Lecture 3 - Volume, variety and sensory-specific satiety PDF

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Taught by Dr Witcomb and guest lecturers. Notes contain content from lectures combined with independent reading, structured as would be written for the exam....

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The Psychology of Eating Behaviour – Lecture 3 Volume, variety and sensory-specific satiety

Learning objectives • Describe factors that contribute towards increased food intake – Volume and energy density – Taste and palatability – Variety – Sensory-specific satiety • Understand key concepts associated with these factors – Passive overconsumption – Liking versus wanting – Satiation and satiety – Habituation and monotony

Mealtimes • Evidence that most food is consumed across three main meals (in the UK). -

Certain foods and certain amounts of food becomes associated with certain mealtimes o This is purely based on learning Link to later evidence that anticipation around mealtimes is associated with reward

• There are different influences on energy intake for self-selected portions vs pre-made portions.

The Psychology of Eating Behaviour – Lecture 3 -

There are different influences on energy intake for self-selected portions vs pre-made portions

What drives you to select specific foods and amounts of foods for a meal? • Hunger • Staving off hunger • Routine choices • Portion size and volume • Liking/wanting • Sensory variety • Traits and emotions • Higher order goals (e.g. dieting) • Social influence • Product branding/labelling

What is hunger? (*more info in L2) • A common misconception is that hunger is due to insufficient energy available in the body. • But humans store months of energy in adipose tissue meaning that short-term fasting has little impact on energy stores (Rogers & Brunstrom, 2016) -

Bathtub model

• Energy continues to be supplied to the body's tissues through a variety of fuels (e.g. from fats, glycogen, ketones) from different sources depending on the duration of the fast.

What is hunger? Previous literature, and health professionals, often describe acute energy depletion in the body as the stimulus for ‘hunger’ (Lowe & Butryn, 2007; Zheng et al., 2009). In this case, ‘hunger’ is the urge to eat in response to an energy deficit. – the phenomenon is more complex than this however… -

Bathtub model also significantly disagrees with this (energy depletion over short time span will be insignificant in comparison to energy stores)

The Psychology of Eating Behaviour – Lecture 3 • A study found that when individuals were full (i.e., not hungry) they explained their perceptions of hunger in relation to their level of fullness since their last meal, the timing and/or size of the previous meal, and the proximity of their next meal (Rogers & Hardman, 2015; Rogers & Brunstrom, 2016). • This suggests that the expression of hunger is actually grounded in an absence of fullness and that it is this feeling that underlies readiness to eat (also anticipation of pleasure as described later). Hunger is not grounded in a lack of energy… -

These criteria (timing, size of previous meal, etc.) could be interpreted as proxies of shortterm energy depletion since they roughly represent the degree of energy expenditure since the last meal. Therefore, these could be the parameters of energy depletion in the body. o However, this degree of energy expenditure will still be low compared to total body energy stores (bathtub). Limiting the scale and impact of inter-meal energy depletion.

‘Normal hunger’ vs hypoglycaemia ‘Hitting the wall’ is a renowned phenomenon in endurance sports. It is a sudden fatigue caused by a depletion of liver and muscle glycogen stores (Rapoport, 2010) which can be relieved by eating carbohydrates (hypoglycaemia). -

However, those who have experienced hypoglycaemia do not describe the experience as ‘normal hunger’ or resembling appetite. Symptoms include shaking, sweating and weakness. o Although these individuals did not experience ‘normal hunger’, they knew they had to consume carbohydrates to relieve these symptoms.

Therefore, Rogers and Brunstrom (2016) suggest that ‘normal hunger’ or appetite may result from having an empty, or not full, upper gut in combination with the anticipation of pleasurable food. This is essentially an incentive model of eating in which food is more pleasurable in the absence of fullness (Rogers & Hardman, 2015). -

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Murray & Vickers (2009) support this notion as they found that British consumers described ‘fullness’ as having physical (e.g. gastric distension) and psychological (e.g. satisfaction, lack of desire to continue eating) components. Therefore eating could be conceptualised as a cycle of reward and satiety is only indirectly related to energy balancing and increase of the body’s energy stores. - Rogers and Brunstrom (2016) o This fits into our daily lives as the approach of mealtime acts as a reminder of the pleasure of eating and usually coincides with an empty gut.

The Psychology of Eating Behaviour – Lecture 3

Evolutionary background to the importance of cognitive influences over eating behaviour (Brunstrom, 2011)

The importance of cooking can be traced back to early homo erectus and it coincides with a decrease in masticatory apparatus and gut size, and an increase in brain size (Wrangham et al., 1999). Cooking can greatly increase the energy that is extracted from food (Wrangham, 2009) and it kills potential pathogens. However, it also requires preparation, fire and time. In this context, it makes little sense to cook food, consume food and then rely on the development of satiation to meter and control further food preparation and intake. Instead, it would seem sensible to acquire a capacity to anticipate future need, and to do this at the point at which food is selected and prepared. This strategy optimises effort, minimises food wastage and protects against hunger and the need to prepare unplanned meals (Brunstrom, Collingwood & Rogers, 2010).

Satiation and satiety The satiety cascade (first drawn up by Blundell, Rogers & Hill, 1987)

The Psychology of Eating Behaviour – Lecture 3

Satiation = within-meal process, feelings of fullness that builds up during a meal that ultimately terminates a meal Satiety = the suppression of hunger after an eating episode, related to the beginning of next eating episode (and duration of time between end of one eating episode and beginning of another)

Models the onset, duration and termination of an eating episode.

The ingestion of food/drink in one instance triggers the succession of a variety of signals that contribute to the inhibition of eating. These sensory, hormonal, cognitive and metabolic signals have overlapping influences.

Whilst eating, sensory factors inhibit further eating through sensory-specific satiety (Rolls et al., 1981) whereby recently ingested foods, and similar foods, lose their hedonic properties. Sensory input such as taste, smell and texture of food in the oral cavity promote intake at the beginning of an eating episode. As eating progresses, sensory-specific satiety (sensory-specific habituation) increases in response to the ingested foods (Hetherington & Havermans, 2013) (more immediate) and signals from the gastrointestinal tract (gastric distention, release of hormones and

The Psychology of Eating Behaviour – Lecture 3 peptides, drop in stomach ghrelin) inhibit the motivation to continue eating (more delayed, postabsorptive stage) (Tremblay and Bellisle, 2015).

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After satiation is achieved for the specific sensory characteristics of a food, other foods with different sensory characteristics maintain their stimulatory influence and can continue to promote eating until satiation signals are strong enough to counteract the sensory appeal of all foods (Tremblay and Bellisle, 2015). Sensory-specific satiety inhibits the intake of foods with overlapping characteristics with previously-ingested foods (smell, taste, shape, colour, texture).

Cognitive factors also affect satiety after eating. People know they have just eaten, and know how big their last meal was, and this knowledge prevents them from continuing to eat (Bellisle, 2008).

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Even before the food arrives in the gut, where it may act on stretch or macronutrient receptors, cognitive and sensory signals originating from the sight and smell of the food, as well as the sensory experience of food in the mouth, influence how much food is eaten in a sitting (moderating satiation) and how long individuals remain ‘full’ for (moderating satiety).

Cognitive factors also contribute to satiation (expectations of the satiety of foods, beliefs, attention/distraction at the time of eating) (Bellisle & Dalix, 2001; Bellisle et al., 2004; Brunstrom, 2011).

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Even non-food-related cognitions play a role in satiation. Demanding cognitive tasks before a meal can increase energy intake at meal time without affecting perceived hunger (Chaput & Tremblay, 2007). o This has been explained as preprandial mental work increases glycaemic instability and cortisolemia, both of which can disturb satiation (Chaput et al., 2008).

Beliefs about the satiating value/energy load of the meal can also affect satiety (Cassady et al., 2012). Eating with attention and recalling foods consumed earlier in the day can reinforce post-meal satiety (Bellisle et al., 2004; Higgs et al., 2008).

Physical factors such as the weight, volume, energy and nutrient content, and energy density of the meal affect satiety (Keller et al., 2013). -

The volume of a meal exerts effects in the early stages of satiety (gastric distension), nutritional content exerts effects in the post-absorptive, later stages of satiety (Tremblay & Bellisle, 2015). o Data has shown that the weight of the food (from previous meal) left in the stomach at the time of meal onset significantly affects the size of the next meal (de Castro, 2010).

The Psychology of Eating Behaviour – Lecture 3 Caloric beverages also have a weaker influence on satiety in comparison to solid foods. This satiety deficit can lead to ‘passive overconsumption’ (Almiron-Roig et al., 2013).

Biological factors, such as hormonal/neural signals in response to nutrient/stretch receptors, originate from the periphery of an organism (Woods, 2013). -

Hormonal signals originate peripherally (e.g. leptin from adipose tissue or insulin from pancreas) and these affect eating behaviour by acting on the central nervous system. Many ‘satiety hormones’ are secreted into the gastrointestinal tract following food consumption (e.g. CCK, peptide YY, gastric inhibitory peptide) – this is in the post-absorptive stage and is relatively delayed.

The satiety cascade also shows how the brain receives signals reflecting energy input and expenditure from the periphery of an organism and integrates these to act as a ‘homeostatic regulator’ (Tremblay & Bellisle, 2015). -

One key feature of the ‘homeostatic regulator’ is the alternation between hunger and satiety states, adjusting the body’s hunger state to maintain energy balance (Berthoud, 2002). However, this signalling is only loosely coupled with appetite control. (look at ‘hitting the wall’ section) – This can be used in reference to ‘appetite not just associated with hypothalamic control’ below

In this model, satiety is the summation of the effects from all sensory signals involved in the ingestion of food which suppress appetite. (Meiselman, 2020) -

The model also acknowledges that satiety does not hold absolute inhibition over eating behaviour, one example being sensory-specific satiety. (mentioned later, also Yeo (2018))

Satiation and satiety – definitions Satiation and satiety are the two causal mechanisms that influence the experience of appetite (such as sensations of hunger) and how eating behaviour manifests. Changes in eating behaviour are often explained through changes physiological and/or psychological processes caused by adjustments in the strength of satiation and satiety.

• The extent to which a food or portion will elicit satiation and satiety can be predicted before a meal begins – based on learning of exposure to particular foods in the past • Expected satiation = the perception, before consumption, of the ability of a food to deliver fullness that will lead to meal termination.

The Psychology of Eating Behaviour – Lecture 3 • Expected satiety = the perception, before consumption, of the ability of a food to stave off hunger/appetite in the post-prandial period through the sensation of fullness caused by the presence of ingested nutrients. (Bellisle & Blundell, 2013; Meiselman, 2020) • Expected satiation and expected satiety are highly correlated. Food that is high in expected satiation is likely to be high in expected satiety.

Together satiation and satiety are involved in biological processes that cause people to 1) begin eating; 2) maintain an episode of eating before bringing it to an end; 3) suppress further motivation to eat following a meal; 4) maintain eating inhibition for a certain amount of time following a meal. (Bellisle & Blundell, 2013) -

It could be suggested that eating behaviour and appetite are controlled by satiety and satiation, however evidence from L2 shows that these control processes are often subverted or manipulated (weaken biological/environmental signals of satiation or satiety) to allow for unhealthy eating habits.

Satiation and satiety – different use of the terms The semantics of the terms ‘satiation’ and ‘satiety’ have shown some inconsistency between researchers. 1) The terms are often described as causal mechanisms that affect the experience of hunger, expression of appetite and structure of eating behaviour. E.g. satiety cascade. 2) The terms are also used without notions of causality, instead they are operationalised to measure patterns of eating behaviour. E.g. satiety refers to effects during the post-prandial period, satiation refers to effects that determine the size of energy intake. 3) The terms have also been described as intervening variables (between other objectively measured variables) that explain changes in behaviour.

Dictionaries themselves have struggled to give a consistent definition of ‘satiety’, Oxford English defines satiety as “feeling or state of being sated” which requires a definition of ‘sated’ and approaches a circular argument! (Meiselman, 2020)

Satiation and satiety – portion size

The Psychology of Eating Behaviour – Lecture 3 • The portion selected to elicit fullness (expected satiation) or to stave off hunger until the next meal (expected satiety) is strongly associated with ideal portion size (Brunstrom & Rogers, 2009; Brunstrom, Collingwood & Rogers, 2010). – I.e., expected satiation/satiety strongly influences pre-meal decisions about food and portion selection! (Hardman et al., 2011; Brunstrom et al., 2012) o

This is often based off past experiences of ‘the degree of fullness produced by a food’.

• Individuals’ expected satiation/satiety per kcal of different foods, and portions of these foods, varies – There can be a 5-to-6-times difference in the perceived satiating abilities of foods when compared calorie-for-calorie (Brunstrom et al., 2011)

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For example, 837 kJ of pasta was expected to confer to the same degree of satiety as 1612 kJ of pizza (Brunstrom et al., 2011). o Generally, more energy dense foods have lower expected satiety and lower energy dense foods have higher expected satiety (evidence later in this doc) These findings were replicated in participants’ ratings of snack foods in a later study (Brunstrom & Shakeshaft, 2009)

From satiety cascade -

The volume of a meal exerts effects in the early stages of satiety (gastric distension), nutritional content exerts effects in the post-absorptive, later stages of satiety (Tremblay & Bellisle, 2015). o Data has shown that the weight of the food (from previous meal) left in the stomach at the time of meal onset significantly affects the size of the next meal (de Castro, 2010).

HOWEVER THERE ARE OTHER PROPOSED MECHANISMS THAT AFFECT PORTION SIZE -

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The size of plates has been investigated. Studies have found, in adults and children, that portion size increased as plate size increased (Wansink & van Ittersum, 2013; DiSantis et al., 2013); another study also found that portion size decreased as the rim of the plate increased in width (McClain et al., 2014). However, results are inconsistent with many studies finding no relationship between portion and plate sizes (Rolls et al., 2007; Yip et al., 2013; Robinson et al., 2014). o Overall, a meta-analysis by Robin et al. (2014) identified a small, positive relationship between plate size and amount eaten. Other proposed mechanisms include people’s difficulty estimating amounts of food (Nørnberg et al., 2014) and lack of awareness of reference portion sizes. Individual differences may play a role here as men are found to perform worse at estimating portion sizes (Lewis et al., 2015).

External factors

The Psychology of Eating Behaviour – Lecture 3 -

“Value for money” has been identified as an important determiner of portion size. Humans are generally willing to pay marginally more for a larger meal as they feel like they are getting more value for their money, this can increase exposure to larger meals (Wansink, 1996; Steenhuis & Vermeer, 2009).

ALSO HOWEVER, PORTION SIZE IS NOT SOLELY AFFECTED BY EXPECTED SATIATION Brunstrom, Collingwood and Rogers (2010) found that expected satiation explained 74.8% of the variance in energy content of individuals’ portions.

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Within this, they only found that 31% of the variance in self-selected portion volume was moderated by expectations around satiation. The remaining 43.8% in variance was not related to the perceived physical dimensions of the food. o This evidences that expected satiation is not a proxy for volume of portions and that foods of equal volume are expected to be equally satiating.

Satiation and satiety – expectations – continue reading brunstrom 2011 A few important findings about expected satiation/satiety:

1. These expectations can be learned. The more familiar a food is to an individual, the higher its expected satiation/satiety per kcal (Hardman et al., 2011; Brunstrom, 2011; Brunstrom, Shakeshaft & Alexander, 2010). – this leads to a reduction in portion size - Learning is relatively rapid and expected satiation can be affected after a single exposure to a new food (Brunstrom, 2011). - The presumed mechanism behind familiarity on expected satiety is associations between flavour characteristics of a food and post-ingestive events dubbed ‘flavour-nutrient learning’ (Yeomans, 2012). This is based on the theory of classical conditioning whereby flavours act as sensory stimuli that are associated with post-ingestive consequences induced by the consumption of a particular food (Brunstrom, 2005). - Evidence of flavour-nutrient learning: Irvine et al. (2013) compared the expected satiation of wine gums before and after eating wine gums to fullness in a laboratory setting. Results showed that participants with greater experience eating wine gums to high levels of fullness expected them to provide greater satiation.

The Psychology of Eating Behaviour – Lecture 3 - Further insight into flavour-nutrient learning: O’Sullivan et al. (2010) manipulated the energy density of a familiar food (spaghetti Bolognese), serving low-energydense and high-energy-dense versions to participants over five consecutive days. - The participants reported no significant differences in expected satiation or expected satiety over the five days. Indicating that individuals may not be able to re-learn pre-existing flavour-nutrient relationships based from past experiences.

One interesting theory ...