Most Australians drink alcohol — 10.5% of males and 5% of females over the age of 14 years drink daily (~1.5 million people) while about 40% of the population (~7 million people) drink weekly [1]. 

The social costs of alcohol abuse in Australia in 2004/05 were estimated at over $15 billion; with $2 billion related to medical costs alone [2]. 

About 29% of adults attending general practice are drinking alcohol at levels that put them at risk of harm in the short-term (eg. accidents and injuries) or long-term (eg liver disease, cognitive impairment) [3]. 

Routine screening for alcohol use in general practice is recommended [4]. 

The Alcohol Use Disorders Identification Test (AUDIT) is a brief screen suitable for use in the primary care setting [5]. 

Brief intervention for alcohol misuse can reduce consumption by about 20% overall [6] which can be sustained in the long term [7]. 

Blood alcohol concentration

Blood alcohol concentration (BAC) is a good indicator of intoxication. BAC is measured in grams of alcohol per 100 ml blood. Therefore, a BAC of 0.05 (Australia’s upper legal limit for driving) indicates 0.05 g of alcohol per 100 ml of blood.

A lethal dose of alcohol is around 4 grams of alcohol per 100 ml of blood (i.e. BAC ≥ 0.4). One standard drink will usually result in a BAC of about 0.01% to 0.02% but varies by build and gender [8]. High BAC with little behavioural change is indicative of high tolerance and or dependence.

Brief intervention

Brief intervention (BI) is offered following screening (AUDIT) for alcohol use in primary care. BI is an effective treatment for hazardous and harmful alcohol use, and can be used to aid referral or an appropriate treatment plan for those who are dependent [9]. BI has been shown to decrease alcohol consumption by about 20% overall [7].

Core components of BI are feedback on assessment followed by information about harmful effects and simple advice to reduce consumption. BI takes only 5-15 minutes to complete. A simple model for BI can be recalled by the acronym FRAMES standing for Feedback, Responsibility, Advice, Menu, Empathy, Self-efficacy [10].


Alcohol dependence is indicated if 3 or more of the following ICD-10 criteria are met:

  • a strong desire to drink 
  • impaired control over drinking
  • withdrawal following reduction or cessation of drinking 
  • tolerance (need more alcohol for usual effect) 
  • disproportionate amount of time is spent obtaining, drinking and recovering from the effects of alcohol 
  • continued drinking despite alcohol-related problems.

In 1997, 3.5% of Australians met criteria for alcohol dependence; 95% of whom reported impaired control over drinking, 73% reported increased tolerance, and 50% reported withdrawal symptoms following alcohol cessation [11]. 

Alcohol dependence ranges in severity from mild to severe. As dependent individuals struggle to control drinking a treatment goal of abstinence is advised [12]. 

Drinking guidelines

National Health and Medical Research Council recommends men and women drink no more than two standard drinks per day to reduce lifetime risk of alcohol-related harm, and no more than four standard drinks on any single occasion to reduce risk of accident and injury on that occasion [12].

A standard drink contains 10 grams of pure alcohol. See the definition of the Australian standard drink:

  • Light beer (2.7%): 1 can or stubbie = 0.8 of a standard drink 
  • Medium light beer (3.5% alcohol): 1 can or stubbie = 1 standard drink 
  • Regular beer (4.9% alcohol): 1 can or stubbie = 1.5 standard drinks 
  • 1 jug = 4 standard drinks 
  • Wine (9.5%–13% alcohol): 750-ml bottle = about 7 to 8 standard drinks 
  • 4-litre cask = about 30 to 40 standard drinks 
  • Spirits: 1 nip (30 ml) = 1 standard drink 
  • Pre-mixed spirits (around 5% alcohol): 1 can (375 ml) = 1.5 standard drinks.

Drug interactions

Alcohol interacts with a range of drugs by:

  1. competing with the drug for the same metabolizing enzyme resulting in prolonged drug activity, higher than usual concentration of the drug and possible toxic reactions
  2. activating drug-metabolizing enzymes resulting in diminished drug effects. 

Possible interactions occur with some prescribed drugs in the following classes [13]:

  • antibiotics – nausea, headache, vomiting, reduced effectiveness 
  • antidepressants – sedation, impaired coordination, increased depression
  • antihistamines – dizziness, over-sedation 
  • anticoagulant Warfin – heamhorrage 
  • diabetic medications – nausea, vomiting, hypoglycaemia 
  • antipsychotic medications – sedation, increased side-effects, lack of effectiveness 
  • antihypertensive medications – dizziness, fainting, reduced effectiveness 
  • narcotic analgesics – respiratory depression, sedation and possible overdose 
  • NSAIDs/asprin – gastrointestinal bleeding 
  • sedatives – over-sedation, accident and injuries.


Alcohol is rapidly absorbed predominantly from the small bowel via portal circulation (~ 80%), and stomach (~20%). It reaches the brain within five minutes of ingestion where it exerts it intoxicating effects before being metabolized primarily by the liver (95%) with the remainder excreted unchanged in saliva, urine, faeces and sweat. Alcohol is rapidly distributed throughout the body and crosses blood–brain and placental barriers [8].

Approximately 10 grams of alcohol (one standard drink) is metabolised by the average person each hour but this can vary based on:

  • age and gender
  • health
  • person's alcohol tolerance (metabolised faster) 
  • liver function (metabolised more slowly in liver disease) [8].

Blood alcohol concentration table

BAC Likely presentation
  • cheerful, relaxed, sense of wellbeing
  • decreased inhibitions
  • increased chance of accidents
  • loss of fine motor skills
  • slurred speech, ataxia, labile mood
  • impaired judgment/loss of self-control/ poor coordination
  • potential for aggression
  • marked ataxia and slurred speech
  • nausea and vomiting, double vision, memory loss
  • stage 1 anaesthesia (sleepiness, poor response to external stimuli, oblivion)
  • memory loss
  • respiratory failure, coma
  • possible death&

Source: Alcohol and Other Drugs: A Handbook for Health Professionals, NCETA, 2004

Risks and consequences

Short-term risks include accident, injury, interpersonal conflict, aggression and violence.

Longer term risks can include [12]:

  • Cardiovascular disease – hypertension, arrhythmias, haemorrhagic stroke, raise high-density lipoprotein cholesterol 
  • Cancers – oral cavity, pharynx, larynx, oesophagus, liver, colorectum and female breast
  • Nutrition-related conditions – to malnutrition, Wernicke-Korsakoff syndrome, folate deficiency, Vitamin A and B3 depletion 
  • Liver disease – fatty liver, cirrhosis, cancer 
  • Mental health problems – depression, self-harm, anxiety disorders 
  • Cognitive impairment 
  • Tolerance and dependence 
  • Foetal alcohol syndrome – characterised by low birthweight, smaller than normal head circumference, small eyes, flattened face and heart defects. Later in life, affected children might experience low IQ, developmental delays, behavioural problems, learning difficulties and memory problems.


A number of screens are available and the Alcohol Use Disorders Identification Test (AUDIT) is recommended and is available on this site. The AUDIT [14] was designed for primary care settings and has been extensively evaluated [15-18]. It can be self administered in 2–3 minutes, is simple to score and has clear cut-offs to identify hazardous, harmful and dependent drinkers. 

Anther brief screen is the CAGE. A positive response to two or more of the following questions is indicative of problem drinking and should trigger a full assessment [19]:

  • Have you ever felt you ought to cut down on your drinking? 
  • Have people annoyed you by criticising your drinking? 
  • Have you ever felt bad or guilty about your drinking? 
  • Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover?


Long-term, heavy use of alcohol can lead to a range of neurobiological adaptations including decreased levels of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits electrical activity in the brain, and to reduced sensitivity of GABA receptors [20]. These effects, coupled with over stimulation of glutamate (an excitatory neurotransmitter) and an increase in glutamate receptors are thought to contribute to the CNS hyperactivity which characterizes many of the symptoms of alcohol withdrawal following reduction or cessation of use [21]. 

The alcohol withdrawal syndrome can be mild to severe, with the onset of symptoms typically occurring within hours after the last drink, peaking in intensity at days 2-3 and subsiding by days 5-6. 

Common symptoms of mild to moderate withdrawal are tremor, restlessness, insomnia, nightmares, sweats, tachycardia, fever, nausea, and vomiting. More severe withdrawal can include seizures, hallucinations (auditory, visual, tactile), severe agitation and tremulousness, while delirium tremens (DTs), cardiac arrest and death can occur in very severe withdrawal [20]. 

Benzodiazepines are most commonly prescribed for alcohol withdrawal and are effective for symptom control.


1. Australian Institute of Health and Welfare, National Drug Strategy Household Survey. 2007, Australian Institute of Health and Welfare.

2. Collins, D.J. and Lapsley, H.M., The avoidable costs of alcohol abuse in Australia and the potential benefits of effective policies to reduce the social costs of alcohol. National Drug Strategy Monograph Series No. 70. 2008, Australian Governement Department of Health and Ageing: Canberra. p. 51.

3. Britt, H., Miller, G.C., Charles, J., Henderson, J., Bayram, C., Pan, Y., Valenti, L., Harrison, C., Fahridin, S., and O'Halloran, J., General practice activity in Australia 2008-09. General practice series no. 25. 2009, Australian Institute of Health and Welfare: Canberra.

4. Seale, J.P., Shellenberger, S., Velasquez, M., Boltri, J., Okosun, I., Guyinn, M., Vinson, D., Cornelius, M., and Johnson, J.A., Impact of vital signs screening & clinician prompting on alcohol and tobacco screening and intervention rates: a pre-post intervention comparison. BMC Family Practice, 2010. 11(1): p. 18.

5. Saunders, J.B., Aasland, O.G., Babor, T.F., De la Fuente, U.R., and Grant, M., Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons With Harmful Alcohol Consumption, Part 2. Addiction, 1993. 88(6): p. 791-804.

6. Chisholm, D., Rehm, J., Van Ommeren, M., and Monteiro, M., Reducing the Global Burden of Hazardous Alcohol Use. Journal of Studies on Alcohol, 2004. 65(6): p. 782-793.

7. Wutzke, S.E., Conigrave, K.M., Saunders, J.B., and Hall, W.D., The longterm effectiveness of brief interventions for unsafe alcohol consumption: a 10-year follow-up. Addiction, 2002. 97(6): p. 665.

8. National Centre for Education and Training on Addiction (NCETA) Consortium, Alcohol and Other Drugs: A Handbook for Health Professionals, ed. A.G.D.o.H.a. Ageing. 2004, Canberra.

9. Babor, T.F. and Higgins-Biddle, J.C., Brief intervention for hazardous and harmful drinking: A manual for use in primary care. 2001, Geneva: World Health Organization, Department of mental health and substance dependence.

10. Bien, T., Miller, W.R., and Tonigan, J.S., Brief interventions for alcohol problems: A review. Addiction, 1993. 88(3): p. 315-336.

11. Teesson, M., Hall, W.D., Lynskey, M., and Degenhardt, L., Alcohol- and drug-use disorders in Australia: implications of the National Survey of Mental Health and Wellbeing. Australian New Zealand Journal of Psychiatry, 2000. 34: p. 206-13.

12. NHMRC, Australian Guidelines to Reduce Health Risks from Drinking Alcohol. 2009, Canberra: National Health and Medical Research Council (NHMRC). 

13. NIAAA, Alcohol alert. 1995, National Institute on Alcohol Abuse and Alcoholism.

14. Saunders, J.B., Aasland, O.G., Babor, T.F., De la Fuente, U.R., and Grant, M., Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons With Harmful Alcohol Consumption, Part 2. Addiction, 1993. 88(6): p. 791–804.

15. Bergman, H. and Källmén, H., Alcohol Use Among Swedes And A Psychometric Evaluation Of The Alcohol Use Disorders Identification Test. Alcohol and Alcoholism, 2002. 37(3): p. 245-251.

16. Reinert, D.F. and Allen, J.P., The Alcohol Use Disorders Identification Test (AUDIT): A Review of Recent Research. Alcoholism: Clinical & Experimental Research, 2002. 26(2): p. 272-279.

17. Piccinelli, M., Tessari, E., Bortolomasi, M., Piasere, O., Semenzin, M., Garzotto, N., and Tansella, M., Efficacy of the alcohol use disorders identification test as a screening tool for hazardous alcohol intake and related disorders in primary care: a validity study. British Medical Journal, 1997. 314(7078): p. 420-424.

18. Shand, F., Gates, J., Fawcett, J., and Mattick, R., The Treatment of Alcohol Problems: A Review of the Evidence. 2003: Commonwealth of Australia.

19. Dawe, S., Loxton, N.J., Hides, L., Kavanagh, D.K., and Mattick, R.P., Review of diagnostic screening instruments for alcohol and other drug use and other psychiatric disorders. 2nd Edition. 2002, Cannberra: Commonwealth Department of Health and Ageing.

20. Ntais, C., Pakos, E., Kyzas, P., and Ioannidis, J.P.A., Benzodiazepines for alcohol withdrawal. The Cochrane Database of Systematic Reviews, 2005.

21. Krupitsky, E.M., Rudenko, A.A., Burakov, A.M., Slavina, T.Y., Grinenko, A.A., Pittman, B., Gueorguieva, R., Petrakis, I.L., Zvartau, E.E., and Krystal, J.H., Antiglutamatergic Strategies for Ethanol Detoxification: Comparison with Placebo and Diazepam. Alcoholism: Clinical and Experimental Research, 2007. Vol 31(4): p. 604–611.