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Lecture 7

PSY240H1 Lecture 7: Substance Use Disorders
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Department
Psychology
Course
PSY240H1
Professor
Christine Burton
Semester
Winter

Description
This lecture is on “Substance-Related & Addictive Disorders” (which is a diagnostic categoy in DSM that includes substance-related disorders and gambling disorders) Psychoactive substances are chemical substances that are ingested to alter mood and/or behaviour. DSM 5 has 10 categories of substances (Caffeine, Cannabis, Hallucinogens, Inhalants, Opioids, Sedatives + Hypnotics + Anxiolytics, Stimulants, Tobacco, Alcohol, Other/Unknownthis last one is usually labelled when a patient has ingested a drug that for ex. is a newly manufactured drug never before been given to humans until now and so only now we are finding out its causing bad effects and it doesn’t fall under any other category) In the brain we have the nucleus accumbens (NA) which is part of the forebrain and is associated with reward. NA is innervated by dopaminergic neurons originating in the ventral tegmental area. These two parts make up the mesolimbocortical dopaminergic pathway. This pathway is a source of reward in “normal” circumstances (in that it’s evolutionarily useful to have – for ex. food and sex stimulate the release of dopamine into NA which reinforces their use). Many psychoactive substances stimulate the mesolimbocortical dopaminergic pathway which causes intense reward experiences and as a result can cause addiction (which is not normal – i.e. not evolutionarily useful). Substance use means moderate ingestion (I am having a glass of wine). Intoxication is clinically significant problematic behavioural or physiological changes (Drunk). Substance abuse is use that interferes with/disrupts aspects of one’s life (ex. Family problems due to my drinking. Also, using under dangerous circumstances like before driving is considered abuse). One can use without abusing. One can abuse without becoming dependent (ex. binge a drug). One can be dependent without abusing (ex. using pain relief drugs that’s not disrupting life but gets withdrawal symptoms. Ex. Addicted to alcohol but functioning fine) A [substance] use disorder involves a pathological pattern of behaviours related to use of the substance. There are many types of [substance] use disorders (as indicated by the fact that you can insert almost any of the 10 substance names in the bracket). Each one pretty much has one essential criteria and it is that it requires distress/impairment as indicated by a number of symptoms (listed as #’s – see Alcohol use disorder later as an example). This new [substance] use disorder encompasses aspects of previously substance abuse and substance dependence disorder (it was not effective having both of these since most people were diagnosed with both). For most of the 10 substance categories, DSM has criteria and diagnoses for 5 main disorders: [substance] use disorder, [substance] intoxication, [substance] withdrawal (the previous two usually diagnosed in a hospital setting since they’re that dangerous), [substance]-induced disorder (ex. alcohol induced MDD), Unspecified [Substance]-related disorder There are some exceptions though: for example there is no such thing as Caffeine use disorder (although it’s in appendix of DSM5) and there is no Tobacco intoxication Depressants are a category of substances that reduce physiological arousal and anxiety. They relax you and give you a sense of well-being. They have a high incidence of tolerance and withdrawal (hence why they are meant for periodical use and not long term use). Examples include alcohol, barbiturates, and benzodiazepines—recall for panic related disorders. Note: Alcohol is also commonly associated with stimulant effects (more later). In addition to dependence these three things specifically cause cognitive/motor side effects (specifically sedative effects which are sleepiness, tired, slowness of thought). Barbiturates (used for anxiety were largely replaced by benzos in 1960s because they are safer in that barbiturates are easier to overdose. Combining drugs of the same category is lethal. The biggest difference between alcohol and substances like cocaine and heroin is that alcohol has been legal for most of history and has been incorporated in many cultures (parties, social gatherings) and religions and thus alcohol is constantly encouraged. When you drink alcohol it gets into the bloodstream and thus circulates through all organs along with your blood. It is gradually metabolized in the liver. Somatic effects depend on persistence and extremity of use – liver, brain, pancreas, and heart all at risk of damage. Withdrawal symptoms can be quite severe (tremor, nausea, vomiting, anxiety, psychomotor agitation, insomnia, sweating, high HR). There is also delirium tremens which basically severe withdrawal and characterized by confusion, hallucinations and seizures. It’s very rare and be fatal due to the seizures or cardiac collapse. Drinking during pregnancy can result in Fetal Alcohol syndrome which causes the child to have learning difficulties, intellectual deficits, and behavioural problems. They also have characteristic facial features. Alcohol is a GABA agonist (recall GABA makes receiving neuron less active by opening Cl ion channels). Alcohol thus causes GABA-receiving neurons to fire even less thus communicating less with other cells. This is consistent with the disruptions in movement, slurred speech, and thought that is characteristic of drinking alcohol. Alcohol also has anxiolytic effects (makes you feel less anxious – this is the stimulant aspect of it). All of these symptoms can also be re-worded to say that alcohol causes sedative effects (the effects are as if you just woke up). There are of course individual differences in how one is impaired by alcohol (how pleasurable it is, how intoxication manifests, how strong the sedative effects are) Alcohol lessens anxiety thus lowering inhibition – It makes you do more riskier and impulsive behaviour. Some people may behave more aggressively which is mediated by this lowering of inhibition. A person’s history of acting aggressive, the context (in a bar scene or with friends), and executive function (the central executive – inhibits behaviour…if this is weak that means you’re impulsive) all predicts chance of acting aggressive under alcohol. It’s not that the alcohol directly increases aggression it’s just that its effects at reducing apprehension and reducing your ability to anticipate consequences cause you to act aggressive. The idea it this: BAC is rising or falling; while in the process of drinking, alcohol acts as a stimulant, but as drinking tapers off it begins to act more as a sedative. Response to the sedative properties of alcohol predicts people’s likelihood of developing dependence. Fewer/lessened sedative effects makes you more likely. Also stronger euphoric/stimulant effects is a risk factor. Alcohol affects glutamatergic (by causing memory changes) and serotonergic (by causing mood and sleep changes and changes in the appetite – people report being able to fall asleep quicker but the sleep quality is poor). It also affects dopaminergic circuits (causing pleasurable effects sometimes euphoric). It also affects the brain’s natural opioid circuits (endogenous opioids) by causing analgesic (pain relieving) effects. Thus, alcohol’s pleasurable effects works through two mechanisms: positive reinforcement and negative reinforcement (hence strong tendency to reuse psychoactive substances). Examples: GABA-ergic anxiolytic effects of alcohol = negative reinforcement Analgesic effects = negative reinforcement dopaminergic effects = positive reinforcement. See DSM for Alcohol Use Disorder (slides 22, 23, 24). Notes: This disorder has caused controversy in that pharm companies have lobbied to make the criteria too broad so that more people would fall under this diagnosis. For #4 the urge can be so strong that you cannot stop thinking about it (like when you’re in a meeting). Alcohol Statistics 23% of Canadians exceed Canadian guidelines (not laws) for low-risk drinking. About 3% of Canadians are alcohol dependent in a given year (9% of adult drinkers have “some level of problem” with alcohol). There are cultural variations as well: More Canadian than American uni students use alcohol but more American students are binge drinkers (likely having to do with the fact that alcohol in the States is cheaper and easier to get – a bartender won’t stop you there). Many Asian countries have lower rates of alcohol-related disorders because 1/3-1/2 of Asian people don’t produce alcohol dehydrogenase so they get symptoms like face flushing and nausea (this is +ve punishment). Men are more likely to drink and drink heavily than women (16% of adult men are heavy drinkers vs. 4%). Young males (18-29) most likely to have alcohol use problems. About 20% of people with severe alcohol dependence experience spontaneous remission without relapse, Common course of alcohol disorders are fluctuating: abstinence, heavy drinking, social drinking. Another common course: steady progression of severity each decade from 20s and on. Alcohol disorders have high comorbidity with: anxiety and depressive disorders, gambling disorder (pathological gambling). However these comorbid patterns could reflect: Chance (all these disorders are very common so it could just be due to chance it happened), Alcohol disorders cause/predispose to others, Other disorders cause/predispose to alcohol-related disorders (alcohol used as a self-medication for ex. to remove anxiety or depression). Etiological factors in alcohol-related disorder: Twin&Adoption studies have shown that there is a genetic influence on alcoholism in men (but in women the studies have produced mixed results). Genes linked to responsivity of dopaminergic circuits to alcohol may be involved. More etiological factors on alcohol-related disorders: Recall that the use of psychoactive substances is strongly reinforcing. Negative reinforcement may be related to forms of self- medication. Negative reinforcement is also relevant to opponent process theory (see next paragraph) (this theory is more for chronic users) The idea is this: Drug-induced spikes in pleasure will lead to corresponding spikes in negative feelings. The more one uses a drug, the more intense the negative after-effects. A person’s motivation for using the drug eventually changes from obtaining pleasurable high to now taking the drug in order to relieve aversive lows (i.e. its course goes from at first a +ve reinforcement to mainly –ve reinforcement later). Recall classical condition
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