Seminar 3: Food addiction / intake Flashcards
(32 cards)
What are the 3 steps to the HPA axis?
- hypothalamus releases CRH
- anterior pituitary releases ACTH
- adrenal cortex releases cortisol
How does your stress response influence the HPA-axis?
- manageable stress = smaller HPA response and quicker to baseline
- overwhelming stress = higher HPA response and longer back to baseline
What are the two main processes involved in eating?
- Hunger - to eat
- Satiety - to stop eating
What is the set-point-theory-of-hunger? Theory of food intake
body uses regulatory mechanisms to keep the weight in check
every person has a predisposed weight range that we maintain on average for optional functioning
weight = stored energy in case we require it
What happens when we eat too much / too little?
- our metabolic rate increases a bit to help burn off the excess of what we have consumed
- if we eat less, our metabolic rate slows to keep energy in our system for a bit longer
What is positive incentive theory?
people are driven to eat based on the anticipatory or reward intake of food
In positive incentive theory, what happens when food as a need becomes a want?
As a behaviour, food becomes a reward for positive behaviour or on rare occasions, forming an association between ‘treats’ and ‘behaviour’
Biological results in dopamine release, causes behavior and biological conditioning where stimulus is paired with dopamine and treats
“You see and want food, you enjoy food, cycle repeats”
Whats the outcome for behavioural and biological conditioning in positive incentive theory?
This desire for food intake can be caused in the absence of hunger, eg. desire for food without being hungry when seeing food, because dopamine has been released as the brain has associated the food with reward
What is stress (affect) regulation theory?
that food intake promotes stress or emotional relief
- stress increases HPA axis
- stress chemicals make people seek out comfort foods such as sugars/fats
- biologically, sugars/fats can dampen cortisol activity, and thus reducing stress
- becomes a learned response and repeats
What does the arcuate nucleus do?
- regulates feeding and metabolism, receptor site for NPY and ghrelin
What does the paraventricular hypothalamus do?
inhibitory control of food intake, receptor site for leptin and HPA axis
What does the laternal hypothalamus do?
responsible for reward related or motivated food intake - responses to highly palatable stimuli
receptor site for dopamine
What is the ventromedial nucleus?
- responsible for satiety and controlling fullness
What are the 3 endocrine hormones for hunger?
- Ghrelin - orexigenic hormone stimulates hunger by causing stomach contractions, sine wave activity, eat and ghrelin drops
- leptin - anorexigenic - appetite suppressant, encourages adipogenesis, opposite of ghrelin, leptin levels increases as you eat food
- dopamine - has central and peripheral pathways that dont crossover due to BBB
- in CNS, dopamine = reward eating,
- in PNS, dopamine = glucose, stress response and emotional eating for relief
What is leptin resistance?
chronically elevated leptin levels result in desensitization to leptin and feelings of satiety, can’t tell when full and often gain weight, thought to be underlying to obsesity
What’s disordered eating?
food intake patterns can be precursor to eating disorders or only a behaviour on its own
What underlies both anorexia and binge eating disorder?
- trying to get a sense of control, dopamine pathways altered to associate starving/overeating as a way to get control, releases dopamine - dopamine is paired with these distorted eating behaviours
Natural bias in BED?
food as a thing to control = natural predisposed bias found in BED
Why do disordered eating occur?
- emotional overeating to relieve distress
- restrained - to prevent weight gain, and then compensation intake, eg. dieting plus occasional treats
- external - food cues increase desire for food intake and attentional bias
- binge eating - rapid intake of food
- restrictive - avoiding certain foods/limited food intake
What is food addiction?
addictive behaviours in association with highly palatable foods, eg. sugars and fats
- not in DSM, used in yale food addiction scale version 2
- prevalence: 5-20% in general, 15-25% in obesity people
Food criteria YFAS 2.0 scale 11 criteria?
note how its similar to substance use disorder
- increased intake from normal
- inability to quit
- increased time to obtain foods
- cravings
- failing to meet other life obligations
- continued use despite problems
- giving up other activities
- physically hazardous use in dangerous situation, eg. driving
- continued use despite psych or health problems
- tolerance - habitating to the increased amount of food being consumed
- withdrawal related symptoms
What’s validity evidences for food addiction?
- links to dopamine CNS and PNS pathways
- similar behaviours to substance use symptoms
- similar reward mediated circuits in brain
- both food and drug addiction is related to stress
- both are linked with poor treatment outcomes
What connects food addiction, substance use addiction?
- stress as the underlying mechanistic pathway to the behaviour
- food/drugs used as coping mechanism
Why isn’t food addiction accepted more?
- can you become addicted to something you need to survive?
- can you call it ‘compulsive overeating’? - but not always compulsive, but rather dependence
- is it additive addition, as it responds to the sugar/fat content, as the things that make food addictive are often added ingredients to food
