habitual behavior in 48 patients with CUD and 42 healthy control participants using a contingency degradation paradigm and the Creature of Habit Scale. In a subgroup of this sample (CUD: n = 21; control participants: n = 22), we also measured glutamate and glutamine concentrations in the left putamen using ultra-high-field (7T) magnetic resonance spectroscopy. We hypothesized that increased habitual tendencies in patients with CUD would be associated with abnormal glutamatergic metabolites in the putamen. RESULTS: Compared with their non-drug-using peers, patients with CUD exhibited greater habitual tendencies during contingency degradation, which correlated with increased levels of self-reported daily habits. We further identified a significant reduction in glutamate concentration and glutamate turnover (glutamate-to-glutamine ratio) in the putamen in patients with CUD, which was significantly related to the level of self-reported daily habits. CONCLUSIONS: Patients with CUD exhibit enhanced habitual behavior, as assessed both by questionnaire and by a laboratory paradigm of contingency degradation. This automatic habitual tendency is related to a reduced glutamate turnover in the putamen, suggesting a dysregulation of habits caused by chronic cocaine use.

Habits may develop when meaningful action patterns are frequently repeated in a stable environment. We measured the differing tendencies of people to form habits in a population sample of n = 533 using the Creature of Habit Scale (COHS). We confirmed the high reliability of the two latent factors measured by the COHS, automaticity and routines. Whilst automatic behaviours are triggered by context and do not serve a particular purpose or goal, routines often have purpose, and because they have been performed so often in a given context, they become automatic only after their action sequence has been activated. We found that both types of habitual behaviours are influenced by the frequency of their occurrence and they are differentially influenced by personality traits. Compulsive personality is associated with an increase in both aspects of habitual tendency, whereas impulsivity is linked with increased automaticity, but reduced routine behaviours. Our findings provide further evidence that the COHS is a useful tool for understanding habitual tendencies in the general population and may inform the development of therapeutic strategies that capitalise on functional habits and help to treat dysfunctional ones.

Background Drug-induced alterations to the dopamine system in stimulant use disorder (SUD) are hypothesised to impair reinforcement learning. Computational modelling enables the investigation of the latent processes of reinforcement learning in SUD patients, which could elucidate the nature of their impairments. Methods We investigated reinforcement learning in 44 SUD patients and 41 healthy control participants using a probabilistic reinforcement learning task that assesses learning from reward and punishment separately. In an independent sample, we determined the modulatory role of dopamine in reinforcement learning following a single dose of the dopamine D2/3 receptor antagonist amisulpride (400 mg) and the agonist pramipexole (0.5 mg) in a randomised, double-blind, placebo-controlled, crossover design. We analysed task performance using computational modelling and hypothesised that reinforcement learning impairments in SUD patients would be differentially modulated by a dopamine D2/3 receptor antagonist and agonist. Results Computational analyses in both samples revealed significantly reduced learning rates from punishment in SUD patients compared with healthy controls, whilst their reward learning rates were not measurably impaired. In addition, the dopaminergic receptor agents modulated reinforcement learning parameters differentially in both groups. Both amisulpride and pramipexole impaired reinforcement learning parameters in healthy participants, but ameliorated learning from punishment in SUD patients. Conclusion Our findings suggest that reinforcement learning impairments seen in SUD patients are associated with altered dopamine function.

Rationale Drug addiction has been suggested to develop through drug-induced changes in learning and memory processes. Whilst the initiation of drug use is typically goal-directed and hedonically motivated, over time, drug-taking may develop into a stimulus-driven habit, characterised by persistent use of the drug irrespective of the consequences. Converging lines of evidence suggest that stimulant drugs facilitate the transition of goal-directed into habitual drug-taking, but their contribution to goal-directed learning is less clear. Computational modelling may provide an elegant means for elucidating changes during instrumental learning that may explain enhanced habit formation. Objectives We used formal reinforcement learning algorithms to deconstruct the process of appetitive instrumental learning and to explore potential associations between goal-directed and habitual actions in patients with cocaine use disorder (CUD). Methods We re-analysed appetitive instrumental learning data in 55 healthy control volunteers and 70 CUD patients by applying a reinforcement learning model within a hierarchical Bayesian framework. We used a regression model to determine the influence of learning parameters and variations in brain structure on subsequent habit formation. Results Poor instrumental learning performance in CUD patients was largely determined by difficulties with learning from feedback, as reflected by a significantly reduced learning rate. Subsequent formation of habitual response patterns was partly explained by group status and individual variation in reinforcement sensitivity. White matter integrity within goal-directed networks was only associated with performance parameters in controls but not in CUD patients. Conclusions Our data indicate that impairments in reinforcement learning are insufficient to account for enhanced habitual responding in CUD. Electronic supplementary material The online version of this article (10.1007/s00213-019-05330-z) contains supplementary material, which is available to authorized users.