Canada’s Guidance on Alcohol and
Health
Update published January 2023
Much chatter in the press/social media about the severe change in
recommendations from earlier iterations

 Previous recommendations:
 10 drinks per week for women, no more than 2 drinks on any given day most days
 15 drinks per week for men, no more than 3 drinks on any given day most days

Canada’s Guidance on Alcohol and
Health

it is recommended that people living in canada consider reducing their alcohol use.

because there is a continuum of risk associated with weekly alcohol consumption

the risk of harm from alcohol is...

low for individuals who consume 2 standard drinks or less per week.

and moderate for those who consume between 3 and 6 standard drinks per week.

risks increase for those that consume 7 standard drinks or more per week.

consuming more than 2 standard drinks per occassion is associated with an increased risk of harms to self an others.

true

when trying to get prego or prego there is no known safe amt of alcohol use

true

sex and gender

above the upper limit of the moderate risk zone for alcohol consumption-the health risks increase steeply for females than males.

DSM-V
Criteria:
Substance Use
Disorder

“A problematic pattern of
[substance] use leading to clinically
significant impairment or distress,
as manifested by at least 2 of the
following, occurring within a 12-
month period:”
-Impaired control
- Social impairment
- Risky use
- Pharmacological criteria

DSM-V Diagnostic Criteria- Alcohol Use Disorder

1. Alcohol is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.
3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.
4. Craving, or a strong desire or urge to use alcohol.
5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home.
6. Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of
alcohol.
7. Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
8. Recurrent alcohol use in situations in which it is physically hazardous.
9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have
been caused or exacerbated by alcohol.
10. Tolerance, as defined by either of the following:
1. A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.
2. A markedly diminished effect with continued use of the same amount of alcohol.
11. Withdrawal, as manifested by either of the following:
1. The characteristic withdrawal syndrome for alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal).
2. Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

1) Have you ever felt you should Cut down on your drinking?
2) Have people Annoyed you by criticizing your drinking?
3) Have you ever felt bad or Guilty about your drinking?
4) Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (Eye-opener)?

Assessment Tool: CAGE

Scoring: Item responses on the CAGE questions are scored 0 for "no" and 1 for "yes" answers, with a higher score being an indication of alcohol problems. A total score of two or greater is considered clinically significant.

Assessment
Tool: AUDIT

AUDIT = Alcohol Use Disorders IdentificationTest

10 questions
Interview or Self-Reported
Developed by the World Health Organization
Must be answered based on STANDARD drinks

Assessment Tool:
AUDIT

- Score 8 or more: Hazardous
Drinking
- Score 13 for females, 15 for
males: Likely presence of
alcohol use disorder

Why the
difference
between sexes?

- Answer lies in physiological difference
between the sexes
- Cis-women and people who were Assigned
Female at Birth (AFAB) generally have a
lower % water in their bodies
- Alcohol is water soluble
- Therefore, less alcohol is needed to cause
intoxication
- New research suggests cis-women and
AFAB may produce less alcohol
dehydrogenase than cis-men or people
assigned male at birth (AMAB)

MOA of Alcohol

Alcohol
Ingestion
-incr GABA (+ incr Glutamate to compensate)
-Disinhibition/
CNS
depression

under normal circumstances

inhibition =excitation

GABA and excitation= glutamate

alcohol causes GABA to .....

increase

with long term alcohol exposure, the brain attempts to restore eqbm by...

compensating for the depressant effects of alcohol aka the brain decreases inhibitory neurotransmission and enhances excitatory neurotransmission.

how does short term alcohol exposure tilt the balance towards inhibition?

by enhancing the function of inhibitory neurotransmitters and neuromodulators i.e GABA, glycine and adenosine

what happens during withdawal?

compesatory changes are no longer opposed by the presence of alcohol-balance shifts towards excessive excitation.

what are the characteristics of the state of hyperexcitation?

seizures

delirium and anxiety

→ Chronic alcohol use leads to chronically elevated

GABA and glutamate

When alcohol quickly removed:

GABA levels drop quickly
glutamate levels remain elevated
Can lead to Delirium Tremens

ALCOHOL ADME

Absorption- oral absorption is rapid- 5-10 mins after ingestion
Peak = 30-90 mins after last drink depending on type of drink
Food slows absorption and increases time to peak
-Distribution- Vd = 0.6-0.7L/kg, less in women
Metabolism
Ethanol (worked on by Alcohol Dehydrogenase) to acetaldehyde which is worked on by Acetaldehyde dehydrogenase to become acetate CO2 + H2O
▪ Elimination- Primarily renal. Lungs can eliminate up to 10% (rely on this for breathalyzer tests)
▪ Elimination rate = 15-20mg/dL/hour (longer in AUD)

Symptoms: Acute
Intoxication

 Slurred speech
 Ataxia
 Disinhibition
 Euphoria (via reward pathway)
 Aggression
 Flushing
 Nausea/vomiting

Severe
Intoxication/Overdose

 Severe intoxication/overdose:
 Blackouts- not creating new
memories
 Coma
 Respiratory depression
 Hypoglycemia
 Hypothermia
 Death

Management:
Acute Intoxication

Provide a safe space
 Fluid balance is very important- oral or IV fluids as
tolerated
 Glucose monitoring
 TIME is the main cure for acute alcohol intoxication
 Antagonists not used
 Alcohol poisoning- the person may pass out and not be
able to vomit→ MAY require stomach pumping etc. No
longer routinely done

Alcohol Withdrawal

More than just a hangover
 Can be life threatening
 Body has compensated for chronically
high levels of GABA by increasing release
of excitatory neurotransmitters like
glutamate
 Abrupt removal of alcohol leads to a
rapid drop in inhibitory neurotransmitters
 Excitatory neurotransmitters take time to
down-regulate and reduce
 CNS in an excitatory state
 Delirium tremens, seizures, death

CIWA-Ar
 Clinical Institute Withdrawal
Assessment- Alcohol (revised)

 Pulse
 Nausea/vomiting
 Tremor
 Paroxysmal sweating
 Anxiety
 Agitation

 Tactile disturbances
 Auditory disturbances
 Visual disturbances
 Headache/fullness
 Orientation/clouding of
sensorium

Clinician assessment tool used to
evaluate the level of alcohol
withdrawal
 Helps dictate treatment of
alcohol withdrawal
 Combines clinician observation
and patient reporting
 Validated tool

CIWA-Ar score of less than ....is the goal

discontinue protcol if score less than 10 for....

10

3 consectutive assessments.

hold benzos and notify prescriber if benzo intoxication occurs e.g..

ataxia

nystagmus

disorientation, RRless than 10/min or systolic BP less than 100mmhg.

notify prescriber if patient has recieved more than....or if sx of wwithdrawal worsen after 2 consecutive doses

60mg diazepam or 12mg lorazepam in a 12h period

Delirium Tremens

Life threatening condition
caused by severe alcohol
withdrawal due to acute
abstinence or reduction in
consumption of alcohol
 Occurs in ~5% of alcohol
withdrawal patients
 Starts ~48-96 hours after last
drink and lasts ~5 days

Delusions
Hallucinations requirement
Tachycardia
Hyperthermia
Hypertension
Diaphoresis

Elevated cardiac markers

Increased O2

Hyperventilation → respiratory
alkalosis

Hypophosphatemia

Rhabdomyolysis

Cardiac failure

Risk factors for DTs

 Previous DT
 Sustained heavy drinking
 >30y/o
 Concurrent illness
 Significant alcohol withdrawal in the
presence of elevated BAC
 Longer period since last drink (ex.
Person presenting >2 days since last
drink)
 Treat with supportive care, benzos,
treatment of underlying conditions, and
frequent monitoring of symptoms

 NO SUCH THING AS MILD DTs(Delirium Tremens)
 DTs are the most severe form
of withdrawal
 Occur after other withdrawal
symptoms
 Withdrawal hallucinosis can
occur well before DTs set in

true

Non-Beverage
Alcohol

 Non-beverage alcohol is alcohol that is not intended for
human consumption as a beverage.
 E.g. hand sanitizer, mouth wash, aftershave, vanilla
extract
 Marginalized people with severe AUD are often forced to
turn to these forms of alcohol due to inability to afford
beverage alcohol
 Can lead to many harms, including severe intoxication,
blindness, and death (especially if it is not ethanol that is
being consumed)
 A harm reduction approach here would be to provide them
with beverage alcohol.
 More on this later

Chronic
Alcohol Use

 Alcohol use disorder
 Different than treating acute withdrawal or
intoxication
 Non-pharm= CBT, group therapy, AA and other
abstinence-based therapies
 Pharmacological = disulfiram, acamprosate,
naltrexone
 All used to help promote prolonged abstinence and
recovery

A Word About AA/NA

 Created in USA by Bill Wilson and Bob Smith
 Originally a faith-based program
 Abstinence- based: believe that use of drugs to
help with abstinence (ex. Diazepam for
alcoholism or methadone for opioid use
disorder) dose not constitute true abstinence
 Historically, people who used medications like
above were not allowed in AA/NA
 Newer groups forming with less emphasis on the
“God” aspect and with medications allowed

Naltrexone

 Aka Revia®
 Mechanism of action: blocks central µ opioid
receptors
 Doing so blocks the reinforcing nature of
alcohol in the nucleus acumbens (reward
pathway) in the brain
 Also has effect on HPA-axis to suppress alcohol
use
 DOES NOT CAUSE PHYSICAL AVERSION TO ALCOHOL
 If the person drinks, they will not vomit etc
 Rather, helps reduce cravings for, and euphoria
caused by alcohol

Naltrexone
 Dosing:

50mg daily (often will see
starting dose of 25mg)
 Efficacy:
 Found to reduce alcohol use in
people with AUD better than
placebo in several SR/MA
 E.g. A 2010 Cochrane review
found the RR to be 0.83 (0.76-
0.9) for heavy drinking for
naloxone compared to placebo.
Also reduced drinking days by 4%

Naltrexone

 IMPORTANT:
 THIS IS AN OPIOID ANTAGONIST
 Therefore, opioid analgesia will be
ineffective
 CONTRAINDICATED IN COMBINATION
WITH METHADONE- several dangerous
cases have occurred as a result of
naltrexone+methadone combination
 THERE IS NO SITUATION IN WHICH THE
COMBO IS WORTH THE RISK
 ADRs: Nausea, headache, dizziness. Can
cause elevation in LFTs- measure at
baseline and then monthly

Acamprosate Aka Campral®

 Mechanism of action: not 100% clear
 Postulated to restore glutamate “tone”
 Modulates the neurotransmission of
glutamate upon alcohol use cessation
 DOES NOT DECREASE WITHDRAWAL
SYMPTOMS- pt is still at risk of DTs
 Patients may do better if already
abstinent x 7 days or so- evidence on
this unclear

Acamprosate
 Dose

2x333mg TID (ADHERENCE ISSUE)
 Evidence:
 Murky here too
 Cochrane Review in 2010 of acamprosate vs
placebo showed NNT of 9 for return to ANY
drinking and increased abstinence duration
by 11%. NO effect on heavy drinking
 Other studies have found it to be less
effective
 ADRs: Diarrhea, flatulence, insomnia, anxiety,
depression
 CI in CrCl <30ml/min

DisulfiramAka Antabuse

▪ Irreversible inhibition of acetaldehyde dehydrogenase (DOA up to 14 days)
▪ Produces severe reaction in combination with alcohol due to build-up of acetaldehyde → approximately 30mins after ethanol exposure
▪ Vomiting, flushing, tachycardia, hypotension, syncope
▪ Reaction severity depends on dose of disulfiram and ethanol

Disulfiram

 Considered aversion therapy
 Helps eliminate positive conditioning
associated with drinking- no longer
associated with euphoria but with negative
consequences
 Best if given under supervision or in highly
motivated patients
 Dosing: 125-500mg daily. often done as
500mg daily for 2 weeks then 250mg once
daily thereafter

Disulfiram
 Evidence

Evidence = mixed at best
 2014 meta-analysis = disulfiram
no better than placebo for
return to drinking (JAMA. 2014
May;311(18):1889-900)
 Other SR/MA have found time to
first drink and other measures of
abstinence to be no better with
disulfiram than placebo
 No longer commercially
available- must be compounded

Other Anti-Craving
Treatment

 Anti-craving treatments work to reduce reward pathway
activity
 Gabapentin- modulates dopamine. Has good evidence,
especially in combination with naltrexone
 Baclofen- GABA agonist
 Topiramate- modulates GABA system

Complications of Alcohol Use

 MANY
 Liver disease: hepatitis, fatty liver,
cirrhosis
 Wernicke’s encephalopathy, Korsakoff’s
dementia
 Peripheral neuropathy
 Stroke (hemorrhagic)
 Cardiomyopathy
 Arrhythmia
 Cancer
 Impotence
 Esophageal varices

Complications
Chronic AUD

 MANY
 Liver disease: hepatitis, fatty liver,
cirrhosis
 Wernicke’s encephalopathy, Korsakoff’s
dementia
 Peripheral neuropathy
 Stroke (hemorrhagic)
 Cardiomyopathy
 Arrhythmia
 Cancer
 Impotence
 Esophageal varices

Chronic Alcohol Use: The Reality

Many of these people are homeless or have experienced homelessness
 “Listerine Bums”
 Imagine how awful the disease must be to have a person stealing mouth wash,
cologne, vanilla extract etc. to support stave off cravings and feed their use disorder
 As pharmacists, we need to get away from this demeaning language and refer to
these people as what they are, PEOPLE WHO NEED OUR HELP
 Will be in and out of the justice system- there is little help available to these
folks
 Often spend many nights in the “drunk tank”
 Given a Cliff bar and a bottle of water
 “dry out”
 Sent back out to the street once sober

What Can Pharmacists Do?

 ASK, in a non-judgemental way, about people’s drinking
 ASK if they feel they would like to change their drinking habits
 USE the CAGE screening tool to aid your discussions
 KNOW where to refer people when they come to you for help

Difficult to get a true picture of stimulant use in Canada

 CTADS historically combined them into “illicit drugs”

-Cocaine/crack
- MDMA
- Hallucinogens
- Methamphetamine
- Heroin
- Past year use of those 5 drugs was 3% in the 2017 CTADS
 However, methamphetamine use is escalating across the country

trauma..>dusconnection...>drug use numb pain....>criminal activity to get access to drug.>arest incarcerate &bac

true

Substance Use Disorder Risk Factors

Personal history of substance use disorder
Family history of substance use disorder
History of psychiatric illness
History of pre-adolescent sexual abuse

DSM-V Criteria: Substance Use Disorder

“A problematic pattern of [substance] use leading to
clinically significant impairment or distress, as manifested
by at least 2 of the following, occurring within a 12-month
period:”
 Impaired control
 Social impairment
 Risky use
 Pharmacological criteria

Impaired control

Using higher doses and/or
using substance over a longer
period of time than initially
intended.

e.g Taking more hydromorphone
pills than prescribed or continuing to seek them out after rx is finished
“I really need to cut back”

Social impairment

Failure to fulfill major roles
(home, school, work etc)
Avoiding family activities in
order to use

Risky use

Using in situations that are
physically dangerous or using
despite knowledge of serious
harm
Drinking and driving.
Continued use of cocaine
despite knowledge of
arrhythmia

Pharmacological criteria
(tolerance and withdrawal)

Increasing doses required to
achieve desired effect
(tolerance). Withdrawal
symptoms occurring when use
abruptly stopped.
e.g Escalating doses of
hydromorphone required to
achieve the “high.” Alcohol
withdrawal syndrome and DTs.

SUD etiology

we find SUD at the intersection of

-learned maladaptive coping

-environment

-drug

-genetics

“Abuse liability

refers to the tendency of a drug to be used in nonmedical situations, even sporadically, due to underlying psychoactive effects it produces (such as euphoria, sedation, or mood changes)” –
Cambridge Cognition

A drug needs to have abuse liability to .....

reinforce the neural
pathways/reward system

SUD is ......whereby the drug “hijacks” the normal reward
pathway and the brain learns that that is easier than normal coping
strategies.

a learning disorder

Lays down neural pathways that say “stress is more easily managed by
using drug X”

CNS Depressants

 Alcohol
 Benzodiazepines/barbiturates
 Opioids
 Volatile Solvents

 Stimulants

 Cocaine/crack
 Amphetamines
 Caffeine
 Nicotine

 Hallucinogens

 LSD
 Psilocybin (mushrooms)
 Mescaline
 Phencyclidine (PCP)
 Ecstasy (MDMA) (also stimulant)
 Cannabis (also depressant)

natural rewards elevate dopamine levels.

food and sex

Basic Pharmacology: Stimulants

 Lead to release of ++ neurotransmitters
 Especially NE, Dopamine, Serotonin
 Hijack the reward pathway

Cocaine:
 Other names: Blow, snow, rock, coke, crack

 Available in 2 main forms:
 Crack= crystalline, smokable form→cheaper than pure cocaine
 Cocaine= pure form→ water soluble. Injected or snorted.

MOA: blocks reuptake of catecholamines to the presynaptic neuron
leading to increased concentrations of 5HT, NE, dopamine and
epinephrine in the synapse.

cocaine use leads to....

Exogenous activation of the reward pathway→euphoria, insomnia,
increased heart rate, reduced appetite
 Directly cardiotoxic- overdose deaths usually caused by cardiac arrest
 Can lead to extreme increases in core body temperature, which is very
dangerous

cocaine kinetics

intravenous onset

<1 minute

peak 3-5 minutes

duration of action 30-60mins

nasal route onset

1-5 mins

peak 20-30mins

duration of action 60-120

smoking onset

< 1 min

peak 3-5 minute

duration 30-60 minutes

gastrointestinal route

onset

onset 30-60minutes

peak 60-90

duration - unknown.

Cocaine: Acute Effects

 Euphoria/extreme happiness
 ++ Energy
 Mental alertness
 Irritability
 Paranoia
 Bizarre, unpredictable behaviour
 Insomnia

 Vasoconstriction
 Dilated pupils
 Nausea
 Increased BT and BP
 Tachycardia
 Tremors/restlessness
 Muscle twitches

Cocaine: Long Term Effects

Of snorting: nosebleeds, frequent runny nose, loss of smell, trouble
swallowing
 Of smoking: Cough, asthma, respiratory distress, increased risk of
pneumonia
 Of injection: Increased risk of HIV and Hep C, other bloodborne illness,
endocarditis, skin/soft tissue infections, collapsed veins
 General:
 Malnourishment due to chronic appetite suppression
 Parkinson’s disease after years of use
 Insomnia/restlessness after binges
 Severe paranoia

Cocaine: Overdose

Overdose:
 Tachycardia
 Hypertensive crisis
 Fever/hyperthermia
 MI
 Death
 Risk of death increases when mixed with other drugs
 Often mixed with EtOH→ party drug
 Heroin + cocaine = speedball = very dangerous and deadly
 No antidote to cocaine overdose- supportive care only

Cocaine: Withdrawal

 Withdrawal:
 Anhedonia
 Depression
 Fatigue
 Increased appetite
 Slowed thinking
 Scary dreams and insomnia
 Anhedonia and depression and persist for YEARS after drug
use stops
 Brain needs to re-learn how to experience normal
pleasure

Methamphetamine:
 AKA Crystal Meth, Crystal, Ice, Speed, Blue, Meth
 ROA: Smoked, swallowed, Snorted, Injecting (powder dissolved in water or
EtOH)
wat is the MOA?

MOA: ++++ dopamine, serotonin, norepinephrine, and epinephrine release in the nucleus acumbens

 Also blocks neurotransmitter reuptake.

Methamphetamine: Pharmacokinetics

Absorption:

rapid via any route (PO, IN,
Inhaled, IM, IV, PR, PV)

Methamphetamine: Pharmacokinetics Distribution:

 Quickly and easily crosses BBB
 Large Vd of 3-4L/kg

Methamphetamine: Pharmacokinetics Onset of action:

 Injection or smoking: seconds
 Intranasal: 5 mins
 Oral: 20 mins

Methamphetamine: Pharmacokinetics Peak plasma [ ]:

 Injection or smoking: 30 mins
 Oral: 2-3 hours

Methamphetamine: Pharmacokinetics Duration of action:

 Plasma T1/2 : 12-34 hours
 Effects commonly persist for >24 hours

Methamphetamine: Acute Effects

Adrenergic activity:

 Adrenergic activity:
 Tachycardia
 Hypertension
 Hyperthermia
 Wakefulness

 Dopaminergic activity:
 Increased movement
 “Tweaking”
 Euphoria/rewarding feeling

Methamphetamine: Acute Effects Serotonergic activity:

Changes in appetite
 Changes in thirst signal
response
 Changes in mood
(expansive)

Methamphetamine: Acute Effects

 Dopaminergic activity:
 Increased movement
 “Tweaking”
 Euphoria/rewarding feeling

Methamphetamine: Long Term Effects

 Increased risk HIV and Hep B&C
 Risky behaviours
 Injury to nerve cells (worsening of
HIV as a result)
 Dental complications (“meth
mouth” see pic)
 Changes in brain structure and
functioning; changes in
dopaminergic pathways
 May be irreversible or may not
recover for a long time after drug
use stops
 Psychosis/hallucinations
 Violent behaviour
 Sleeping problems
 Changes in bone structure
 Overdose = death from cardiac
arrest or due to hallucination

Methamphetamine: Formication

 sense of bugs crawling all over the
skin accompanied by extreme
itchiness.
 Leads to intense sessions of
scratching and subsequent
scabbing and scars.

MDMA (Ecstasy): AKA: Ecstasy, Molly (slang for molecular, implying purity/scientific)
3,4-Methylenedioxymethamphetamine
is a ....

A sympathomimetic amphetamine

MDMA (Ecstasy):

 Considered a social/party drug- people report feeling close to others,feeling loved, feeling more social and having improved sensory perception
 Often sold at parties and in bars, part of “rave” culture
 Sold in pill form with “cute” designs to appeal to party goers

 MOA: Indirect serotonergic agonist- leads to increased concentration of
serotonin in the synapse. Also leads to release of NE and dopamine.
 Similar effects to amphetamines- euphoria

MDMA Pharmacokinetics

Absorption: readily absorbed from GI tract
Distribution:
 Peak within 2 hours
 Duration: 4-6 hours
Elimination:
 75% excreted intact via urine
 Remainder metabolized via CYP 2D6

MDMA: Short Term Effects

With onset of action comes:
 Increased energy/activity
 HTN/tachycardia
 Euphoria/expansive mood
 Closeness with others and increased sexual libido
 Increased trust/empathy
 Nausea
 Muscle cramping
 Chills

MDMA: Short Term Effects

 Hyponatremia:
 +++sweating
 +++thirst
 MDMA causes persistent secretion of antidiuretic
hormone which slows water excretion
 MDMA users also often believe that drinking lots of
water will reduce risk of hyperthermia
 All leads to hyponatremia which can be very dangerous

MDMA: Short Term Effects

 Serotonin Syndrome:
MDMA is ++ serotonergic
Characterized by a triad of symptoms:
Autonomic dysfunction
Abnormal neuromuscular activity
Altered mental status
Potentially life threatening

MDMA: Long Term Effects

 Many of these can persist for YEARS
 Especially anything to do with
pleasure
 Brain needs to re-learn how to
experience pleasure in response to
normally pleasurable experiences
like yummy food, a hug from a
loved one, or sex.

 Irritability
 Impulsivity
 Aggression
 Depression
 Sleep problems
 Anxiety
 Memory and attention issues
 Decreased appetite
 Decreased interest in and pleasure
from sex

MDMA Overdose

 Serotonin syndrome
 Hyponatremia
 Hepatotoxicity
 Life-threatening increases in HR, BT, and BP
 No antidote
 Supportive measures only

Stimulant Use Disorder Treatment

 Not much to offer folks
 Not a lot of evidence on what to use
 Non-Pharm: CBT, CBT, Group Therapy, Motivational incentives
(aka $$)

Pharmacological trtment for stimulant use disorder

(May see):
 Benzodiazepines (diazepam)- issues with efficacy and risk of
developing BZD use disorder
 Methylphenidate or dextroamphetamine (Dexedrine)
 Some emerging evidence that these MAY help with stimulant
withdrawal

Hallucinogens

Drugs:
 LSD
 Psilocybin
 Peyote
 Dextromethorphan
 Salvia
 PCP and Ketamine (dissociative
hallucinogens)

Hallucinogens-effects

 Sleep changes
 Hallucinations/delusion
 Change in sexual behaviour
 Changes in perception of time and
place
 Spiritual experiences
 Relaxation
 Paranoia and overt psychosis (short
and long term

hallucinogen Dissociative:

changes in pain
perception, perception of past
trauma
 Some being studied for tx of
tx resistant depression etc

 Hallucinogen Persisting
Perception Disorder (HPPD):

 Flashbacks to when patient
was on hallucinogen
 Happen without warning
 Can happen days to years
after last drug use

Hallucinogen “Abuse Liability”

 Hallucinogen use disorders are in the DSM-V
 However, there is some debate about whether a true hallucinogen use disorder can occur at a brain level
 They do not cause a release of NTs in the nucleus acumbens
 They do not then “hijack” the reward pathway
 Without doing that, can a person have a true use disorder?
 Rarely hear of someone using LSD over and over again to the detriment of their
family, work, or school commitments
 Hallucinogens are often taken in addition to other substances
 Those substances are usually the ones for which the person has the true use disorder
 Food for thought!

Volatile Solvents/Inhalants

Solvents (become gas at RT)
 Aerosol sprays
 Gases (including petroleum gas)
 Nitrites (ex. Nitroglycerine)
 Work to slow/reduce brain activity

Volatile Solvents/Inhalants

Acute Effects:

 Slurred speech
 Ataxia
 Euphoria
 Dizziness

 Long term effects:

 Liver and kidney damage
 Hearing loss
 Bone marrow damage
 Loss of coordination
 Muscle damage
 Delayed behavioural development
 Brain damage

Hallucinogen/Solvent Use Disorder
Treatment

 Not much to offer folks
 Not a lot of evidence on what to use
 Non-Pharm: CBT, CBT, Group Therapy, Motivational
incentives (aka $$)