Lecture 3: food, cannabis and opioids

Question 1

What is food addiction?

Answer 1

The concept of FA is widely accepted among the general public, In recent years, FA started to gain some credibility in the scientific literature and is linked with obesity. Focus on binge eating. Not to be equated with eating disorders (e.g., binge eating disorder)

Question 2

What is the yale food addiction scale

Answer 2

Created to study severity of food addiction,Version 2.0. Questionnaire items correspond to DSM-v substance related and addictive disorders symptom criterion or clinical impairment/distress

Question 3

The yale food addiction scale criteria

Answer 3

People sometimes have difficulty controlling how much they eat of certain foods such as:

• Sweets (e.g., ice cream, chocolate)
• Starches (e.g., white bread, rolls, pasta)
• Salty snacks (e.g.,chips, pretezels and crackers)
• Fatty foods (e.g., steak, bacon, hamburgers, pizza)
• Sugary drinks (e.g. soda pop, sports drinks). When the following questions ask about “certain foods” please think of any foods or beverages similar to those listed in the food or bevreage groups above or ANY other foods you have has difficulty with in the past year

Question 4

What are the DSM-IV over arching criteria for food addiction?

Answer 4

• Taking the substance in larger amounts or for longer thanintended
• Wanting to cut down or stop using the substancebut not managing to
• Important social, occupational or recreational activities given up or reduced
• Cravings and urges to use the substance
• Continuing to use, even when it causes problems in relationships
• Recurrent use of substance in situations that are physically hazardous
• Use continues despite knowledge of adverse consequences
• tolerance (marked increase in amount; marked decrease in effect)
• Withdrawal symptoms and/or substance used to alleviate/avoid withdrawal
• Use causes clinically significant impairment or distress

Question 5

What is the prevalence of food addiction?

Answer 5

Used Yale Food Addiction Scale (YFAS), 25 studies were identified with a total of 196,211 predominantly female, overweight/obese participants (60%). Using meta-analysis, the weighted mean prevalence of YFAS food addiction diagnosis was 19.9%. FA was found to be higher in adults aged >35 years, females, and overweight/obese participants

Question 6

What has research shown about Food addiction and the brain?

Answer 6

Prior research has shown that food and drug use both result in DA release in mesolimbic regions and the degree of release correlates with subjective reward from both food and drug use

Question 7

How do the reward learning regions respond to food and substances?

Answer 7

Although obese and substance dependent individuals show hyperresponsivity of reward learning regions to food and substance cues, respectively, actual intake of food and drugs is associated with reduced reward circuitry activation. Strong parallels In the brain regions that encode reward from drugs and palatable food and in neural abnormalities associated with addiction and obesity

Question 8

Have studies testing food addiction found similarities to substance addiction?

Answer 8

Tested the idea that elevated “food addiction” scores based on the YFAS are associated with similar patterns of neural activation as substance addiction

Question 9

What was hypothesized about participants experiencing a food addiction? (Gearhardt et al.)

Answer 9

Hypothesized that participants exhibiting elevated FA symptoms would show greater activation in response to food cues in the amygdala, striatum, OFC, DLPFC, thalamus, midbrain, insula, and anterior cingulate gyrus.

Also hypothesized that, during consumption of a highly palatable food, the high FA group would demonstrate less activation in the dorsal striatum and OFC, analogous to the reduced activation demonstrated in substance-dependent participants on receipt of a drug.

Question 10

What was the method of the study? (Gearhardt et al.)

Answer 10

Participants: 48 healthy young women. Examined the association of YFAS scores with neural activation in response to…

1) Cues signaling impending delivery of a highly palatable food (chocolate milkshake) vs. a tasteless control solution
2) Intake of a chocolate milkshake vs. a tasteless solution

Question 11

What were the results? (Gearhardt et al.)

Answer 11

They saw that the brain regions that were hypothesizing would light up did and there was a moderate correlation between food and those regions

Question 12

Food addiction and the brain: conclusions (Gearhardt et al.)

Answer 12

Support theory that compulsive food consumption may be driven in part by an enhanced anticipation of the rewarding properties of food
Like how addicted individuals are more likely to be physiologically, psychologically, and behaviorally reactive to substance-related cues
May be due to incentive salience (cues may begin triggering the release of DA)

Question 13

What were the Limitations of the study? (Gearhardt et al.)

Answer 13

only 48 people and restricted to only “healthy” people and only women thus cannot determine if it would generalize to men

Question 14

What were the aims in Davis et al. study food addiction and obesity?

Answer 14

Investigate the legitimacy of FA in humans. Extend the validation of YFAS

Question 15

What was the method of the study by Davis et. al?

Answer 15

Obese adults (aged 25–45 years) 
Retrospective design Assessed clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance

Question 16

results of Davis et al. study?

Answer 16

Participants with FA…Had a greater co morbidity with binge eating disorder, depression, and ADHD compared to their age and weight equivalent counterparts
Were more impulsive and displayed greater emotional reactivity than obese controls
Displayed greater food cravings and the tendency to self soothe with food

Question 17

What are some limitations of the food addiction concept?

Answer 17

Is addiction the best framework to study FA? addiction has a natural history and course, and a set of vulnerability or risk factors. If we are to consider that FA is a disorder then it would need to be similarly characterized
Close scrutiny of the transitions from use to abuse to addiction will be critical in elucidating the development of the syndrome
SUD may not be the best framework to characterize FA

Question 18

What is considered legal use of opioids?

Answer 18

Most are classified as schedule I drugs under the controlled drugs and substances Act (CDSA). Legal when they are prescribed by licensed practitioners and used by the person for whom they are prescribed

Question 19

What is illegal use of opioids?

Answer 19

Illegal possession of opioids and “double doctoring” (i.e., obtaining a prescription from more than one practitioner without telling the prescribing practitioner about other prescriptions received in the past 30 days) can result in years of imprisonment.Trafficking, importing, exporting or producing opioids can result in life imprisonment

Question 20

What is the prevalence of opioids in Canada?

Answer 20

More prevalent in older adults. People with vulnerability factors are at a higher risk for opioids

Question 21

What is an appropriate use of Opioids?

Answer 21

opioids for pain management is an important and effective intervention for managing acute pain However since some people are at higher risk for developing opioid addiction, it is important to conduct a comprehensive assessment of risk factors before initiating prescription opioid pain management
People with a family or personal history of substance use problems are at higher risk

Question 22

Opioid related deaths in Canada

Answer 22

are rising

Question 23

Fentanyl related deaths in Canada

Answer 23

Are rising and peaking in 2017 and 2018

Question 24

What happens to the neurotransmitters and in the synapse when opiates are consumed?

Answer 24

Prior to use, inhibtory neurotransmitters are active in the brain, these NT’s inhibit DA from being released. When the body’s natural opiates activate opiate receptors, the release of inhibitory neurotransmitters is shut down. Without inhibition, DA can be released . The consumed opiate mimics natural opiates in the body and binds to opiate receptors, turning off DA inhibition. DA is allowed to flood the synapse, producing immediate feelings of sedation and wellbeing

Question 25

What can long term use of opioids do to the brain?

Answer 25

Long-term use of opioids can impair speed of cognitive processing and working memory

Question 26

How opiates cause overdose deaths ?

Answer 26

Overdose deaths caused by activated opioid receptors in the brain stem that suppress or stop the breathing reflex

Question 27

How do fentanyl and other opioid drugs lead to maladaptive learning?

Answer 27

essentially hijack the brain’s natural motivation and reward system, leading to a strong, maladaptive form of learning

Question 28

What is the prevalence of cannabis use and addiction?

Answer 28

on the rise relative to previous years. Higher amongst people ranging from 18-24 years old (28.4%). The older population, 65 or older are also consistently using (17.5%). It is less commonly used by people in their mid life

Question 29

How do we screen for cannabis use?

Answer 29

The cannabis use disorders identification test revised (CUDIT-R). A brief eight item screening measure. Has good psychometric properties in clinical populations. If you score 12 or more that is considered a possible cannabis use disorder or engaging in hazardous behaviour

Question 30

How does Cannabis effect neurotransmitters and the brain?

Answer 30

Before cannabis enters the body, inhibitory neurotransmitters are active in the synapse. These NT’s inhibit DA from being released
When activated by the body’s own native cannabinoid (called anandamide) cannabinoid receptors turn off the release of inhibitory NT’s. Without inhibition, dopamine can be released.
Tetrahydrocannabinol (THC), the active chemical in cannabis, mimics anandamide and binds to cannabinoid receptors. Inhibition is then turned off and DA is released into the synapse

Question 31

Describe the binge intoxication stage

Answer 31

Characterized by an excessive impulsivity and compulsivity to use drugs despite negative consequences associated with such use. Hyperactivation of the mesocorticolimbic dopaminergic reward pathway of the brain associated with the positive reinforcement of the rewarding effects of drugs; Viewing environmental cues (like where you took this drug) increases release of dopamine.
Impairment in incentive salience

Question 32

What is the withdrawal/negative affect stage?

Answer 32

Triggered by opponent-process responses following binge episodes Within-systems and between-systems neurobiological changes (i.e., neuroadaptations) that drive the loss of motivation towards non-drug rewards and impaired emotion regulation

Question 33

Describe within systems (withdrawal/negative affect stage)

Answer 33

changes in the function of brain reward systems (e.g., decreased dopaminergic signaling in the NAcc and dorsal striatum) that result in an elevation of reward thresholds for non-drug reinforcers, which contributes to amotivation

Question 34

Describe the between systems

Answer 34

dysfunction of neurochemical systems that are not primarily involved in the rewarding effects of drugs of abuse (e.g., HPA-axis)

Question 35

What is the preoccupation/anticipation stage?

Answer 35

Reinstatement of substance use following abstinence. Executive control over craving and impulsivity is key in maintaining abstinence and is mediated by the PFC
Stage is marked by dysregulation of signaling between the PFC and areas of the brain that control decision making, self-regulation, inhibitory control and working memory

Question 36

What is the binge/intoxication stage for cannabis

Answer 36

Hyperactivation seems to be present in cannabis addiction but to a lower extent
Unlike other drugs (e.g., cocaine), research indicates no differences in baseline DA receptors between cannabis users and healthy controls. Dopamine release differences are usually a biological marker of addiction.
However, chronic cannabis use still results in blunted dopamine reactivity to a stimulant challenge. Consistent with the concept of tolerance

Question 37

What is the withdrawal/negative affect stage for cannabis

Answer 37

Blunted stimulant-induced DA reactivity has been associated with negative emotionality Chronic cannabis use has been associated with affect dysregulation that may involve changes in amygdala functioning
Like other drugs, cannabis seems to disrupt HPA axis function

Question 38

Cannabis use and depression/anxiety

Answer 38

associated with an increased risk for developing depressive and anxiety disorders. There’s a small relationship between cannabis use and increase in depression, does not assess causality (very small correlation)

Question 39

Cannabis use and psychosis

Answer 39

Bullying by peers and cannabis use are associated with adolescents’ reports of increasing psychotic experiences over time.

Question 40

study on bullying, cannabis use and Psychosis: method

Answer 40

Participants: adolescent boys and girls in the UK. Relational bullying and being physically attacked. Measured cannabis through categories of use (e.g., heavy user)
Longitudinal study: over a 2 year period
Completed questionnaires

Question 41

study on bullying, cannabis use and Psychosis: results

Answer 41

Uncovered 3 trajectories of psychosis in the data: Low, increasing and elevated
Bullying and cannabis use were associated with elevated and increasing psychotic symptoms vs. low. These results do not mean that smoking cannabis causes psychosis.