Motivation and emotion/Book/2018/Alcohol addiction and emotional growth

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Alcohol addiction and emotional growth:
How does alcohol addiction affect emotional growth?

Overview[edit | edit source]

This is both a personal and academic exercise: from the age of 14 until I was 51, I struggled with addiction to alcohol.  I want to know how I was able to get an Upper Second Class Honours Degree in Civil Engineering, a Master’s Degree in Foundation Engineering, a Post Graduate Diploma in Construction Management, work around the world, run a 2 hour 43 minute marathon, find myself in a 20 plus year relationship, with three adult step-children, and yet have no idea about who I was, who may wife was, and what I actually felt about anything!  Although the song is about sleep walking through life, the lyrics of Once in a Lifetime summed up nicely the position I found myself in, and I asked myself “How did I get here?"

Once in A Lifetime - Talking Heads

“And you may find yourself

And you may find yourself

In another part of the world

And you may find yourself

Behind the wheel of a large automobile

And you may find yourself in a beautiful house

With a beautiful wife

And you may ask yourself, well

How did I get here?”

Byrne & Eno, 1981, Sire Records

Watch Talking Heads perform song

What is addiction?[edit | edit source]

Addiction is defined by the American Psychological Association (2009) as a “state of psychological or physical dependence (or both) on the use of alcohol or drugs”. Addictions generally take time to develop, and not every person who tries a highly addictive drug, heroin for instance, will become addicted to the substance.  Millions of people can enjoy a glass of wine with dinner, or a beer whilst watching the football, without becoming an alcoholic.

Addiction is a progressive disease, and can impact anyone, irrespective of gender, race, social status, or religious belief.  There are several models of addiction, which can include anything from 3 to 5 stages as the disease develops.  Simply because a person reaches one stage, does not necessarily mean that continued usage will ensure progression to the next stage.  A person can remain a heavy, and risky drinker, without becoming dependent. One such model, used by the Australian Institute of Professional Counsellors is:

Stage 1: Experimentation

Stage 2: Regular use – Misuse

Stage 3: Risky use - Abuse

Stage 4: Dependence

Stage 5:  Addiction

Risk factors for addiction[edit | edit source]

As reported by the National Institute of Alcohol Abuse and Alcoholism (NIAAA) in the United States, there are five primary categories of risks associated with the development of alcoholism:

  • Genetic – although no specific ‘addiction gene’ has been identified, researchers believe that a predisposition to alcohol addiction can be passed from parent to child through DNA
  • Biological – some people may be biologically predisposed to drink more or less – AA argues that alcoholics have an ‘allergy’ to alcohol (The Doctor's Opinion pp xxv-xxxii, AA, 1939)
  • Environmental – children raised in homes where one or more parent, or significant care giver, drinks alcoholically are more likely to engage in risky drinking than children raised in homes where no parent or caregiver drinks alcoholically. The behaviour of siblings, other family members and peers can also influence behaviour
  • Psychological – a lack of care, neglect, abuse, exposure to violence and other forms of trauma are a significant factor in increasing the risk of developing an alcohol abuse disorder
  • Socio-cultural – how society portrays drinking, endorsement of alcohol products by ‘role models’, e.g. sports, music, film or TV personalities, exposure to advertising.

These factors can result in an addiction at any time during a person’s life.  However, for the purposes of this chapter, I am interested in how alcohol can adversely affect emotional development.  Since emotional development is a significant part of adolescence, with the associated angst and other emotional pains of the teenage and young adult years, I will focus of the adolescent drinker and how drinking at an early age may adversely affect emotional development.

Theories on emotions[edit | edit source]

Carroll Izard (2010) as reported in Reeve (2018) developed a definition of emotions that included the following:

“Emotion consists of neural circuits (that are at least partially dedicated), and response systems, and a feeling state/process that motivates and organizes cognition and action.”

Biological perspective[edit | edit source]

A lot of early research into emotions focussed on the biological reactions of the body to specific stimuli, or events.  These recognisable reactions, such as increased heart rate, increased blood flow in large muscles, increased release of hormones such as adrenaline, are identified with perceived presence of a threat and fear.  These are very basic coping mechanisms that would facilitate a fight or flight response in the presence of a threat out on the savannah in the early days of mankind’s development.  These same reactions, however, are still built-in to the human physiology.[factual?]

The biological perspective on emotions focusses on a small number of basic emotions.  The number of emotions included in this perspective depends on the researcher and ranges between: two - fear and euphoria (Soloman, 1980); three - fear, joy and anxiety (Gray, 1994); to eight - anger, disgust, sadness, surprise, fear, acceptance, joy, and anticipation (Plutchik, 1980). Whilst researchers do not agree on the actual number of basic emotions, they share the belief that these basic emotions are common to all humans, irrespective of culture, and that they result from evolution and biology.  The biological perspective takes the position that these emotions are hard-wired into our systems, and are, therefore, not necessarily the products of learning and experience. Emotions such as gratitude, pride, shame and guilt are ‘second-order’ emotions, that are learned through experience.[factual?]

Cognitive perspective[edit | edit source]

A lot of early research into emotions focussed on the biological reactions of the body to specific stimuli, or events.  These recognisable reactions, such as increased heart rate, increased blood flow in large muscles, increased release of hormones such as adrenaline, are identified with perceived presence of a threat and fear.  These are very basic coping mechanisms that would facilitate a fight or flight response in the presence of a threat out on the savannah in the early days of mankind’s development.  These same reactions, however, are still built-in to the human physiology.[factual?]

The cognitive perspective on emotions argues that emotions are generated by learned responses to situations and events, i.e. a person places a value or meaning to a situation/event, and a resulting emotion depends on how that situation or event transpires. So, if a person feels that they have done well in an important exam, they may feel pride.  Conversely, if they do poorly in the exam, they may feel disappointment, shame or guilt.  If the exam was, however, not considered to be important, the emotion may be very different.  So, a specific outcome could result in a different emotion, dependent upon the value that a person places on the outcome.  This is clearly different from the biological perspective, which would predict the same emotion, regardless of the value placed on the outcome.[factual?]

Besides the basic emotions, researchers have identified many second-order emotions.  For example, amongst many other sub-emotions, anger can be subdivided into:

  • Irritation
  • Annoyance
  • Frustration
  • Rage
  • Ire
  • Fury
  • Resentment

This is a bit like the numerous subtle colours that interior designers and real estate agents try to sell us, but they can all look red to an angry person who has not learned to discern subtle differences.  This is the same with their emotions; because they didn't learn to identify, appraise, modify and accept their emotions the basic, biological emotions discussed above, control. The differences between them are subtle, and difficult to distinguish.  It may need extensive exposure and learning, of our own bodily reactions, feelings and consequences, to recognise the difference between frustration and resentment, say[awkward expression?] (e.g., Palmer, Donaldson, & Stough, 2002).

Complex emotions[edit | edit source]

If the basic emotions come ready to use in every person, what about the more complex emotions? Cognitive theory recognises that biology contributes to a person’s emotions, but also incorporate the role of past experiences and thinking in the generation of specific emotions. Thus, the generation of an emotion could follow the process proposed by Arnold (1960):

Situation e.g. a visit to the dentist

Appraisal -  Have I done this before?  What happened? Was it a good or a bad experience?

Emotion – fear or relaxed, depending on the appraisal

Action – Go to the dentist or avoid going to the dentist

As events and emotions become more nuanced, then every greater awareness of how one is feeling, what is causing that feeling, how to manage the feeling, and how to adapt the situation to a positive is required.  These skills are usually developed at home, with parents and family and in the classroom or on the playground with friends and school colleagues. As we get older, we learn to work with people that we do not particularly like because we learn that there are rewards and consequences associated with cooperating or not cooperating. As we mature, we (hopefully) learn to accept the transition from being the centre of a parent’s world, to being a member of a group (friends and other family), to being a member of a school class, possibly a team member, and eventually a functioning member of society. This process is facilitated greatly by developing an awareness of our own and others emotions and developing appropriate responses.

If subtle emotions need to be learned, and this learning takes place as a person grows, especially during adolescence, when a person is exposed to puberty, and all the associated hormonal changes, what will happen to emotional development if a person starts to abuse alcohol during this critical period?

Emotional intelligence[edit | edit source]

Emotional Intelligence (EI) has defined as “the ability to monitor one’s own and other people’s emotions, to discriminate between different emotions and label them appropriately, and to use emotional information to guide thinking and behaviour” (Salovey & Mayer, 1990).  Whilst this definition has subsequently been expanded and refined, it is appropriate for this discussion as it sets out the basic precepts of Emotional Intelligence.  Goleman (2006) argues that whilst IQ is inherent and can be manipulated only slightly be learning and experience, Emotional Intelligence is almost entirely learned. Early experiences with primary care givers (usually the mother) are critical to the development of Emotional Intelligence and how a person develops coping skills.  By developing Emotional Intelligence, Goleman (2006) argues that a person learns how to recognise situations and evaluation his experiences and reactions to similar situations, to develop coping strategies, to identify which ‘fights are worth fighting’, to negotiate, and learn to ‘give-and-take’ to avoid loss of face to others.  Thus, Emotional Intelligence, may be considered an essential element of a person’s repertoire of skills for living. 

It is important to note that emotional intelligence and academic intelligence or other skills, such as carpentry, can be developed fully, separate from Emotional Intelligence.  Therein lies a clue to one of my questions at the start of this chapter.

Emotional Intelligence and the risk of developing an alcohol use disorder or addiction was investigated by Trinidad & Johnson (2000), who found that EI was negatively correlated with alcohol (and tobacco) use in early adolescents.  They postulated that teens with higher EI could develop effective strategies to resist unwanted peer pressure.   Person’s with high Emotional Intelligence, are also likely to develop effective strategies for managing and controlling their emotions, realistically evaluating their own performance, and learning to recognise and accept constructive criticism.

Emotions and decision making[edit | edit source]

The Somatic Marker theory (Damassio (1996) and Bechara & Damassio (2005) provides a theory of decision making that combines emotions and cognitive factors.  The authors argue that decision making must include an emotional factor, based on previous experience.  The Somatic Markers are signals issued as biological processes in response to events, choices being encountered.  This is similar, to the processes discussed under the Biological Perspective on Emotions.  These signals permit rapid decision making, based on emotional stimuli from previous experience.  Damassio (1996) demonstrated that damage to the ventromedial prefrontal cortex inhibited the initiation of these somatic marker signals, thus preventing a change in somatic state to and emotionally charged stimulus.  Could alcohol abuse be associated with damage to the ventromedial prefrontal cortex?

Garcia, Garcia & Bechara (2006) noted that persons with a substance dependence often displayed poor decision making, frequently opting for an immediate reward, even if the long-term consequences were severe.  They reported on numerous behavioural studies, which confirmed that persons with a substance dependence had impaired decision making capacity.  The authors wanted to investigate whether this impaired decision making was attributable (partially or completely) to a disruption of the somatic marker model of decision making.  The results of imaging studies showed that persons with a substance dependence also demonstrated impaired function of the ventromedial prefrontal cortex, the amygdala and other areas important for emotions and decision making.

Adolescence and the developing brain[edit | edit source]

Research has shown that adolescence is a critical phase in brain development, both in forming new synapses and neural networks and in developing memory circuits that are important in recognizing and managing emotions. If subtle emotions need to be learned, and this learning takes place as a person grows, especially during adolescence, when a person is exposed to puberty, and all the associated hormonal changes, what will happen to emotional development if a person starts to abuse alcohol during this critical period?

Age at first exposure to alcohol[edit | edit source]

In the UK and Australia, the legal age for purchase of alcohol is 18 and in many states of the USA the legal age is 21.  However, many parents permit their children to consume alcohol at home, often in the belief that early, and controlled exposure will lead to moderate and controlled drinking.  Whilst this may be a successful strategy for some, DeWit et al (2000) reported that exposure to alcohol between the ages of 11 and 14 resulted in a significant increase in the risk of developing an alcohol use disorder, compared to people who delay exposure to alcohol until they are older. 

Role of brain glucose metabolism[edit | edit source]

Chugani (1998) reported on the importance of local cerebral metabolic rates of glucose utilisation (LCMRglc) in learning and emotional development, especially during middle childhood and early adolescence, after which the rates fall towards adult levels.   Chugani also discussed the importance of LCMRglc to the development of new synapses, hence not only is it important in learning and emotional development, but it plays a crucial role in building neural networks and developing brain plasticity. 

Effect of alcohol on the developing brain[edit | edit source]

The adolescent brain is still developing, and major changes occur during this period (NIAAA, undated). Many of these changes comprise the development of new neural networks in response to the adolescent person’s experiences, and these connections will depend upon which neurons are stimulated. During adolescence, unused pathways are pruned and discarded. Hence, this is a critical time in the brain’s development.  Exposure to alcohol during this period can adversely affect how neural pathways, which subsequently control emotional responses, are laid-down. This can impair cognitive and emotional learning, as neural circuits used to embed emotional reactions and strategies to events may not be developed.

Volkow et al (2015) showed that heavy alcohol usage reduces the metabolism of brain glucose, favouring alternative energy sources (acetate).  This effect was only evident during alcohol usage and in the early stages of sobriety. However, what would the effect of long-term, heavy alcohol usage look like in terms of brain glucose metabolism? Could the early onset of alcohol abuse result in a significantly reduced rate of LCMRglc and hence a loss of emotional memory and development?  Volkow et al (2015) did find that the baseline brain glucose metabolism of heavy drinkers was lower than normal or non-drinkers.

Watch a short video on the effects of alcohol on the adolescent brain.[1]

The role of the amygdala[edit | edit source]

The amygdala is part of the limbic system and is known to have an important role in memory, emotion, the perception of threat and learning fear (APA 2012). The amygdala was one of the earliest parts of the human brain to develop (Goleman, 2006). Together with the hippocampus, it was part of what has been called the ‘nose-brain’, because it helped humans differentiate odours from safe and dangerous, edible and non-edible, potential mate and not a potential mate, etc., and remembered the appropriate emotional reactions to each scent. The amygdala is still important for learning and remembering emotional matters. Damage to the amygdala can result in a loss of emotional stimulus. The amygdala provides the immediate emotional response to a stimulus. Work by LeDoux (e.g. 2003) has shown that the brain forms neural pathways that can bypass the cognitive thought centres in the event of a perceived threat and go straight to the amygdala. The amygdala then issues the urgent, all-consuming messages of fear that overcome rational thought. In addition to facilitating emergency responses faster than the cortex could process them, the amygdala also plays an important part in developing memories that have intense emotions associated with them (Goleman, 2006). This is due to neurotransmitters released in moments of stress, or intense emotion, being received by the amygdala, which then issues signals to other areas of the brain.

The amygdala is critical to assigning emotional importance to events and memories (Wand, 2005, Gilpin, Herman, & Roberto, 2015). Neurotransmitters that affect the amygdala and can be impacted by alcohol use include CREB, GABA and dopamine (Zielgler et al (2008), Koob (2005), Roberto et al (2010). Thus it can be seen that the amygdala is important for the ‘rapid response’ that is needed whilst the cortex gets on with the cognitive processing and later takes over the response.

Alcohol and memory[edit | edit source]

As discussed above, alcohol interferes with functioning of the amygdala, which then affects emotional memory. Binge drinking and cause a state known as a blackout. In this state, as person may appear to be functional, but no memories are recorded. The person can have a conversation, but will not remember what has been said after a short period. A person in a blackout could drive, operate machinery and do many other tasks that are already embedded as memories. However, on exiting the state, they will have no memory of what has happened and they will never recover the memory, because it was not recorded (White, 2003). Blackouts are caused by the rapid consumption of alcohol, rather than the actual volume of alcohol consumed. Blackouts are extremely dangerous, as a person may do things that they would not normally do. A recent case in the UK is likely a tragic example of what can happen during a blackout:

Experiencing blackouts is another cause of anxiety, as the person may be worried about who they may have offended, what they had done, etc. during the blackout state.

Withdrawal from chronic alcohol abuse[edit | edit source]

It is important to remember that in early recovery, feelings of anxiety are likely to be high, which can exacerbate the risk of relapse (e.g. Wand, 2005). Withdrawal from alcohol can also cause delirium tremons (DTs) and seizures, which can be fatal[factual?]. Withdrawal from chronic alcohol abuse should not be attempted without medical advice and preferably supervision[factual?].

Conclusion[edit | edit source]

From a biological perspective, a few basic emotions such as fear and joy, are inherent across mankind and utilise rapid neural networks to prepare the body for a response to a stimulus. The cognitive perspective shows that as people mature, the basic emotions become more nuanced and responses require appraisal and assessment of what the stimulus was, what feelings were associated with it, what the outcomes were, etc., which is a learned process. Often, an immediate reaction to a stimulus may be intense (a basic emotion at play) and then the reaction reduces as the cognitive appraisal takes over. We have seen how adolescence is a critical period in the formation of new neural networks and the pruning of networks that are not being used; networks associated with the development of the nuanced emotions are, therefore, included in this development. However, alcohol is known to interfere with this development, and the functioning of parts of the brain, especially the amygdala, resulting in a significant risk of emotional development being impaired by the consumption of alcohol during adolescence. As such, persons who abuse alcohol during adolescence are at risk of not developing their emotional intelligence and being 'controlled' by their basic emotions. Thus, as is often observed in addicts, they may be quick to anger, dominated by fear, and display low empathy.

See also[edit | edit source]

References[edit | edit source]

Alcoholics Anonymous. (1939) Alcoholics Anonymous - The Big Book. New York. Alcoholics Anonymous Inc.

American Psychological Association. (2009). APA College Dictionary of Psychology. Washington : American Psychological Association

Arnold, M.B. (1960). Emotion and Personality (Vols 1 & 2). New York: Columbia University Press

Australian Institute of Professional Counsellors (8 August 2012), The Five Stages of Addiction, retrieved from

Bechara, A. & Damassio, A.R. (2005). The somatic marker hypothesis: A neural theory of economic decision. Games and Economic Behaviour, 52, 336-372.

Berridge, K.C., & Robinson, T.E. (1998).  What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?  Brain Research Reviews, 28, 309-369

Chugani, H.T. (1998).  Biological basis for emotions:  Brain systems and brain development.  Pediatrics, 102, 1225-

Cooper, M. L. (1994). Motivations for alcohol use among adolescents:  Development and validation of a four-factor model. Psychological Assessment, 6, 117-128.

Cox, W. M., & Klinger, E. (1988).  A motivational model of alcohol use.  Journal of Abnormal Psychology, 168-180

Damasio, A. R., Everitt, B.J., & Bishop, D. (1996).  The somatic marker hypothesis and the possible functions of the prefrontal cortex.  Philosophical Transactions:  Biological Sciences, 351, 1413-1420

Five Stages of Addiction, retrieved from

Gilpin, N.W., Herman, M.A., & Roberto, M. (2015).  The central amygdala as an integrative hub for anxiety and alcohol use disorders.  Biological Psychiatry, 77, 859-869.

Goleman, D. (2006).  Emotional Intelligence: Why it can matter more than IQ. (10th Anniversary Edition), New York.: Bantom

Gray, J.A. (1994). Three fundamental emotion systems. In Ekman, P., & Davidson, R.J. (Eds), The nature of emotion: Fundamental questions. pp 243-247, New York : Oxford University Press.

Hiller-Sturmhofel, S., & Swartzwelder, H.S. Alcohol's effect on the adolescent brain - what can be learned from animal models? (Undated) Published on line by National Institute on Alcohol Abuse and Alcoholism

Izard, C.E. (2010). The many meanings/aspects of emotions: Definitions, functions, activations, and regulation. Emotion Review, 3363-370

Koob, G.F. (2015).  The dark side of emotion: the addiction perspective.  European Journal of Pharmacology, 753, 73-87.

LeDoux, J. (2003). The emotional brain, fear, and the amygdala. Cellular and Molecular Neurobiology, 23, 727-738.

Miltenberger, R.G. (2016). Behaviour Modification: Principles and Procedures (6th Edition). Boston. Cengage Learning.

Palmer, B., Donaldson, C., & Stough, C. (2002). Emotional intelligence and life satisfaction. Personality and Individual Differences, 33, 1091-1100.

Plutchik, R. (1980). Emotion: A psychoevolutionary analysis. New York : Harper & Row

Reeve, J. Understanding Motivation and Emotion. (7th Edition).  Hoboken :  John Wiley & Sons

Roberto, M., Cruz, M.T., Gilpin, N.W., Sabino, V., Schweitzer, P., Bajo, M., Cottone, P., Madamba, S.G., Stouffer, D.G., Zorrilla, E.P., Koob, G.,

Siggins, G.R., & Parsons, L.H. (2009).  Corticotropin releasing factor-induced amygdala gamma-aminobutyric acid release plays a key role in alcohol dependence.  Biological Psychiatry, 67, 831-839.

SMART Recovery Australia (2015). SMART Recovery Facilitator Training Manual. Sydney. SMART Recovery Australia

Salovey, P., & Mayer, J.D. (1990).  Emotional intelligence. Imagination, Cognition, and Personality, 9 185-211

Soloman, R.L. (1980). An opponent-process theory of motivation: The costs of pleasure and the benefits of pain. American Psychololgist, 35, 691-712

Spear, L. (2004). Modeling adolescent development and alcohol use in animals. Alcohol Research and Health, 24, 115-

Trinidad, D.R. & Johnson, C.A. (2002).  The association between emotional intelligence and early adolescent tobacco and alcohol use.  Personality and Individual Differences, 32, 95-105.

Volkow, N.D., Wang, G.J., Kojori, E.S., Fowler, J.S., Benveniste, H. & Tomasi, D. (2015).  Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases.  The Journal of Neuroscience, 35, 3248-3255.

Verdejo-Garcia, A., Perez-Garcia, M., & Bechara, A. (2006).  Emotion, decision making and substance dependence:  A somatic marker model of addiction.  Current Neuropharmacology, 4, 17-31

Wand, G. (2005). The anxious amygdala: CREB signalling and predisposition to anxiety and alcoholism. Journal of Clinical Investigation, 15, 2697-2699.

White, A.M. (2003). What happened? Alcohol, memory blackouts, and the brain. Alcohol Research & Health, 27, 186-196

deWit, D.J., Adlaf, E.M., Offord, D.R., & Ogborne, A.C. (2000). Age at first alcohol use: A risk factor for the development of alcohol disorders. American Journal of Psychiatry, 157, 745-750

Wrase, J., Makris, N., Braus, D.F., Mann, K., Smolka, M.N., Kennedy, D.N., Caviness, V.S., Hodge, S.M., Tang, L., Albaugh, M., Zielgler, D.A., Davis, O.C., Kissling, C., Breiter, H.C., & Heinz, A. (2008). Amygdala volume associated with alcohol abuse relapse and craving. American Journey of Psychiatry, 165, 1179-1184.

External links[edit | edit source]