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Psychopathology > Seminar 3: Food addiction / intake > Flashcards

Seminar 3: Food addiction / intake Flashcards

1
Q

What are the 3 steps to the HPA axis?

A
  1. hypothalamus releases CRH
  2. anterior pituitary releases ACTH
  3. adrenal cortex releases cortisol
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2
Q

How does your stress response influence the HPA-axis?

A
  1. manageable stress = smaller HPA response and quicker to baseline
  2. overwhelming stress = higher HPA response and longer back to baseline
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3
Q

What are the two main processes involved in eating?

A
  1. Hunger - to eat
  2. Satiety - to stop eating
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4
Q

What is the set-point-theory-of-hunger? Theory of food intake

A

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

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5
Q

What happens when we eat too much / too little?

A
  1. our metabolic rate increases a bit to help burn off the excess of what we have consumed
  2. if we eat less, our metabolic rate slows to keep energy in our system for a bit longer
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6
Q

What is positive incentive theory?

A

people are driven to eat based on the anticipatory or reward intake of food

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7
Q

In positive incentive theory, what happens when food as a need becomes a want?

A

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”

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8
Q

Whats the outcome for behavioural and biological conditioning in positive incentive theory?

A

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

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9
Q

What is stress (affect) regulation theory?

A

that food intake promotes stress or emotional relief

  1. stress increases HPA axis
  2. stress chemicals make people seek out comfort foods such as sugars/fats
  3. biologically, sugars/fats can dampen cortisol activity, and thus reducing stress
  4. becomes a learned response and repeats
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10
Q

What does the arcuate nucleus do?

A
  1. regulates feeding and metabolism, receptor site for NPY and ghrelin
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11
Q

What does the paraventricular hypothalamus do?

A

inhibitory control of food intake, receptor site for leptin and HPA axis

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12
Q

What does the laternal hypothalamus do?

A

responsible for reward related or motivated food intake - responses to highly palatable stimuli

receptor site for dopamine

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13
Q

What is the ventromedial nucleus?

A
  1. responsible for satiety and controlling fullness
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14
Q

What are the 3 endocrine hormones for hunger?

A
  1. Ghrelin - orexigenic hormone stimulates hunger by causing stomach contractions, sine wave activity, eat and ghrelin drops
  2. leptin - anorexigenic - appetite suppressant, encourages adipogenesis, opposite of ghrelin, leptin levels increases as you eat food
  3. 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
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15
Q

What is leptin resistance?

A

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

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16
Q

What’s disordered eating?

A

food intake patterns can be precursor to eating disorders or only a behaviour on its own

17
Q

What underlies both anorexia and binge eating disorder?

A
  1. 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
18
Q

Natural bias in BED?

A

food as a thing to control = natural predisposed bias found in BED

19
Q

Why do disordered eating occur?

A
  1. emotional overeating to relieve distress
  2. restrained - to prevent weight gain, and then compensation intake, eg. dieting plus occasional treats
  3. external - food cues increase desire for food intake and attentional bias
  4. binge eating - rapid intake of food
  5. restrictive - avoiding certain foods/limited food intake
20
Q

What is food addiction?

A

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
21
Q

Food criteria YFAS 2.0 scale 11 criteria?

note how its similar to substance use disorder

A
  1. increased intake from normal
  2. inability to quit
  3. increased time to obtain foods
  4. cravings
  5. failing to meet other life obligations
  6. continued use despite problems
  7. giving up other activities
  8. physically hazardous use in dangerous situation, eg. driving
  9. continued use despite psych or health problems
  10. tolerance - habitating to the increased amount of food being consumed
  11. withdrawal related symptoms
22
Q

What’s validity evidences for food addiction?

A
  1. links to dopamine CNS and PNS pathways
  2. similar behaviours to substance use symptoms
  3. similar reward mediated circuits in brain
  4. both food and drug addiction is related to stress
  5. both are linked with poor treatment outcomes
23
Q

What connects food addiction, substance use addiction?

A
  1. stress as the underlying mechanistic pathway to the behaviour
  2. food/drugs used as coping mechanism
24
Q

Why isn’t food addiction accepted more?

A
  1. can you become addicted to something you need to survive?
  2. can you call it ‘compulsive overeating’? - but not always compulsive, but rather dependence
  3. 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
25
Q

Whats the type of correlation between chronic disease and MDD?

A

bidirectional - but stronger evidence that MDD precedes the onset of chronic disease

unsure since MDD is highly heterogeneous

26
Q

What’s the main vulnerability factor for MDD?

A
  1. repeated exposure to stress, causing altered activity in the HPA-axis
  2. repeated exposure is called the KINDLING EFFECT, a big life stressor results in enduring neurochemical changes with cortisol - causes MDD symptoms less linked to specific triggers, causing repeated depressive episodes, raises vulnerability
27
Q

Recap on weight changes and subtypes of MDD - what is linked with what?

A
  1. weight gain/hyperphagia =
    atypical depression
  2. weight loss/hypophagia = melancholic depression

changes to weight is greatest predictor to depressogenic subtype

28
Q

What was Mill’s et al. (2018) paper findings? FIRST STUDY

A
  1. higher overeating behaviours in MDD people vs. controls, more in women
  2. 24% of depressed sample met YFAS 2.0 for food addiction
  3. Leptin levels were positively linked with BMI, emotional and restrained eating
29
Q

What was Mill’s et al. (2019) paper findings? SECOND STUDY

A
  1. problematic eating behaviours higher in depression vs. control, higher in women, 28% met food addiction
  2. leptin resistance linked with BMI, emotional restrained, and subscales of the food addiction scale
  3. ghrelin is negatively linked with restrained eating and BMI
30
Q

What was Mill’s et al. (2020) paper findings? THIRD STUDY

A
  1. split into MDD + food addiction, and MDD without food addiction
  2. higher MDD in those depressed with food addictions, more women, 29% met food addiction
  3. dopamine linked with food addiction symptoms in WOMEN ONLY
31
Q

Mills et al. (2021)

A

cortisol is negatively linked with BMI weight circumference, unrelated to any overeating behaviours

cortisol linked with melancholic subtype of MDD

32
Q

Findings on Barschi and Greenwood (2023)?

A
  1. food addiction as mediator between MDD and BMI, more in atypical MDD, no sex differences
  2. 22% of food addiction in subclinical samples

Psychopathology (9 decks)

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