Lecture 3 - Volume, Variety & SSS Flashcards
Describe what portion distortion is?
Amount of food presented at meal times is on an increase.
We are eating 40% more outside the home where cannot control portion size.
This is 500 more calories than 1990s.
Using evidence from Rolls et al 2002, Explain howPortion Size affect Food Intake?
Manipulated amount of Mac & Cheese. Consumed 30% more when given the large portion (1000g) compared to the small (500g) with self-reported levels of fullness were equal.
Replicated with sandwiches in 2004, so it was a discrete item; 6inch vs 12inch ate more larger portion with similar ratings of fullness.
Shows we rely on external cues instead of internal.
Why does portion size affect food intake?
Our ability to regulate food intake changes as we age. Children under three are better at regulating intake as use internal cues.
Internal physiological mechanisms ca be easily overridden by learned behaviours.
Describe the over-consumption of fat.
Fat is highly palatable due to the texture, flavour and cross-modal sensory effects.
There is a similar effect of CHO and Fat on subsequent FI when palatability and energy density are matched.
According to Bell et al 1998, describe how energy density affects satiation.
If the amount of food plays a role on FI, we may over-consume fat due to its high energy density despite differences in volume.
Similar weights of food eaten but low energy density meals ate 30% less compared to high ED but with similar appetite “I’m Full”.
Poor at recognising ED of foods and adjusting FI accordingly
Due to Fat not being as satiating, we experience High fat hyperphagia.
Can we alter our predisposition to consume energy dense foods?
There are individual differences in self-control and in the rewarding nature of foods.
High/Low Self-Control Vs High/Low Desire.
Food Response Inhibition Training (Lawrence et al 2015) has been shown to strengthen self-control and reduce propensity to energy dense foods, showing reduction in weight at 1 and 6 month follow up.
Outline the brains control of taste and palatability.
Taste and palatability is not just down to hypothalamic control.
Instead, there is a cross-modal sensory experience with associated emotions and memory:
- Parabrachical Nucleus: opioid compounds associated with pleasure
-Prefrontal cortex: motivation and desire to select foods, associated with behavioural conditioning
-Amygdala: Emotion & Memory of food expereinces
- Nucleus Accumbens: pleasure and taste of food types.
- VTA: Dopamine reward systems.
Referring to research from Berridge 1996, explain the process of liking and wanting.
Non-homeostatic hedonic processes are also involved in FI.
Affect (Liking) determined by facial expressions (tongue protrusions)
Motivation (Wanting) determined by instrumental behaviour such as desire ratings.
Lesion studies demonstrated L&W are activated in different areas of the brain.
- Liking: Opioid & GABAnergic systems. Opioid blockers reduce pleasantness but not hunger.
Wanting: Dopaminergic NTs. Dexfenfluramine reduces hunger but not pleasantness.
We have poor awareness of hedonic changes.
Explain how we can dissociate between liking and wanting.
Finlayson et al 2007, Liking Vs Wanting:
Liking: visual analog scale. Wanting: forced choice paradigm, assessed pre & post meal.
When hungry- wanted high fat savoury, no different in liking. Liked high fat sweet, no difference in wanting.
When Satiated - liked high fat savoury, no difference in wanting. Wanted high fat sweet no difference in liking= REVERSED.
What are the problems with dissociating between liking and wanting.
Study has failed to be replicated.
Test meal = pizza which is high fat savoury. This may change how much food is liked/wanted when satiated.
Forced choice = no option to say neither.
Explain how variety enhances intake with supporting evidence.
Roll et al 1984, 4 different courses vs 4 same courses = 40% increase in FI in different courses condition.
Wisnewski et al 1992, PPS asked to eat to satiety Presented with same or different food. 3 fold increase in consumption of new food.
Relates to SSS and “Pudding Tummy”.
Explain Sensory Specific Satiety, according to Rolls 1986.
SSS is evolutionary as an access to variety utilises a balanced diet. Where food is scarce, we are motivated to seek change and gain more food for balance.
Rolls et al 1989 found changes in pleasantness occur rapidly across sensory dimensions - within 2 minutes of consumption and lasting up to an hour.
Suggests this occurs as a result of sensory stimulation rather than post-absorptive effects.
This has an important impact on meal termination and overall meal intake as variety undermines processes and promotes increased consumption.
How specific is SSS?
Intake increases with changes in sensory properties; texture, flavour & shape.
For example, variation in pasta shapes gives a 15% increase in intake.
Decrease in pleasantness occurs similar sensory flavour, cognitively the same type of food or similar macronutrient content.
What are the 3 mechanisms of SSS?
- Habituation & Monotony
- Central Mechanisms
- Opioid Mediation
According to Epstein et al 1993, explain how habituation and monotony are mechanisms of SSS.
Measured salivation and hedonic judgements.
Reduction of pleasantness and salivation to lemon juice over 10 trials but the presentation of a new stimulus dishabituated the response.
