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

Chronic harms of substance misuse: Effects of substances

A bio-psycho-social perspective

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.

The bio-psychosocial model: mapping harms and strengths.

psycho-logical

social

biological

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.

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).

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.

Alcohol

Let’s stay with alcohol and look at the physiological effects.

Alcohol is toxic to the liver (hepatotoxic). It is a poison.

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.

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.

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).

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.

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).

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.

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.

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.

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.

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.

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.

Opiate dependency: long term effectsBiological: • 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.

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.

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.

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.

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.

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.