Alcohol Addiction

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Alcohol Addiction

• Hana Tariq Janice Jansen

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OVERVIEW

• Introduction
• Symptoms
• Epidemiology
• Comorbidity
• Etiology Studies
• Neuroanatomy
• Neurochemistry
• Treatment
• Conclusion

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What is Alcoholism?

• Chronic (lifelong) disease
• Keep on drinking despite legal, family or health
  problems
• Different from alcohol abuse (involves frequent
  over-consumption without being dependent although
  many of the effects are the same)

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SYMPTOMS

• It includes the following symptoms
• Craving (intense need to drink)
• Loss of control (inability to stop)
• Tolerance (need increasing amounts to
  achieve a high)
• Large amount of time spent on obtaining, using,
  or recovering from substance

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SYMPTOMS contd

• Important activities and responsibilities are
  given up or reduced as a result
• Physical dependence (withdrawal symptoms once you
  stop drinking nausea, sweating, shaking,
  anxiety)
• Hiding alcohol or sneaking drinks
• Denial

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Effects of Alcohol

• CNS depressant
• Reduces anxiety, inhibition, guilt
• Impairs perception, memory, judgment, motor
  coordination, speech, vision, reaction time
• Can cause liver cirrhosis, brain damage, fetal
  alcohol syndrome
• At the highest levels loss of consciousness,
  coma, or death from respiratory arrest

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EPIDEMIOLOGY (Canada)

• Declining trend in alcohol sales during the
  1980s early 1990s increase since late
  1990s
• One in 10 adult drinkers report having problems
  with their drinking (health and/or financial)

• 14.5 billion Total sales of alcohol in Canada in
  2001-2002

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EPIDEMIOLOGY (U.S.)

• Almost 1 of 4 Americans admitted to general
  hospitals have alcohol problems, or are
  undiagnosed alcoholics being diagnosed for
  alcohol-related consequences.
• Alcohol alcohol-related problems cost the U.S.
  economy at least 100 million in health care
  lost productivity each year.
• Over 15 million Americans are dependent on
  alcohol. 500,000 of them are between the age of 9
  12.

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EPIDEMIOLOGY contd

• NOTE Gender may influence a persons risk for
  developing alcoholism.
• Adoption studies present some info about possible
  sex differences in the heritability of
  alcoholism, but overall results have been
  inconclusive.
• Twin studies have steadily supported the role of
  genetic risk factors in the heritability of
  alcoholism in men.

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COMORBIDITY

• Alcohol dependence often co-occurs with other
  psychiatric disorders.
• Mental health and substance abuse facilities are
  expanding their services for patients with dual
  disorders, but further research is needed to
  guide their treatment.
• The NCS (National Comorbidity Survey) found that
  the median age of onset for comorbid psychiatric
  disorders (11 years) preceded the median age of
  onset for all addictive disorders (21 years)
• Most of the respondents who had both a
  psychiatric disorder and an addictive disorder
  reported that they started suffering from at
  least one psychiatric disorder before the
  addictive disorder started

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COMORBIDITY contd

• May be related to other disorders in many ways
• Can co-occur with a second disorder, either
  sequentially or simultaneously, by coincidence.
• Can cause various medical psychiatric
  conditions or increase their severity.
• Comorbid disorders might cause alcoholism/increase
  its severity.
• Both alcoholism the comorbid disorder may be
  caused, separately, by some third condition.
• Alcohol use or alcohol withdrawal can produce
  symptoms that mimic those of an independent
  psychiatric disorder.

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COMORBIDITY contd
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NEUROANATOMY

• overall studies show that alcoholics have
  shrunken brains and enlarged ventricles

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• FRONTAL LOBE
• MRI and CT scan of alcoholics show extensive
  brain shrinkage
• after age 40 shrinkage my be irreversible
• MRI images of alcoholics who continued drinking
  over a 5-year period showed progressive brain
  shrinkage that significantly exceeded normal
  age-related shrinkage
• MRI studies show decreased activity
• causes confusion, lack of judgment, clouded
  thinking, etc.

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• BASAL GANGLIA
• alcohol has inhibitory effect on basal ganglia
• person becomes more talkative, more
  self-confident and less socially inhibited

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• CEREBELLUM
• MRI and fMRI studies show shrinkage and decreased
  activity
• causes lack of coordination and balance
  (tipsiness)

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• LIMBIC SYSTEM
• decreased volume and lower activity in
  hippocampus
• results memory loss and learning problems
• individuals predisposed to alcohol have a smaller
  amygdala
• amygdalas close connection with the nucleus
  accumbens

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• RETICULAR FORMATION
• lowers body temperature (can lead to hypothermia
  in extreme cold)
• interferes with normal sleep patterns excessive
  sleepiness or insomnia
• lowers heart rate, blood pressure, breathing rate
• these conditions can be fatal

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NEUROCHEMISTRY

• GABA and Glutamate
• Beta-Endorphins
• Dopamine
• Serotonin

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• GABA AND GLUTAMATE
• the brain attempts to restore equilibrium after
  long-term alcohol abuse
• short-term alcohol consumption increases GABA
  activity BUT prolonged drinking decreases GABA
  receptor levels and receptor sensitivity
  (down-regulation)
• short-term alcohol consumption decreases
  glutamate activity, prolonged drinking increases
  glutamate activity (up-regulation)
• Alcohol Withdrawal Syndrome

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• BETA-ENDORPHINS
• alcohol stimulates the release of beta-endorphins
  from the hypothalamus
• animal studies show even greater release of
  endorphins in alcohol-preferring rats compared to
  non-preferring rats
• causes the high associated with alcohol,
  thereby reinforcing alcoholism

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• BETA-ENDORPHINS contd
• alcohol stimulates the formation of opiate-like
  compounds, called Tetrahydrolsoqulnoline (THIQ)
• acetaldehyde serotonin/dopamine
  tetrahydrolsoqulnoline (THIQ) like opiates
• like opiates, THIQ promote lethargy, mental
  cloudiness and fogginess, depression, apathy,
  inability to concentrate, etc.

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• DOPAMINE
• alcohol increases the dopamine activity in the
  mesocorticolimbic dopamine pathway (reward
  pathway) VTA to medial PFC to nucleus accumbens
• individuals predisposed to alcoholism have
  decreased dopamine activity
• the increase in dopamine release after the
  alcohol consumption is much higher in
  alcohol-preferring rats than in non-preferring
  rats
• alcoholics given dopamine precursors in clinical
  trials reported fewer cravings for alcohol

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• DOPAMINE contd
• interaction with GABA and opioid peptide
  neurotransmitter systems regulates the release of
  dopamine

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• SEROTONIN
• individuals predisposed to alcoholism have
  decreased 5-HT levels in CSF
• same findings in alcohol-preferring rats
• differences particularly pronounced in the
  nucleus accumbens links with DA system
• tryptophan depletion studies with at-risk youth

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• SEROTONIN contd
• alcohol increases serotonin levels
• serotonin metabolites in the urine and blood
  increase after a single drinking session
• during withdrawal, depression is common due to
  decreasing serotonin levels
• links with depression
• lower serotonin also causes depression do people
  drink to self-medicate?

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• SUMMARY NEUROCHEMISTRY
• GABA
• In the short-term, alcohol increases GABA
  activity (more inhibition), but after prolonged
  use, GABA activity decreases in order to
  compensate for the depressant effects of alcohol.
• Originally causes sedation, incoordination.
• Glutamate
• In the short-term, alcohol decreases glutamate
  activity (decreased excitation), but after
  prolonged use, glutamate activity increases in
  order to compensate for the depressant effects of
  alcohol.
• Originally causes sluggishness and sedation, but
  after prolonged use, contributes to the Alcohol
  Withdrawal Syndrome.

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• SUMMARY NEUROCHEMISTRY contd
• Beta-endorphins
• Alcohol increases production of beta-endorphins
  in the hypothalamus.
• Causes the high associated with alcohol,
  thereby reinforcing alcoholism.
• Dopamine
• Alcohol increases dopamine activity. Those
  predisposed to alcoholism have lower than normal
  dopamine activity.
• Makes alcoholism rewarding.
• Serotonin
• Alcohol increases serotonin activity. Those
  predisposed to alcoholism have lower than normal
  serotonin activity.
• Contributes to the high associated with
  alcohol, and impulsive and violent behaviours.

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TREATMENT

• Complications in evaluating effectiveness
• Approximately 20 of addicts spontaneously
  achieve long-term abstinence with no obvious
  relationship to treatment/self-help group
  participation.
• May work less effectively or preferentially on
  individuals with comorbid disorders.

• No single universally acknowledged definition of
  efficacy or the best way to determine outcome.

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TREATMENT contd

• Inpatient rehabilitation programs usually last 28
  days provides highly structured treatment
  services (including group therapy, individual
  therapy, alcoholism education).
• Majority of treatment occurs in outpatient
  setting.
• Can initially result in alcohol withdrawal
  syndrome (ranges from mild irritability,
  insomnia, and tremors to potentially
  life-threatening medical complications, such as
  seizures, hallucinations, and delirium tremens).

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MEDICATIONS

• Benzodiazepines (i.e. Valium)
• Most popular choice of medication
• Sedative affects same areas in brain as alcohol
• Prevents development of delirium tremens
• Only used during initial withdrawal period
  because highly addictive
• enhances GABA activity

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MEDICATIONS contd

• Naltrexone (i.e. ReVia)
• Helps remain sober
• Opioid antagonist
• Blocks alcohol-induced release of dopamine
• Better results in certain subtypes effective for
  reducing alcohol dependence in the short term for
  people with low to moderate alcohol dependency

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MEDICATIONS contd

• Disulfiram (i.e. Antabuse)
• Anti-craving medication
• Produces sensitivity to alcohol
• Discourages drinking by making the person feel
  sick if he or she drinks
• Targets the brains reward circuits
• Use may not have any effect on abstinence (but it
  does reduce frequency of drinking)

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MEDICATIONS contd

• Acamprosate (Campral)
• Anticraving medication
• Widely used in Europe
• Works on different brain circuits to ease
  physical discomfort
• Works on the glutamate system
• GABA inhibitor

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MEDICATIONS contd

• Ondansetron (i.e. Zofran)
• Effective therapy for patients with early-onset
  alcoholism
• Serotonergic agent (imbalance between serotonin
  and dopamine is believed to create craving)
• Differentially affects some of the 15 specific
  serotonin-receptor subtypes, including the 5HT3
  receptor (offers promising results)
• Better results in certain subtypes (early onset
  alcoholics, who a biological predisposition
  towards alcoholism)

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MEDICATIONS contd

• Fluoxetine (i.e. Prozac)
• General serotonergic agent
• Reduces cravings desire
• Produces mixed results
• Effective in treating depressive symptoms as well
  as reducing alcohol consumption in patients with
  these comorbid illnesses

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MEDICATIONS contd

• Sertraline (i.e. Zoloft)
• SSRI (serotonin inhibitor)
• Very weak effects on norepinephrine dopamine
  reuptake
• Down regulates brain norepinephrine serotonin
  receptors
• Better results in certain subtypes (those with
  lower risk/severity of alcoholism and
  psychopathology)

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CONCLUSIONS

• many neurotransmitters are affected by alcohol
• alcohol is a depressant so it has an inhibitory
  effect on the frontal lobe, basal ganglia,
  cerebellum, limbic system, reticular formation
• different medications target different subtypes
  of the alcoholic population
• the best treatment is medication paired with
  counselling