Volume, variety and sensory specific satiety - week/lecture 6 Flashcards

1
Q

biology behind hunger

A
  • Months of energy stored in adipose tissue; short-term fasting has little impact on energy stores
    • Energy continues to be supplied to the body’s tissues through a variety of fuels (fats, glycogen, ketones), from different sources, depending on the duration of the fast
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2
Q
  • Rogers and Hardman (2015) - what do individuals explain their perceptions of hunger as?
A

○ When full, individuals explained their perceptions of hunger in relation to their level of fullness since their last meal, the timing and/or size of the previous meals, and the proximity of their next meal

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3
Q

what is the expression of hunger?

A
  • The expression of hunger is actually grounded in absence of fullness; and it is this that underlies the readiness to eat (Rogers & Brunstrom, 2016)
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4
Q

satiety

A

Satiety: feeling full after eating, inhibiting intake between meals

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5
Q

satiation

A

Satiation: within meal process determining when you stop eating

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6
Q

expected satiety

A
  • Expected satiety: perception, before consumption, of the ability of a food to stave off hunger
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7
Q

expected satiation

A
  • Expected satiation; perception, before consumption, of the ability of a food to deliver fullness
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8
Q

what can expected satiety/satiation predict?

A
  • Experimental evidence to suggest that expected satiation/satiety of foods can strongly influence pre-meal decisions about food and portion selection (e.g. Brunstrom, Shakeshaft & Alexander)
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9
Q

what determines expected satiation/satiety?

A
  • Can be learned
    ○ More familiar food, more filling it is expected to be (routines)
    • Influenced by perceived volume of food
      ○ Larger volume, more filling expected (volume)
    • Exposure to varieties of food reduces expected satiety/satiation (variety)
    • Energy density negatively correlated with expected satiety
      ○ Higher the foods energy density, less filling it is perceived to be (energy density)
    • Routine decisions and automatic processing can lead to passive overconsumption of foods.
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10
Q

does portion size affect food intake?

A
  • Rolls, Morris & Roe (2022)
    ○ 30% more energy for largest portions (1000g) compared to the smallest (500g)
    • Rolls et al., (2004)
      ○ Replicated with sandwiches
      ○ Gender differences
      ○ Similar ratings of fullness
    • Meta-analysis of 65 studies found that doubling the portion served to individuals, increases food intake by ~35% (Zlatevska, Dubelaar & Holden, 2014)
    • More pronounced in males
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11
Q

what do larger portions do in terms of satiation/satiety?

A

○ Encourage consumption past satiation
○ Indicates socially appropriate amount to consume
○ Adjust biological signals and cognitive perceptions over time about what portion elicits satiety
○ Driven by primal instincts to consume as much food as possible when available

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12
Q

why does portion size affect food intake?

A
  • Ability to regulate food intake changes as we age - children <3 years old better at regulating intake and less affected by external cues
    • Experimental evidence indicates significant impact on food intake in the short term; similar effects in naturalistic settings
    • Longitudinally - limited adjustment for increases in intake (e.g., Rolls, 2006; Vermeer et al., 2011)
      ○ The upper end ‘set point’ intervention to reduce intake is much weaker than the lower end intervention to increase intake.
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13
Q

are there individual differences in the portion size effect? evidence

A
  • Cunningham et al., (2023).
    ○ Repeated measures over four weeks.
    ○ Macaroni cheese served in 400g to 700g portion sizes (increases by 100g)
    ○ N = 44 (29 female)
    ○ Explored how elements of eating microstructure (e.g., meal duration, bite count, mean bite size, and mean eating rate) were linked to portion size increases.
    ○ Faster eating rate and larger bite sizes were related to greater food consumption as larger portion sizes are served; but did not moderate the degree of increase in food intake across larger portions.
    ○ Serving larger portions, eating faster, and taking larger bits all combine to contribute to greater food intake.
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14
Q

why do increased portion sizes lead to increased consumption?

A
  • External cues
    • Physiological regulatory mechanisms overridden by learned behaviours
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15
Q

why do we overconsume fat?

A
  • Highly palatable: texture, flavour, cross-modal sensory effects
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16
Q

satiety signals for fat consumption

A

○ Preload studies (early work): Pro > CHO > fat
○ Later work: similar effect of CHO and fat on subsequent intake of test meal when palatability and energy density matched

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17
Q

energy density of fat

A
  • Energy density of fat is high – 9kcal/g (4kcal/g CHO & protein). Small portions of fatty food can therefore have a high energy content.
18
Q

effects of satiation on fat consumption

A

○ Tendency to consume constant weight of food; regardless of
macronutrient content. E.g., Stubbs et al., 1996, Saltzman, 1997.
○ Therefore, we may overconsume fat due to its high energy density in comparison to other foods.
○ We are poor at recognising energy density of foods and adjusting intake.

19
Q

palatability of fats and their traceability

A
  • Palatability of fats can be traced to our primal roots
    ○ Foods high in fat contribute the most (in energy) to satisfy our biological drive to have the necessary energy for survival.
    ○ We are highly motivated therefore to seek out foods high in fat, sugar, salt and energy density to ‘ensure our survival’.
20
Q

what is the most satiating macro?

A

Protein is most satiating and then carbs and fat are pretty similar next.

21
Q

passive overconsumption

A
  • We tend to consume a constant weight of food, despite variations in macronutrient content
    • High energy density of highly liked, high-fat foods → overconsumption of fat
    • Fat has a relatively weak effect on satiation and satiety (relative to protein)
    • Passive overconsumption (high fat hyperphagia)
22
Q

Can we alter our predisposition to consume energy dense foods?

A
  • Individual differences in self-control and in rewarding nature of food
    Food response inhibition training
23
Q

Lawrence et al., 2015. Appetite, 95(1) 17-28

Food response inhibition training task:

findings

A
  1. Reduced liking of no-go food
    1. Reduced consumption of no-go
      food
    2. Less likely to choose the no-go
      food
    3. Reduced portion sizes of no-go food.
      - Preliminary evidence to suggest reduction in weight among trained group at 1 and 6 month follow up.
      - Jones et al., (2016) Meta-analysis. Robust evidence to suggest that participants exposed to inhibitory control training consume significantly less food/drink than control.
24
Q

what is appetite associated with?

A
  • Appetite not just associated with hypothalamic control
    • Texture, flavour, cross-modal sensory experiences
    • Associated emotions and memory of foods are also important
25
Q

brain regions for appetite and eating?

A

○ PFC (planning and decision making)
○ Nucleus accumbens (pleasure and aversive taste memories)
○ Amygdala (memory)
○ VTA (dopamine reward system)
○ Parabrachial nucleus (release of pleasure based substances like endorphins)

26
Q

what is palatability?

A
  • “Palatability is the hedonic component of food reward, and results from a central integrative process that can incorporate aspects not only of the taste, but of the physiological state and of the individual’s associative history” (Berridge, 1996).
27
Q

what are the 2 Hedonic (non-homeostatic) reward mechanisms

A

○ Affect (liking)
○ Motivation (wanting)

28
Q

what is liking measured through in studies? Berridge (2009)

A

pleasure responses (facial expressions) in animals and subjective ratings of pleasantness in humans

29
Q

what is wanting measured through in studies? Berridge (2009)

A
  • Wanting is measured through incentive motivation (instrumental behaviour) in animals and desire to eat in humans.
30
Q

neuropsychology and responses of liking and wanting

A
  • Berridge (1996): Lesion studies demonstrated liking & wanting activated different areas of the brain in animals
31
Q

evidence from pharmacological studies of liking and wanting

A
  • Evidence from pharmacological studies in humans suggest activation of different systems and neurotransmitters.
    ○ Liking: – opioid and GABAnergic systems
    § Opioid blockers reduce pleasantness but not hunger (e.g., Cambridge et al., 2013; Drewnowski et al., 1995).
    ○ Wanting: – Dopaminergic neurotransmitters
    § Dexfenfluramine –reduce hunger but no effect on pleasantness (e.g.,
    Blundell & Hill, 1992)
    • Much more difficult to dissociate using self-report; poor awareness of hedonic changes
32
Q

dissociating liking and wanting

A
  • Finlayson, King & Blundell (2007).
    ○ 53 participants; mean age 21.4
    ○ Photos of 20 foods (high fat, low fat, savoury, sweet)
    § Liking–Visual Analog Scale
    § Wanting – Forced choice
    “Which of these foods would you most like to eat now?”
    ○ Changes in food liking and wanting assessed pre & post meal.
    • When hungry…
      ○ Wanted high fat savoury over low fat savoury; no differences in liking.
      ○ Liked high fat sweet more than low fat sweet, but no differences in wanting.
    • When satiated, the pattern was reversed:
      ○ Liked high fat savoury over low fat savoury, but no differences in wanting
      ○ Wanted high fat sweet foods over low fat sweet foods, but no differences in liking
33
Q

evidence for the fact that - Increasing variety in taste, texture, appearance and choice of foods can increase food intake, and is linked with higher weight.

A
  1. Pliner et al (1980) – different spreads on bread
    2. Bellisle & LeMagnen (1980) – Pizza, sausage rolls & egg
    roll (together or singularly)
    3. Rolls, van Duijvenvoorde & Rolls (1984) – Four different courses vs. four courses of the same food (40% increase)
    4. Wisniewski et al (1992) – Eat to satiety. Presented with the same or a different food. 3-fold increase in consumption of new food.
34
Q

evidence for sensory specific satiety

A
  • (Rolls, 1986)
    ○ Changes in pleasantness occur rapidly (within 2 minutes of consumption) and last up to an hour (Hetherington, Burley, & Rolls, 1989).
    ○ The decrease in enjoyment and intake of the already-consumed food is driven by a reduction in both liking and wanting of the food (Brunstrom & Mitchell, 2006; Havermans et al., 2009; Raynor & Epstein, 2001).
    ○ Suggests that it occurs a result of sensory stimulation rather than postabsorbtive affects (largest changes occur before meal absorbed).
    ○ Important impact on meal termination (and overall intake). Variety undermines the process and promotes increased consumption.
35
Q

how specific is SSS?

A
  • Greatest changes in palatability occur for the food eaten
    • Decreases in pleasantness of other foods may also occur, due to:
      ○ Similarity in sensory properties or flavour
      ○ Cognitively the same ‘type’ of food
      ○ Similarity in macronutrient content
      § E.g., sweet versus savoury foods; orange jelly & raspberry jelly
    • Intake increases with changes in sensory properties
      ○ E.g., flavour, shape, texture. Variation in pasta shapes→15% increase in intake over 3 courses
36
Q

what does variety do to SSS?

A
  • Variety promotes switching between foods, which may delay SSS.
37
Q

impact of fluids on SSS

A
  • Cunningham et al., (2023)
    ○ Video recordings of meal consumption
    ○ Assessed patterns of bites, sips and the number of
    switches between them; also assessed SSS
    • Switching between bites and sips more frequently was linked with greater food consumption
    • Overall water intake was also linked with greater food intake.
    • Suggestion that switching between food and water may promote energy intake by attenuating the development of SSS
38
Q

mechanisms of SSS

A
  1. Habituation & monotony (Epstein et al, 1992; 1993)
    • Reduction in pleasantness of, & salivation to lemon juice over 10 trials;
      presentation of new stimulus dishabituated response
    • Pleasantness of water reduced among those who tasted it AND those
      who drank it (Rolls, 1982).
    • Habituation regardless of energy content or ingestion.
  2. Central mechanisms - neurophysiological explanation (Rolls, 1993)
    • Satiety linked to decreased OFC neuronal response
  3. A role for endogenous opioids
    • Hypothalamic release of opioid peptides associated with reward
    • Blocking the release or the reuptake of these peptides (via drugs) disrupts SSS
39
Q

the appetizer effect

A
  • The Appetizer Effect (Yeomans, 1996)
    ○ High initial ratings of highly liked food
    ○ Offered bland, palatable and strong flavoured
    food (pasta + oregano).
    ○ Palatable flavour → enhanced intake, eating rate
    and reported appetite (the appetizer effect)
    ○ Decline in pleasantness & desire to eat still
    follows – reflects satiation
    ○ So, sensory stimulation explains initiation not termination
40
Q

what is hunger

A
  • “The expression of hunger is actually grounded in an absence of fullness and it is this feeling that underlies readiness to eat”
    • BUT you can be ready to eat while being full (e.g., the dessert effect in SSS).
    • “Hunger reflects the readiness to eat in the absence of fullness and in anticipation of pleasure” (Rogers & Brunstrom, 2016).