Lecture 5, Substance Use Flashcards

1
Q

DSM Criteria for Substance Use Disorder (SUD)

A

SUD diagnosis reflects the impact of substance use on functioning in everyday life, rather than just the frequency or dose of substance use
Harmful consequences can occur without meeting dependence criteria, especially for those with mental health problems who may be more sensitive to the effects of substances

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2
Q

Consequences of Substance Use

A

Physical health: direct damage to liver, heart, and lungs, increased cancer risk; indirect harm from illness, injury, risky behaviors
Financial: cost of drugs/alcohol, lost income due to intoxication and after-effects
Social and interpersonal: conflict with others, exclusion/stigma, poor educational attainment, homelessness
Mental health: transient psychosis, depression, anxiety, worsened symptoms for those with established mental illness, increased suicidality and aggression
Societal and economic burden: rising NHS and welfare costs, criminal activity, increased rates of mental health problems

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3
Q

Prevalence/Epidemiology of SUD

A

Estimates vary by location and methodological differences; UK AUD estimate = approx 600,000 (1%)
35% of UK adults have used drugs at some point in their lifetime, with 9% using in the last year and 21% of young adults aged 16-24 using in the last year
Drug use fell 1995-2013 but is now rising again, with increased use of class A drugs in 16-24 year olds
65% of UK men and 50% of women have drunk alcohol in the past week, with prevalence increasing with age
More people are abstaining from alcohol and binge drinking is decreasing, particularly among young adults

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4
Q

Comorbidity and Dual Diagnosis

A

Substance use and mental health problems are highly comorbid (occur frequently together)
Dual diagnosis is a term used to describe those with severe mental illness and problematic drug/alcohol use (referred to as “dually diagnosed”)

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5
Q

Epidemiological Catchment Area (ECA) Study (Regier, 1990) Lifetime prevalence of SUD

A

The ECA study reported higher rates of substance use disorders (lifetime and current) in individuals with mental illness, compared to the general population. This finding is consistent across different studies and countries.

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6
Q

Schizophrenia/Psychosis and Substance Use

A

Individuals with psychosis have higher rates of substance use, including drugs, alcohol, and tobacco. Approximately 50% of individuals with psychosis use substances, while 85% smoke cigarettes. Substance use in individuals with psychosis is associated with poorer outcomes, such as more symptoms, relapses, hospitalizations, poorer functioning, and increased suicidality. There may be a causal role of substances, particularly cannabis, in the development of psychosis.

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7
Q

Why Psychosis and Not Bipolar Disorder?

A

Psychosis is more common than bipolar disorder in the UK, and there is a larger evidence base regarding the relationship between substance use and psychosis. Cannabis use has been linked to the development of psychosis, and individuals with schizophrenia are more vulnerable to the effects of THC.

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8
Q

Definition of Psychosis

A

Psychosis is a loss of contact with reality and may include false beliefs about what is taking place or who one is (delusions) and seeing or hearing things that aren’t there (hallucinations). Schizophrenia is diagnosed when an individual experiences two of the following: delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, negative symptoms, and social/occupational dysfunction, lasting 6 or more months.

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9
Q

Causes of Comorbidity between Psychosis and Substance Use

A

There are several potential causes of the comorbidity between psychosis and substance use. These include:

  1. Substance use causing psychosis
  2. Substance use as a consequence of psychosis (self-medication)
  3. Common origin (e.g., genetic vulnerability)
  4. Bidirectional – psychosis and substance use interact and maintain one another
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10
Q

Evidence I - Substances as a Cause of Transient Psychosis

A

There is evidence that some substances, such as amphetamine, cocaine, and cannabis, can cause transient psychosis. For example, tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, has been shown to produce schizophrenia-like positive symptoms in healthy individuals and transiently increase symptoms in people with schizophrenia. Individuals with schizophrenia may also be more vulnerable to the effects of THC.

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11
Q

Evidence II - Substance Use (Cannabis) Preceding Psychotic Symptoms

A

Longitudinal prospective cohort studies, such as Andreasson et al. (1987), Ferdinand et al. (2005), Henquet et al. (2005), van Os et al. (2002), and Zammit et al. (2002) have shown that substance use, particularly cannabis, often precedes the onset of psychotic symptoms. For example, Andreasson et al. found that individuals who used cannabis more than 50 times before the age of 18 were six times more likely to be hospitalized for schizophrenia at age 33.

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12
Q

Evidence III - Substance Use as Self-Medication

A

There is evidence that individuals with psychosis may use substances to self-medicate. Gregg et al. (2009) and Spencer et al. (2002) found that individuals with psychosis reported using substances to alleviate symptoms such as anxiety, depression, and insomnia.

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13
Q

Main Reasons for Substance Use in Individuals with Psychosis

A

According to Gregg et al. (2009), the main reasons for substance use in individuals with psychosis include:

  1. To alleviate symptoms
  2. Social
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14
Q

Genetic vulnerability

A

Genetic factors may predispose individuals to both mental illness and substance use.
Adolescents with the COMT polymorphism (Val allele) are 10 times more likely to have schizophreniform disorder at age 26, and genetic predisposition may moderate the risk of developing psychosis after cannabis use.

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15
Q

Bidirectional relationship between substance use and psychosis

A

Simple causal models are too simplistic to explain the relationship between substance use and psychosis.
The most likely explanation is that the relationship is bidirectional, with multiple risk factors (genetic, environmental, individual differences) playing a part.

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