This document discusses the bio-psychosocial model for understanding chronic harms of substance misuse. It uses alcohol as an example to show the interactions between biological, psychological, and social factors. The biological effects of substances like alcohol, opioids, stimulants are then outlined, including liver disease, addiction, overdose risk, and infections. Lastly, harm reduction strategies are proposed focusing on prevention, screening, and safer use.

1. Chronic harms of
substance misuse:
Effects of substances
A bio-psycho-social
perspective

2. The bio-psycho-social model
• To structure this material, we will use the bio-psychosocial model to
(artificially) separate the different types of chronic harms associated
with problem substance use.
• As you will see in the next section, there are three ways we can view
‘harm’. We can also see the strengths a person has in the different
sections of the model.

3. The bio-
psychosocial
model:
mapping
harms and
strengths.
psycho-
logical
social
biological

4. An example of the interaction
of the model
• Let’s look at alcohol for an example of the interactions of biological,
social and psychological or behavioural factors.
• Biological: could be genetic or someone’s existing health status.
• Psychological: could be the attitudes or beliefs, or behaviour/habits
the person has about substances or themselves.
• Social: could be the culture, social environment that governs
exposure to substances.

5. Alcohol: an example of bio-
psychosocial factors (Cook & Gurling, 2001)
Alcohol is metabolized by the liver by the enzyme alcohol
dehydrogenase (ALDH2).
• Some people have an inactive version of the enzyme (ALDH2-2).
This is inefficient in metabolizing alcohol resulting in bad hangovers!
(see Shibuya, 1993, Higuchi et al 1992).
• This means that some people will avoid alcohol (psychological).
• People who have active ALDH2 are very good at processing alcohol
(biological). This gene type is more highly prevalent in Caucasian
populations (Agarwal & Goedde, 1991).
• This means they can drink heavily and are more likely to drink
heavily with few side effects (psychological).
• Cultures that approve of alcohol give easy access to alcohol to the
population (social).

6. Alcohol: an example of bio-
psychosocial factors:
• Populations which have a high incidence of ALDH2, and live in an
accepting culture are more prone to heavy drinking, drunkenness
and alcoholism than others.
• An example of this bio-psychosocial ‘perfect storm’ is Scotland
which has the highest rates of alcohol harms in the UK.
• A high proportion of the population of Scotland have the genetic
propensity for active ALDH2.
• Alcohol use is embedded in the Scottish way of life; drinking is
expected at social events.
• Alcohol is part of the Scottish and UK culture generally and is easily
available.

7. Alcohol
Let’s stay with alcohol and look at
the physiological effects.
Alcohol is toxic to the liver
(hepatotoxic). It is a poison.

8. Alcohol: hepatic effects
(Heather et al. 2001)
Alcohol causes liver disease.
• It overburdens the liver’s capability to metabolize ethanol – leaves
liver cells exposed to toxin.
• Liver cells become ‘fatty’ = inefficient and damaged, then become
cirrhosed – dead.
• Liver function reduced and inefficient in extracting essential minerals
and vitamins, especially Thiamine (vitamin B1) – essential for
neuronal function.
• Inefficient liver also = portal hypertension, ascites, gastric &
oesophageal varices & risk of death from oesophageal bleeding.

9. Alcohol dementia
• Lack of thiamine due to liver disease can result in neural damage.
• This can affect the peripheral nervous system, i.e. neuropathy of
fingers, hands, feet.
• It also causes cerebral damage and specific dementia...
– Wernicke –Korsakoff syndrome – specific anterograde amnesia.

10. Alcohol-related cancers and
cardiovascular disease
• Alcohol is a causal factor in mouth, throat, stomach, liver and breast
cancers (Alcohol Concern, 2015).
• Heavy drinking, especially bingeing, makes platelets more likely to
clump together into blood clots which can lead to heart attack or
stroke (Mukamal et al, 2005).

11. Alcohol: neurological effects
(Heather et al, 2001)
Alcohol is a depressant:
• longer-term effect reduces motivation, mood,
causes sleep deprivation, sexual dysfunction,
reduces blood flow (vaso-restriction).
• Sleeplessness is often a maintaining factor for
continued drinking: people continue to drink in
order to get to sleep.

12. Alcohol: foetal alcohol syndrome
disorder (BMA, 2007)
Drinking alcohol can cause neural damage to the foetus.
• Foetal alcohol syndrome causes cognitive/learning and behavioural
difficulties and abnormal facial features in the baby.
• There are vulnerable periods of when the foetus is more at risk from
heavy maternal drinking especially at the early stage of pregnancy.
• Even low level drinking at the early stages may affect the foetus
(Sayal et al 2007).
• Government advice is for women to avoid alcohol during or when
planning pregnancy to keep avoid potential health risks to the
unborn child (DH 2016).

13. Prevention of foetal alcohol
syndrome (BMA, 2007; DH 2016)
• Advice from the British Medical Association and the Department of
Health is that expectant mothers and women considering pregnancy
should be abstinent from alcohol.
• Ante-natal services should be screening and advising on alcohol
consumption rates.
• All professionals in contact with at-risk mums or mums-to-be should
be able to deliver brief intervention on alcohol consumption and
foetal alcohol syndrome disorder.
• Health promotion in schools should include foetal alcohol syndrome
within wider alcohol harm reduction teaching.
• Reduced drinking reduces the damage to the foetus, so any effort by
the practitioner is valuable harm reduction.

14. Alcohol: long term bio-psycho-
social effects
Biological:
– Liver disease, neuropathy, hypertension, brain damage, foetal
alcohol syndrome, cardiomyopathy, gastritis, cancer.
– Tolerance (nervous system) – withdrawal effects & increased
anxiety & depression.
Behavioural:
– All-day drinking, salience (prioritizing the substance), motivation,
relapse.
Social:
– Conflict with family, employers, friends, the law, financial
problems, social exclusion, child-care risks, low self-esteem.

15. Simple alcohol harm reduction &
prevention (Drinkaware, 2015; NICE 2011)
Give parenteral thiamine to anyone at risk of alcohol-related dementia.
Give advice for heavy alcohol drinkers aims to reduce the ‘load’ on their
livers, for example:
• Help someone realise how much they are drinking.
• Advise reduction or alcohol free days – to let the liver recover.
• Have smaller measures – cuts down the units drunk.
• Eat well to absorb alcohol and nourish the liver.
• Give information about the harm alcohol does to the liver.

16. Problem stimulant use
• Stimulants raise the body’s arousal system so longer
term effects are associated with cardiovascular
damage.
• Also, some stimulants are smoked. This route of use
caused lung damage, sometimes known as ‘crack
lung’. When a chronic condition it can resemble
emphysema but often in people under 50.
• Freebase cocaine, crack and cannabis are also
associated with asthma and lung cancer due to way
they are taken (smoked).
• Injected cocaine and amphetamines largely present
the same risks as other injected drugs.

17. Problematic stimulant use
• This can include problematic use of cocaine, amphetamines, ecstasy,
methamphetamine.
• Biological:
– cardiovascular & respiratory problems, psychosis (self-limiting -5
days approx), flashbacks, depression (crash & withdrawal – 96
hrs), anxiety, suicidal thoughts, risk-taking behaviour when high.
• Behavioural:
– salience, compulsive drug-seeking, social avoidance, lack of
motivation, anti-social behaviour. Strong cueing effects.
• Psychosocial:
– Psychological dependency, paranoia, social exclusion, social
withdrawal, poverty, exploitation.

18. Opiates
• This group of drugs incldues
heroin, morphine, diamorphine,
codeine, diclofenac, co-codamol,
etc
• The main chronic physical
problems associated with
injecting opiates are the blood
borne viruses such as HIV,
Hepatitis B & C.
• It is also common to inject other
infectious agents which can
cause chronic infections and
damage - commonly chronic
endocarditis.

19. Opiate dependency: long term
effects
Biological:
• tolerance, HIV, Hepatitis, overdose, endocarditis,
amputation.
Psychological, Behavioural:
• Depression and low self esteem, drug-seeking, lack of
motivation, acquisitive crime.
Social:
• Social exclusion, prison, exploitation (i.e. sex work,
stealing), loss of family & social support.

20. Harm reduction and prevention
strategies for injected drugs
Harm reduction and prevention for injected drugs tends to focus on
avoiding, reducing and detecting blood borne viruses (BBVs). See
‘resources’ for information on HIV for care professionals.
• Safer injecting – through advice and needle exchange schemes.
• Protected sex – offering advice, free condoms and testing in the sex
industry and beyond.
• Screening for infections – ensuring at-risk individuals are offered
testing for BBVs – low threshold access.

21. Ecstasy and associated new
psychoactive substances
There is some evidence to suggest that longer term
use of ecstasy can cause chronic memory loss as
brain cells shrink away from each other (Wagner et al
2013).
This neuronal ‘pruning’ effect of synapses associated
with memory and recall – associated with periods of
low serotonin. Damage appears permanent.

22. Reduction & prevention of chronic
harm: ecstasy and NPS (Talk to Frank, 2015).
One of the key problems with pills is not knowing
what is being taken. Advice on short term use is...
• Know what you are taking – obtain any pills from
a ‘reliable’ source, not a stranger.
• Use pill testing if available.
• Drink moderately to combat dehydration. Don’t
drink too much water. Don’t drink alcohol at all.
• NPS (or legal highs) are NOT safer than banned
substances.

23. References
• Agarwal D & Goedde H (1991) The role of alcohol metabolising enzymes in alcohol
sensitivity. In: Palmer (Ed) The Molecular Pathology of Alcoholism. Oxford University
Press, Oxford.
• Alcohol Concern (2015) Statistics on alcohol. https://www.alcoholconcern.org.uk/help-
and-advice/statistics-on-alcohol/
• Cook C. & Gurling H. (2001) Genetic predisposition to alcohol dependence and
problems. In: Heather et al. (Eds), Int. Handbook of alcohol dependence and
problems. Chichester, Wiley.
• Department of Health (2016) UK Chief Medical Officers’ Alcohol Guidelines Review.
Summary of the proposed new guidelines. Available online at:
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/489795
/summary.pdf
• Drinkaware (2015) Alcohol and Liver Disease. Available at:
https://www.drinkaware.co.uk/check-the-facts/health-effects-of-alcohol/effects-on-the-
body/alcohol-and-your-liver
• Heather N Timothy J Peters T & Stockwell T( eds) (2001) International handbook of
alcohol dependence and problems. Chichester, UK: John Wiley.

24. References cont.
• Higuchi, S Muramatsu, Shigemori K. Saito M. Kono H. Dufour M. & Hartford T. (1992)
The relationship between low K aldehyde dehydrogenase phenotype and drinking
behaviour in Japanese. Journal of Studies on Alcohol, 53, 170-175.
• Mukamal et al (2005) Binge drinking and mortality after acute myocardial infarction.
Circulation, 112: 3839-3845.
• NICE Guidelines CG115 (2011) Alcohol-use disorders: diagnosis, assessment and
management of harmful drinking and alcohol dependence. Available at:
http://www.nice.org.uk/guidance/cg115/chapter/1-recommendations
• Shibuya A. (1993) Genotypes of alcohol dehydrogenase and aldehyde
dehydrogenasie and their significance for alcohol sensitivity. Nippon Rinsho, 51, 394-
399.
• Talk to Frank: Ecstasy. Available at: http://www.talktofrank.com/drug/ecstasy
• Wagner et al (2013) A prospective study of learning, memory and executive function
in new MDMA users. Addiction, 108(1), 136-145.