What is food addiction?
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)
What is the yale food addiction scale
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
The yale food addiction scale criteria
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
What are the DSM-IV over arching criteria for food addiction?
- 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
What is the prevalence of food addiction?
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
What has research shown about Food addiction and the brain?
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
How do the reward learning regions respond to food and substances?
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
Have studies testing food addiction found similarities to substance addiction?
Tested the idea that elevated “food addiction” scores based on the YFAS are associated with similar patterns of neural activation as substance addiction
What was hypothesized about participants experiencing a food addiction? (Gearhardt et al.)
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.
What was the method of the study? (Gearhardt et al.)
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
What were the results? (Gearhardt et al.)
They saw that the brain regions that were hypothesizing would light up did and there was a moderate correlation between food and those regions
Food addiction and the brain: conclusions (Gearhardt et al.)
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)
What were the Limitations of the study? (Gearhardt et al.)
only 48 people and restricted to only “healthy” people and only women thus cannot determine if it would generalize to men
What were the aims in Davis et al. study food addiction and obesity?
Investigate the legitimacy of FA in humans. Extend the validation of YFAS
What was the method of the study by Davis et. al?
Obese adults (aged 25–45 years) Retrospective design Assessed clinical co-morbidities, psychological risk factors, and abnormal motivation for the addictive substance
results of Davis et al. study?
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
What are some limitations of the food addiction concept?
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
What is considered legal use of opioids?
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
What is illegal use of opioids?
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
What is the prevalence of opioids in Canada?
More prevalent in older adults. People with vulnerability factors are at a higher risk for opioids
What is an appropriate use of Opioids?
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
Opioid related deaths in Canada
Fentanyl related deaths in Canada
Are rising and peaking in 2017 and 2018
What happens to the neurotransmitters and in the synapse when opiates are consumed?
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
What can long term use of opioids do to the brain?
Long-term use of opioids can impair speed of cognitive processing and working memory
How opiates cause overdose deaths ?
Overdose deaths caused by activated opioid receptors in the brain stem that suppress or stop the breathing reflex
How do fentanyl and other opioid drugs lead to maladaptive learning?
essentially hijack the brain’s natural motivation and reward system, leading to a strong, maladaptive form of learning
What is the prevalence of cannabis use and addiction?
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
How do we screen for cannabis use?
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
How does Cannabis effect neurotransmitters and the brain?
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
Describe the binge intoxication stage
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
What is the withdrawal/negative affect stage?
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
Describe within systems (withdrawal/negative affect stage)
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
Describe the between systems
dysfunction of neurochemical systems that are not primarily involved in the rewarding effects of drugs of abuse (e.g., HPA-axis)
What is the preoccupation/anticipation stage?
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
What is the binge/intoxication stage for cannabis
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
What is the withdrawal/negative affect stage for cannabis
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
Cannabis use and depression/anxiety
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)
Cannabis use and psychosis
Bullying by peers and cannabis use are associated with adolescents’ reports of increasing psychotic experiences over time.
study on bullying, cannabis use and Psychosis: method
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
study on bullying, cannabis use and Psychosis: results
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.