Identifying viable theoretical frameworks with essential parameters for real-time and real world alcohol craving research: a systematic review of craving models

Figures & data

Table 1. Descriptions of craving models, as reviewed by Skinner and Aubin (2010). The left column presents the model name and its founding publication as identified by Skinner and Aubin (2010). The central column briefly describes the model, and the right column shows Skinner and Aubin’s (2010) critical appraisal of the various models.

Model	Description	Criticisms of Model according to Skinner and Aubin (2010)
Conditioning-based Models
1. Withdrawal model Wikler (1948)	Symptoms of withdrawal become associated with a stimulus. As a result, this stimulus will result in an urge to drink to relieve these withdrawal symptoms.	‘These [conditional] models were discredited, (…) by numerous studies that found fault with some of their basic assumptions’ (p. 609).
2. Compensatory model Siegel (1983)	Over time an addict develops tolerance, this leads to a contrary reaction rather than the pleasure of the substance. Craving occurs to escape this process of discomfort.	”
3. Opponent-process model Solomon and Corbit (1974)	Craving is a stimulation to use the substance and to give relief from withdrawal symptoms.	”
4. Incentive model Stewart et al. (1984)	Craving promotes individuals to seek the substance as a reward. An addict experiences pleasure just by thinking of the expected reward.	”
Cognitive models
5. Outcome expectancy model Marlatt (1985)	Environmental cues can trigger powerful expectations about the effects of alcohol. These expectations can be a craving for reward or relief. This craving can be followed by urge, which is the actual intention to drink.	‘Little research exists to validate the outcome expectancy model and the attempts to confirm the theory have not been conclusive perhaps because more specifications of the features of the model are needed’ (p. 610). ‘The relationship between outcome expectancies and urges, however, is still unknown’ (p. 610).
6. Dual-affect model Baker et al. (1986)	This model assumes that craving can be induced by a positive or negative affect, but not together. Negative affect craving can be triggered by: (1) negative emotions, (2) aversive events, (3) withdrawal or cues associated with withdrawal, and (4) no availability of an alcohol cue. Positive affect craving can be triggered by: (1) positive emotions, (2) small alcohol dosage, (3) cues paired with alcohol use, or (4) availability of an alcohol cue.	‘Baker et al. (1986) admitted that it did not explain why some drug users do not become addicted’ (p. 611). ‘(…) they had primarily considered data from smoking studies, reducing the theory’s external validity’ (p. 611). ‘One challenge to the model is that the induction of positive mood states generally did not affect urge when cues were not presented’ (p. 611).
7. Affective processing model of negative reinforcement Baker et al. (2004)	Craving occurs to escape from the negative effect of withdrawal symptoms. This effect is increased by additional stressors.	‘Some addicts relapse long after withdrawal symptoms should have ceased’ (p. 611). ‘The relief of aversive withdrawal symptoms cannot be an important determinant of addiction because some drugs (e.g., tobacco, cocaine, and buprenorphine) are highly addictive without producing highly unpleasant syndromes’ (p. 611).
8. Cognitive processing model Tiffany (1999)	Alcohol use is an automated conditioned process for an alcoholic who is not trying to quit. Only when the process is blocked by a situation (for example, when a bar is closed) is a non-automatic process activated which then causes craving. The process can also be blocked by a person’s attempt to abstain from alcohol.	No criticisms reported.
Psychobiological models
9. Three-pathway psychobiological model Verheul et al. (1999)	Three types of craving come from three causes, which all have their individual neurobiological process: need for reward (dopamine/opioidergic dysregulation), need for relief (GABAergic/glutamatergic dysregulation), and lack of control (serotonergic dysregulation).	‘Verheul et al. equate craving with the intention to consume, they do not attempt to explain how craving occurs without consumption (a frequent occurrence in treatment units) or, for that matter, how consumption occurs without craving’ (p. 614).
10. Incentive sensitization Robinson and Berridge (1993)	A psychological process termed 'incentive salience' occurs, which is the increase in the perceived value of the substance, making the substance more attractive and the craving stronger.	No criticisms reported.
11. Theory of neural opponent motivation Koob and Le Moal (1997)	A combination of the (1) Incentive sensitization model, (2) Opponent-process model and (3) Affective processing model of negative reinforcement, this theory integrates the processes of sensitization, counter adaption and the predominance of the influence of negative affect.	No criticisms reported.
12. Temporal-difference reinforcement learning model Redish (2004)	Actions are selected that maximize future reward and a person learns the reward value of each action. Drugs influence this learning process causing a person to choose actions leading to rewards of drug-use over non-drug-use.	‘The model explains how an addict over-selects actions that lead to probable use, but it is yet to be empirically proven’ (p. 613).
13. Unified framework for addiction Redish et al. (2008)	Craving is caused by a change in the allostasis and an overvaluation of the outcome and the reward of drug use.	‘Several peer commentators have pointed out a major omission which is the absence of affective processes as a vulnerability’ (p. 614). ‘The overvaluation of the habit system (vulnerability 7), (…) which has not been empirically proven’ (p. 614).
14. Neuroanatomical model Anton and Carolina (1999)	Chronic alcohol exposure leads to sensitization, which can contribute to a subjective feeling of discomfort and craving during abstinence. Stress can enhance this process and trigger reward memory.	No criticisms reported.
15. Model of interoceptive dysregulation Paulus et al. (2009)	Drug-use itself is a repeated perturbation of the current body state, which becomes associated with conditioned stimuli that contribute to the sensitization of the body prediction error. Craving comes from the motivation to use drugs and interoceptive body sensations.	No criticisms reported.
Motivational models
16. Motivational model of alcohol use Cox and Klinger (1988)	Drinking is fundamentally a choice. Persons choosing to drink are motivated by their expectations that their current affect state will improve.	‘The model accounts less well for the irrational aspects of craving in the alcohol dependent’ (p. 618).
17. Multidimensional ambivalence model Breiner et al. (1999)	Approach (craving) and avoidance are two pathways in the brain that respond independently to various moderators.	No criticisms reported.
18. Prime theory West and Hardy (2006)	There are two moderators of craving, namely impulses and motives.	‘What remains to be accomplished is the validation of hypotheses generated by this model’ (p. 620).

Figure 1. Schematic representation of the extraction of decision criteria. M represents the number of models included or excluded at each step of the procedure.

Figure 2. Flowchart of the literature search strategy. N represents the number of articles included of excluded at each step of the procedure.

Table 2. Results from snowballing and keyword extraction literature search strategy to identifying craving models. The first column shows the model with its founding publication. The second column shows the number of articles found with snowballing, and the third column shows the number of articles remaining after applying inclusion and exclusion criteria. The overview of key terms, the number of articles found on their basis, and the final number of relevant articles found are presented in the fourth column.

Models (founding publication)	Step 1. Number of articles found after snowballing the founding publication	Step 2. Number of articles after applying inclusion and exclusion criteria^a	Step 3 & 4. Key word extraction^b (Number articles found | Number articles relevant)
Cognitive models
5. Outcome expectancy model* Marlatt (1985)	111	44
6. Dual-affect model* Baker et al. (1986)	74	13
7. Affective processing model of negative reinforcement Baker et al. (2004)	615	125	Negative affect (37|17)
8. Cognitive processing model Tiffany (1999)	1054	290	Attentional bias (34|20) Working memory (15|8)
Psychobiological models
9. Three-pathway psychobiological model Verheul et al. (1999)	220	105	Reward (17|6) Withdrawal (9|4)
10. Incentive sensitization Robinson and Berridge (1993)	3890	331	Attentional bias (55|20)
11. Theory of neural opponent motivation Koob and Le Moal (1997)	1393	156	Stress (17|12)
12. Temporal-difference reinforcement learning model* Redish (2004)	216	15
13. Unified framework for addiction* Redish et al (2008)	169	23
14. Neuroanatomical model* Anton and Carolina (1999)	137	61
15. Model of interceptive dysregulation* Paulus et al. (2009)	40	6
Motivational models
16. Motivational model of alcohol use Cox and Klinger (1988)	512	333	Drinking motives (157|20)
17. Multidimensional ambivalence model* Breiner et al. (1999)	68	37
18. Prime theory* West and Hardy (2006)	290	19

^a The frequency tables were not included in the paper because of their length. These tables can be requested from the authors.

^b Only the articles that have key terms in their title or author keywords are included. Models excluded are marked with an asterisk (*).

Table 3. Effect of drinking motives on dependence or drinking.

Motive	Articles that found an effect on dependence or drinking
Enhancement	Lyvers et al. 2010; Doyle et al. 2011; Hasking et al. 2011; Drerup et al. 2011; Kristjansson et al. 2011, 2012°; Glavak Tkalić et al. 2013; Piasecki et al. 2014; Cadigan et al. 2015*.
Coping	Agrawal et al. 2008; Beseler et al. 2008; Lyvers et al. 2010; Doyle et al. 2011; Littlefield et al. 2011°; Mackie et al. 2011; Mezquita et al. 2011; Kristjansson et al. 2011, 2012°; Fitzgerald and Long 2012; Gilson et al. 2013; Glavak Tkalić et al. 2013; Piasecki et al. 2014*; Rodriguez et al. 2014; Cadigan et al. 2015; Levitt and Leonard 2015.
Social	Agrawal et al. 2008; Beseler et al. 2008; Lyvers et al. 2010; Drerup et al. 2011; Mackie et al. 2011; Kristjansson et al. 2011; Mezquita et al. 2011; Gilson et al. 2013; Cadigan et al. 2015.
Conformity	Agrawal et al. 2008; Kristjansson et al. 2011; Fitzgerald and Long 2012.

°These studies are all on the same dataset. *Effect on experiences outcomes.

Table 4. Results for each model on the decision criteria in order to determine the most suitable model.

Affective processing model of negative reinforcement (Baker et al. 2004)	Cognitive processing model (Tiffany 1999)	Three-pathway psychobiological Model (Verheul et al. 1999)	Incentive sensitization (Robinson & Berridge 1993)	Theory of neural opponent motivation (Koob & Le Moal 1997)	Motivational model of alcohol use (Cox & Klinger 1988)
1. The model should incorporate negative affect as a predictor of relapse.
Yes: The negative affect model acknowledges this as the most prominent predictor of the relapse process. Baker et al. (2004) see negative affect as a withdrawal signal, meaning that next to tremors or extensively sweating, a person in rehabilitation experiences fear, depression and other negative affect symptoms.	Unclear: The cognitive processing model does not specify negative affect as specific cue for relapse. Tiffany (1999) mentions that cues can come forward from a personals emotional state, possibly including negative affect.	Yes: The three-pathway model mentions both positive and negative affect as equally relevant predictors. This model is therefore either partly incorrect according to the review or partly irrelevant for a system where dependent drinkers are the target population.	No: The incentive sensitization model states that a person starts drinking for positive reasons, but because of repeated drug intake an incentive sensitization process is activated, leading to compulsive craving. Robinson and Berridge (1993) mention stress as a possible initiator of a relapse process.	Yes: The theory of neural opponent motivation has negative affect as important reason of relapse. Negative affect is seen as a withdrawal effect.	Yes: One important motivation in the motivational model is to avert negative situations. However, another equally important motivation is to enhance a positive situation.
2. The model should explain that dependent drinkers have a higher attentional bias towards alcohol cues than nondependent drinkers.
Yes: The negative affect model argues that if there is no immediate relief from distress, the individual is biased towards response options (alcohol use) that most effectively have alleviated negative affect in the past. Whether this bias is the same attentional bias found in the empirical studies from this review is debatable, however the model does not seem to pose a contradiction to the finding of attentional bias.	Yes: The cognitive processing and incentive sensitization model are often mentioned as explanations for the attentional bias effects in a Stroop task. The cognitive processing model accounts for attentional bias, but it remains unclear whether attentional bias gives foundation to the cognitive processing model.	Unclear: Verheul et al. (1999) give no explicit explanation for attentional bias. However, when assumed that attentional bias explains compulsive addiction, then the three-pathway model has support for the compulsive path of the model.	Yes: Attentional bias is explained in the model. However, it is unclear whether attentional bias gives foundation to the incentive sensitization model.	Unclear: Koob and Le Moal (1997) indicate that the process of wanting (as they call craving) is compulsive, but whether this causes attentional bias is unclear.	Unclear: Cox and Klinger (1988) give no explicit explanation for attentional bias.
3. The model should incorporate stress as an increased risk of relapse.
Yes: Stress is an important predictor of negative affect according to the affective processing model of negative affect.	Unclear: Stress could be a cue for the relapse process coming from a person’s emotional network. However this is not specified.	Yes: Stress is the initiator of the second pathway called need for relief, leading to a motive for drinking.	Yes: Robinson and Berridge (1993) claim that stress activates a similar process as alcohol priming, increasing the chance on relapse.	Yes: Stress is a trigger of relapse.	Unclear: Stress is not explicitly mentioned.
4. The model explains why some people experience craving and relapse even after long periods of abstaining.
Partly: This is the major argument against this model according to Skinner and Aubin (2010) because it is entirely built around the idea of withdrawal affect. Baker et al. (2004) claim that withdrawal symptoms are more prolonged than once thought.	Yes: The cognitive processing model explains that feelings of craving after long abstinence can be caused by a configuration of cues that can trigger a person back into automatic consumption. This only happens on some very specific and rare occasions.	No: Verheul et al. (1999) do not explain this.	Yes: Robinson and Berridge (1993) claim that the brain of an addicted individual is permanently altered, making them always vulnerable.	Yes: The brain of an addicted individual is permanently altered, making them always vulnerable.	Unclear: Cox and Klinger (1988) do not explicite explain why people relapse after long periods of time. Maybe relapse is due to the change in the individual’s current situation expectations of what drinking might change in the situation.
5. The irrational/compulsive side of craving is explained by the model.
Yes: The irrational side of addiction is explained by the growth of negative affect causing a transition from cold to hot cognition. This idea infers that people with a higher negative affect level tend to be more emotionally (and not rationally) driven. Such individuals focus on the short-term relief of their distress and not on the long term effects on family, job, etc.	Unclear: Tiffany (1990) claims that the process of drinking is automatized, and might therefore be claimed to be compulsive. However, when somebody is abstaining this person forms a blockage in this automatized process, which leads the craving. It is not explained why people choose to drink compulsively above everything else.	Yes: The three-pathway psychobiological model has a compulsive pathway as one of its three pathways.	Yes: Sensitization is the process of giving a higher incentive to alcohol every time alcohol is consumed. This concepts infers that alcohol is perceived to have a high reward over a period of time, which explains the irrational/compulsive side of craving.	Yes: The irrational side is explained by sensitization and counter adaptation.	No: The motivational model claims that drinking is always a motivated choice and, as such, ignores the irrational side of craving. This is generally seen as an unacceptable deficiency of this model.
6. The model should explain how craving can occur without consumption or how consumption occurs without craving.
Yes: Baker et al. (2004) claim that negative affect is highly determinant of relapse. However, this process may occur without craving.	Yes: The cognitive processing model assumes that addicts drink automatically, without experiencing craving. Only when this automatic process is blocked, does craving occur (which would not always lead to consuming).	No: Craving is assumed to cause relapse. This is the critique of this model.	No: Craving (wanting) is assumed to cause relapse.	No: Craving (wanting) is assumed to cause relapse.	Yes: Choice is always a mediating variable, meaning that a person always makes a rational choice whether or not to drink. This idea implies that craving triggers a rational decision process, not always leading to relapse.

Table 5. Parameter selection from the different models in the theoretical frameworks defined.

Affective processing model of negative reinforcement (Baker et al. 2004)	Cognitive processing model (Tiffany 1999)	Incentive sensitization (Robinson & Berridge 1993)	Theory of neural opponent motivation (Koob & Le Moal 1997)
1. The parameters describe the continuous and cyclical process of craving and relapse in an enduring addiction, rather than the process of developing an addiction.
Yes: The negative affect model is predominantly about the process of relapse.	Yes: The cognitive processing model merely describes the process of being addicted.	Both: The main focus of the model is about becoming addicted and not about the process of relapse. However, it also gives some triggers for the relapse process.	Both: The theory of neural opponent motivation describes both the processes of becoming and being addicted.
2. The parameters are episodic states that fluctuate over time.
Yes: Baker et al. (2004) state that negative affect grows over time, leading to an increase of craving.	Yes: The cognitive processing model assumes that cues are triggers for the automated drinking process. These triggers are not always present and, therefore, differ over time.	Yes: The incentive sensitization model assumes that alcohol receives a higher incentive by drinking. This incentive value grows over time.	Yes: According to Koob and Le Moal (1997) a first self-regulation failure leads to emotional distress and negative affect which causes relapse.
3. The parameters can be operationalized in a natural environment.
Yes: The negative affect model suggests negative affect, stress and as parameters.	Unclear: The cognitive processing model describes that multiple processes can be automatized and therefore 'trigger' drinking behavior. However, Tiffany (1999) is not specific about what these are. Arguably, these may differ between subjects. However, this also complicates translation into generic monitoring parameters.	Yes: According to the incentive sensitization model triggers are can be operationalized into stress and priming by alcohol or other drugs.	Yes: The model can be operationalized into stress and negative affect.

Skinner MD, Aubin HJ. 2010. Craving’s place in addiction theory: contributions of the major models. Neurosci Biobehav Rev. 34:606–623.

 PubMed Web of Science ®Google Scholar

Wikler A. 1948. Recent progress in research on the neurophysiologic basis of morphine addiction. Am J Psychiatry. 105:329–338.

 PubMed Web of Science ®Google Scholar

Siegel S. 1983. Classical conditioning, drug tolerance, and drug dependence. In: Research advances in alcohol and drug problems. New York: Springer; p. 207–246.

 Google Scholar

Solomon RL, Corbit JD. 1974. An opponent-process theory of motivation. I. Temporal dynamics of affect. Psychol Rev. 81:119–145.

 PubMed Web of Science ®Google Scholar

Stewart J, de Wit H, Eikelboom R, Wit H, De, Eikelboom R. 1984. Role of unconditioned and conditioned drug effects in the self-administration of opiates and stimulants. Psychol Rev. 91:251–268.

 PubMed Web of Science ®Google Scholar

Marlatt G. 1985. Cognitive factors in the relapse process. In. Marlatt J, Gordon G, editors. Relapse prevention: maintenance strategies in the treatment of addictive behaviors. New York: Guilford Press; p. 128–200.

 Google Scholar

Baker TB, Morse E, Sherman JE. 1986. The motivation to use drugs: a psychobiological analysis of urges. Nebr Symp Motiv. 34:257–323.

 PubMed Web of Science ®Google Scholar

Baker TB, Piper ME, McCarthy DE, Majeskie MR, Fiore MC. 2004. Addiction motivation reformulated: an affective processing model of negative reinforcement. Psychol Rev. 111:33–51.

 PubMed Web of Science ®Google Scholar

Tiffany ST. 1999. Cognitive concepts of craving. Alcohol Res Health. 23:215–224.

 PubMedGoogle Scholar

Verheul R, van den Brink W, Geerlings P. 1999. A three-pathway psychobiological model of craving for alcohol. Alcohol Alcohol. 34:197–222.

 PubMed Web of Science ®Google Scholar

Robinson TE, Berridge KC. 1993. The neural basis of drug craving: an incentive-sensitization theory of addiction. Brain Res Rev. 18:247–291.

 PubMed Web of Science ®Google Scholar

Koob GF, Le Moal M. 1997. Drug abuse: hedonic homeostatic dysregulation. Science. 278:52–58.

 PubMed Web of Science ®Google Scholar

Redish a. D. 2004. Addiction as a computational process gone awry. Science. 306:1944–1947.

 PubMed Web of Science ®Google Scholar

Redish AD, Jensen S, Johnson A. 2008. A unified framework for addiction: vulnerabilities in the decision process. Behav Brain Sci. 31:415–437.

 PubMed Web of Science ®Google Scholar

Anton RF, Carolina S. 1999. What is craving? Models and implications for treatment. Alcohol Res Health. 23:165–173.

 PubMedGoogle Scholar

Paulus MP, Tapert SF, Schulteis G. 2009. The role of interoception and alliesthesia in addiction. Pharmacol Biochem Behav. 94:1–7.

 PubMed Web of Science ®Google Scholar

Cox WM, Klinger E. 1988. A motivational model of alcohol use. J Abnorm Psychol. 97:168–180.

 PubMed Web of Science ®Google Scholar

Breiner MJ, Stritzke WGK, Lang AR. 1999. Approaching avoidance. A step essential to the understanding of cravingAlcohol Res Health. 23:197–206.

 PubMedGoogle Scholar

West R, Hardy A. 2006. Theory of addiction. Alcohol and alcoholism. Vol. 42 [Internet]. Oxford (UK): Blackwell Publishing. Available from: https://doi.org/10.1093/alcalc/agl107

 Google Scholar

Lyvers M, Hasking P, Hani R, Rhodes M, Trew E. 2010. Drinking motives, drinking restraint and drinking behaviour among young adults. Addict Behav. 35:116–122.

 PubMed Web of Science ®Google Scholar

Doyle SR, Donovan DM, Simpson TL. 2011. Validation of a nine-dimensional measure of drinking motives for use in clinical applications: the desired effects of drinking scale. Addict Behav. 36:1052–1060.

 PubMed Web of Science ®Google Scholar

Hasking P, Lyvers M, Carlopio C. 2011. The relationship between coping strategies, alcohol expectancies, drinking motives and drinking behaviour. Addict Behav. 36:479–487.

 PubMed Web of Science ®Google Scholar

Drerup ML, Johnson TJ, Bindl S. 2011. Mediators of the relationship between religiousness/spirituality and alcohol problems in an adult community sample. Addict Behav. 36:1317–1320.

 PubMed Web of Science ®Google Scholar

Kristjansson SD, Agrawal A, Littlefield AK, Pergadia ML, Lessov-Schlaggar CN, Sartor CE, Bucholz KK, Madden PA, Cooper ML, Sher KJ, Heath AC. 2011. Drinking motives in female smokers: factor structure, alcohol dependence, and genetic influences. Alcohol Clin Exp Res. 35:345–354.

 PubMed Web of Science ®Google Scholar

Kristjansson SD, Agrawal A, Lessov-Schlaggar CN, Madden PAF, Cooper ML, Bucholz KK, Sher KJ, Lynskey MT, Heath AC. 2012. The relationship between rs3779084 in the dopa decarboxylase (DDC) gene and alcohol consumption is mediated by drinking motives in regular smokers. Alcohol Clin Exp Res. 36:162–170.

 PubMed Web of Science ®Google Scholar

Glavak Tkalić R, Sučić I, Dević I. 2013. Motivation for substance use: why do people use alcohol, tobacco and marijuana? Drustvena Istrazivanja/ J Gen Social Iss. 22:601–625.

 Web of Science ®Google Scholar

Piasecki TM, Cooper ML, Wood PK, Sher KJ, Shiffman S, Heath AC. 2014. Dispositional drinking motives: associations with appraised alcohol effects and alcohol consumption in an ecological momentary assessment investigation. Psychol Assess. 26:363–369.

 PubMed Web of Science ®Google Scholar

Cadigan JM, Martens MP, Herman KC. 2015. A latent profile analysis of drinking motives among heavy drinking college students. Addict Behav. 51:100–105.

 PubMed Web of Science ®Google Scholar

Agrawal A, Dick DM, Bucholz KK, Madden PAF, Cooper ML, Sher KJ, Heath AC. 2008. Drinking expectancies and motives: a genetic study of young adult women. Addiction (Abingdon, Engl). 103:194–204.

 PubMed Web of Science ®Google Scholar

Beseler CL, Aharonovich E, Keyes KM, Hasin DS. 2008. Adult transition from at-risk drinking to alcohol dependence: the relationship of family history and drinking motives. Alcohol Clin Exp Res. 32:607–616.

 PubMed Web of Science ®Google Scholar

Littlefield AK, Agrawal A, Ellingson JM, Kristjansson S, Madden PAF, Bucholz KK, Slutske WS, Heath AC, Sher KJ. 2011. Does variance in drinking motives explain the genetic overlap between personality and alcohol use disorder symptoms? A twin study of young women. Alcohol Clin Exp Res. 35:2242–2250.

 PubMed Web of Science ®Google Scholar

Mackie CJ, Conrod PJ, Rijsdijk F, Eley TC. 2011. A systematic evaluation and validation of subtypes of adolescent alcohol use motives: genetic and environmental contributions. Alcohol Clin Exp Res. 35:420–430.

 PubMed Web of Science ®Google Scholar

Mezquita L, Stewart SH, Ibáñez MI, Ruipérez MA, Villa H, Moya J, Ortet G. 2011. Drinking motives in clinical and general populations. Eur Addict Res. 17:250–261.

 PubMed Web of Science ®Google Scholar

Fitzgerald K-A, Long CG. 2012. The influence of drinking motives and anxiety on low-, moderate- and high-risk drinkers. J Subst Use. 17:240–248.

 Web of Science ®Google Scholar

Gilson K-M, Bryant C, Bei B, Komiti A, Jackson H, Judd F. 2013. Validation of the Drinking Motives Questionnaire (DMQ) in older adults. Addict Behav. 38:2196–2202.

 PubMed Web of Science ®Google Scholar

Rodriguez LM, Knee CR, Neighbors C. 2014. Relationships can drive some to drink: relationship-contingent self-esteem and drinking problems. J Social Personal. 31:270–290.

 Web of Science ®Google Scholar

Levitt A, Leonard KE. 2015. Insecure attachment styles, relationship-drinking contexts, and marital alcohol problems: testing the mediating role of relationship-specific drinking-to-cope motives. Psychol Addict Behav. 29:696–705.

 PubMed Web of Science ®Google Scholar

Tiffany ST. 1990. A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychol Rev. 97:147–168.

 PubMed Web of Science ®Google Scholar