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Information on Alcohol

3. Alcohol


At-risk groups and social factors
Alcohol and physical disease

Fundamentally, 'alcohol dependence' is a longitudinal development, a series of events (problems) correlated with the consumption of alcohol and associated with the phenomena of tolerance, loss of control and dependency.

The natural history of alcohol dependence is therefore a continuum, evolving from hazardous to harmful patterns of drinking, causing a series of alcohol-related disorders or problems, and the development of a dependency on the use of alcohol.


  • Bouts of heavy alcohol consumption - a variety of patterns may evolve.
  • Early problems are mainly psychosocial: drink driving offences, loss of jobs, marital disharmony, civil or criminal offences.
  • Dependence can begin to develop relatively early.
  • Physical complications tend to occur later: earliest are trauma, hypertension and gout, later ones are cirrhosis, cardiomyopathy and brain damage.
  • Alcohol-related physical disease begins to constitute a threat to life and there is a significant annual mortality rate once severe dependence has developed.
  • Loss of control of drinking habits emerges about midway.
  • With further progression, problems multiply and dependence becomes consolidated.
  • Social and psychological disintegration becomes manifest.
  • Progression is not inevitable.
  • Many factors may accelerate progression or alter its direction.
  • Many heavy drinkers change course, modify their drinking or become abstinent without any professional help.
  • There are at-risk groups and contributing social factors.

At-risk groups and social factors

  • Family history of alcohol dependence, especially in close relatives and males
  • peer group heavy drinking - distortion of perception of drinking norms
  • antisocial personalities
  • anxious or depressed persons
  • significant life events causing psychological stress
  • cultural norms of heavy drinking, eg particular occupations
  • tolerated patterns of heavy drinking and of intoxication.

The presence of positive outcome indicators need to be considered when planning treatment programs. Examples may include:

  • when a person begins to notice the harmful effects of his/her drinking behaviour
  • if the person seeks help or joins support groups such as Alcoholics Anonymous
  • if rewarding and sustaining relationships exist
  • if a growth of positive personal values occur
  • if satisfying new interests and relationships are developed
  • if social supports remain intact, such as family structure and employment.


  • Often minimal intervention is all that is required.
  • Abstinence is not the sole criterion of recovery.
  • Many people adopt low risk drinking patterns, especially those in controlled environments or who have not progressed far along the road of dependence.
  • Goals of management should be realistic, individually tailored, frequently reassessed and often staged. Staging is often determined by the development of social supports and of emotional stability.


Any drinking is potentially deleterious to the foetus but major abnormalities are the sequel of heavy drinking (five or more drinks in a day). Women should be advised not to consume alcohol during pregnancy. Very early pregnancy (less than 6-8 weeks) and late pregnancy (third trimester) appear to be times of greatest foetal risk.

Alcohol and physical disease

  • Physical disease due to alcohol does not occur in a simple dose-response relationship.
  • Some diseases, eg Wernicke's encephalopathy, are due to nutritional deficiency states, secondary to heavy alcohol consumption.
  • The best researched physical complication is liver disease.
  • Studies have established the concept of the aggregate dose, the product of the average daily dose and the number of years. The higher the aggregate dose, the more likely is the development of serious liver disease.
  • The lower levels of risk for liver disease appear with sustained average daily intakes of 40 grams for women and 60 grams for men.
  • It is unknown whether the same values apply to other physical diseases, eg pancreatitis, cardiomyopathy.
  • Cerebral dysfunction seems to occur at lower levels of alcohol intake than liver disease.
  • Cerebral dysfunction is a clinical syndrome in which abnormalities of cerebral function can be demonstrated by psychometric testing. Function may recover in whole or in part once drinking has ceased. Maximal recovery may be delayed by weeks or months. Damage and recovery may be demonstrated by serial computerised tomography.
  • Foetal alcohol syndrome may occur in children born of drinking mothers.
  • Changes short of foetal alcohol syndrome also occur. Measurable defects have been found in infants of mothers drinking as little as 20 g per day. The risk of full blown foetal alcohol syndrome has been shown to be very marked if the mother consumes 50 g or more per day.
  • It is not known whether a single episode of heavy drinking can damage the foetus but animal studies have shown this to be so.


Certain diseases and conditions may be present which are not specific or consistently diagnostic of heavy alcohol consumption. However, suspicion should be raised particularly when more than one is present.

Note: They usually appear later than the social and psychological complications.

* = common; E = early (may also be late); L = late

  • Cardiovascular
  • Respiratory
  • Gastrointestinal
  • Haematological
  • Neurological
  • Chronic disorders
  • Nutritional
  • Metabolic
  • Endocrine
  • Skin
  • Facial
  • Musculoskeletal
  • Traumatic and accidental


  • Hypertension (*E)
    • usual improvement with abstinence
    • non-compliance treatment problems in established hypertension.
  • Cardiac arrhythmias after heavy drinking (*L) but may occur (E)
    • tachycardia – sinus and paroxysmal
    • ectopic beats
    • atrial fibrillation – chronic and paroxysmal
    • may be responsible for a higher incidence of sudden death among heavy drinkers.
  • Cardiomyopathy (L)
    • left ventricular failure and lowered cardiac output
    • beriberi heart disease – high output cardiac failure as a consequence of thiamine deficiency.


  • Hoarseness
    • oedema of the vocal chords.
  • Especially in heavy smokers (*L)
    • chronic bronchitis (*L)
    • poor immune response (L)
    • carcinoma of the lung (L).
  • Aspiration pneumonia (L)
    • lung abscess
    • emphysema.
  • Bacterial pneumonia (L)
    • impaired lung defence mechanisms.
  • Tuberculosis (L)
    • carcinoma of the upper airways
    • obstructive sleep apnoea syndrome.
  • Mouth wash or alcohol on breath (*E) at routine consultation (E).


  • Carcinoma (L)
    • mouth, pharynx or oesophagus most common, especially when combined with smoking.
  • Unhealthy furred tongue (*E).
  • Alcoholic dysphagia (L).
  • Reflux oesophagitis (*E)
    • diminished lower oesophageal sphincter tone.
  • Haemorrhage (*E)
    • rupture of oesophageal varices (L)
    • Mallory-Weiss syndrome (E).
  • Gastritis (acute or chronic) (*E)
    • dyspepsia, vomiting and morning nausea
    • gastric erosions and haemorrhage, especially when combined with aspirin.
  • Peptic ulcer (E) (in drinkers who smoke).
  • Small intestine
    • diarrhoea - chronic or acute (E)
    • malabsorption
      • vitamins
      • amino acids
      • carbohydrates
      • minerals (Mg, Zn, Fe).
  • Liver disease (*E)
    • abnormal liver function tests, gamma GT, AST, ALP, ALT
    • fatty enlargement and tenderness
    • alcoholic hepatitis
    • cirrhosis (*L)
    • hepatoma

    with portal hypertension, ascites – hepatic coma – at an advanced stage.

  • Pancreas (*E)
    • pancreatitis
      • acute, relapsing or chronic
    • steatorrhoea
    • pancreatic diabetes.


  • Red cells
    • anaemia following blood loss – varices and peptic ulcer (E)
    • iron deficiency anaemia – nutritional (L)
    • megaloblastic anaemia – folate deficiency
      • nutritional (L)
      • malabsorption
    • sideroblastic anaemia – ringed sideroblasts in marrow (L)
    • macrocytosis (MCV > 96) (*E)
      • thick macrocytosis
        • folate deficiency
        • haemolytic anaemic
        • specifically alcohol-induced
      • thin macrocytosis
        • alcoholic cirrhosis
    • haemolytic anaemia
      • alcoholic liver disease (L)
      • stomatocytosis
    • haemochromatosis
      • may worsen with primary familial type (L)
      • alcoholic cirrhosis occasionally associated with secondary type.
  • White cells (E)
    • granulocytopaenia
      • with acute infection
      • low grade chronic granulocytopaenia
    • impaired lymphocyte/macrophage function.


Alcohol should be included in the differential diagnosis of all acute, confusional and coma states.

  • Acute alcoholic intoxication (*E)
    • confusion, coma and death with respiratory depression, often combined with other drugs.
  • Hyponatraemic coma (*L)
    • beer drinkers' water intoxication.
  • Platelets (*L)
    • thrombocytopaenia

      – with acute and chronic intoxication
      – folate deficiency
      – hypersplenism in cirrhosis.
  • Coagulation (*L)
    • factor deficiency in alcoholic liver disease.
  • Hyperosmolar coma
    • with hypernatraemia in acute intoxication.
  • Sub-dural haematoma (*L) (can be *E)
    • accidents common in alcoholics especially head injury and fractures.
  • Metabolic coma (*L) (can be *E in diabetics)
    • alcohol-induced hypoglycaemia, keto- and lactic acidosis.
  • Convulsions (*L)
    • usually grand mal
    • acute intoxication
    • acute withdrawal
    • brain damaged chronic alcoholic
    • alcohol-induced fits, in idiopathic epilepsy.
  • Alcoholic withdrawal syndrome (*L).

Chronic disorders

(These may coexist.)

  • Wernicke's encephalopathy (*L) (can be E in a heavy drinking bout)
    • ophthalmopegia
    • ataxia – nystagmus
    • mental disturbance – confusion – coma
    • responsive to thiamine.
  • Korsakoff's psychosis (*L)
    • disorder of recent memory
    • lack of judgment
    • confusion
    • confabulation
    • not usually thiamine responsive.
  • Alcohol-related brain damage (*L) (frontal lobe syndrome) (some signs are E)
    • cerebro-cortical degeneration and atrophy
    • more obvious in the frontal and prefrontal cortex (*E)
    • probably the commonest form of alcoholic brain damage
    • more apparent since CAT scanning and sophisticated psychometric testing used
    • may be more common than alcoholic liver disease
    • subtle changes may be present even in early hazardous drinking
    • may have implications for treatment success
    • early features
      • visuo-motor, visuo-spatial skill impairment
      • impaired adaptive abilities and new concept formation
      • impaired self-criticism
      • impaired problem solving
      • intelligence and verbal skills may remain intact
    • late features – serious intellectual impairment
      • marked loss of judgment
      • memory impairment.
  • Cerebellar degeneration (*L).
  • Ataxia – combination of cerebellar and peripheral neuropathies.
  • Polyneuropathy (*L)
    • common peripheral sensory-motor neuropathy
    • including autonomic neuropathy
    • peripheral nerve pressure palsies, eg radial nerve
    • Saturday-night palsy (neuropraxic nerve injury).


  • Vitamin deficiencies (*L)
    • B1, B6, folate – most common, Vitamin A, C and B12 also.
  • Mineral deficiencies (*L)
    • Mg, Zn, Fe, Ca, PO4.
  • Malnutrition (*L)
    • low serum albumin and prealbumin.


  • Alcohol induced
    • hypoglycaemia – with fasting
    • hyperglycaemia – transient elevation of blood glucose with or without diabetes
    • ketoacidosis – with fasting and dehydration with or without diabetes
    • lactic acidosis – associated liver disease with or without diabetes
    • hypertriglyceridaemia (*E)
    • elevated – high density lipoprotein cholesterol HDL-C (*E)
    • hyperuricaemica – provocation of gout (*E)
    • attacks of porphyria – in vulnerable persons
    • hyperosmolality – in acute intoxication.
  • Poor diabetic control
    • with insulin or oral hypoglycaemics, or reducing diets (*E).


  • Adrenal
    • ACTH-mediated alcohol-induced rise in plasma cortisol (L)
    • pseudo-Cushing's syndrome in some people with severe alcohol dependence
    • primary or secondary chronic adrenocortical insufficiency
    • alcohol-induced medullary catecholamine hypersecretion
    • possible cause of sweating, tachycardia and hypertension.
  • Thyroid
    • in alcoholic cirrhosis, low serum thyroid binding protein and T4 levels simulate hypothyroidism but TSH and free thyroxine index are normal. Peripheral conversion of T4 to T3 is also diminished resulting in low T3 levels (L).
  • Gonadal
    • decreased serum testosterone levels – even in the absence of liver disease (*L)
    • direct testicular effect
    • low testosterone and high oestrogen levels in alcoholic cirrhosis (*L)
    • feminisation – gynaecomastia, testicular atrophy, spider naevi (*L)
    • loss of libido (*E).
  • Pituitary
    • suppression of ADH with water diuresis (*E)
    • inhibition of oxytocin release – this may result in premature labour. In this situation oxytocin replacement may be required.


    • Abrasions (*E)
    • Lacerations (*E)
    • Infections (*L)
    • Boils (*L)
    • Unexplained bruising (*L)
    • Paronychia (*L)
    • Clubbing of fingers (*L)
    • Dupuytren's contracture (*L)
    • Hyperpigmentation (*L)
    • Vascular spiders (naevi) (*L)
    • Palmar erythema (*L)
    • Sweating of hands and feet (*L).


    • Puffiness (*E)
    • Vasodilation and flushing (*E)
    • Parotid hyperplasia (L).
  • Conjunctivae (*E)
    • vessels engorged
    • corkscrew vessels in sclera.


  • Muscle (*L)
    • acute rhabdomyolysis
    • chronic myopathy
    • raised muscle enzymes.
  • Skeletal (*L)
    • osteoporosis and aseptic bone necrosis.

Traumatic and accidental (*E)

  • Increased tendency to accident – trauma. More than 43% outpatient fractures (Elvy and Rose, 1983)
  • Motor vehicle accidents
  • Repeated accidents
  • Pedestrian and cycle accidents
  • Drinking and driving offences
  • Hypothermia
  • Drowning in adults
  • Unexplained falls
  • Accidental falls
  • Industrial accidents
  • Unexplained burns
  • Unexplained house fires.



The alcoholic personality as such does not exist. There is no difference between the mental health and pre-morbid personality of the alcohol-dependent person and the non-dependent person. Most, but not all, psychological problems in alcohol-dependent people are secondary to the effects of drinking. In some a psychiatric disorder (eg affective disorder, antisocial personality disorder) is primary and precedes the abnormal drinking behaviour.

There are almost no psychological symptoms or syndromes which cannot be caused or exacerbated by alcohol and other drug misuse. These must be considered in every psychological presentation. The diagnostic possibilities cover the whole field of psychiatry and only the most common can be listed here.

Common psychological presentations

  • Suicide attempts and suicide
  • Depression
  • Loss of memory or blackout
  • Anxiety
  • Phobic states
  • Fugue states
  • Hyperexcitability and rage states
  • Morbid jealousy
  • Paranoid reactions
  • Atypical psychosis
  • Schizophrenia
  • Insomnia
  • Antisocial behaviour.

Cognitive and memory defects

It is important to consider alcohol use every time a tranquilliser, antidepressant or hypnotic is prescribed.

Sexual problems

  • Loss of libido
  • Hypogonadism
  • Impotence and premature ejaculation, ejaculatory incompetence
  • Forcing sexual relations on partner
  • Sexual deviancy, eg incest, sexual molestation of children, rape.


Social disorders are usually the earliest and most frequent complications of alcohol misuse. A complete range of these can be produced by, or associated with, alcohol misuse.


  • Isolation from family and community activities
  • Life revolving around drinking activities
  • Increased frequency of driving accidents
  • Increase in acts of violence and crime
  • Financial problems
  • Legal problems.

At work

  • Frequent absenteeism, especially Monday and Friday and after pay day
  • Frequent and varied medical reasons for absence from work
  • Promotion failure, impaired job performance
  • A history of gaps in work, frequent changes of employment and the threat of job loss
  • Industrial accidents
  • Early retirement.

Common effects of excessive alcohol consumption within the family

The alcohol-dependent person:

  • denies the alcohol problem, blames others, forgets and tells stories for self defence and protection against humiliation; receives criticism from others in the family
  • spends money needed by the family on alcohol
  • ignores bills, debts pile up
  • is unpredictable and impulsive
  • resorts to verbal and physical abuse in place of honest, open talk
  • loses the trust of family, relatives and friends
  • experiences increased sexual arousal but reduced function
  • has unpredictable mood swings – Jekyll and Hyde personality
  • uses devious and manipulative behaviour to divert attention from drinking problem
  • suffers depression, guilt, shame.

The spouse or partner:

  • often tries to hide and deny the problem of the partner
  • takes on the other person's responsibilities, carrying the load of two and perpetuating the spouse/partner dependence
  • takes a job to get away from the problem and/or to maintain financial security
  • finds it difficult to be open and honest because of resentment, anger, hurt and shame
  • avoids sexual contact and may seek separation or divorce
  • may overprotect the children, neglect and/or use them for emotional support
  • shows gradual social withdrawal and isolation
  • may lose feelings of self-respect and self-worth
  • may use alcohol or prescription drugs in an effort to cope
  • may present to the doctor with anxiety, depression, psychosomatic symptoms or evidence of domestic violence.

The children

The children have an increased risk of developing alcohol dependency themselves. They may:

  • be victims of birth defects (from maternal alcohol use)
  • be torn between two parents
  • be deprived of emotional and physical support and lack trust in anyone
  • avoid peer group activities, especially in the home, out of fear and shame
  • learn destructive and negative ways of dealing with problems and getting attention
  • lose sight of values, standards and goals because of a lack of consistent, strong parenting
  • be a failure in school and indulge in petty crime
  • suffer a diminishing sense of self-worth as a significant member of the family
  • present with learning difficulties, school refusal, enuresis or sleep disorders.


Early indicators

Psychosocial factors

  • Heavy drinking (more than six drinks per day, ie greater than 60 grams per day of ethanol for men, and more than four drinks per day for women, ie greater than 40 grams of ethanol)
  • Concern about drinking by self or family or both
  • Intellectual impairment, especially in the abstracting, planning, organising and adaptive skills
  • Eating lightly or skipping meals
  • Drinking rapidly
  • Increased tolerance to alcohol
  • Accidents related to drinking
  • Absence from work related to drinking
  • Majority of friends and acquaintances are heavy drinkers; most leisure activities and sports relate to drinking
  • Attempts to cut down on drinking have had limited success
  • Frequent use of alcohol to deal with stressful situations
  • Frequent drinking during the working day, especially at lunch break
  • Heavy smoking.

Investigation factors

  • Macrocytosis (MCV of red cells more than 100) in the absence of anaemia
  • An elevated GGT (gamma-glutamyl transpeptidase)
  • Elevated serum uric acid level
  • Elevated high density lipoprotein
  • Random blood alcohol level greater than BAC 0.05 g %.

Clinical symptoms and signs

  • Trauma
  • Scars unrelated to surgery
  • Hand tremor and sweating
  • Alcohol smell on the breath during the day
  • Dyspepsia
  • Morning nausea and vomiting
  • Recurring diarrhoea
  • Pancreatitis
  • Hepatomegaly
  • Impotence
  • Palpitations
  • Hypertension
  • Insomnia
  • Nightmares.


Routine                      Specific

* MCV Red cell count            * WBC Diff., platelet count ESR

  - MCV must be included in       - if MCV raised, anaemia liver

    blood count                     pathology or acute infection


                                * CPK

                                  - if myopathy suspected

* Liver function tests          * Prothrombin time

  - must include GGT, ALP,        - if liver pathology suspected

    ALT, AST

* Blood alcohol level           * Amylase

  - if any indication of          - if abdominal symptoms

    current alcohol ingestion

* Lipids                       * Folate

  - fasting                      - if anaemia, macrocytosis

                                   or poor nutrition present

* Uric acid                    * Transketolase (thiamine assay)

                                 - if poor nutrition, neuropathy,

                                   cardiomyopathy or CNS changes

                               * Urea, Electrolytes, Mg, Ca, Glucose,

                                 pH, Osmolarity

                                 - if acutely ill

                               * Hepatitis B surface antigen,

                                 hepatitis C and HIV antibody

                                 - if liver pathology confirmed or

                                   illicit drug use suspected

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