Ireland has a longstanding relationship with alcohol dating back many centuries. This small nation ranks highly internationally in terms of alcohol consumption. In 2003 alcohol consumption in Ireland was 13.4 litres per adult, ranking third highest behind Hungary and Luxembourg in a comparison of 26 countries in the expanded European Union.¹ While the latest statistics from the World Health Organisation show that consumption has reduced to 11.3 litres per adult, there is little room for complacency; in the period 1980-2009 there has been an overall increase in alcohol use of 18%.²

Alcohol-related harm has steadily increased over the past 20 years. The effects of drinking have taken their toll and the statistics behind this fallout are quite staggering. In a major national study, which included six large hospitals, it was found that 28% of all emergency department admissions were alcohol related; over 50% of these involved people between the ages of 18 and 30 years and 75% were male.³ Between 1995 and 2003 there was an estimated 85% increase in the number of hospital discharges due to alcohol-related intentional injuries, with over 70% in the 15-34 year age group.⁴

It is clear that if the burden of alcohol abuse is to be reduced, then any national alcohol strategy needs to be particularly aimed at young drinkers, as it is this group that is particularly vulnerable to the negative effects of alcohol. Adolescence is a period of physical and psychological development and the introduction of alcohol can impede that process, sometimes profoundly. A 2012 report into the drinking and substance use trends of a group of 15-16 year olds showed that about 50% had drunk alcohol, 40% had consumed more than five drinks on a single sitting, and 23% had been intoxicated on more than one occasion.⁵

The ‘brain reward system’ explains why humans derive pleasure from the regular use of alcohol. Essentially, alcohol has positively reinforcing or pleasurable properties that make its repeated use more likely. When alcohol is consumed, beta-endorphins are produced in the arcuate nucleus. This in turn stimulates the release of dopamine in the nucleus accumbens by inhibiting the release of GABA (gamma-aminobutyric acid) in the ventral tegmental area (VTA). The production of these hormones is believed to result in the pleasurable effects of alcohol.⁶

GABAergic neurotransmission, under normal circumstances, leads to inhibition. Interestingly, in chronic alcohol use, adaption occurs in response to the increase in GABAergic activity resulting in a reduction in the number of GABA_A receptors. At low doses, alcohol inhibits glutaminergic (excitatory neurotransmitter) function. The body adapts by upregulating NMDA receptors and this increases glutamate function. Therefore in higher, chronic doses, the GABAergic and glutaminergic systems are dysregulated. In these circumstances, where alcohol is suddenly discontinued, CNS hyperactivity occurs.^7,8

Serotonin (5HT) is believed to play a role in the pleasurable, positively reinforcing qualities of alcohol. Intoxication is associated with higher levels of 5HT, while alcohol dependence is associated with lower 5HT levels which may have a role in alcohol cravings.^7,8

The opioidergic system is also believed to play an important role in the rewarding and reinforcing effects of alcohol and this is evidenced by an increase in the coverage of µ-opioid receptors in the ventral striatum in patients with alcohol dependence on PET scanning, relative to healthy controls.⁹

Alcohol dependence has a genetic predisposition, with inheritance rates of 50-65%.¹⁰ In a study of 169 same-sex pairs of twins (both male and female) where at least one of the twins had undergone treatment for alcohol dependence, a greater concordance rate was found in identical rather than in fraternal twins.¹¹

The physical complications of alcohol abuse

The long-term, chronic use of alcohol comes with significant complications. Liver problems include fatty liver, alcoholic hepatitis and cirrhosis. Fatty liver is the most common injury caused by alcohol and is usually an incidental finding. It is characterised by the accumulation of triglycerides in liver cells. Alcoholic hepatitis may be asymptomatic or it may present as painless jaundice.

It is estimated that 20% of alcohol dependent patients (120-180g alcohol intake per day) will eventually develop cirrhosis, which is an irreversible change in liver architecture.¹² There is also a significantly increased risk of hepatocellular carcinoma, a condition that carries a particularly poor prognosis. 

Chronic alcohol use is also associated with cancers of the gastrointestinal tract (GIT), although smoking appears to be a strong confounder in research into GIT cancers and alcohol use. It may be that alcohol abuse facilitates tobacco products to cause cancerous change by reducing the availability of vitamin A.¹² For example, in a large Swedish study investigating the role of heavy alcohol use in pancreatic cancer amongst alcoholic patients it was found that smoking was the likely cause rather than alcohol.¹³

Other well-recognised GI complications of heavy alcohol use include stomatitis, glossitis (indirectly due to vitamin B, vitamin C and iron deficiency), gastritis, duodenitis, oesophageal varices, malnutrition due to change in small bowel function, acute and chronic pancreatitis, reduced salivary production and enlarged parotid glands; chronic inflammation of the oropharyngeal mucosa can result in leukoplakia, erythroplakia and submucous fibrosis.¹⁴ There is also an increased incidence of gastro-oesophageal reflux disease (GORD).

There are a number of well recognised cardiovascular complications of heavy alcohol intake. Amongst them is an increased risk of hypertension which in turn increases the risk of stroke. Atrial fibrillation is probably the most common form of arrhythmia.¹² Heavy alcohol use has been associated with reduced left ventricular function and cardiac failure, although the research is equivocal.¹⁵ In patients with alcoholic cardiomyopathy one study showed that patients who reduced their alcohol intake to below 60g/day showed demonstrable improvements in cardiac function.¹⁶

Chronic alcohol use also has a number of effects on breathing by reducing respiratory rate, airflow and oxygen transport. There is an increased risk of obstructive sleep apnoea and aspiration pneumonia. It is believed that these changes are medicated through the GABA system. At levels of alcohol above 300mg/ml death can occur through respiratory depression.¹⁷

Alcohol can also adversely affect the lung’s ability to fight infection which increases the risk of pneumonia in chronic drinkers (particularly gram negative, pneumococcal and TB infections) and there is an association with adult respiratory distress syndrome (ARDS).

Other systems affected by chronic alcohol use include the endocrine (eg. glucose intolerance, hypoglycaemia, impotence, menstrual irregularities, gynaecomastia) and haemopoetic systems (eg. anaemia, thrombocytopenia, altered platelet function) as well as the skin (eg. psoriasis and superficial skin infections).

Neuropsychiatric complications

Chronic alcohol abuse is associated with a number of neuropsychiatric sequelae.

Alcohol intoxication

Intoxication/drunkenness results from the consumption of significant quantities of alcohol, although there is significant interindividual variation. For example, drinkers with severe alcohol dependence can drink inordinately large amounts of alcohol without displaying obvious signs of extreme intoxication due to a raised tolerance to alcohol. Obvious features include dysarthria, ataxia and facial flushing. 

Alcohol withdrawal

The severity of withdrawal symptoms depends on the severity of dependence. Essentially, when a dependent drinker stops alcohol abruptly, the depressant effects of alcohol are lost and CNS over-stimulation occurs, resulting from a down-regulation of GABA_A receptors and an upregulation of NMDA receptors. Withdrawal effects can range from mild (eg. anxiety, sweating, palpitations) to severe (eg. hallucinations, seizures, circulatory collapse – in cases of delirium tremens). The mainstay of treatment for alcohol withdrawal is benzodiazepines (usually chlordiazepoxide) in reducing doses over five to seven days. 

Approximately 5% of alcoholic patients hospitalised for alcohol withdrawal develop delirium tremens symptoms which develop one to three days after the last drink.¹⁸ The onset is heralded by worsening agitation and illusions. Florid symptoms include changing levels of consciousness, cognitive deterioration and sweating, palpitations and tremor, as well as feelings of fear. Treatment is with benzodiazepines often augmented with haloperidol (where hallucinations are a feature). Delirium tremens comes with a mortality which may be as high as 5-15%.¹⁸

Wernicke’s encephalopathy (WE)

First described in 1881 by Carl Wernicke, this condition occurs as a result of thiamine (vitamin B1) deficiency. It is associated with alcoholics and is most commonly found on autopsy in non-alcoholics.¹⁹ It consists of a triad of features including encephalopathy (notably confusion), oculomotor changes and ataxia. It requires prompt intervention with parenteral vitamins. Improvement in confusion occurs within a couple of days, while recovery from ophthalmoplegia and ataxia is variable ranging from days to weeks.

Kosakoff’s syndrome (KS)

KS can occur as a result of WE or independently of it. It is characterised by amnesia with a deficit in short term memory. Intellectual function remains relatively intact. Recovery tends to occur in quarters: 25% exhibit no recovery of memory, 25% recover their memory slightly, 25% significantly and 25% fully recover memory.²⁰

Pellagra

Pellagra occurs as a result of niacin (vitamin B3) deficiency. Memory becomes impaired and sufferers can develop psychotic features such as delusions and hallucinations and also dementia and delirium. Skin and GI changes may also occur. The condition usually responds to niacin replacement.

Central pontine and extrapontine myelinolysis

This can occur in alcoholics due to the inappropriate and rapid correction of hyponatraemia. Demyelination and oligodendrocyte toxicity occurs. Symptoms include dysarthria, dysphagia and psychiatric symptoms. The outcome is usually poor.

Marchiafava-Bignami disease

This condition results from demyelination and necrosis of the corpus callosum in patients with alcohol dependence and poor nutrition. It can present acutely with coma or seizures or in a chronic fashion with dementia and ataxia. It is diagnosed on MRI scan and treatment is difficult.

Hepatic encephalopathy

This results from the accumulation of toxic substances normally removed by the liver in circumstances of liver failure, which results in confusion, altered levels of consciousness and coma, and is associated with a significant risk of mortality. The condition may become a medical emergency and require hospitalisation; treatment is aimed at identifying obvious causative factors and treating the sequelae of liver failure.

Alcohol and depression

Alcohol is strongly correlated with mood disorder. An epidemiological catchment area study found that 40% of patients with alcohol-use problems also met the criteria for a psychiatric disorder, notably anxiety and major depression.²¹ This figure reduces to 5-10% when drinking discontinues, which strongly suggests that alcohol causes depression rather than the other way around, although it is accepted that depressed individuals often use alcohol (among other psychoactive drugs) to cope with symptoms of low mood. The National Comorbidity Survey (NCS), a nationally representative survey in the US, found that compared with non-depressed respondents in the NCS, the lifetime odds of alcohol dependence were significantly elevated for both men (2.95) and women (4.05) with major depression.²² Alcohol abuse also plays a significant role in many cases of suicide.²³ The treatment of ‘dual diagnosis’ is often fragmented and many alcohol-related bouts of depression remain outside clinical practice. A co-ordinated and collaborative response is needed by psychiatric, general practice and addiction treatment services.

Identifying and screening problematic drinking

There are a number of ways of identifying an alcohol problem in clinical practice, although interestingly few alcohol problems are picked up directly. Brief interventions are a simple and cost effective way of exploring the patient’s relationship with alcohol but are rarely used in everyday practice. In fact, only 5.5% in a population-based study said they were ever counselled for their alcohol problem.²⁴ There are many reasons for this including time restraints, adequate resources and the attitudes of GPs towards addicted patients. Furthermore, it is often perceived that unless an intervention is intensive and sustained, it is unlikely to be effective.

Proper clinical assessment is the cornerstone of good treatment. A brief intervention is defined as any therapeutic intervention of short duration (one to five sessions) designed to influence patients to think more actively about their alcohol consumption. They usually include five stages: assessment, feedback, information, advice and providing self-help materials.²⁵ The patient may be attending you for a problem which on the surface creates little suspicion of an underlying problem with alcohol. For example, they may be depressed or be suffering abdominal symptoms such as heartburn or epigastric pain. This provides an excellent opportunity to ask about alcohol consumption. Phrasing the question is crucial. Sensitive queries are sometimes best asked in passing such as “Do you take a drink at all?” If the patient elicits a positive response then this provides the GP with a window of opportunity to delve further. The CAGE questionnaire is a simple, well established brief intervention tool that is well known to GPs and takes only a few minutes to carry out. 

Other screening tools include the Severity of Alcohol Dependence Questionnaire (SADQ), which is a simple 20 item checklist of alcohol withdrawal symptoms that patients can complete in a few minutes. This gives a patient a score of severity which can determine the level of treatment that is required. The Maudsley Addiction Profile (MAP) and the Five Item AUDIT are other useful tools.²⁶

Referral to specialist services

While GPs are in a unique position to identify alcohol problems, there will be occasions where alcohol misusing patients will need referral to specialist services such as cases of severe alcohol dependence or where the extent of the alcohol problem is beyond the expertise of the GP.  There will also be medical and neuropsychiatric complications that may necessitate hospital admission.

Treatment of alcohol misuse can be safely and effectively delivered in an outpatient setting in the vast majority of cases. Research has consistently shown that there is no significant difference in outcomes for patients treated as outpatients compared to those treated as inpatients. Relapse, at some point, is almost inevitable with addiction and the quality of the treatment programme is a far greater factor in influencing outcome than the setting of the treatment. Patient characteristics are also an important factor in determining outcomes.²⁷

The real difference between the two treatment settings is cost. Outpatient treatment is much less expensive, not only in terms of the cost of the programme but also, for example, the cost to employers. Residential treatment precludes people from continuing work, while treatment as an outpatient can result in earlier return to employment. In most cases, patients can continue to work throughout the duration of the programme as the sessions are flexible and will work around the needs of the patient. 

Despite the cost-effectiveness of outpatient treatment, most acute treatment for alcohol problems in Ireland is delivered as inpatient rehabilitation.

Summary

Alcohol abuse is a significant problem in Ireland with significant health and social implications. Alcohol is an attractive drug due to its positive reinforcing properties and works on the brain reward system through a complex interplay of the drug with the body’s natural neurotransmitters. With chronic alcohol use this balance is upset and can lead to unpleasant side effects such as withdrawal.

There are many physical and neuropsychiatric complications associated with alcohol abuse which range in severity and prognosis. Most of these complications are discovered late and not usually in the context of addiction treatment.

Brief interventions are a cost effective way of flagging alcohol problems. GPs are excellently placed to provide brief interventions to alcohol-misusing patients, although this form of therapy is underused in general practice. Furthermore, there is a dearth of medical referral options should an alcohol problem require specialist intervention.  

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