Webb Therapy Uncategorized What Alcohol does to the Human Body

What 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

Related Post

Albert Ellis’s “Irrational Belief’s about Life” and Self-stereotypingAlbert Ellis’s “Irrational Belief’s about Life” and Self-stereotyping

Albert Ellis, in his Rational Emotive Behaviour Therapy (REBT), identified a number of dysfunctional beliefs that people often hold. Ellis intentionally adopts extreme views to emphasize how people often exaggerate their perspectives irrationally. He referred to this tendency as “awfulizing,” where we negatively overgeneralise situations. This behaviour can stem from a strong desire for certainty, causing us to perceive things in extreme terms rather than viewing them as part of a nuanced spectrum. Consequently, this leads to the formation of self-stereotypes.

A self-stereotype refers to the process of applying generalised beliefs or stereotypes about a group to oneself, especially when one identifies as part of that group. For instance, if someone belongs to a specific cultural or social group (gay men) and internalises the commonly held stereotypes about that group (partying and casual sex), they may unconsciously start viewing and behaving in ways that align with those generalisations.

AIPC (2021). Busting Common Myths About Anger. Issue 355 // Institute Inbrief. Retrieved June 17, 2021.AIPC (2021). Busting Common Myths About Anger. Issue 355 // Institute Inbrief. Retrieved June 17, 2021.

All human beings experience anger at least occasionally. It’s a natural emotion helping us recognise that we or someone or something we care about has been violated or treated badly. When we feel threatened or our goals are thwarted, anger is a coping mechanism that enables us to act decisively, especially in situations where there is little time to reason things out. It can motivate problem-solving, goal-achievement, and the removing of threats. It serves a protective function and is not always a problem (Lowth, 2018; Stosny, 2020; Zega, 2009).

But anger is a complex emotion, and all too often manifests maladaptively in clients’ lives, when they perceive excessive need for protection, protect the “wrong” things, or use anger to thwart their longer-term best interests. The result is problem anger.

Perhaps because it is so multi-faceted, misperceptions about anger abound, and the question arises: how shall we regard anger? How do we advise the client to think about it? Folk wisdom often would say that the best thing to do is just let it all out, but is it? Clients complain that they cannot control it, that the tendency to be easily angered is inherited, but again, is there evidence for that? Here are common myths people tend to hold about anger, and factual statements following them that you can use to clarify for the client why learning to deal with problem anger is time well spent.

Myth 1: “Anger is inherited.”

This is the client that may try to claim that their father was short-tempered and they have inherited that trait from him, so there is nothing they can do. Such a stance implies an attitude that the expression of anger is a fixed, unalterable set of behaviours. Research shows, however, that expression of anger is learned, so if we have – say, through exposure to aggressive influential others, such as parents – learned to be violent in our expressions, we can also learn healthier, more appropriate, pro-social ways of dealing with it.

Myth 2: “Anger and aggression are the same thing.”

Fact: Nope. Anger is a felt emotional state. Aggression is a behaviour, sometimes carried out in response to anger, but not the same as it. A person can be angry, yet use healthy methods of expression without resorting to violence, threats, or other aggression. Anger does not always lead to aggression. In fact, some experts claim that most daily anger is not followed by aggression. When it does result in aggression the “I3 Model” (pronounced “I cubed”) is deemed responsible. This suggests that aggression emerges as a function of three interacting factors, which all begin with “I”:

Instigation, an event which instils an urge to aggress as a result of, say, being addressed rudely or learning that one’s partner has had an affair (or a relatively “minor” event, such as being cut off in traffic);

Impellance, meaning a force that increases the urge to act in response to an instigating stimulus. These could be strong hormonal releases or a belief system which says that the instigating event should not be tolerated, or even a sociocultural norm which demands that instigating stimuli be responded to immediately and harshly (such as punching back someone who has hit you);

Inhibition, referring to forces that typically work to counter aggression, such as cultural norms, awareness of negative consequences, or perspective-taking or empathy (Kassinove & Tafrate, 2019).

Myth 3: “Other people make me angry.”

Fact: How often in common parlance do we say things like, “He made me so angry!” or “You make me so mad I could kill you!”? Even though we may occasionally speak about people causing emotions other than anger, it is far more frequent to hear such statements in regard to anger. We can choose whether or not we let someone else’s behaviour make us happy, sad, or something else, but we often think and talk about it as if anger is caused directly by others. With the undiscerning listener, an angry person thus gets to use anger as an excuse for unacceptable behaviour. Ultimately, it is not the other person’s behaviour that causes our anger, and in fact, it’s not even their intention, though that may influence our behaviour. Being precise, we must acknowledge that it is our interpretation of their intention, expressed in their behaviour/language, which is causative.

Myth 4: “I shouldn’t hold anger in; it’s better to let it out” (either by venting or catharsis).

Fact: If by “holding it in” someone means that they suppress anger, it’s true; ignoring it won’t make it go away and squashing it down is not a healthy choice. Neither, however, is venting. Blowing up in an aggressive tirade only fuels the fire, reinforcing the problem anger. Ditto the use of pillow-punching or other means of catharsis; this may come as a surprise to therapists trained a few years ago, when catharsis was an anger management technique in good standing. Now researchers have found that, even though we feel better in the moment after hitting something, our brain notices, subtly changing its wiring. Then the next time we are angry it softly whispers, “Hit something; you’ll feel better”. The time after that, the wiring is stronger in the brain towards a hitting catharsis, and the angry-brain-voice speaks a little louder. Continuing in this vein means that eventually, we could decide to hit something more alive than a pillow. Rather than either angry venting or catharsis is the use of skills to manage the angry impulse.

Myth 5: “Anger, aggression, and intimidation help me to earn respect and get what I want.”

Fact: People may be afraid of a bully, but they don’t respect those who cannot control themselves or deal with opposing viewpoints. Communicating respectfully is a far superior way to get (most) people to listen and accommodate one’s needs. While the momentary power that comes with successful intimidation may feel heady in the moment, it does not help build the healthy relationships that most people coming to counselling yearn to have.

Myth 6: Anger affects only a certain category of people.

Fact: Anger is a universal emotion that affects everyone. It does not discriminate against people of any particular age, nationality, race, ethnicity, socioeconomic status, education, or religion. It is tempting for some people in the educated middle classes to believe that anger is more prevalent among the poor, or those who are less educated or lacking in social skills. Reality does not bear this out, although the expressions of anger do vary among different social groups. Remember, anger is just an emotion, one which does not make people “good” or “bad” for having it.

Myth 7: “I can’t help myself. Anger isn’t something you can control.”

We don’t always get to control the situations of our lives, and some of them may trigger our anger. In fact, it’s also agreed by experts that we don’t (in the short-term) control whether we have angry feelings or not; they just come – although there are longer-term ways to work with clients that see them less easily provoked, and therefore less prone to have the experience of anger. What we do have the short-term choice to control is how we express that anger. Continuing in sessions with you (the therapist) for the purpose of learning how to better handle anger means having more choices of response, even in highly provocative situations.

Myth 8: “When I’m angry I will say what I really mean.”

Fact: This is rarely true. Uncontrolled angry expressions are more about gaining control of or hurting others, not saying what a person’s deepest truth is. 

Myth 9: “By not saying what I’m thinking in the moment, I’m being dishonest and will be even angrier later.”

Fact: There is a strong pull to “speak our mind” when angry. But it is at this time that a person’s judgment is most severely flawed. To speak from anger is to allow the impulsive part of the brain to overrule the rational part. Better for relationships, career, and pretty much everything else to wait until that reasoning part can regain control.

Myth 10: “Men are angrier than women.”

Fact: The sexes experience the same amount of anger, says research; they just express it differently. Men often use aggressive tactics and expressions, whereas women (often constrained culturally) more frequently choose indirect means of expression, such as found in passive-aggressive tactics. This could mean getting back at someone by talking negatively about them or cutting them out of their lives (categories adapted from: Therapist Aid LLC, 2016; Segal & Smith, 2018; Morin, 2015; Morrow, n.d.; Better Relationships, 2021; Gallagher, 2001).

Thought for reflection

Anger has many facets to it, and we have introduced some information here that may seem either startling or counterintuitive. As you think back over the myths we just debunked, which aspect has surprised you the most? Do you have any sense of why that might be? One woman, for example, was very surprised to hear that “men are angrier than women” was only considered a myth; it turned out that in her family, women “never got angry” (we hypothesise that perhaps they were socialised to not show anger), and the men got angry all the time (perhaps more allowed in that woman’s family/culture). In what ways, if at all, might your views about anger have shaped how you behave? How you respond to others? 

And here’s the ultimate question if you share this material with a client: what are their responses to the above questions? How might hearing these myths help them seek more adaptive ways to deal with problem anger? 

The upcoming Mental Health Academy course, “Helping Clients Deal with Problem Anger” draws from numerous therapies and neuroscience to help clinicians and clients collaboratively create a program to address each client’s unique challenges with this universal human emotion.

References:

  1. Better Relationships. (2021). Common myths about anger. Anglicare Southern Queensland. Retrieved on 13 April, 2021, from: Website.
  2. Gallagher, E. (2001). Anger. eddiegallagher.com.au. Retrieved on 13 April, 2021, from: Website.
  3. Kassinove, H., & Tafrate, R.C. (2019). The practitioner’s guide to anger management: Customizable interventions, treatments, and tools for clients with problem anger. Oakland, CA: New Harbinger Publications, Inc. 
  4. Lowth, M. (2018). Anger management. Patient. Retrieved on 7 April, 2021, from: Website.
  5. Morin, A. (2015). 7 myths about anger and why they’re wrong. Psychology Today. Retrieved on 13 April, 2021, from: Website.
  6. Morrow, A. (n.d.). Anger myths. Stress and Anger Management Institute. Retrieved on 13 April, 2021, from: Website.
  7. Segal, J., & Smith, M. (2018). Anger management: Tips and techniques for getting anger under control. Helpguide.org. Retrieved on 9 April, 2021, from: Website.    
  8. Stosny, S. (2020). Beyond anger management. Psychology Today. Retrieved on 9 April, 2021, from: Website.
  9. Therapist Aid, LLC. (2016). Anger warning signs. Therapist Aid LLC. Retrieved on 7 April, 2021, from: Website.
  10. Zega, K. (2009). Holistic Psychotherapy (159). Retrieved on 7 April, 2021, from: Website.

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