Webb Therapy Uncategorized Addiction – What You Need To Know

Addiction – What You Need To Know

Addiction fundamentally alters the brain’s reward and decision-making systems through well-documented neurobiological mechanisms. When substances like drugs (including alcohol and nicotine) are consumed, they trigger massive releases of dopamine in the brain’s reward circuit, particularly in areas like the nucleus accumbens and ventral tegmental area. With repeated exposure, the brain adapts by reducing natural dopamine production and decreasing the number of dopamine receptors, creating tolerance and requiring increasingly larger amounts of the substance to achieve the same effect. This neuroadaptation hijacks the brain’s natural reward system, making everyday activities less rewarding while the addictive substance becomes disproportionately important.

Over time, addiction also impairs the prefrontal cortex, the brain region responsible for executive functions like decision-making, impulse control, and weighing long-term consequences. This creates a neurological double-bind: the midbrain structures driving craving and drug-seeking behaviour become hyperactive, while the prefrontal systems that would normally regulate these impulses become weakened. Chronic substance use also disrupts stress response systems, making individuals more vulnerable to relapse during difficult periods. These changes help explain why addiction is recognised as a chronic brain disease rather than simply a matter of willpower – the neuroplastic changes can persist long after substance use stops, though the brain does have remarkable capacity for recovery with sustained abstinence and appropriate treatment.

The Challenge of Stopping

The challenge of stopping stems from the profound neurobiological changes addiction creates in the brain’s fundamental survival systems. The brain essentially learns to treat the addictive substance as necessary for survival, similar to food or water. When someone tries to quit, they face intense physical withdrawal symptoms as their neurochemistry struggles to return to homeostasis, combined with psychological cravings that can persist for months or years. The damaged prefrontal cortex makes it extremely difficult to override these powerful urges with rational decision-making, while stress, environmental cues, and emotional states can trigger automatic drug-seeking responses that feel almost involuntary. This creates a cycle where attempts to quit often lead to temporary success followed by relapse, which many interpret as personal failure rather than recognising it as part of the neurological reality of the condition.

Addiction appears progressive because tolerance drives escalating use over time, while the brain’s reward system becomes increasingly dysregulated. What begins as recreational use gradually shifts to compulsive use as natural dopamine production diminishes and neural pathways become more deeply entrenched. The condition typically follows a predictable pattern: initial experimentation leads to regular use, then to use despite negative consequences, and finally to compulsive use where the person continues despite severe impairment in major life areas. Additionally, chronic substance use often damages the brain regions responsible for insight and self-awareness, making it harder for individuals to recognise the severity of their condition. The progressive nature is also influenced by external factors – as addiction advances, people often lose social supports, employment, and housing, creating additional stressors that fuel continued use and make recovery more challenging.

Understanding addiction when you’re not “addicted” to alcohol or other drugs

The difficulty in understanding addiction, even among people with their own compulsive behaviors, stems from several key differences in how these conditions manifest and are perceived. While behaviors like sugar consumption, social media use, or shopping can indeed activate similar dopamine pathways, they typically don’t create the same level of neurobiological hijacking that occurs with substances like alcohol, opioids, or stimulants. Addictive drugs often produce dopamine surges 2-10 times greater than natural rewards, creating more profound and lasting changes to brain structure and function. Additionally, many behavioral compulsions allow people to maintain relatively normal functioning in major life areas, whereas substance addiction typically leads to progressive deterioration across multiple domains – relationships, work, health, and legal standing.

The social and cognitive factors also create barriers to understanding. Most people can relate to losing control occasionally – eating too much dessert or spending too much time scrolling their phone – but these experiences usually involve temporary lapses that can be corrected relatively easily through willpower or environmental changes. This creates a false sense of equivalency where people think “I can stop eating cookies when I want to, so why can’t they just stop drinking?” They don’t grasp that addiction involves a qualitatively different level of brain change where the substance has become neurobiologically essential, not just psychologically preferred. There’s also often a moral lens applied to addiction that doesn’t exist for other compulsive behaviours – society tends to view overconsumption of legal, socially acceptable things as personal quirks or minor character flaws, while addiction to illegal substances or excessive alcohol use carries heavy stigma and assumptions about moral failing, making it harder to see as a medical condition requiring treatment rather than simply better self-control.

A Word On Nicotine (Tobacco Products)

Yes, nicotine absolutely does release large amounts of dopamine, making it highly addictive despite being legal and socially accepted in many contexts. Nicotine causes an increase in dopamine levels in the brain’s reward pathways, creating feelings of satisfaction and pleasure.Research shows that nicotine, like opioids and cocaine, can cause dopamine to flood the reward pathway up to 10 times more than natural rewards.

This helps explain why nicotine addiction can be so powerful and difficult to overcome, even though people often view smoking or vaping as less serious than other forms of substance addiction. Repeated activation of dopamine neurons in the ventral tegmental area by nicotine leads not only to reinforcement but also to craving and lack of self-control over intake. The addiction develops through the same basic mechanisms as other substances – as people continue to smoke, the number of nicotine receptors in the brain increases, requiring more of the substance to achieve the same dopamine response.

What makes nicotine particularly insidious is its legal status and social acceptance, which can make people underestimate its addictive potential. The rapid delivery of nicotine to the brain (within 10-20 seconds when smoked) creates an almost immediate reward that strongly reinforces the behaviour. This is why many people who successfully quit other substances still struggle with nicotine, and why nicotine addiction often serves as a gateway that primes the brain’s reward system for addiction to other substances.

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Why We Choose Now Over Later: Instant vs Delayed Gratification and CostWhy We Choose Now Over Later: Instant vs Delayed Gratification and Cost

We all know the feeling of eating the last Tim Tam even though we said we’d stop, or putting off the gym even though we know we’ll feel better after. There’s a simple psychological framework behind this tug-of-war, and it’s more nuanced than “willpower” or “laziness.”

Four combinations, not two

Most people think of this as one axis — instant vs delayed — but really there are two separate questions: when something happens, and whether it’s a reward or a cost. That gives four combinations:

  • Instant gratification: reward now (a cigarette, a scroll through social media, a splurge on payday)
  • Delayed cost: the price paid later (lung damage, lost hours, an empty bank account)
  • Instant cost: effort or discomfort now (a hard training session, saying no to dessert)
  • Delayed gratification: the pay-off later (fitness, health, savings)

These naturally pair up in everyday life — instant gratification tends to travel with a delayed cost (gluttony, addiction, procrastination), and instant cost tends to travel with delayed gratification (discipline, exercise, saving). But they’re not the same thing by definition; they’re just common bundles. Sometimes you get gratification with barely any real cost (an afternoon nap), or cost with barely any real reward (over-saving to the point of never enjoying your money).

Why the future feels so much less real

The underlying mechanism is called temporal discounting — our tendency to value a reward less the further away it sits. Offer someone $50 today or $100 in a year, and plenty will take the $50. The future reward gets “discounted” in the mind, even though it’s objectively worth more. This isn’t a flaw exclusive to people struggling with addiction or avoidance — everyone discounts the future to some degree. What differs from person to person is how steeply.

A more specific quirk sitting inside this is present bias — an extra, disproportionate pull toward anything happening right now, over and above normal discounting. The classic sign of it is a preference reversal: someone might happily choose $100 in 31 days over $50 in 30 days when both options are off in the future. But offer them $50 today versus $100 tomorrow, and many flip to taking the smaller amount immediately. Nothing about the maths changed — only whether “now” was on the table. This is the same mechanism behind grand plans made the night before that evaporate the next morning: the plan looked easy when “now” was still hypothetical.

Why does this happen? Economists originally assumed we discount the future smoothly and consistently — a steady, predictable decline in value the further out a reward sits. Real behaviour doesn’t work that way. Instead, people follow what’s called a hyperbolic discounting curve — value declines really fast for anything in the near future (i.e., pushing a reward from today to next week costs it a lot of its appeal) then flattens out for anything further away. But pushing a reward from five years away to six years away barely changes how appealing it feels at all. The decline is steep early and flat later. That steep early drop is what makes “right now” so magnetic, and the flat tail is why consequences six months away can feel almost as unreal as consequences five years away, even though they’re nothing alike in real terms.

Where this shows up in society

This isn’t just an economics quirk — it explains a lot of everyday human struggle:

  • Addiction runs almost entirely on this pattern: an intensely immediate reward (a drink, a hit, a bet) paired with a cost that’s not just delayed but sitting on that flat, barely-felt part of the curve.
  • Avoidance behaviours (procrastination, dodging a hard conversation, skipping medical checkups) work in reverse — the relief of avoiding discomfort is instant, while the cost of avoidance quietly compounds somewhere out on the flat tail.
  • Overeating or “gluttony” fits the same shape — the pleasure of eating is immediate and vivid; weight gain or health decline is real but distant and abstract, so it barely registers in the moment of choosing.
  • Under-saving and impulse spending are the financial version — a purchase feels good today; retirement or a rainy-day fund is decades away and easy to discount to near zero.

Why this matters practically

The useful reframe here is that struggling with this isn’t a personal failing or a lack of insight — it’s the human valuation system doing exactly what it evolved to do, just more steeply in some people than others. That points toward practical fixes that work with the curve rather than fighting it: shrinking the delay before a good choice pays off (visible progress, milestone rewards), making the cost of a bad choice show up sooner rather than later (a streak, a check-in, immediate feedback), or removing the in-the-moment choice altogether through precommitment (automatic savings transfers, not keeping temptation in the house). Trying to simply convince someone to “care more” about the distant future tends not to work, because the problem was never a lack of caring — it’s that the future is quietly, structurally, worth less to the mind than the present.

Comparison table of four relationship dependency types: Dependence, codependence, independence, and interdependence, across seven psychological characteristicsComparison table of four relationship dependency types: Dependence, codependence, independence, and interdependence, across seven psychological characteristics

CharacteristicDependenceCodependenceIndependenceInterdependence
Overall patternUnbalanced — reliantDysfunctional — enmeshedDisconnected — isolatedHealthy — mutually supportive
RespectExcessive deference to the other; own views and preferences are regularly abandoned to avoid conflict or disapprovalRespect is extended to the other at the direct expense of self-respect; personal autonomy and needs are consistently sacrificedSelf-respect is strong, but regard for others’ needs, feelings, or boundaries may be limited — a “my way” orientationGenuine, mutual recognition of each person’s worth, needs, and autonomy; respect flows in both directions without self-erasure
ReciprocityOne-sided reliance — one person leans heavily; the other is often left carrying the emotional or practical loadChronic one-sidedness: the codependent person gives and enables, while the other takes; sustained by the giver’s need to be neededLittle appetite for mutual exchange; interaction tends to be transactional or self-focused rather than genuinely reciprocalBalanced give-and-take that flexes with circumstances; neither person keeps a tally, but both feel the exchange is broadly fair
AutonomyLittle or no independent decision-making; the dependent person habitually outsources choices, often due to anxiety or low self-efficacyAutonomy is outsourced — the codependent’s sense of self is defined by, and contingent on, the other person’s state, needs, and approvalStrong individual autonomy, but exercised in ways that exclude or override others; autonomy as self-sufficiency rather than self-directionEach person retains a secure, stable sense of self while choosing to share their life; autonomy and closeness are seen as compatible, not competing
BoundariesWeak or absent; the dependent person struggles to assert needs or limits, often fearing rejection or abandonment if they doBlurred or non-existent; emotional enmeshment is central — one person feels responsible for the other’s inner world and vice versaRigid and inflexible; protective walls rather than healthy limits, often rooted in avoidant attachment or past relational hurtClear, flexible, and openly negotiated; allow genuine intimacy and breathing room to coexist; adjusted as the relationship evolves
CommunicationMarked by fear of expressing needs, disagreement, or vulnerability; communication is often indirect, placating, or suppressedFrequently indirect, enabling, or controlling; may include people-pleasing, hinting, or managing the other person’s emotional state rather than direct dialogueReluctant to disclose personal matters or emotional needs; communication tends to be functional, guarded, or focused on problem-solving rather than connectionOpen, honest, and emotionally safe; needs, feelings, and disagreements are expressed directly and received without fear of destabilising the relationship
ResponsibilityPersonal responsibility is ceded; the dependent person relies on the other to manage decisions, emotions, or practical life tasksThe codependent assumes responsibility for the other’s emotions, wellbeing, and behaviour — often enabling harm in the process; both people’s growth is stuntedResponsibility is taken for oneself but rarely sought or accepted collaboratively; help-seeking is resisted even when it would be adaptiveResponsibility is appropriately owned and shared; each person takes accountability for their own actions while supporting, but not managing, the other
Self-esteemFragile and externally anchored; feelings of worth are contingent on the other person’s approval, presence, or positive regardChronically low and outsourced; the codependent’s self-worth is tied to their caretaking role — they feel valuable only when they are needed or usefulCan appear high, but is often defended rather than genuine; may be maintained through achievement, self-sufficiency, or emotional distancing rather than authentic self-acceptanceStable and internally grounded; does not depend on the partner’s approval or on performing a particular role; resilient to relational stress
SupportConstant and disproportionate support is sought; the dependent person struggles to self-soothe or function without frequent reassurance from the otherOne party is chronically over-reliant on the other for emotional regulation; the codependent may also subtly require the other to remain dependent in order to feel neededSupport is rarely sought, even when genuinely needed; self-reliance is prioritised to the point of isolation, and vulnerability is experienced as threateningSupport is both offered and sought fluidly and appropriately; neither person feels burdened by the other’s needs, and both feel safe to ask for help

Sources: APA Dictionary of Psychology (2023); Mental Health America; Rusbult & Van Lange, Annual Review of Psychology (2003); research on attachment theory, interdependence theory, and the “dependency paradox” (Feeney & Van Vleet). The goal state in healthy adult relationships is interdependence — not independence.

Addiction TheoriesAddiction Theories

There have been various theories and models proposed over time to help us understand why individuals use alcohol and other drugs, and why some people become dependent or ‘addicted’ but not others. The following are several models or theories of addiction. They reflect the political, medical, spiritual, and social forces of those times in history.

The Moral Model

Alcohol and tobacco was introduced in the Western countries during the 1500’s. The widespread use and misuse of chemical substances resulted in a range of social problems and it was thought by some that substance use was “problematic” and “morally wrong” (Lassiter & Spivey, 2018). The moral model viewed AOD dependency as a moral and personal weakness that involved a lack of self-control, and was often viewed as a potential danger to society (Stevens & Smith, 2014).

The moral model considered addiction a “sin” and a result of free, yet irresponsible, choice. Therefore, many politically conservative groups, religious groups, and legal systems tended to punish the individual who uses AOD. The moral model or attitude towards addiction can still be seen today in certain cultures. Those who still believe addiction is morally “wrong” tend to perceive the most appropriate way to treat the individuals who use AOD are through legal sanctions, such as imprisonment and fines. For example, in many countries, drivers who are caught under the influence of alcohol or other drugs are not considered for treatment programs but instead receive court sentences as punishments (Fisher & Harrison, 2017).

This model has been rejected by alcohol and other drugs professionals as unscientific and contributes to the stigma surrounding addiction and substance use (White, 1991, cited in Fisher & Harrison, 2017).

The Disease Model

This model takes up the medical viewpoint and proposes addiction as a disease or illness that an individual has. It proposed that addiction is a disease that is progressive and chronic whereby the individual holds no control as long as the substance use continues. In other words, their addiction will continue to deteriorate with the continuous AOD (Thombs & Osborn, 2019). It also proposes that individuals who uses AOD can never be cured from addiction, though it can be readily treated through sustained abstinence such as self-help fellowships and treatment community. 

In the 1940s, Jellinek proposed a disease model in relation to alcoholism, arguing that it is a disease caused by a physiological deficit in an individual, making the person permanently unable to tolerate the effects of alcohol (Stevens & Smith, 2014). Jellinek identified signs and symptoms and clustered them into stages of alcoholism, as well as progression of the disease, which form the basis of 12-step or Anon-type programs (e.g., Alcoholics Anonymous and Narcotics Anonymous; Stevens & Smith, 2014). 

Under the disease model, treatment requires complete abstinence. Once an individual has accepted the reality of their addiction and ceased substance use, they are labelled as being in recovery, but are never ‘cured’ (e.g., “Once an alcoholic, always an alcoholic”; Thombs & Osborn, 2019). Whilst originally applied to alcohol dependency, it has now been generalised to other substances and many traditional substance use treatment models are based on this model (Capuzzi & Stauffer, 2020; Stevens & Smith, 2014).

The disease model offered an alternative to the moral theory, helping to remove the moral stigma attached to addiction and replacing it with an emphasis on treatment of an illness (Capuzzi & Stauffer, 2020). Disease theory helped to explain how some people experience the physiological effects of addiction such as dependence, tolerance, and withdrawal more than others, and how these mechanisms are caused by a biochemical abnormality in an individual which increases their likelihood of developing a dependency (DiClemente, 2018). 

While the disease model was well received by a range of professionals, many criticised it because research did not find that the progressive, irreversible progression of addiction through stages always occurs as predicted (Capuzzi & Stauffer, 2020). Additionally, many in the AOD field argued that the model did not address the complex interrelated factors that accompany dependency (Stevens & Smith, 2014). Finally, some professionals argued that the concept of addiction being a disease may also convey the impression to some individuals that they are powerless over their dependency and/or not responsible for the consequences of destructive addictive behaviours, which can be counteractive to treatment (Capuzzi & Stauffer, 2020).

Genetic and Neurobiological Theories

These theories suggest that some people may be genetically predisposed to develop drug dependency. For example, individuals usually begin substance use on an experimental basis. They then continue using because there is some reinforcement for doing so (e.g., a reduction of pain, experience of euphoria, social recognition, and/or acceptance, etc.). Some people may continue to use substances in a controlled or recreational manner with limited consequences while others progress to non-medical use and eventually develop a dependency. Why? Genetic and neurobiological theories propose that this is the result of a genetic predisposition to drug dependency (Fisher & Harrison, 2017). 

Factors being considered by researchers in the genetic transmission of dependency on alcohol include neurobiological features such as an imbalance in the brain’s production of ‘feel good’ neurotransmitters or in the metabolism of ethanol, which is the key component of alcohol (Stevens & Smith, 2014). Other researchers explored genetic differences in temperament and personality traits which they argued may lead to certain individuals becoming more vulnerable in the face of challenging environmental circumstances, leading to AOD use (Stevens & Smith, 2014). Genetic predispositions such as these may explain why some individuals develop dependency on AOD while others in similar situations do not.

The Psycho-dynamic Model

This model proposes that substance use may be due to an unintentional response to some difficulties that an individual experienced in their childhood. This explanation is based on the theory that was put forward by Sigmund Freud, whereby the problems of whether we are able to cope with difficulties as adults are linked to our childhood experience. Many counselling approaches today are based on this theory which aim to seek understanding of people’s unconscious motivations and to enhance how they view themselves (Capuzzi & Stauffer, 2020).

The Psycho-dynamtic model also believes that AOD use is often secondary to a primary psychological issue. In other words, alcohol and other drugs is a symptom rather than a disorder, and AOD use is a means to temporarily relieve or numb emotional pain. For example, an individual suffering from depression might self-medicate with stimulants to relieve the enervating effects of depression or manage their anxiety by using benzodiazepines (Fisher & Harrison, 2017). 

There is evidence to support this model, whereby childhood traumatic events are associated with mental health problems and substance use disorders. Wu et al. (2010) conducted a study among 402 adults who were receiving substance use disorder treatments. They revealed that almost all (95%) of the participants experienced one or more childhood traumatic events, and 65.9% of them experienced emotional abuse and neglect from their childhood. The authors also reported that the higher the number of childhood traumatic events experienced, the higher the risk of substance use disorders and mental health problems such as post-traumatic stress disorder. 

Personality Traits

Some theorists suggest that certain individuals have certain personality traits that are linked to AOD dependency. For example, dependency on alcohol has been associated with traits such as developmental immaturity, impulsivity, high reactivity and emotionality, impatience, intolerance, and inability to express emotions (Capuzzi & Stauffer, 2020).

Social Learning Model

This model suggests that social learning processes such as observing other peoples behaviours (i.e., modelling) and cultural norms are important in the process of learning behaviours. Albert Bandura proposed Social Learning Theory which would argue that substance use is initiated by environmental stressors or modelling people around you with “perceived status”. For example, a child observes their parents use alcohol in social situations and the child is therefore more likely to perceive that AOD use for social situations is appropriate (Harrison & Fisher, 2017); the association between socialisation and alcohol has been established.

The social learning model also recognises the influence of cognitive processes such as coping, self-efficacy, and outcome expectancies. Some researchers are currently focusing on how an individuals expectation of the effects of drugs influence the pattern of AOD use and resulting dependency. Russell (1976, cited in Wise & Koob, 2013) suggested that dependency on substance is not only chemical (biological) but also behavioural and social in nature. 

It has also been suggested that substance use occurs when an individual thinks substance use is a coping mechanism. This can be learned from television and film, social medial, peer influence, or messages from caregivers during childhood. The individual hopes the AOD use will relieve from them from stress (Stevens & Smith, 2014). 

Socio-cultural Model

Different from the previous models, the socio-cultural model perceives substance use as an issue of society as a whole instead of focusing only on the individual. People tend to overestimate the influence of internal and psychological factors while underestimating the external and environmental factors, even among some alcohol and other drugs workers (Gladwell, 2000, cited in Lewis, Dana, & Blevins, 2015). Thus, this model highlights the importance of how society shapes substance use behaviours, such as cultural attitudes, peer pressures, family structures, economic factors, and more (Bobo & Husten, 2000). For example, Coffelt et al. (2006) found that parents’ alcohol use are associated with their children’s drinking behaviour, whereby when the adult’s alcohol problems increased, the likelihood of their adolescent child’s alcohol use increased. 

The Biopsychosocial Model

Substance use behaviour cannot be explained or understood scientifically or spiritually based on a single variable, antecedent, or “cause”. Biological, psychological, learning, social and cultural context all contributes to explaining why addiction develops and maintains. The interactions between these factors are presented in The Biopsychosocial Model – arguably the most commonly used model to explain addiction today. The model suggests that substance use and the progression of substance dependency can be explained by recognising that the body and mind are connected within a social and cultural context (Skewes & Gonzalez, 2013).

The model allows any combination of biological, psychological, social and cultural factors to contribute to AOD misuse and dependency, rather than a single dominating factor. This is much more holistic and integrative when attempting to understand the determinant of addiction (Stevens & Smith, 2014).

References:

  1. Bobo, J. K., & Husten, C. (2000). Sociocultural influences on smoking and drinking. Alcohol Research and Health, 24(4), 225-232. 
  2. Capuzzi, D., & Stauffer, M. D., Sharpe, C. W. (2020). History and etiological models of addiction. In D. Capuzzi, & M. D. Stauffer (Eds.), Foundations of addictions counseling (pp. 1-22). Pearson Education.
  3. Coffelt, N. L., Forehand, R., Olson, A. L., Jones, D. J., Gaffney, C. A., Zens, M. S. (2006). A longitudinal examination of the link between parent alcohol problems and youth drinking: The moderating roles of parent and child gender. Addictive Behaviours, 31, 4, 593-605. https://doi.org/10.1016/j.addbeh.2005.05.034 
  4. DiClemente, C. C. (2018). Addiction and change: How addictions develop and addicted people recover. The Guilford Press.
  5. Fisher, G. L., & Harrison, T. C. (2017). Substance abuse: Information for school counsellors, social workers, therapists, and counsellors. Pearson Education. 
  6. Lassiter, P. S., & Spivey, M. S. (2018). Historical perspectives and the moral model. In P. S. Lassiter, & J. R. Culbreth (Eds.), Theory and practice of addiction counselling. (pp. 27-46). Sage Publications. 
  7. Lewis, J. A., Dana, R. Q., & Blevins, G. A. (2015). Substance abuse counselling. Cengage Learning.
  8. Skewes, M. C., & Gonzalez, V. M. (2013). The biopsychosocial model of addiction. In P. M. Miller, A. W. Blume, D. J. Kavanagh, K. M. Kampman, M. E. Bates, M. E. Larimer, N. M. Petry, P. D. Witte, S. A. Ball (Eds.), Principles of addiction: Comprehensive addictive behaviours and disorders (pp. 61-70). Academic Press.
  9. Stevens, P., & Smith, R. L. (2014). Substance abuse counselling: Theory and practice. Pearson Education. 
  10. Teesson, M., Hall, W., Proudfoot, & Degenhardt, L. (2012). Addictions. Taylor & Francis Group.
  11. Thombs, D. L., & Osborn, C. J. (2019). Introduction to addictive behaviours. The Guilford Press. 
  12. Wise, R. A., & Koob, G. F. (2013). The development and maintainance of drug addiction. Neuropsychopharmacology, 39, 254-262.
  13. Wu, N. S., Schairer. L. C., Dellor, E., & Grella, C. (2010). Childhood trauma and health outcomes in adults with comorbid substance abuse and mental health disorders. Addictive Behaviors, 35(1). 68-71. https://doi.org/10.1016/j.addbeh.2009.09.003