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Alcohol - An Overview
- By Schaffer Library
- Published 01/5/2006
- Addiction Research
- Unrated
Schaffer Library
The Schaffer Library of Drug Policy site includes studies and histories of drugs and drug laws, medical marijuana research, government publications on drugs and drug policy.
View all articles by Schaffer LibraryNatural history of alcohol dependence
Physical complications
Psychological complications
Social complications
Early recognition of alcohol-related problems
Blood tests when alcohol dependence is suspected
NATURAL HISTORY OF ALCOHOL DEPENDENCE
Progression
At-risk groups and social factors
Recovery
Pregnancy
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.
Progression
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.
Recovery
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.
Pregnancy
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.
PHYSICAL COMPLICATIONS
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
Cardiovascular
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.
Respiratory
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).
Gastrointestinal
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.
Haematological
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.
Neurological
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).
Nutritional
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.
Metabolic
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).
Endocrine
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.
Skin
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).
Facial
Puffiness (*E)
Vasodilation and flushing (*E)
Parotid hyperplasia (L).
Conjunctivae (*E)
vessels engorged
corkscrew vessels in sclera.
Musculoskeletal
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.
PSYCHOLOGICAL COMPLICATIONS
General
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 COMPLICATIONS
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.
General
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 RECOGNITION OF ALCOHOL-RELATED PROBLEMS
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.
BLOOD TESTS WHEN ALCOHOL dependence IS SUSPECTED
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
present
* 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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