Webb Therapy Uncategorized The stages of change model

The stages of change model

‘The stages of change model’ was developed by Prochaska and DiClemente. Heard of them? It informs the development of brief and ongoing intervention strategies by providing a framework for what interventions/strategies are useful for particular individuals. Practitioners need an understanding of which ‘stage of change’ a person is in so that the most appropriate strategy for the individual client is selected.

There are five common stages within the Stages of Change model and a 6th known as “relapse”:

1. In the precontemplation stage, the person is either unaware of a problem that needs to be addressed OR aware of it but unwilling to change the problematic behaviour [or a behaviour they want to change. It does not always have to be labelled as “problematic”].

2. This is followed by a contemplation stage, characterized by ambivalence regarding the problem behaviour and in which the advantages and disadvantages of the behaviour, and of changing it, are evaluated, leading in many cases to decision-making.

3. In the preparation stage, a resolution to change is made, accompanied by a commitment to a plan of action. It is not uncommon for an individual to return to the contemplation stage or stay in the preparation stage for a while, for many reasons.

4. This plan is executed in the action stage, in which the individual engages in activities designed to bring change about and in coping with difficulties that arise.

5. If successful action is sustained, the person moves to the maintenance stage, in which an effort is made to consolidate the changes that have been made. Once these changes have been integrated into the lifestyle, the individual exits from the stages of change.

6. Relapse, however, is common, and it may take several journeys around the cycle of change, known as “recycling”, before change becomes permanent i.e., a lifestyle change; a sustainable change.

(Adapted from Heather & Honekopp, 2017)

Related Post

What Alcohol does to the Human BodyWhat Alcohol does to the Human Body

1. Alcohol (ethanol) enters the body through the oral cavity (i.e., the mouth). The inner surface of the oral cavity is mucosal tissue to keep the cavity lubricated and it is capable of absorbing alcohol into the bloodstream. This absorption is considered “insignificant”.

2. Alcohol flows down the oesophagus to the stomach where 10-20% of ethanol will be absorbed into the bloodstream. Alcohol enters the bloodstream via the mucosal tissue of the stomach wall, and travels straight to the liver. Alcohol can take 5-10 minutes to reach the brain because of the ethanol absorbed via the stomach. If you drink alcohol on an empty stomach, the pyloric sphincter [gateway between the stomach and the small intestine] is going to be more open, and the alcohol is going to immediately enter the small intestine after reaching the stomach. If food is also present in the stomach, the sphincter will open and close at a rate that allows food to enter the small intestine gradually, therefore if alcohol is also in the stomach, it will gradually enter the small intestine.

3. Alcohol flows through the pyloric sphincter into the small intestines where most alcohol absorption occurs. Human intestines are attached the to the posterior abdominal wall by a fold of membrane called the mesentery. Alcohol is absorbed into the mesentery via veins and then travels to the liver.

4. One function of the liver is that it detoxifies toxic elements into non-toxic elements before passing it to the heart and then the rest of the body. The liver sustains considerable “abuse” from a variety of toxic elements and chemicals, and therefore it needs to be capable of full regeneration. NOTE: Many diseases and exposures can harm it beyond the point of repair. These include cancer, hepatitis, certain medication overdoses, and fatty liver disease.

In the liver, ethanol is met with an enzyme called alcohol dehydrogenase and converts ethanol into acetaldehyde [ass-eh-tal-de-hide]. This chemical is more toxic than ethanol, so the liver uses another enzyme to convert acetaldehyde into acetate, which is non-toxic to the human body. NOTE: the amount of alcohol consumed + the timeframe it is consumed [and a variety of other factors] will influence the ability of the liver to effectively convert acetaldehyde all the way into acetate. The liver can’t handle the entire workload effectively therefore ethanol (before being metabolised) will go straight from the liver to the bloodstream and make its way directly to the heart.

NOTE: Genetics will play a role! Certain people do not produce the liver enzymes in enough quantity to properly breakdown ethanol.

5. Blood leaves the liver through the hepatic veins. The hepatic veins carry blood to the inferior vena cava—the largest vein in the body—to the right side of the heart. The heart will beat and send the incoming blood to the lungs to oxygenate and expel carbon dioxide as we breath out. This is how ethanol can be on your breath. Inside the lungs, at the very end of the bronchioles, are hollow air sacs called alveoli where there is a gas exchange. Ethanol evaporates through capillaries into the air sacs and exhaled out of the body. Breathalysers can detect the quantity of ethanol in a person’s system based on the quantity of ethanol in our breath.

6. Not all the ethanol will expel from the body via the breath. The rest will flow back to the heart, with newly oxygenated blood, and then get pumped all the way up to the brain and around the body. NOTE: Ethanol is water soluble. It will be distributed to every cell in the body except bone and fatty tissue [some will enter fat cells but not easily]. Ethanol will interact with every other cell i.e., every organ, gland, nerve, muscle etc.

7. Ethanol will affect and compromise protein synthesis inside muscle tissue. Therefore, if you have been training at the gym, running, swimming etc., your muscles will not effectively be able to repair.

8. Once ethanol has reached the brain, it will cross the blood-brain barrier and begin to affect chemical messengers [neurotransmitters] in the grey matter of the brain. It affects serotonin, dopamine, gamma-amino-butyric-acid (aka GABA), glutamate, endorphins etc. The person will experience pleasure, euphoria, lowered inhibitions [related to dopamine], lowered cognitive ability (e.g., decision making/problem solving, emotion regulation) and lowered coordination and reflexes.

The more ethanol ingested, the more dopamine is secreted and communicated between neurons (i.e., nerve cells). One of dopamine’s functions is to make you feel pleasure or ‘rewarded’ for doing things that are good for humans, hence, from an evolutionary perspective, we are likely to do them again to help us thrive in our environment and social world. Dopamine is secreted when we:

  • eat healthy foods (but also recently developed processed foods that are high in sugar and salt)
  • exercise
  • achieve goals
  • be productive (e.g., finish a task like cleaning, cooking, work-related tasks)
  • master new skills (e.g., learning an instrument or a new talent), and
  • have positive and stimulating social interactions

Ethanol influences so much dopamine secretion and communication that the brain becomes unable to make responsible decisions cognitively. The simultaneous experience of euphoria and lowered cognitive ability means we are more likely to be “happy” about making irresponsible decisions.

Increased dopamine is how drinking alcohol “blocks” unpleasant emotions like fear, stress, anxiety, and insecurity. When we don’t feel these unpleasant, yet necessary, emotions we will behave in ways that are dangerous, abnormal, potentially embarrassing, and generally problematic.

Another significant brain region affected by ethanol is the hypothalamus and the pituitary glad [together known as the hypothalamic-pituitary axis]. These structures control the entire hormonal system. The hypothalamus monitors the body, and it will send instructions to the pituitary gland based on information it receives from the hypothalamus. The hypothalamus is aware that ethanol is flooding the brain and it starts adjusting the secretion of hormones via the pituitary gland.

One of the instructions it gives the pituitary gland is to start modulating the adrenal glands to secrete cortisol (i.e., stress hormone) and epinephrine and norepinephrine (i.e., adrenaline).

Now, our cognitive capacity is diminished, inhibitions are lowered, and we will experience a rush of stress hormones and adrenaline coursing through the body. Cortisol and adrenaline will provide a boost of energy. It will increase the heart rate, blood pressure, body sweat, sugar levels in the bloodstream, and enhances the brain’s ability to use glucose. Glucose is a “fuel” source for brain functioning, including the generation of neurotransmitters. Behaviourally, we can see this in children when we say they are “hyperactive” because they’ve ingested too much sugar.

The pituitary gland will also slow the secretion of anti-diuretic hormone (aka. vasopressin). A diuretic is something that makes us urinate. If the anti-diuretic hormone (also called vasopressin) slows down, then we won’t be “holding on” to water as effectively, hence we begin to urinate more. People call this “breaking the seal”.

9. South of the body, blood is pumped into the kidneys via the renal artery which spreads through the renal cortex. The blood is then filtered into urine and expelled from the body. The lowered anti-diuretic hormone will dilate (become wider/bigger or more open) blood vessels in the kidneys which means more blood gets passed through and filtered, but it also means we lose a lot more body water which leads to dehydration. Vasopressin is essential in the control of osmotic balance, blood pressure regulations, and kidney function, therefore, when vasopressin is lowered, we are losing essential water and minerals/electrolytes. Electrolytes are involved in urination because the kidneys need them to make the process of filtering blood more efficient.

The loss of water and electrolytes will contribute to a hangover. Electrolytes play a role in cellular water absorption so if we are losing more water than we are bringing in, and we are losing the electrolytes that support the absorption of water, we become dehydrated very quickly.

10. The Hangover

Symptoms: nausea, fatigue, diarrhoea, vomiting, paranoia, anxiety, anorexia (i.e., loss of appetite), increased thirst, muscle weakness, irritability, sweating, increased blood pressure, and headache.

The exact cause of a “hangover” is not yet known however variables affecting the hangover are:

  • individual differences such as sex, size, body fat, genetics etc
  • lack of sleep
  • general health
  • drinking behaviour e.g., frequency, duration, quantity
  • food intake before and during
  • water intake before and after
  • your body’s ability to metabolise alcohol i.e., excessive amounts of acetaldehyde due to fewer enzymes to metabolise alcohol in the liver before entering the bloodstream
  • general behaviour while drinking e.g., poly-substance use, dancing, sexual activity, risk-taking behaviours etc.

Strategies for Controlled Drinking

  • Setting personal drinking limits and sticking to it
  • Alternating alcoholic drinks with soft drinks i.e., one alcoholic drink then a water, soft drink, or juice
  • Have a meal before drinking
  • Switching to low alcohol drinks
  • Having regular alcohol-free days/weeks/months
  • Identifying high risk situations for heavy drinking and creating a management plan

Engaging in alternative activities to drinking

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 

Sigmund Freud’s classic Defence Mechanism’sSigmund Freud’s classic Defence Mechanism’s

Projection: Attributing one’s unacceptable feelings or desires to someone else. For example, if a bully constantly ridicules a peer about insecurities, the bully might be projecting his own struggle with self-esteem onto the other person.

Denial: Refusing to recognize or acknowledge real facts or experiences that would lead to anxiety. For instance, someone with substance use disorder might not be able to clearly see his problem.

Repression: Blocking difficult thoughts from entering into consciousness, such as a trauma survivor shutting out a tragic experience.

Regression: Reverting to the behaviour or emotions of an earlier developmental stage.

Rationalization: Justifying a mistake or problematic feeling with seemingly logical reasons or explanations.

Displacement: Redirecting an emotional reaction from the rightful recipient to another person altogether. For example, if a manager screams at an employee, the employee doesn’t scream back—but the employee may yell at her partner later that night.

Reaction Formation: Behaving or expressing the opposite of one’s true feelings. For instance, a man who feels insecure about his masculinity might act overly aggressive.

Sublimation: Channelling sexual or unacceptable urges into a productive outlet, such as work or a hobby.

Intellectualization: Focusing on the intellectual rather than emotional consequences of a situation. For example, if a roommate unexpectedly moved out, the other person might conduct a detailed financial analysis rather than discussing their hurt feelings.

Compartmentalization: Separating components of one’s life into different categories to prevent conflicting emotions.