BRIE F I N G PA P E R

Satiation, satiety and their effects on

eating behaviour nbu_1753 126..173

B. Benelam
British Nutrition Foundation, London, UK

Summary
1. Introduction
2. Physiological mechanisms of satiation and satiety
2.1 Physiological mechanisms of satiation
2.1.1 Gastric mechanisms of satiation
2.1.2 Intestinal mechanisms of satiation
2.2 Physiological mechanisms of satiety
2.2.1 Gut hormones – episodic signals of satiety
2.2.2 Tonic satiety signals
2.3 The integration of satiety signals in the brain
2.3.1 Anorexigenic pathways in the hypothalamus
2.3.2 Orexigenic pathways in the hypothalamus
2.3.3 Other areas of the brain involved in satiation and satiety
2.3.4 Reward pathways
3. Measuring satiation and satiety
3.1 Measuring satiation
3.2 Measuring satiety
3.2.1 Free living vs. laboratory studies
3.2.2 Preload studies
3.2.3 Self-reported measures of satiety
3.2.4 Measuring food intake
3.2.5 Quantifying satiety
3.3 Confounders in satiety research
3.3.1 Physiological confounders
3.3.2 Behavioural confounders
4. The effects of foods and drinks on satiety
4.1 Protein and satiety
4.2 Carbohydrates and satiety
4.3 Fibre and satiety
4.4 Intense sweeteners and satiety
4.5 Fat and satiety
4.6 Liquids and satiety

Correspondence: Bridget Benelam, Nutrition Scientist, British Nutrition Foundation, High Holborn House, 52–54 High Holborn, London
WC1V 6RQ, UK.
E-mail: b.benelam@nutrition.org.uk

126 © 2009 The Author

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 Satiation, satiety and their effects on eating behaviour 127

4.7 Alcohol and satiety

4.8 Energy density and satiety
5. The effect of external factors on satiation and satiety
5.1 Palatability
5.2 Variety
5.3 Portion size
5.4 Sleep
5.5 Physical activity
5.6 Television viewing and other distractions
5.7 Social situations
6. Satiation, satiety and weight control
6.1 Obesity genes and satiety
6.2 Physiological differences in satiation and satiety responses in obese people
6.3 Behavioural differences in the response to satiation and satiety in obesity
7. Conclusions

Summary In the context of the rising prevalence of obesity around the world, it is vital to
understand how energy balance and bodyweight are controlled. The ability to
balance energy intake and expenditure is critical to survival, and sophisticated
physiological mechanisms have developed in order to do this, including the control
of appetite. Satiation and satiety are part of the body’s appetite control system and
are involved in limiting energy intake. Satiation is the process that causes one to
stop eating; satiety is the feeling of fullness that persists after eating, suppressing
further consumption, and both are important in determining total energy intake.
Satiation and satiety are controlled by a cascade of factors that begin when a food
or drink is consumed and continues as it enters the gastrointestinal tract and is
digested and absorbed. Signals about the ingestion of energy feed into specific areas
of the brain that are involved in the regulation of energy intake, in response to the
sensory and cognitive perceptions of the food or drink consumed, and distension of
the stomach. These signals are integrated by the brain, and satiation is stimulated.
When nutrients reach the intestine and are absorbed, a number of hormonal signals
that are again integrated in the brain to induce satiety are released. In addition to
these episodic signals, satiety is also affected by fluctuations in hormones, such as
leptin and insulin, which indicate the level of fat storage in the body.
Satiation and satiety can be measured directly via food intake or indirectly via
ratings of subjective sensations of appetite. The most common study design when
measuring satiation or satiety over a short period is using a test preload in which the
variables of interest are carefully controlled. This is followed by subjects rating
aspects of their appetite sensations, such as fullness or hunger, at intervals and then,
after a predetermined time interval, a test meal at which energy intake is measured.
Longer-term studies may provide foods or drinks of known composition to be
consumed ad libitum and use measures of energy intake and/or appetite ratings as
indicators of satiety. The measurement of satiation and satiety is complicated by the
fact that many factors besides these internal signals may influence appetite and
energy intake, for example, physical factors such as bodyweight, age or gender, or

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128 B. Benelam

behavioural factors such as diet or the influence of other people present. For this
reason, the majority of studies on satiation and satiety take place in a laboratory,
where confounders can be controlled as much as possible, and are, therefore, of
short duration.
It is possible for any food or drink to affect appetite, and so it is important to
determine whether, for a given amount of energy, particular variables have the
potential to enhance or reduce satiation or satiety. A great deal of research has been
conducted to investigate the effect of different foods, drinks, food components and
nutrients on satiety. Overall, the characteristic of a food or drink that appears to have
the most impact on satiety is its energy density. That is the amount of energy it
contains per unit weight (kJ/g, kcal/g). When energy density is controlled, the
macronutrient composition of foods does not appear to have a major impact on
satiety. In practice, high-fat foods tend to have a higher energy density than
high-protein or high-carbohydrate foods, and foods with the highest water content
tend to have the lowest energy density. Some studies have shown that energy from
protein is more satiating than energy from carbohydrate or fat. In addition, certain
types of fibre have been shown to enhance satiation and satiety. It has been suggested
that energy from liquids is less satiating then energy from solids. However, evidence
for this is inconsistent, and it may be the mode of consumption (i.e. whether the liquid
is perceived to be a food or drink) that influences its effect on satiety. Alcohol appears
to stimulate energy intake in the short-term, and consuming energy from alcohol does
not appear to lead to a subsequent compensatory reduction in energy intake.
The consumption of food and drink to provide energy is a voluntary behaviour,
and, despite the existence of sophisticated physiological mechanisms to match
intake to requirements, humans often eat when sated and sometimes refrain from
eating when hungry. Thus, there are numerous influences on eating behaviour
beyond satiation and satiety. These include: the portion size, appeal, palatability
and variety of foods and drinks available; the physiological impact on the body of
physical activity and sleep; and other external influences such as television viewing
and the effect of social situations.
Because satiation and satiety are key to controlling energy intake, inter-individual
differences in the strength of these signals and responsiveness to their effects could
affect risk of obesity. Such differences have been observed at a genetic, physiological
and behavioural level and may be important to consider in strategies to prevent or
treat obesity.
Overall, it is clear that, although the processes of satiation and satiety have the
potential to control energy intake, many individuals override the signals generated.
Hence, in such people, satiation and satiety alone are not sufficient to prevent
weight gain in the current obesogenic environment. Knowledge about foods, ingre-
dients and dietary patterns that can enhance satiation and satiety is potentially
useful for controlling bodyweight. However, this must be coupled with an under-
standing of the myriad of other factors that influence eating behaviour, in order to
help people to control their energy intake.

Keywords: appetite, behaviour, obesity, satiation, satiety

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1. Introduction
Maintenance of energy balance and a healthy body-
weight has been critical to human survival, and sophis-
ticated physiological mechanisms exist in the body to
maintain homeostasis (the maintenance of a constant
internal environment in the body) (Woods & D’Alessio
2008). The control of energy intake is vital to energy
balance, and satiation and satiety are part of a complex
system of appetite control, which regulates how much
we consume. Definitions of satiation and satiety are
shown in Box 1.
Box 1 Definitions
Satiation The process that leads to the termination
of eating, which may be accompanied by
a feeling of satisfaction
Satiety The feeling of fullness that persists after
eating, potentially suppressing further
energy intake until hunger returns
Over the course of a day, people typically have a
number of eating occasions including meals, drinks and
snacks. Satiation is important in controlling the amount
of energy consumed at each of these eating occasions,
while satiety affects the period of time between eating
occasions and potentially the amount consumed at the
next. Total daily energy intake is a function of both the
number of eating occasions that day and their size.
Hence, both satiation and satiety affect energy intake.
In the context of the rising prevalence of obesity, it is
important to consider the impact of satiation and satiety
on energy balance, and whether they can be enhanced in
order to facilitate the reduction of energy intake, aiding
weight control. However, although this briefing paper
will focus on the relationship of satiation and satiety to
obesity, it is worth remembering that there are many
instances where low energy intake is of concern, for
example, in the elderly or those with eating disorders. In
these cases, it may be desirable to reduce the effects of
satiation and satiety in order to allow greater energy
intake.
The factors affecting satiation and satiety from the
start of eating to late satiety have been characterised by
Blundell et al. (1987) in the satiety cascade, showing
sensory, cognitive, post-ingestive and post-absorptive
stages shown in Figure 1.
As this figure demonstrates, satiation and satiety are
initially affected by sensory and cognitive factors includ-
ing expectations about what is to be consumed, the
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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 129
Satiety Cascade (Blundell et al, 1987)
Post-absorptive
Sensory Cognitive
Post-ingestive
FOOD Early Late
Figure 1 The satiety cascade showing the influences on satiation and
satiety over time (Source: Blundell et al. 1987. reproduced with permission).
taste, texture and smell of the food or drink and any
associations with previous experience that arise. Once
the food or drink reaches the stomach, post-ingestive
factors start to take effect. Initially, the distension of the
stomach sends signals to the brain, initiating satiation.
As digestion continues in the intestines, hormones that
promote satiation and satiety are released from the gut.
In the post-absorptive stage of the satiety cascade, nutri-
ents themselves are detected by specialist receptors in
various sites of the body, including the brain, providing
information about nutrient status that also affects
satiety (Blundell et al. 1987). In the longer term, satiety
may also be affected by signals such as leptin, which
convey information about the level of fat storage in the
body (Wynne et al. 2005a).
Thus, the body has a complex network of signals
involved in the development of satiation and satiety.
However, for free-living humans, choices about what
and how much to eat are affected not only by internal
appetite signals such as satiation and satiety but also by
many other factors including the palatability of the
food in question, the portion size provided, the time of
day and the presence of other people (Bellisle 2003).
The amount of energy we consume is completely
accounted for by voluntary behaviour, namely the acts
of eating and drinking, influenced by physiological,
psychological and cultural factors. This is in contrast to
energy expenditure, between 20% and 40% of which
is under behavioural control via voluntary physical
activity (Blundell 2006). Thus, the study of appetite,
including satiation and satiety, must take account of
both physiological and behavioural evidence in order
to gain a full picture of how satiation and satiety affect
eating behaviour.
This briefing paper aims to give an overview of how
satiation and satiety develop in the body, the factors
that affect this and how satiation and satiety interact
130 B. Benelam
with external influences to impact on eating behaviour,
particularly with regard to excessive energy intake and
obesity. The physiological mechanisms of satiation and
satiety will first be outlined, followed by a description of
the different techniques used to measure satiation and
satiety. There is a potential for any food or drink to
induce satiety. Thus, it is important to gain evidence as
to whether, for a given energy content, particular foods,
drinks or their components are more satiating than
others. The evidence for the effect of a number of foods,
food components and nutrients on satiety is reviewed.
Humans may eat when sated and refrain from eating
when hungry, so it is clear that internal appetite controls
are not the only influence on energy intake. Some of the
potential external influences on energy intake are then
discussed. Appetite control is one of the potential
factors that could affect the risk of obesity (Foresight
2007). In light of the current prevalence of obesity, it
may be important to consider whether differences in
satiation and satiety or sensitivity to these signals can
increase the risk of obesity. There is evidence that this
may be the case, and this is outlined in the final section.
This Briefing Paper does not examine functional foods
and ingredients and satiety in detail, as these have
recently been reviewed elsewhere (Thomas & Chapman
2008). Changes in satiation and satiety in those with
eating disorders or other clinical conditions (other than
obesity) are also not included. In addition, the area of
health claims, satiation and satiety, with reference to the
European Commission regulation that came into force
in 2007 (EC/1924/2006), is not included in this paper
because this is currently the subject of the Institute of
Life Sciences International, Europe Appetite Regulation
Task Force, which will provide a thorough investigation
of the methodologies, relevant food components and
appropriate physiological biomarkers to provide scien-
tific substantiation to a satiety claim. This paper does
not constitute a systematic review but aims to give a
picture of the research in the area of satiation, satiety
and eating behaviour.
2. Physiological mechanisms of satiation
and satiety
Early animal experiments characterised areas of the
brain involved in satiation and satiety by observing the
effects of damage in particular locations in the brain, on
food intake behaviour. In this way, a number of areas
within the hypothalamus were identified as important in
the control of hunger and energy balance (Morgane &
Jacobs 1969). More recently, the way the body commu-
nicates influx, circulation and storage of nutrients and
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
the integration of these signals in the brain to affect
satiation and satiety have become more fully under-
stood. An outline of the pathways involved in commu-
nication of satiation and satiety between the body and
the brain is described in Figure 2.
This section describes the mechanisms by which satia-
tion and satiety signals affect specific areas of the brain
to maintain energy homeostasis. It also highlights the
possibility that hedonic systems within the brain (i.e.
those affected by the pleasurable aspects of food) may
interact with homeostatic systems and may override
satiation and satiety signals.
2.1 Physiological mechanisms of satiation
Satiation is the feeling of satisfaction that signals eating
to stop. The time course of satiation means that factors
affecting it must occur early in the satiety cascade, when
the food is selected, smelled and eaten and in the first
stages of digestion. Satiation appears to be a very basic
animal function that even rats with only a hindbrain
exhibit (Ritter 2004).
2.1.1 Gastric mechanisms of satiation
When food or drink reaches the stomach, nerves com-
municate an increase in gastric volume to the brain
(Ritter 2004). It appears that gastric distension pro-
motes satiation, independently of nutrient content
(Phillips & Powley 2000). In addition, there is evidence
that when food is removed from the stomach after inges-
tion, satiation does not occur. In experiments where
cannulas are fitted that allow food to drain from the
stomach, animals eat continuously, but quickly reach
satiation when the cannula is closed allowing food to fill
the stomach normally (Davis & Smith 1990).
There is the possibility that gastric distension could be
used as a biomarker of satiation. There are a number of
possible indirect methods for measuring gastric disten-
sion, for example, measuring changes in water pressure
in the stomach, which are outlined in a review of biom-
arkers in satiation and satiety by De Graaf et al. (2004).
Although further work is needed to develop direct
markers of gastric distension, this is a possible marker
for future research on satiation.
2.1.2 Intestinal mechanisms of satiation
From the stomach, food and drink are released into the
small intestine where digestion continues and nutrients
are absorbed. It appears that information about the
absorption of nutrients can be communicated to the
© 2009 The Author

Adipose
tissue
Figure 2 A schematic representation of
physiological satiation and satiety signalling.
When food is consumed, the gastric distension
is communicated to the brain via the vagus
nerve, which connects the gastrointestinal tract
to the brain, initiating satiation. Gut hormones
from the stomach and intestine are released
when food is consumed and act on areas of
the brain involved in appetite. Leptin from
adipose tissue and insulin from the pancreas are
related to the amount of fat stored in the body
and act on the brain to modulate satiation and
satiety in the longer term. All signals are
integrated in the brain to affect energy intake
and expenditure (Adapted from Wynne et al.
2005a).
brain and contributes to satiation. Experimental infu-
sions of fat, carbohydrates and proteins directly into the
intestine promote satiation. In the case of protein, car-
bohydrate and fat, digestion to their respective building
blocks of amino acids, sugars and fatty acids is neces-
sary in order for satiation to take place (Ritter 2004).
The gut hormone cholecystokinin (CCK) appears to
be involved in satiation. The satiating effects of CCK
were first demonstrated in 1973, when Gibbs et al.
showed that administering CCK reduces subsequent
meal size in a dose dependant manner in rats (Gibbs
et al. 1973). This has since been confirmed in humans
(Kissileff et al. 1981; Muurahainen et al. 1988),
although the distension of the stomach by food or drink
is necessary for this effect to take place (Lieverse et al.
1995).
CCK is mainly synthesised by the endocrine L cells in
the duodenum and jejunum (the beginning and middle
of the small intestine) and is rapidly released into the
circulation in response to the presence of nutrients in the
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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 131
Effects on energy intake
Brain
Insulin
Leptin
Pancreas
Vagus
nerve Gut
hormones
Gut Stomach
hormones
Intestines
gut, particularly after fat- or protein-rich meals (Wren
& Bloom 2007). CCK’s effects on satiety appear to be
mediated via receptors in the vagus nerve (the nerve that
connects the gut to the brain) and are blocked when this
nerve is removed in rats (Smith et al. 1981). The mecha-
nisms by which signals from CCK are integrated within
the brain are discussed in section 2.3.
CCK is a potential biomarker for satiation (De Graaf
et al. 2004). However, it must be noted that changes in
the levels of this gut hormone are only one part of the
process leading to satiation and cannot be seen as a
direct marker of satiation.
In addition to effects on satiation, CCK also delays
gastric emptying and stimulates pancreatic enzyme
secretion and gall bladder contraction (Liddle et al.
1985; Moran & Schwartz 1994), thus playing a role in
co-ordinating digestion. CCK is also found in the brain,
where it acts as a neurotransmitter involved in reward
behaviour, memory and anxiety, as well as satiety
(Crawley & Corwin 1994). CCK may act synergistically
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Table 1 Gut hormones and their actions
Name Site of production
Ghrelin Stomach
Cholecystokinin (CCK) Duodenum and jejunum
Glucagon-like peptide-1 (GLP-1) Intestine and brain
Oxyntomodulin (OXM) Intestine and brain
Peptide YY (3-36) (PYY 3-36) Ileum, colon and rectum
Pancreatic polypeptide (PP) Pancreas
with the hormone leptin, which signals the level of fat
storage in the body. This is discussed in section 2.2.2.
In summary, there are a number of variables that
influence satiation and thus the amount of food eaten at
one sitting. When nutrients reach the small intestine,
satiety signalling, which affects the time interval before
hunger and the desire to eat returns, is initiated.
Although the distinction between satiation and satiety is
an important one, they are part of a continuum in the
ingestive process, and there may be some overlap
between the later stages of satiation signalling and that
of early satiety. The next section outlines the mecha-
nisms affecting satiety.
2.2 Physiological mechanisms of satiety
Broadly, satiety is influenced both by short term or
‘episodic’ signals in response to the consumption of food
and by longer term or ‘tonic’ signals indicating the levels
of energy stores in the body. These act in various ways
on the hypothalamus in the brain, which in turn pro-
duces signals that affect energy intake and expenditure.
This section explores the satiety signals from the body
and their effects in the brain.
2.2.1 Gut hormones – episodic signals of satiety
A number of hormones are secreted from the gut to
indicate that food has been consumed. These act directly
or indirectly on specific areas of the brain to promote
satiety. A summary of gut hormones and their actions is
shown in Table 1. Ghrelin is the only known gut
hormone that causes hunger and, as its suppression
Effect on appetite Mechanism Additional effects
↑ Hunger Via ghrelin receptors in the brain Long-term effect on energy balance
↑ Satiation Via vagus nerve Delays gastric emptying
Stimulates pancreatic enzyme secretion
Stimulates gall bladder contraction
Acts as a neurotransmitter
↑ Satiety Via GLP-1R in brain Incretin (stimulates insulin production)
Slows gastric emptying
↑ Satiety Via GLP-1R in brain Slows gastric emptying
Via reductions in ghrelin
↑ Satiety Via Y2 receptors in brain Slows gastric emptying and intestinal
transport
Reduces gastric secretions
↑ Satiety Via Y5 receptors in brain –
Via vagus nerve
is relevant to the onset of satiety, it has also been
included for discussion. These hormonal signals are
termed as ‘episodic’ signals of satiety as they occur
alongside episodes of eating. These are considered sepa-
rately from tonic signals, which signal the level of energy
storage in the body, but it is important to note that there
may be interactions between tonic and episodic satiety
signalling. The way in which all these signals are inte-
grated by the brain are discussed in section 2.3.
Ghrelin is a peptide hormone mainly produced in the
stomach and, when administered experimentally to
animals and humans, stimulates appetite and increases
food intake (Tschöp et al. 2000; Wren et al. 2001). When
released, ghrelin acts on receptors in specific areas in the
brain. The integration in the brain of signals from gut
hormones is described in detail in section 2.3.
Ghrelin levels rise before meals, suggesting that it may
play a role in meal initiation in humans (Cummings
et al. 2001), although studies have not found that
ghrelin levels predict the interval between meals
(Callahan et al. 2004). The mechanisms causing release
of ghrelin from endocrine cells in the stomach are not
yet known. However, the suppression of ghrelin after
meals is proportional to the energy intake at the meal
(Callahan et al. 2004). In addition, on a per-kilojoule
basis, fat appears to be less effective than carbohydrate
or protein at suppressing ghrelin (Monteleone et al.
2003; Overduin et al. 2005).
Ghrelin may also play a role in long-term energy
balance. In humans, ghrelin levels are inversely
correlated with levels of body fatness; that is, they are
low in obese subjects (Tschöp et al. 2001), higher in lean
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subjects (Shiyya et al. 2002) and abnormally high in
subjects whose energy intake is chronically restricted,
such as those suffering from anorexia nervosa (Tolle
et al. 2003).
Glucagon-like peptide-1 (GLP-1) and oxyntomodulin
(OXM) are both products of the preproglucagon gene,
which is expressed in the brain, pancreas and intestine.
In the pancreas, the preproglucagon gene product is
processed to produce the hormone glucagon, whereas,
in the intestine and brain, GLP-1 and OXM are pro-
duced (Murphy & Bloom 2004).
Both GLP-1 and OXM are released into the circula-
tion in response to nutrients in the gut (Le Quellec et al.
1992; Herrmann et al. 1995) and appear to have an
effect on satiety. Experimental administration of GLP-1
to humans reduces food intake, decreases ratings of
hunger and increases ratings of fullness in normal-
weight, diabetic and obese subjects (Flint et al. 1998,
2000a; Näslund et al. 1998, 1999a; Gutzwiller et al.
1999a, 1999b; Toft-Nielsen et al. 1999). There is some
evidence that GLP-1 is reduced in obese subjects (Holst
et al. 1983; Ranganath et al. 1996; Näslund et al.
1999a) and that levels are restored by weight loss
(Verdich et al. 2001). Receptors for GLP-1 (GLP-1R)
can be found in areas of the brain involved in appetite,
and it is thought that GLP-1 mediates its effects on
satiety by acting directly upon these areas (Yamamoto
et al. 2003). GLP-1 also slows gastric emptying and
modulates gastric acid secretion, contributing to the
‘ileal brake’ mechanism of the upper gastrointestinal
tract, a combination of effects that controls the transit
of food from the stomach into the intestines, allowing
effective digestion (Näslund et al. 1999b).
In addition to its effects on satiety and digestion,
GLP-1 is a potent incretin, in that it potentiates the
production of insulin (MacDonald et al. 2002). Thus,
GLP-1 appears to have multiple roles in promoting
satiety, in the ileal brake and in encouraging the release
of insulin.
GLP-1 is a potential biomarker for satiety (De Graaf
et al. 2004). GLP-1 can be measured from blood
samples and is seen to rise for two hours after a meal,
compared with the fasting level (Orskov & Holst 1987).
More work is needed to establish whether or not GLP-1
is a reliable marker of appetite. A recent study on
protein and satiety found that, despite an increase in
ratings of satiety after a high-protein vs. low-protein
preload, GLP-1 levels were unchanged between the two
conditions. Other peptide hormones, peptide YY (PYY)
and ghrelin (also discussed in section 2.2.1), were also
found to be unaffected (Smeets et al. 2008).
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Satiation, satiety and their effects on eating behaviour 133
OXM has also been found to reduce food intake in
humans (Cohen et al. 2003) and enhance weight loss
(Wynne et al. 2005b) and appears to increase energy
expenditure (Wynne et al. 2006). OXM can bind to the
GLP-1R found in areas of the brain involved in appetite
control (Dakin et al. 2001) and reduces plasma ghrelin
concentrations in rats (Dakin et al. 2004) and in human
subjects. A study using physiological doses, adminis-
tered intravenously, found that fasting levels of ghrelin
were suppressed by 40% compared with those in con-
trols when OXM was administered (Cohen et al. 2003),
and this might be a factor in its satiating properties.
Similar to GLP-1, OXM also slows gastric emptying
(Schjoldager et al. 1989).
Overall, GLP-1 and OXM have similar actions on
satiety and gastric emptying, although OXM, as well as
the GLP-1R, may work via effects on ghrelin. OXM does
not have the incretin effects of GLP-1 but may have more
potent effects on weight loss (Wren & Bloom 2007).
The PP fold peptides include peptide YY (PYY), pan-
creatic polypeptide (PP) and neuropeptide Y (NPY). PYY
and PP are produced in the gut and are discussed below.
NPY is produced in the brain and is described in section
2.3 on the integration of satiety signals in the brain.
PYY is produced in the L cells of the ileum, colon and
rectum (Adrian et al. 1985a; Ekblad & Sundler 2002)
and is released into the circulation in proportion to the
amount of energy consumed, reaching a plateau after
1–2 hours and remaining elevated for approximately six
hours (Adrian et al. 1985a). This release begins before
the nutrients reach the distal portion of the gut where
PYY is produced, so it appears that PYY secretion may
initially be stimulated indirectly, possibly via the vagal
nerve (Fu-Cheng et al. 1997). Fasting suppresses the
secretion of PYY (Adrian et al. 1985a). The main form
of stored and circulating PYY is known as PYY(3-36) (a
truncated version of the full peptide) (Grandt et al.
1994).
The administration of PYY has been found to reduce
food intake both in rodents (Batterham et al. 2002;
Adams et al. 2004; Chelikani et al. 2005) and in
humans (Batterham et al. 2003a; Degen et al. 2005).
Batterham et al. investigated the effects of PYY(3-36) on
both lean and obese subjects and found that, in both
cases, energy intake at a buffet lunch two hours after
administration was reduced by approximately 30% and
that there was also a significant decrease in energy
intake during the 24 hours after treatment. In addition,
fasting PYY levels were lower in obese than in lean
subjects, and body mass index (BMI) correlated
134 B. Benelam
negatively with PYY levels. Post-prandial PYY release
was also lower in the obese subjects, despite the fact that
they consumed more energy (Batterham et al. 2003a).
This raises the possibility that a deficiency in circulating
PYY could be involved in the development of obesity,
although it is currently unclear whether low levels of
PYY are a cause or an effect of obesity.
PYY also inhibits gastric emptying, increases transit
time through the intestine (Savage et al. 1987) and
reduces gastric secretions (Adrian et al. 1985b), indicat-
ing it may play a role in the ilieal brake mechanism.
PYY, like other PP fold peptides, binds to Y1-Y5 recep-
tors (Larhammar 1996). PYY(3-36) binds most strongly
to the Y2 receptor and it is thought that its effects on
satiety are mediated by binding to this receptor in the
brain.
PP is mainly produced by the pancreas but also in
small amounts in the colon and rectum (Adrian et al.
1976). Like PYY, it is released into the circulation after
eating, in proportion to the amount of energy consumed
(Track et al. 1980). Experiments have also shown that
PP administration reduces food intake in humans. When
administered two hours before a buffet meal, PP
reduced energy intake by 22% at this meal and through-
out the evening and the following morning, leading to a
25% decrease in energy intake over the 24-hour period
(Batterham et al. 2003b). PP, like PPY, signals to the
brain via the Y family of receptors and is thought to act
on Y5 receptors. It may also signal to the brain via the
vagus nerve (Wynne et al. 2005a).
Interestingly, both basal and post-prandial levels of
PP are suppressed in those with Prader–Willi Syndrome
(PWS), a genetic condition associated with hyperphagia
(overeating) and obesity (Zipf et al. 1981). Administra-
tion of PP reduces food intake in some PWS subjects
(Berntson et al. 1993), indicating that an altered PP
response may be a component of this syndrome.
2.2.2 Tonic satiety signals
Tonic satiety signals communicate the levels of fat
storage in the body to the brain, so that energy intake
and expenditure can be balanced to maintain a relatively
constant bodyweight. These signals act over the longer
term than episodic satiety signals that are activated at
each eating occasion.
Leptin is a peptide hormone, mainly produced by the
adipose tissue. It is a product of the ob gene, which was
first identified and cloned in a severely hyperphagic
(over-eating) and obese strain of mutant mouse (Zhang
et al. 1994). Circulating leptin levels are proportional to
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
fat mass and BMI, and are reduced by weight loss.
However, there is inter-individual variation in the
amount of leptin produced at a given percentage of body
fat (Maffei et al. 1995).
Leptin appears to influence bodyweight via its effect on
energy intake and expenditure. Chronic administration
of leptin to rodents causes increased energy expenditure,
reduced food intake and loss of bodyweight and fat mass
(Halaas et al. 1995). Reduction in leptin levels as a result
of weight loss is associated with increased hunger in
humans (Keim et al. 1998). Leptin may have a synergistic
interaction with CCK, a gut hormone involved in satia-
tion (see section 2.1.2), in that small doses of CCK (which
are not effective alone) decrease food intake when leptin
is administered at the same time (Barrachina et al. 1997).
A mutation of the ob gene, resulting in a lack of
circulating leptin, causes severe obesity in humans
(Montague et al. 1997), which can be reversed by
administering exogenous leptin both in children
(Farooqi et al. 1999) and adults (Licinio et al. 2004). In
addition, in those with a heterozygous leptin deficiency
(i.e. one rather than two functional copies of the ob
gene), there is a greater prevalence of obesity and a
higher percentage body fat than in subjects with a fully
functional ob gene (Farooqi et al. 2001).
The leptin receptor is expressed in areas of the brain
involved in appetite control, and leptin is thought to
mediate its effects by acting directly on these receptors
(Flier 2004). The effect of leptin in the brain will be
discussed in section 2.3. Leptin is transported across the
blood–brain barrier via a saturable process (Banks et al.
1996). This appears to be affected by energy balance in
that starvation reduces leptin transport across the
blood–brain barrier, and refeeding increases it (Kastin &
Pan 2000).
Although, as mentioned above, a very small propor-
tion of obesity cases involve impaired leptin secretion,
most obese people have relatively high levels of circu-
lating leptin (Maffei et al. 1995), and the administration
of exogenous leptin has only a modest effect on body-
weight (Heymsfield et al. 1999; Fogteloo et al. 2003).
This indicates that leptin resistance, rather than defi-
ciency, may be associated with obesity. The mechanisms
by which this could occur are not yet clear, but impaired
transport across the blood–brain barrier may be
involved (Kastin & Pan 2000). Blood–brain barrier
transport of leptin in mice is reduced by diet-induced
obesity (Banks et al. 1999). There is also some evidence
in animal models to suggest that neurones in the brain
that respond to leptin may become resistant to its effects
after chronic exposure to high levels of leptin (Sahu
2002).
© 2009 The Author

Leptin has been suggested as a biomarker for satiety
(De Graaf et al. 2004). However, because high leptin
levels do not appear to reliably increase satiety, it cannot
be assumed that changes in leptin will cause a corre-
sponding change in appetite. Thus, leptin might be useful
as a biomarker of satiety in the longer term but may not
be useful in subjects with chronically high leptin levels.
Thus, while a lack of leptin causes severe obesity,
high circulating levels do not have a similarly dramatic
effect in reducing body fat, which has been described as
leptin resistance. It is also important to consider that
leptin’s ineffectiveness in preventing obesity at high
levels may be a result of internal satiety signals being
ignored in the face of easily available, energy-dense and
palatable foods.
Insulin is a metabolic hormone produced by the pan-
creas. Unlike leptin, which does not rise directly
in response to food intake, insulin secretion increases
rapidly after meals (Polonsky et al. 1988) and acts to
control blood glucose levels. However, over the longer
term, levels of plasma insulin are directly related to
changes in adiposity, so that levels increase with obesity
(Bagade et al. 1967).
In animal models, experimental administration of
insulin results in a decrease in food intake and loss of
bodyweight (Woods et al. 1979; Ikeda et al. 1986), and
inhibition of insulin’s actions leads to increased energy
intake and weight gain (McGowan et al. 1992). This
suggests that insulin contributes to satiety. Obesity and
lack of physical activity are associated with insulin resis-
tance, which may be accompanied by dislipidaemia
(high plasma triglycerides, and low high density lipo-
protein (HDL) (‘good cholesterol’), central fat deposi-
tion and high blood pressure (Coppack et al. 2005). It is
also possible that obese subjects are less sensitive to the
satiating effects of insulin. In a study investigating
passive over-consumption of high-fat foods in lean and
obese males, hyperinsulinaemia in the obese subjects
was associated with a lack of appetite control compared
with lean subjects (Speechly & Buffenstein 2000). The
results of a study that measured responses to insulin in
the specific parts of the brain involved in satiety, sug-
gested that insulin resistance may attenuate the effect of
insulin on these areas (Anthony et al. 2006).
Insulin crosses the blood–brain barrier and is thought
to act on insulin receptors that are found in the brain
(Corp et al. 1986). The signalling pathways activated by
insulin are discussed in section 2.3.
Interestingly, it has been suggested that there is cross
talk between leptin and insulin. Although leptin levels
are associated with fat mass, there appear to be other
factors involved, and insulin may play a role in stimu-
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 135
lating leptin production. In turn, the leptin receptor is
expressed in the pancreatic b cells that produce insulin,
raising the possibility that leptin affects insulin produc-
tion (for a review see Kieffer & Habener 2000).
2.3 The integration of satiety signals in the brain
Both tonic and episodic signals of appetite control act
directly through receptors in the brain or indirectly via
the nervous system on areas of the brain involved in
appetite control. Neurones within these areas express
neuropeptides that have downstream effects on energy
homeostasis. This section describes how these signals
are integrated to affect energy intake and expenditure.
Early animal experiments involving stimulation or
damage to different brain regions established the hypo-
thalamus as a centre for appetite control (Morgane &
Jacobs 1969), and this picture has since been developed
by establishing pathways originating within the arcurate
nucleus area of the hypothalamus, which controls
feeding and satiety. These pathways can broadly be
divided into anorexigenic (inhibit feeding) and orexi-
genic (stimulate feeding) pathways. Each pathway can be
both stimulated and inhibited by signals from the
gut, pancreas and adipose tissue. The overall effect is to
increase feeding and decrease energy expenditure or vice
versa, depending on the availability of nutrients and
the levels of energy storage in the body. The pathways
involved and how they integrate the tonic and episodic
signals that have been described in previous sections
are summarised in Figure 3. Other areas of the brain are
also involved in satiation and satiety, and these are briefly
outlined in section 2.3.3. In addition, reward pathways,
conveying the pleasurable qualities of food, may also
influence satiety and are discussed in section 2.3.4.
2.3.1 Anorexigenic pathways in the hypothalamus
Neurones that express the neuropeptides pro-
opiomelanocortin (POMC) and cocaine-and-
amphetamine-related transcript (CART) have an
anorexigenic effect and are stimulated by leptin. POMC
is a precursor for the neuropeptide a-melanocyte-
stimulating hormone (aMSH), which acts on melano-
cortin 3 (MC3) and melanocortin 4 (MC4) receptors
(Ellacott & Cone 2004). Administration of aMSH to
rats inhibits feeding (Rossi et al. 1998) and increases
energy expenditure (Pierroz et al. 2002); humans and
animals that have a mutant POMC or MC4 gene are
hyperphagic and obese (Yang & Harmon 2003). CART
is co-expressed with POMC in the hypothalamus.
Administration of CART to rats inhibits feeding both
136 B. Benelam
Arcurate nucleus
Stomach Grehlin
NPY/AgRP
PPY(3-36)
GLP-1
Intestine OXM
PP
Pancreas Insulin
PP POMC/CART αMSH
CART
Adipose tissue Leptin
under normal conditions and during starvation. Con-
versely, inhibiting the actions of CART increases feeding
(Kristensen et al. 1998).
2.3.2 Orexigenic pathways in the hypothalamus
Neurones that express NPY and agouti-related peptide
(AgRP) are orexigenic and are stimulated by ghrelin
and inhibited by PYY 3-36, GLP-1, OXM, PP, insulin
and leptin. Administration of NPY in animal models
causes hyperphagia and obesity (Stanley et al. 1986) and
reduces energy expenditure (Billington et al. 1991).
NPY is thought to increase food intake and decrease
energy expenditure by acting on Y1 and Y5 receptors in
the hypothalamus (Gehlert 1999). NPY may also have
an inhibitory effect on neurones, producing POMC
(Roseberry et al. 2004), therefore having a dual effect of
stimulating feeding while inhibiting pathways that
reduce feeding. AgRP is an antagonist of the MC3 and
MC4 receptors, inhibiting the reductive effects of
aMSH on appetite, so injection of AgRP causes an
increase in food intake in rats (Rossi et al. 1998).
2.3.3 Other areas of the brain involved in
satiation and satiety
Neurones that express POMC/CART and NPY/AgRP
connect with other areas in the hypothalamus and
Increased food
intake and decreased
energy expenditure
NPY
Y1 &Y5
receptors
AgRP
Figure 3 Circulating hormones influencing
energy homeostasis via the arcuate nucleus
(adapted from Murphy & Bloom 2004).
MC3 & MC4
Continuous lines indicate stimulatory effects,
receptors
and dashed lines indicate inhibitory effects.
AgRP, agouti-related peptide; CART, cocaine-and
amphetamine-related transcript; GLP-1,
glucagon-like-peptide 1; aMSH,
Decreased food alpha-melanocyte-stimulating hormone; NPY,
intake and
neuropeptide Y, OXM, oxyntomodulin; POMC,
increased energy
expenditure pro-opiomelanocortin; PP, pancreatic
polypeptide; PYY, peptide YY.
convey their signals downstream, producing the effects
on energy homeostasis described in section 2.3. A
detailed description of the neurotransmitters and path-
ways involved is beyond the scope of this paper, but see
Wynne et al. (2005a) for a review.
The brainstem is also an important area of the brain
for energy homeostasis. It receives signals from the gut
via the vagus nerve (Sawchenko 1983) regarding gastric
volume and information about the presence of nutrients
in the gut via signals from CCK (Schwartz et al. 1993;
Mathias et al. 1998). The brainstem is thought to affect
energy homeostasis both through downstream signals in
response to input from the vagus nerve, peripheral cir-
culating signals and via reciprocal connections with the
hypothalamus (Wynne et al. 2005a).
2.3.4 Reward pathways
Reward pathways, which are involved in signalling the
hedonic qualities of food and drink, may also influence
satiety, at least in the short-term. Several signalling
systems are involved in the hedonic response to food.
Opioids appear to affect food intake. In mice, a lack of
opioids removed the reinforcing quality of foods (the
amount of work subjects are prepared to put in to
obtain food), in the fed but not the fasted condition
(Hayward et al. 2002). Similarly, opioid antagonists
have been found to decrease palatability but not to
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
 Satiation, satiety and their effects on eating behaviour 137

Key points
• Satiation is induced via a number of mechanisms, including gastric distension and the gut hormone CCK.
• Satiety is controlled by both episodic (following an eating episode) and tonic (longer-term) signals.
• Episodic satiety signals are made by gut hormones. Release of ghrelin, which is associated with hunger, is
suppressed after energy intake. A number of gut hormones are released from the gastrointestinal tract when energy
is consumed, inducing satiety.
• Tonic satiety signals provide information about the amount of fat stored in the body. Leptin is secreted in
proportion to the amount of body fat, although there are inter-individual differences in leptin levels at comparable
body compositions. Although low leptin levels strongly stimulate energy intake, obese people have chronically high
levels of leptin, suggesting that leptin resistance is developed. Baseline levels of insulin also vary according to
adiposity, and insulin can impact on satiety.
• Specific areas in the brain, particularly the hypothalamus, are involved in integrating signals of satiation and
satiety.
• In these areas, populations of orexigenic and anorexigenic neurones translate signals of satiation and satiety via
downstream pathways to modulate energy intake.
• In addition to the pathways controlling energy intake, reward pathways involved in the pleasurable perception
of food may interact with homeostatic controls and could also affect eating behaviour.

affect hunger or satiety in humans (Yeomans et al.
1990). However, in one study, subjects prone to binge
eating consumed fewer snacks when given opioid
antagonists, despite ratings of hunger and satiety being
unaffected by the treatment (Drewnowski et al. 1992).
The dopaminergic system is also involved in feeding-
reward behaviour. Mice that cannot produce dopamine
die because they do not feed, and dopamine replacement
restores preferences for palatable foods (Szczypka et al.
2001).
Endocannabinoids appear to act on both the homeo-
static and hedonic systems controlling feeding behav-
iour via the hypothalamus and other areas of the brain.
They act on receptors throughout the body, including
the brain, adipose tissue, muscle and gastrointestinal
(GI) tract, increasing energy intake and fat deposition
and decreasing energy expenditure. In the presence of
palatable food, they affect appetite by both stimulating
the desire to eat and blocking signals to terminate eating
(Woods 2007). The ability to block these actions was
exploited by using the cannabinoid 1 receptor (CB1)
inverse agonist known as Rimonabant (Sanofi-Aventis).
This prevented the effects of endocannabinoids, which
reduced appetite and aided weight loss (Poirier et al.
2005). However, Rimonabant was withdrawn from the
European market in 2008 because of the incidence of
psychological side effects, such as depression, associated
with its use.
Both homeostatic and hedonic pathways in the brain
are complex, and it is not clear whether they operate
independently or interact. Indeed, these possibilities are
not mutually exclusive and either process may occur
under particular circumstances. It is self-evident that the
pleasurable sensory aspects of food can override internal
satiety signals, and increased sensitivity to hedonic
stimuli might be a risk factor for over-consumption and
obesity (Blundell & Finlayson 2004).
3. Measuring satiation and satiety
Both satiation and satiety are processes that affect
eating behaviour. They can be measured directly via
food intake or indirectly via subjective sensations. The
methods used and the issues that must be considered
when using them are outlined below.
3.1 Measuring satiation
The satiating qualities of foods and drinks can be mea-
sured by allowing subjects to consume them ad libitum
and monitoring how much is eaten before satiation is
reached, compared with a control food. Because the
termination of a meal may be affected by factors other
than physiological signals, measurement of satiation is
usually performed in a laboratory setting, where the
environment can be controlled to eliminate confounding
effects. These include the variety of foods offered, the
dietary restraint (tendency to consciously restrict the
amount of food eaten) of subjects or the appeal and
palatability of the food (Mattes et al. 2005). Confound-
ers are discussed further in section 3.3.

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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
138 B. Benelam
3.2 Measuring satiety
The measurement of satiety can be achieved through
methods that allow subjects to record feelings of satiety
or hunger, and/or by measuring food intake directly.
Studies on satiety are complicated by the psychological
and environmental factors that can conjointly affect
eating behaviour, and these may be controlled where
possible in studies on satiety. Some of the methods for
studying satiety are outlined below.
3.2.1 Free living vs. laboratory studies
In attempting to measure satiety and eating behaviour,
there has to be a compromise between being able to
measure these precisely and making the results appli-
cable to the ‘real world’. Because of potential confound-
ing by behavioural and environmental factors on satiety
and energy intake, studies are often conducted in a
laboratory environment. This allows the greatest pos-
sible degree of control over the external conditions of
the study and this means that the endpoints of interest
can be measured accurately.
However, when extrapolating the results of labora-
tory studies to free-living subjects, where conditions are
not subject to the same rigorous control, it may be
difficult to determine how relevant these are. In particu-
lar, short-term laboratory studies generally make efforts
to reduce the effect of learning about the post-ingestive
effects of consuming a particular food or drink, for
example that hunger returns more quickly after a
reduced energy version of a product. These effects might
have a meaningful impact on eating behaviour in the
longer term (Livingstone et al. 2000).
In practice, free-living studies require subjects to self-
report dietary intakes, and these measurements are
prone to bias. In particular, the underreporting of
energy intakes (Black et al. 1993; Goldberg & Black
1998) and misreporting of macronutrient consumption
(e.g. underreporting of fat consumption) (Pomerleau
et al. 1999; Goris et al. 2000) can be problematic in
obtaining an accurate picture of dietary intakes. In
addition, the lack of control over the subjects’ environ-
ment may make it difficult to interpret results and draw
conclusions about the effects of the dietary manipula-
tion in question.
Thus, although it is desirable to conduct studies
whose results are relevant to free-living populations, in
reality, it is extremely difficult to gain meaningful results
in uncontrolled conditions. Therefore, the vast majority
of studies on satiety have been conducted in the labo-
ratory under controlled conditions. Many studies use a
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
preload design, which is discussed in the following
section.
3.2.2 Preload studies
Studies that aim to measure the effects of a particular
variable or variables on the short-term regulation of
food intake and appetite often follow a preload design,
generally carried out over part or all of a single day. This
involves first giving subjects a preload food or drink
where the variable of interest is manipulated in order to
monitor subsequent effects.
The test and control preloads are matched (as far as
possible) for taste, appearance, texture and other
sensory qualities that might affect palatability. However,
they may be different in energy content, macronutrient
or ingredient composition, depending on the hypothesis
to be tested. The subjects should be blinded to the
differences between control and test preloads if the
investigators wish to measure only the physiological
effects of the manipulation. If the purpose of the study is
to measure both physiological and cognitive effects of
the changes made, the subjects may be told how the
preloads differ. The formulation of the preload is very
important in the ability of the study to measure a dif-
ference between the test and control preloads. Energy
content appears to be particularly important. Small dif-
ferences in the energy content of test and control pre-
loads or comparisons of preloads containing relatively
small amounts of energy, but differing in their compo-
sition, may mean that no effect of the test preload is
detected; whereas, if the same variables are changed in
preloads with higher energy content, significant effects
may be seen (Livingstone et al. 2000)
Typically, visual analogue scales (VAS), a type of self-
reported measure of appetite, are used to monitor
hunger, fullness and motivation to eat (see section
3.2.3). VAS may be recorded both before and at inter-
vals after the preload is given to monitor changes in
reported satiety.
After a pre-determined time interval after the preload,
a test meal is given, and energy intake is measured. The
time interval between the preload and the test meal is
critical to the results of the study because different
physiological mechanisms play a role in satiety during
the sensory, cognitive, post-ingestive and post-
absorptive phases of the satiety cascade (see Fig. 1). If
sensory, cognitive or gastrointestinal factors are of inter-
est, then the time delay must be 30 minutes or less. A
longer time interval is needed to measure post-
absorptive effects on satiety. However, if the interval is
too long, differences between the test and control
© 2009 The Author

preloads may not be detected (Livingstone et al. 2000).
The measurement of food intake in studies of satiety is
discussed further in section 3.2.4.
Depending on the study, another meal may be offered
to test the effect of the preload over a longer time period
and subjects may also be asked to self-report their food
intake for an allotted time after the study. Preload
studies generally have a crossover design, meaning sub-
jects consume both the control and test preloads on
separate occasions, so that effects of inter-individual
differences are minimised. Differences in self-reported
ratings of satiety and energy intakes after consumption
of the control and test preloads are then analysed to
establish whether the variable in question had an effect
on satiety.
3.2.3 Self-reported measures of satiety
VAS Originally developed in the field of pain research,
VAS are a simple tool to allow subjects to rate their level
of hunger, fullness or desire to eat. The scale consists of
a line, usually 100 or 150 mm, anchored by an extreme
answer to the question posed at either end, for example
‘How hungry are you?’, ‘Not at all hungry’ vs. ‘As
hungry as I have ever felt’ (see Fig. 4). Subjects make a
mark on the line, indicating how they feel at that
moment, and this is quantified by measuring the dis-
tance from the left end of the line to the mark. Because
there may be inter-individual differences in the way the
VAS are completed, a ‘within subject’ study design,
rather than separate groups of control and test subjects,
is generally used where subjects act as their own
controls.
How hungry are you?
Not at all hungry As hungry as I have ever felt
How satisfied are you?
Completely empty Cannot eat another bite
How much could you eat?
Nothing at all A lot
Figure 4 Examples of visual analogue scales for hunger/satiety (from Flint
et al. 2000).
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 139
VAS are generally completed at intervals throughout a
study to monitor changes in appetite. Traditionally, VAS
have been paper based but can now also be administered
by using portable electronic notepads, which have the
advantage of logging the results automatically. Elec-
tronic notepads can also provide alarms to prompt
subjects to complete the VAS (Stratton et al. 1998).
However, because the scale appears smaller on the elec-
tronic notepad than on paper and subjects appear to be
more reluctant to use the extremes of the scale when in
electronic form, paper and electronic VAS, although
equally reliable, should not be used interchangeably
(Stubbs et al. 2001).
VAS are relatively easy to use and process and have
been found to be reproducible and valid on a short-
term basis, in that the satiety/hunger ratings correlate
with energy intake (Flint et al. 2000a). However, there
are concerns that this association with food intake is
modest and that caution should be taken in interpret-
ing the results of studies by using VAS, especially if this
is the only measure of appetite used (Mattes et al.
2005).
There are some issues with the interpretation of VAS.
Although subjects make a mark on a continuous scale
and this is quantified, it cannot be assumed that a mark
of 40 mm along a satiety scale indicates a sensation of
half the magnitude of a mark that is 80 mm along the
scale. It has also been suggested that subjects may be
reluctant to make full use of the scale, either avoiding
use of the extremes of the scale or preferring them
(Livingstone et al. 2000). Despite these issues with VAS,
they remain one of the most widely used tools in
research on satiety and are often used alongside mea-
sures of food intake (see section 3.2.2 on preload
studies).
Category scales Category scales work on the same
principle as VAS – subjects self-report their feelings of
hunger or satiety in response to questions. However,
instead of a continuous line, numbered categories
(usually from 1 to 9) are provided. These may go from
the absence of a factor to its extreme (e.g. ‘How hungry
are you?’ 1 = not at all, 9 = extremely hungry) or repre-
sent the extremes of two variables (e.g. 1 = extremely
hungry, 9 = extremely full).
As with VAS, there are interpretation issues. Although
statements appear on a linear numerical scale, it cannot
be assumed that the associated statements have a linear
relationship; for example, the difference between state-
ments 3 and 4 might not be equivalent to that between
5 and 6. As with VAS, there may also be a tendency for
users to avoid extremes.
140 B. Benelam
Satiety-labelled intensity magnitude (SLIM) scale The
SLIM scale was developed by Cardello et al. (2005) in
order to provide better quantitative data from self-
reported measures of satiety, using a series of experi-
ments designed to quantify the meaning of a number of
statements on hunger and satiety. The responses were
used to select and quantify a number of phrases to label
a magnitude scale from +100 through zero to -100.
When compared with VAS, the SLIM scale was found to
be more sensitive and reliable (Cardello et al. 2005).
However, this scale requires further development (e.g.
translations of terms into different languages) before it
can be widely used.
3.2.4 Measuring food intake
Measuring food intake is a common way to assess
satiety, but eating patterns may be affected by factors
other than internal appetite signals. Humans eat in the
absence of hunger for a number of reasons (e.g. the
availability of palatable foods, boredom or emotional
stress). They may also refrain from eating when hungry
if psychological, social or environmental factors prevent
them from consuming food (Mattes et al. 2005).
Because eating behaviour can be affected by numer-
ous different variables, studies on satiety tend to be
conducted in a laboratory setting where the environ-
ment can be closely controlled. This allows subjects’
eating patterns to be monitored directly by keeping a
record of foods consumed and using a nutritional analy-
sis software to calculate energy and nutrient intakes.
The amount of food or drink consumed can also be
measured covertly and automatically by using a univer-
sal eating monitor (UEM), which consists of a set of
weighing scales concealed under a table cloth, connected
to a computer that measures the amount of food con-
sumed over time (Kissileff et al. 1980).
In these studies, it is important to consider the kinds
of foods offered and the way these are presented to
subjects in the laboratory, as this potentially affects how
much will be consumed. Obviously, foods must be
acceptable to subjects in the study or they will not be
consumed, and it is advisable to first conduct pilot
studies to test the palatability of test meals. Buffet type
meals are often offered to allow subjects to choose from
a variety of foods. However, it is known that offering a
wide variety of foods can increase energy intake through
sensory specific satiety (i.e. a subject may feel sated with
by one kind of food but will consume more when alter-
native foods are offered) (Rolls 1984). This should be
taken into account when designing and interpreting
studies (Livingstone et al. 2000).
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
After a study in a laboratory, participants may be
asked to record their food intake and/or appetite ratings
(using VAS or another self-reported method) when they
leave the laboratory, for a period after the study to
monitor any subsequent changes in appetite (e.g. for the
rest of the day, after a morning spent under laboratory
conditions or for the following 24 hours after a day’s
study). The problems of an uncontrolled environment
and misreporting of food intake persist, but the results
gained in the laboratory provide a context in which to
interpret this. Longer-term studies may provide food to
be consumed ad libitum and monitor the amount eaten
and may also measure changes in bodyweight. If it is
assumed that subjects eat until they are full when eating
ad libitum, which may not always be the case, energy
intake and any changes in bodyweight can give an idea
of the satiating properties of the diet as a whole.
3.2.5 Quantifying satiety
By using the preload design described in section 3.2.2,
methods have been developed to quantify satiety.
Satiating efficiency A test of ‘satiating efficiency’ was
developed by Kissileff in 1984 and aims to determine the
satiating power of foods according to particular factors
such as nutrient composition and energy content. A
number of preloads are given, varying one factor at a time
to different degrees (e.g. increasing the energy content
while keeping the proportions of macronutrients con-
stant). These are followed by a test meal at which energy
intake is measured. The energy intake at the test meal is
then plotted against the factor in question, and the slope
of this line is the ‘satiating efficiency’ per unit of the factor
in the food in question (Kissileff 1984).
The satiety index The satiety index (SI), designed by
Holt et al. (1995), involves giving the food to be mea-
sured as a preload, then taking VAS every 15 minutes
after the preload for the next two hours. Subjects are
then given a selection of food and drink to consume ad
libitum. A ‘satiety response curve’ is plotted by using the
change in satiety ratings on the VAS from baseline over
time. This is shown in Figure 5.
The SI score is calculated by dividing the area under
the satiety response curve (AUC) of the test food by the
group average AUC of the reference food (white bread),
which contains the same amount of energy (1000 kJ),
and multiplying the resulting number by 100. Thus, the
SI compares foods relative to white bread to allow the
satiating properties of foods to be ranked (Holt et al.
1995).
© 2009 The Author

Satiety response curve
Change in satiety rating scale units
3
2.5
2
White bread
1.5
Test food
1
0.5
0 because their energy requirements are different – the
0 15 30 45 60 75 90 105 120
Time (minutes)
Figure 5 A schematic example of a satiety response curve as used by
Holt et al. (1995) to calculate the satiety index (adapted from Holt et al.
1995).
The satiety quotient The satiety quotient (SQ), devel-
oped by Green et al. (1997), provides a measure of a
food’s ability to decrease motivation to eat. It is calcu-
lated by measuring the motivation to eat immediately
before a test preload then at intervals afterwards. The
SQ is calculated from the difference between these
pre- and post-consumption motivations divided by the
weight or energy content of the food or drink being
tested. This gives a measure of the rate at which the
motivation to eat returns, by weight of food or by
energy content (Green et al. 1997).
These methods provide a way to compare the effects
of different foods on satiety. However, they are only as
reliable as the measures taken to calculate them and, as
discussed in section 3.2.3, self-reported measures to
indicate satiety have potential problems, which need to
be considered when using satiating efficiency, SI and SQ.
In addition, comparisons using these methods can only
be made either within a study or between studies that
have exactly the same study design. A comparison
between studies with different designs would be mis-
leading, as the values obtained are dependent on this.
3.3 Confounders in satiety research
Research into satiety generally aims to investigate the
effects of a particular food/nutrient on eating behaviour
(e.g. whether fibre-rich foods enhance satiety, causing a
decrease in energy intake). Indeed, energy intake can be
used as a measure of satiety. However, this is complicated
by the fact that other factors can affect how much people
eat and how satisfied they feel after eating. If researchers
do not wish these to impact on results, then they need to
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 141
be controlled for. Some possible confounders in satiety
research are outlined below, subdivided into physiologi-
cal and behavioural factors. Some studies may measure
the effects of these factors on their results, and, in these
cases, the factors of interest will not be controlled for.
3.3.1 Physiological confounders
Bodyweight Obese and lean subjects may respond dif-
ferently to tests of appetite and energy intake, not least
energy requirements of obese subjects are generally
higher than those of lean subjects. There is also some
evidence to suggest that there may be differences in
some aspects of physiological appetite control between
lean and obese people that could potentially affect the
results of studies on satiety (see section 6). For these
reasons, studies may choose to include lean, overweight
or obese subjects only. In some cases, however, the dif-
ferences between these populations may be of interest,
and satiety and energy intake may be compared in lean,
obese or overweight subjects.
Age The age of subjects may impact on satiety respon-
siveness, in particular to sensory specific satiety. This is
the phenomenon whereby satiety is reached for a par-
ticular food or type of food, but, when different foods
are presented, appetite returns, stimulating further
energy intake (Rolls 1984). This is discussed further in
section 5.2. Sensitivity to sensory specific satiety appears
to decline with age (Rolls & McDermott 1991), and this
may be particularly important if the test meal offered is
in the form of a buffet where subjects are offered a
variety of foods.
Gender The gender of participants in studies may affect
their appetite and energy intake. First, simply because
women have lower energy requirements than men, they
are likely to eat less, and this must be considered if
energy intake is an endpoint of the study.
In addition, if female participants of childbearing age
are included, it is important to take the menstrual cycle
into account. Women’s energy intake fluctuates within
the menstrual cycle, with two distinct periods of
elevated energy intake that appear to be related to
hormonal fluctuations. The difference in energy intake
between these two phases and baseline intakes (364 kJ
or 87 kcal/day) has the potential to confound research
on satiety that uses energy intake as an indicator, and
this should therefore be noted and controlled for
(Lissner et al. 1988).
142 B. Benelam

3.3.2 Behavioural confounders
Habitual diet, alcohol and physical activity The
habitual diet, alcohol consumption and physical activity
of subjects can also affect satiety and eating behaviour.
Attempts may be made to ensure that participants are
not significantly different with regard to these factors
before studies commence, and subjects may be excluded
on this basis or asked to refrain from physical activity
and alcohol consumption the day before a study.
Control of diet before a study may be particularly
important in those who may not be in energy balance
before the study, for example, obese subjects or those on
a weight loss diet (Livingstone et al. 2000). However,
Gregersen et al. (2008) found that standardising the diet
of subjects prior to the study did not improve the repro-
ducibility of ad libitum energy intakes and actually led
to an increased energy intake on the following day. This
issue may require further clarification.
Dietary restraint Dietary restraint refers to the ten-
dency to restrict food intake in order to maintain or
lose bodyweight and is often associated with dieting
behaviour. Dietary restraint may be associated with
‘disinhibition’, where control over eating is lost, result-
ing in binge eating. Obviously, this type of behaviour in
the subjects of a study on satiety could affect the
results, and investigators commonly use questionnaires
such as the Dutch eating behaviour questionnaire (Van
Strien et al. 1986) or the three-factor eating question-
naire (Stunkard & Messick 1985) to assess potential
dietary restraint behaviour in study subjects. These use
a series of questions on aspects of eating behaviour,
providing a score indicating the degree of dietary
restraint exhibited by the subject. Those who score
above a threshold level are commonly excluded from
studies on satiety that wish to exclude the effect of
dietary restraint on results.
Prior knowledge and beliefs about test foods Most
studies on satiety manipulate the content of test meals
covertly in order to control the influence of beliefs or
knowledge about the foods or drinks in question on
subsequent intake. However, this is very difficult to do
comprehensively, and subjects may still be able to detect
differences between the control and test meals. If the
study requires a number of visits to the laboratory to
test different formulations, subjects will become accus-
tomed to the conditions of the experiment and what is
expected of them, and this may also affect their response
(Livingstone et al. 2000).
Studies that have tested the effect of prior knowledge
about differences in the energy or fat content of foods
have found that these can affect both subsequent energy
intake and feelings of satiety. When subjects are given
identical preloads but told that one is high in fat and
the other low in fat, more energy is consumed after the
preload labelled as low fat (Caputo & Mattes 1993;
Shide & Rolls 1995). In addition, in a study of restrained
eaters, sensations of hunger and fullness were affected by
the perceived energy content of a liquid preload even
when this information was incorrect (Ogden & Wardle
1990). Thus, although difficult to do, it is essential that
these factors are controlled as far as possible, unless the
effect of prior knowledge and beliefs about the foods in
question is one of the variables to be measured.
The effect of other people It has been observed that
people consume more energy when eating with others,
although the nature of the relationship with these other
people may modulate this effect (De Castro 1994, see
section 5.7). For this reason, subjects in satiety studies

Key points
• The effects of foods and drinks on satiation can be measured by the amount consumed ad libitum.
• Satiety can be measured directly via recording energy intake and indirectly by using self-reported measures of
appetite.
• Visual analogue scales (VAS) are the most commonly used method of self-reporting appetite.
• Many studies on satiety use a preload design where a food or drink of interest or a control is given, generally
followed by VAS at selected intervals. Then, after a predetermined period of time, a meal is given, and energy intake
is measured.
• A number of physiological and behavioural factors can potentially confound studies on satiety and, as far as
possible, are controlled for in studies that wish to exclude their effects.
• In order to create a controlled environment, satiety studies are generally conducted in a laboratory. However, this
can make it difficult to extrapolate results to the ‘real world’, where conditions are not controlled for in this way.

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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173

generally eat alone or in separate booths to minimise
the social effects of the presence of others on eating
behaviour.
4. The effects of foods and drinks on satiety
It is possible for anything we eat or drink to affect
satiety, so it is important to understand whether, relative
to their energy content, different foods or components
of foods may have consistently differing and meaningful
effects on satiety and subsequent energy intake, at a
feasible level of consumption.
This section looks at the effects on satiety of particu-
lar nutrients and food components, for example, fat and
fibre, and other variables such as energy density and the
degree of hydration (liquid vs. solid). Satiety, rather than
satiation, is the main focus, as this is where the most
research has been conducted. It should be noted that this
section does not systematically review the evidence in
this area but aims to present an overview of the effects
of different foods and drinks on satiety.
Studying the effects of one variable in food or drink
while keeping others constant is inherently difficult,
especially if researchers do not want the differences to
be discernable to subjects. For example, adding fibre to
a food can also decrease its energy density and palat-
ability, both of which could affect satiety. Conversely,
adding fat could have the opposite effect. Laboratory
studies control test foods, so that only the factors of
interest are varied. However, this may generate differ-
ences in the attributed effects of specific macronutrients
between laboratory situations (where many confound-
ing factors are largely controlled) and the real-food envi-
ronment (where they are not).
Although studies generally make efforts to control for
confounding variables, it may not always be possible to
keep all factors constant, and this should be considered
when looking at the results. Many short-term studies in
this area follow the preload design, monitoring appetite
ratings and energy intake after a test food or drink. In
the longer term, changes in bodyweight in subjects
eating ad libitum may be measured to draw inferences
about the effects of particular dietary patterns on satiety.
Often these studies do not include measurements of
appetite, so, although it is assumed that subjects who
are not consciously restricting their intake will eat to
fullness, caution must be exercised in drawing conclu-
sions about satiety in these cases. Finally, epidemiologi-
cal studies may find associations between particular
dietary patterns and bodyweight, and, although these
cannot demonstrate a causal effect of a particular diet
on satiety, they can lend weight to a line of evidence.
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 143
4.1 Protein and satiety
Many studies have investigated the effects of protein on
satiety, and most but not all have found that, at suffi-
ciently high levels, protein has a stronger effect on
satiety than equivalent quantities of energy from carbo-
hydrate or fat. Most studies investigating the effects of
protein on satiety have followed a preload design, where
the protein content of the preload is varied and the
effects on subsequent self-reported ratings of appetite
and/or energy intake are measured.
A review of studies on protein, satiety and weight
loss by Halton and Hu (2004) looked at both short-
term and longer-term studies on satiety, energy intake
and bodyweight change. The studies were selected on
the basis of making a comparison between higher and
lower protein preloads or diets monitoring satiety,
energy intake and bodyweight change. The authors
highlighted that the methodologies used were too dif-
ferent for a systematic comparison to be made and
that the review was qualitative in nature. Out of 14
short-term studies, 11 found that the higher protein
preload significantly increased ratings of satiety, and 8
out of 15 studies found that the subsequent energy
intake was significantly lower in the higher protein
condition than in the control (Halton & Hu 2004).
The test period in the different studies ranged from 1
to 24 hours, and the proportions of macronutrients in
the test and control preloads also varied with 29% to
100% protein in the high protein test and a variety of
higher carbohydrate or fat preloads for the control.
The form of the preload also varied, from mixed meals
to single drinks (Halton and Hu 2004). Another study,
(not included in the Halton and Hu review) found
that, in the short-term (over 5 hours), when the
macronutrient content of a test meal was varied but
the energy density was kept constant, there were no
differences in appetite ratings or subsequent energy
intake (Raben et al. 2003).
Halton and Hu (2004) also looked at the effect of
high-protein diets on weight loss. Of the 15 studies
identified, seven found a significant weight loss after a
high-protein diet compared with the control. Of the
studies selected, all 5 of those that allowed ad libitum
intake found a significant weight loss, whereas only 2 of
the 10 studies that provided isocaloric high- vs. low-
protein diets had significant weight loss results (Halton
& Hu 2004). Although appetite ratings were not taken
during these studies, it may be that increased satiety on
the high protein diets vs. the control diets mediated
lower energy intakes in the ad libitum studies, resulting
in weight loss.
144 B. Benelam
A subsequent study that looked at the effects of
both isocaloric and ad libitum high-protein diets lends
support to this theory. Subjects were given a diet that
provided either 15% or 30% energy from protein (car-
bohydrate was kept constant at 50% of energy and fat
varied from 35% to 20% of energy). For the first four
weeks of the study, the high- and low-protein diets were
isocaloric, and subjects reported significantly higher
ratings of satiety on the high-protein diet than on the
low-protein diet. For the following 12 weeks, the
macronutrient proportions of the diet remained con-
stant, but subjects were allowed to eat ad libitum from
foods provided. This resulted in a spontaneous reduc-
tion in energy intake on the high-protein compared with
the low-protein diet of 1852 kJ (441 kcal) per day on
average and an average weight loss at the end of the
study period of 4.9 kg. This reduction in energy intake
did not appear to cause a reduction in satiety according
to self-reported appetite ratings (Weigle et al. 2005).
Lejeune et al. (2006) conducted a study on protein
and satiety in respiration chambers, allowing energy
expenditure to be assessed. For four days, subjects were
fed either an adequate-protein diet (10% energy from
protein) or a high-protein diet (30% energy from
protein), which were isocaloric. VAS measurements
showed that satiety was significantly increased and
hunger was significantly reduced on the high-protein
diet, compared with the adequate protein diet, despite
energy intakes being the same. Sleeping metabolic rate
and diet-induced thermogenesis (DIT) were significantly
higher on the high-protein than on the adequate-protein
diet (Lejeune et al. 2006). These results confirm those of
a similar study performed by this research group in
1999 (Westerterp-Plantenga et al. 1999). In a subse-
quent review on the effect of protein intake on weight
management, Westerterp-Plantenga et al. (2007) high-
light the relationship between DIT and satiety, both of
which are increased on high-protein diets. It is suggested
that the associated increase in body temperature and
oxygen consumption when on the high-protein diet may
enhance satiety (Westerterp-Plantenga et al. 2007).
A feature of some popular high-protein diets that
are also very low in carbohydrate is the induction of
ketosis. This is the state where ketone bodies are gen-
erated from fat stores in response to reduced glucose
availability when carbohydrate intake is very low. An
intervention study with obese male subjects by
Johnstone et al. (2008) was designed to test whether
high-protein, low-carbohydrate (LC), ketogenic diets
were more satiating and caused greater weight loss
than high-protein, medium-carbohydrate (MC), non-
ketogenic diets. The study compared a high-protein,
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
LC, ketogenic diet (30% energy from protein, 4%
energy from carbohydrate) with a high-protein, MC,
non-ketogenic diet (30% energy from protein, 35%
energy from carbohydrate). The energy density of the
LC and MC diets were the same, but the carbohydrate
and fat contents varied reciprocally. The study had a
crossover design, so that subjects consumed both diets.
The foods for each diet were provided, and the subjects
instructed to eat ad libitum for four weeks. Hunger and
energy intakes were found to be significantly lower on
the LC ketogenic diet than on the MC non-ketogenic
diet, and subjects lost significantly more weight on the
LC ketogenic diet. Other measures of appetite were
tested, such as fullness and prospective consumption
(how much subjects thought they could eat), but were
not found to be significantly different between the two
diets (Johnstone et al. 2008). It is not possible to con-
clude whether it was the ketosis on the LC diet or the
difference in fat content between the two diets that
caused the reduction in hunger and energy intake, and
the relevance of ketosis to satiety may warrant further
investigation. It should be noted, however, that there
are safety concerns about very-high-protein diets and
that caution should be exercised in promoting them
(Eisenstein et al. 2002).
Some studies have investigated the short-term effects
of different protein sources on satiety. Uhe et al. (1992)
measured the relative satiating effects of protein in beef,
chicken and fish over a period of three hours. VAS
measures of satiety were found to be significantly higher
after subjects consumed fish than beef or chicken (Uhe
et al. 1992). Subsequent energy intake was not mea-
sured. Similarly, Borzoei et al. (2006) also looked at the
satiating effects of beef and fish and found a non-
significant increase in satiety and a significant decrease
in energy intake at a subsequent meal after the fish
compared with the beef (Borzoei et al. 2006). However,
both studies were relatively small (6 and 23 subjects,
respectively) and included only lean men. The mecha-
nism by which fish protein might exert greater effects on
satiety is not known, but the authors hypothesised that
it might be a result of differences in amino acid content
or in the slower rate of digestion of fish protein.
Mycoprotein, which is a high-protein food produced
from a fungal source, has also been tested for its effects
on satiety. Burley et al. (1993) and Turnbull et al. (1993)
compared the effects on satiety of a mycoprotein-based
meal with those of a chicken meal, with the same
protein content. In both studies, subsequent energy
intake was lower after the mycoprotein than after the
chicken meal. Although the meals were matched for
energy and protein, it should be noted that the
© 2009 The Author

mycoprotein meal was higher in fibre, which may have
affected the satiety response. It is therefore not possible
to draw conclusions about the specific the effects of
protein on satiety in this case (Burley et al. 1993;
Turnbull et al. 1993). Williamson et al. (2006) com-
pared the effects on satiety of a mycoprotein preload
with those of chicken and tofu, with matched protein
contents. Energy intake at the test lunch was reduced
after both the tofu and mycoprotein preloads, compared
with the chicken preload. There was no significant dif-
ference in this reduction in energy intake between the
tofu and mycoprotein preloads. There were also no
significant differences between any of the three preloads
on the ratings of appetite or energy intake at the evening
meal. However, this does mean that subjects did not
compensate for eating less at lunch time (after the tofu
or mycoprotein preloads) by eating more at the evening
meal (Williamson et al. 2006).
Different types of isolated protein added to meals
have also been investigated for their potential effects
on satiety. Lang et al. (1998) looked at the effects of egg
albumen, casein, gelatin, soy protein, pea protein and
wheat gluten on satiety, using a preload design, and
found no significant differences in their effects on appe-
tite (Lang et al. 1998). The doses used in this study were
extremely high (70 g of protein per meal), and this was
followed up with a similar study using casein, gelatin
and soy protein at lower doses (50 g and 25 g).
However, again, there were no significant differences
found between the different types of protein (Lang et al.
1999).
Hall et al. (2003) compared the effects of drinks con-
taining very large amounts (48 g per serving) of whey vs.
casein (both milk proteins) and found that energy intake
was reduced by 19% at a subsequent meal by the whey
compared with the casein preload (Hall et al. 2003).
Anderson et al. (2004) compared the effects of 45–50 g
of protein in liquid preloads from whey, soy protein, egg
albumen, sucrose and a control (water) on subsequent
energy intake. Whey and soy protein suppressed energy
intake at a meal provided one hour later, but egg
albumin and sucrose did not, resulting in a greater
energy intake overall (preload plus meal). Whey was
more effective at suppressing subsequent energy intake
than soy, resulting in compensation for the energy in the
preload of 96% and 59% respectively, after the whey
protein preload and the soy preload.
In a separate experiment, the effect of 50 g of soy
protein was compared with a combination of 25 g of
soy protein and 25 g of carbohydrate (either glucose or
amylose) on energy intake at a meal one hour later. Soy
protein alone caused a significant reduction in energy
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 145
intake, but when the protein content was reduced and
carbohydrate was added, there was no significant reduc-
tion in energy intake (Anderson et al. 2004). Overall,
evidence suggests that the source of protein itself, at
levels feasible in foods, does not have a large and con-
sistent effect on subsequent appetite and food intake.
In summary, there is relatively consistent evidence
that energy from protein, in a sufficient dose, has a
greater effect on satiety than an equivalent amount of
energy from carbohydrate or fat, in the short-term,
although it is important to note that this effect has
not always been observed in studies that have matched
the energy densities of macronutrient preloads. This
appears to translate into larger amounts of weight loss
in longer-term studies when ad libitum high-protein
diets are compared with lower-protein diets. This may
be a result of a higher satiating effect of protein,
although appetite measures are often not taken in these
studies, making it difficult to confirm this.
Differences in study design make it difficult to pin-
point the optimum dose or percentage of energy needed
to observe significant effects of protein on satiety.
Anderson and Moore (2004) suggest that at least 50 g
of protein in a food or meal is necessary to see a signifi-
cant effect on satiety, but that there is not currently
sufficient information to describe a dose–response rela-
tionship. There is currently no formal definition of ‘high
protein’ as a percentage of energy in a meal or diet. In a
review of the safety and efficacy of high protein diets,
Eisenstein et al. (2002) suggested that protein intakes
higher than 25% energy should be defined as ‘high’ and
over 35% energy as ‘extremely high’ based on the US
dietary recommended intakes which give 10–35% as the
acceptable range of protein intake (Eisenstein et al.
2002).
4.2 Carbohydrates and satiety
Carbohydrates are a diverse group that includes mono-,
di- and oligosaccharides and starches made from long
chains of glucose. The rate at which sugars (mono and
disaccharides) and starches are digested, absorbed and
metabolised are different because the longer chain length
of starches increases the time needed for digestion com-
pared with sugars. In addition, there are a number of
monosaccharides (e.g. glucose, fructose, galactose) that
are combined to make disaccharides, such as sucrose,
lactose and maltose, and there are also variations in the
metabolism of different monosaccharides. Therefore, the
effect of a carbohydrate on satiety depends on the form
of the carbohydrate and other aspects of the food (e.g.
fibre content) from which it is delivered.
146 B. Benelam
In the 1950s, the glucostatic theory of appetite regu-
lation was developed by Mayer (1953), which hypoth-
esised that blood glucose levels determined appetite,
initiating energy intake when low and causing satiety
when increased. Although the effect of nutrients on
appetite is now understood to be far more complex
(Stubbs 1996), glucose concentration does play a role in
appetite control. Because the brain depends heavily on
glucose as a source of energy, glucose levels are tightly
controlled, and there are multiple sites in the body
where glucose levels are detected. This information is
integrated in the brain, feeding into a number of neu-
ronal pathways, including those affecting energy intake
(Marty et al. 2007). Thus, appetite regulatory systems
appear to be directly affected by glucose in addition to
the hormonal signals discussed in section 2.
A number of sugars have been investigated for their
effects on satiety. As with studies on protein, a preload
design is commonly used, and, in order to assess the
effects of individual sugars, the preload is often a drink
with the sugar in question added. With regard to
sucrose, (a disaccharide of glucose and fructose), review
studies have found that 25 g as a single dose appears to
be the lower detection limit in terms of inducing satiety
(Anderson & Woodend 2003), and 50 g or more of
sucrose has been shown to increase satiety and reduce
food intake in the following 20–60 minutes in adults
and children, although the reduction in energy intake
does not fully compensate for the additional energy
from the sucrose preload (Anderson 1995). It should be
noted that the studies included in these two reviews
were relatively small and short-term and so conclusions
about the longer-term effects of sucrose consumption on
satiety or energy intake cannot be drawn.
In a review of the effects of refined carbohydrates on
satiety and mood, Hammersley et al. (2007) emphasised
the difficulty in disentangling the physiological effects of
refined carbohydrates on satiety and the psychological
effects of sweetness. Results from the short-term studies
on carbohydrate and satiety were inconsistent, and the
authors of the review highlighted the fact that a number
of studies had not blinded subjects to the content of the
test foods/drinks. With the longer-term studies on car-
bohydrate and satiety included, it was also difficult to
draw overall conclusions because of the influence of
the inherent palatability of sweetness on food intake
(Hammersley et al. 2007).
Reid et al. (2007) investigated the effects of drinks
containing sucrose vs. those containing aspartame on
satiety and energy intake for a period of four weeks in
133 free-living female subjects with healthy body-
weights. Subjects were provided with drinks each week
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
but were blinded as to their composition. The drinks
provided were actually diet and sugar-sweetened ver-
sions of a well-known brand of soft drink. However,
subjects were told that the drinks had been created
especially for the study to minimise any associations
subjects might already have with this particular brand.
The study had a crossover design so that subjects were
tested with both the sucrose and aspartame containing
drinks and acted as their own controls. The weekly
allocation (comprised of four 250 ml bottles to be con-
sumed over the course of the week) of sucrose-sweetened
drinks provided 1800 kJ, whereas the aspartame-
sweetened drinks provided 170 kJ/week. No effect was
seen on ratings of satiety, but the timing of appetite
ratings was not designed to detect short-term changes
in appetite after the drinks. In the sucrose condition,
subjects reduced their energy intake, partly compensat-
ing for the additional energy from sucrose. However,
because compensation was approximately 50%, con-
sumption of sucrose-containing drinks resulted in an
increased energy intake compared with the baseline mea-
surement. Consumption of the aspartame-containing
drinks resulted in a small reduction in energy intake,
compared with the baseline (Reid et al. 2007).
Glucose and fructose preloads have also been found
to reduce subsequent energy intake (Anderson &
Woodend 2003). There is some uncertainty regarding
the relative effects of glucose and fructose on satiety.
Studies comparing the two tend to be small and short-
term and have yielded conflicting results as to which is
the more satiating (Anderson 1995; Anderson &
Woodend 2003). Glucose and fructose are absorbed and
metabolised differently and may act differently on
satiety pathways. Glucose itself is detected in the brain
and causes insulin release, which also acts on appetite
centres in the brain to induce satiety (see section 2.1.2).
The way in which fructose feeds into satiety pathways is
less clear, and some studies have found that leptin levels
are reduced and ghrelin levels are not suppressed in
response to fructose ingestion (Teff et al. 2004). This
might be expected to lead to impaired satiety although,
because there are many other factors involved in satiety-
signalling pathways, this cannot be assumed.
A number of studies have compared the effects of
sucrose and high-fructose corn syrup (HFCS) on satiety.
HFCS is typically comprised of 55% fructose and 45%
glucose, although other proportions exist, and so is not
that dissimilar to sucrose in terms of its composition.
During the storage of soft drinks, sucrose (50% glucose
and 50% fructose) is 90% inverted to glucose and fruc-
tose within three months (Hein et al. 2005). So, in this
case, the composition of sugars in drinks sweetened with
© 2009 The Author

sucrose compared with HFCS may not be that different.
A number of studies have investigated whether drinks
sweetened with HFCS compared with sucrose have
different effects on satiety, and a significant difference
between the two types of sweetener has not been found
(Akhavan & Anderson 2007; Monsivais et al. 2007;
Soenen & Westerterp-Plantenga 2007). For more infor-
mation on liquids and satiety, see section 4.6.
Aside from sugars, much research on carbohydrates
and satiety has focused on the impact of glycaemic
index (GI) or glycaemic load (GL). GI is a measure of
the capacity of carbohydrate-containing foods to raise
blood glucose compared with a standard, usually
glucose or white bread. GI is defined as the incremental
area under the blood glucose curve of a test food con-
taining 50 g of carbohydrate, expressed as a percentage
of the response to a portion of the reference food con-
taining 50 g of carbohydrate, taken by the same subject
on a different day (FAO/WHO 1998). A high-GI food is
one that is absorbed from the gastrointestinal tract rela-
tively rapidly, resulting in a sharp peak in blood glucose,
rather than in the more gradual rise over time seen with
low GI foods.
GL is calculated by multiplying the available carbo-
hydrate (the total carbohydrate minus fibre) in a serving
of the product by its GI and then dividing by 100. This
was introduced for providing a measure of glycaemic
response that was relevant to a realistic portion of a
food, rather than a constant amount of carbohydrate
(Jenkins et al. 2002). For example, a carrot has a high
GI but a low GL, as the amount of carbohydrate per
portion is relatively small. When considering the effects
of GI or GL, it is important to note that there are a
number of different factors that influence GI and GL,
including fibre content and fat or protein content, all of
which may have independent effects on satiety. In par-
ticular, low GI foods may also be high in fibre, which
can enhance satiety (see section 4.3), and this can be a
confounding factor. Thus, the literature on GI/GL and
satiety is complicated by the fact that, unless the com-
position of test foods is very carefully controlled, any
observed effects on appetite or energy intake may not be
a result of differences in glycaemic response per se, but
due to other factors, such as macronutrient composi-
tion, fibre content and palatability.
A review by Bornet et al. (2007) examined a number
of studies that had investigated the relationship between
the glycaemic response to foods and its impact on satiety
and weight management. Confounding factors were
taken into account when selecting studies for this
review. However, the authors commented that there was
difficulty in distinguishing the effects of GI from those of
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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 147
fibre. Both short-term studies (one day or less) with
liquid carbohydrates (e.g. glucose or fructose in water)
or foods and longer-term studies (2 weeks – 6 months)
were included. Twenty-six short-term studies using
foods were selected. While some studies were inconclu-
sive, 16 out of the 26 studies concluded that satiety was
increased with low-GI vs. high-GI foods. The authors of
the review concluded that, despite some possible con-
founding factors, such as the fibre content and palat-
ability of the foods, there was evidence that low-GI
foods had greater satiating effects than high-GI foods in
the short-term. However, seven longer-term studies were
identified, and their results did not suggest that the
increased satiety seen in the short-term studies had an
effect on energy intake or bodyweight over the longer
time periods studied (Bornet et al. 2007).
A study by Alfenas & Mattes (2005) compared ad
libitum high- and low-GI diets over a period of 8 days.
A selection of high-GI and low-GI foods were provided,
and subjects ate only those foods for the duration of the
study. The high- and low-GI foods were matched for
macronutrient composition and palatability, but the
low-GI diet was higher in fibre. Appetite ratings were
taken on days 1 and 8 after breakfast and lunch, and
energy intake was recorded throughout the study. No
differences were observed in appetite ratings or in
energy intakes between the high-GI and low-GI diets
(Alfenas & Mattes 2005). This suggests that, under
carefully controlled conditions, the GI of foods does not
affect satiety or energy intake.
Das et al. (2007) conducted a randomised controlled
trial (RCT) that looked at the effects of two energy-
restricted diets, one high- and one low-GL. All foods
were provided for the first six months of the trial, and
subjects were guided by individual eating plans prepared
during discussions with dietitians. The researchers
designed the diets to avoid confounding factors, such as
the palatability and variety of the diet. Satisfaction, with
the quantity and types of food provided, hunger, and
desire to eat foods that were not included in the study
were measured during the first three months of the
study. There was a significant decrease in satisfaction
with the foods provided, within the high GL group, but
not within the low-GL group, but there were no signifi-
cant differences over time between the high- and
low-GL groups. Both groups decreased their energy
intakes, compared with baseline, and lost weight and
body fat, but, again, there were no significant differ-
ences between the high- and low-GL groups (Das et al.
2007).
Aston et al. (2008) performed an RCT measuring
the effect of a higher- vs. lower-GI ad libitum diet on
148 B. Benelam
appetite, dietary intake and bodyweight using a cross-
over design (subjects were tested with both diets and
acted as their own controls). The diets were matched for
energy content, macronutrient composition and fibre
content. No differences were found between the higher
and lower GI conditions for any of the endpoints mea-
sured (Aston et al. 2008). Overall, the evidence suggests
that, when potential confounding factors are controlled,
the GI or GL of foods does not have a significant impact
on satiety.
Thus, carbohydrates are a diverse group of com-
pounds, and it is difficult to make generalisations about
their effects on satiety. Although carbohydrates have
been suggested to be intermediate in their impact on
satiety – less satiating than protein, but more so than fat
– comparisons between the satiating power of carbohy-
drates and fats have provided inconsistent results (see
section 4.5).
4.3 Fibre and satiety
The term ‘dietary fibre’ encompasses a variety of com-
pounds that reach the colon undigested, including
insoluble fibres such as wheat bran, soluble fibres from
oats and fruits, resistant starches and oligosaccharides.
These may be found naturally in foods or isolated and
used as functional ingredients (for more information,
see Lunn & Buttriss 2007; Buttriss & Stokes 2008). The
effect that a type of fibre has on satiety depends on its
physical properties when eaten and its physiological
effects in the gut.
The literature on dietary fibre and satiety was
reviewed by Slavin and Green in 2007. They looked at
studies using high-fibre diets, whole foods and isolated
fibres that can be added to foods. With regard to high-
fibre diets, two studies in this review looked at the effect
of a high-fibre breakfast on subsequent energy intake
at lunch (Burley et al. 1987; Silberbauer et al. 1996).
Neither study detected an impact of fibre on energy
intake but Burley et al. found that the high-fibre break-
fast caused greater fullness in subjects’ appetite ratings.
Another study compared the effects of ad libitum high-
and low-energy density diets on satiety, energy intake
and eating time over five days. The high-energy density
diet was achieved by using products that were high in fat
and sugar and by avoiding fibre. The low-energy density
diet was made up of high-fibre foods and was low in fat.
Subjects consumed half the amount of energy per day on
the low- compared with the high-energy density diet,
and eating time was 33% longer on the low-energy
density diet (Duncan et al. 1983). However, it is not
possible to discern from this study whether the results
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
were specifically due to the fibre content of the low-
energy density diet or to the effect of energy density
overall or to some other factor.
Studies on a number of whole foods, such as fruit,
vegetables, oats, barley and bread, were included in the
review. Most, but not all, studies showed an effect of
fibre on satiety and subsequent energy intake. The
amount of fibre was important, and larger doses were
more effective at promoting satiety and reducing energy
intake. Other factors also appeared to play a role, such
as the extent to which the food was refined or processed,
the particle size in grain-based foods and energy density
(Slavin & Green 2007).
Many types of isolated fibre were included in this
review, and some, but not all, had a significant effect on
satiety and/or energy intake. Generally, those studies
that used high doses of fibre (e.g. more than 10 g in one
dose or 30 g over the course of a day) had more positive
results. However, in some cases (e.g. when using poly-
dextrose), even high doses had no effect. The more
viscous fibres, such as pectin, psyllium and guar gum,
were the most effective at increasing satiety and had an
impact on satiety even at relatively low doses. Slavin and
Green (2007) suggested that viscous fibres could
prolong the digestion of food and absorption of nutri-
ents, extending the time available to stimulate pre- and
post-absorptive mechanisms of satiety. The bulking
effect of fibre can increase chewing time and gastric
distension, promoting satiation. Adding fibre also
reduces energy density, which may also promote satiety
(see section 4.8) (Slavin & Green 2007).
Novel fibres, which form gels in the stomach because
of a chemical reaction with stomach acid, have been
developed and tested with respect to their effect on
satiety and energy intake. Hoad et al. (2004) tested the
effects of drinks containing alginate fibres (one that
formed a gel in the stomach and one that did not)
compared with drinks containing guar gum (a fibre
whose viscosity is unaffected by stomach acid) and a
control (a sweetened milk drink) in 12 overweight and
obese subjects. All the drinks containing added fibres
were significantly more satiating over a 240-minute
period than the control, and there was a trend for
increasing satiety with increased viscosity (the gel-
forming alginate being the most viscous) (Hoad et al.
2004).
Pelkman et al. (2007) compared the effects on energy
intake of drinks providing two different levels (1 and
2.8 g) of a gelling pectin-alginate fibre in a drink, com-
pared with a control drink without added fibre, in 29
overweight and obese subjects. The drinks were con-
sumed twice a day over 7 days, and energy intake at an
© 2009 The Author

evening meal was recorded. The 2.8 g dose of pectin-
alginate caused a decrease of approximately 10% in
energy intake at the evening meal, which was not com-
pensated for by an increase in energy intake later. The
1 g dose reduced energy intake in some, but not all
subjects (Pelkman et al. 2007). Paxman et al. (2008)
tested a gelling alginate fibre vs. a control in 68 men
and women for 7 days. Daily consumption of the fibre
resulted in a 7% reduction in energy intake in these
subjects (Paxman et al. 2008). Thus, this novel action of
gelling fibres appears to be effective in inducing satiety
and reducing energy intakes, but more studies may be
needed to confirm these effects. It should also be noted
that some consumers might find products containing
these fibres unpalatable (Hoad et al. 2004).
4.4 Intense sweeteners and satiety
Intense sweeteners provide a sweet taste in foods or
drinks without delivering energy. There has been some
debate surrounding their effects on satiety and energy
intake, in particular whether they help to reduce energy
intake overall or disrupt appetite regulatory systems,
resulting in a loss of appetite control and overeating.
Because there are a number of different intense sweet-
eners that can be used in a variety of products, this is a
complex area and effects may depend on the sweetener
used and the product containing it.
Drewnowski and Bellisle (2007) reviewed this area
and highlighted that, as energy density is an important
determinant of energy intake (see section 4.8), the effect
of intense sweeteners on energy density of foods is an
important factor. In those soft drinks in which the
energy content is provided by sugars, the replacement of
sugar with intense sweeteners produces a large reduc-
tion in energy density, to almost zero. In solid foods
where energy is also provided by protein and fat,
replacement of sugars with intense sweeteners has less
impact on energy density. The studies investigating the
impact of intense sweeteners on satiety and energy
intake, reviewed by Drewnowski and Bellisle, had
mixed results, with some finding increases in appetite
and/or energy intake, some a decrease, but the majority
finding no significant effect on these parameters. Differ-
ences in study design make it difficult to reach any
overall conclusions about the effect of intense sweeten-
ers on satiety, but it appears that intense sweeteners do
not enhance satiety. The reduction in energy intake
because of the reduced energy density of foods/drinks
containing intense sweeteners does not seem to be com-
pensated for by an increase in subsequent energy intake.
However, this could only be helpful in reducing energy
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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 149
intake within the context of a controlled diet
(Drewnowski & Bellisle 2007).
Appleton and Blundell (2007) investigated the effects
of intense sweeteners and sugars on habitual high (HC)
and low consumers (LC) of drinks containing intense
sweeteners. In LC subjects, subsequent energy intake
was increased in response to the sweet tastes of both
preloads containing intense sweeteners and sugar,
whereas, in HC subjects this increase was not observed.
This suggested that HC subjects had learnt to dissociate
sweetness from energy provision, whereas LC subjects
had not (Appleton & Blundell 2007). This study indi-
cates that previous experience with intense sweeteners
may affect appetite and energy intake after their
consumption.
4.5 Fat and satiety
Dietary fat affects satiety by slowing gastric emptying,
stimulating the release of satiating gut hormones and
suppressing the release of ghrelin (Little et al. 2007) (see
section 2.2.1). However, it has been suggested that the
effect of fat on satiety is weaker than that of either
protein or carbohydrate (Rolls et al. 1988; Westerterp
2004). This view is not supported by all studies, and it
is important to note that an increase in the fat content of
a food or diet tends to increase palatability and energy
density, both of which can also affect satiety and energy
intake (Rolls & Hammer 1995). Some of the studies
that have investigated the effects of fat on satiety are
outlined below.
Blundell et al. (1993) investigated the effects on sub-
sequent energy intake of the addition of either a carbo-
hydrate or fat supplement of 1.52 MJ (362 kcal) to a
standard breakfast in lean male subjects, 90 and 270
minutes after eating the breakfast. The carbohydrate
supplement resulted in a reduction in energy intake after
90 minutes but not after 270 minutes, but the fat supple-
ment produced no reduction in subsequent energy intake.
Although the fat and carbohydrate supplements were
matched for energy content, the higher energy content
per gram of fat than of carbohydrate results in a higher
energy density (kJ/g; kcal/g) in the fat supplement. So it is
not possible to discern whether the results in this study
were due to the specific effects of fat on satiety or
differences in energy density.
In a further study, obese female subjects were fed
either a high- (4.12 MJ/985 kcal) or low-(2.21 MJ/
527 kcal) energy lunch, and then given an evening meal
where they were allowed to choose from either a range of
high-fat foods (minimum 50% energy from fat) or a
range of high-carbohydrate foods (minimum 50%
150 B. Benelam
energy from carbohydrate). There was a non-significant
increase in energy intake at the evening meal after the
low- vs. the high-energy lunch of 0.59 MJ (139 kcal).
However, exposure to the choice of high-carbohydrate
or high-fat foods caused a significant difference in energy
intake with subjects consuming an average of 2.84 MJ
(677 kcal) and 5.59 MJ (1336 kcal) on the high-
carbohydrate and high-fat meals, respectively (Blundell
et al. 1993). Thus, providing foods with a higher fat
content stimulated passive over-consumption of energy
at the evening meal. However, again, increasing the fat
content of foods also increased their energy density com-
pared with the high carbohydrate foods, and it might be
energy density, not the fat content per se, that led to the
increased energy intakes observed in this study.
Stubbs et al. (1996) looked at the effects of breakfasts
high in protein (HP), carbohydrate (HC) or fat (HF) on
appetite ratings and energy intake at a test lunch, five
hours later and for the rest of the day (until 11 pm). The
breakfasts were matched for energy density and palat-
ability. They found that hunger was highest after the HF
breakfast compared with the HP and HC breakfasts,
and that the HP breakfast was the most effective at
suppressing hunger throughout the day. However, these
differences did not translate into significant differences
in energy intake either at the lunch or during the rest of
the study day (Stubbs et al. 1995b).
Bell and Rolls (2001) compared the effects of meals
containing varying amounts of fat, matched at two dif-
ferent levels of energy density. This created six different
experimental conditions: lower-energy density with a
low-, medium- or high-fat content or higher-energy
density with a low-, medium- or high-fat content.
Thirty-six subjects attended the laboratory on six occa-
sions (to test each experimental condition) and ate
breakfast, lunch, dinner and an evening snack. Ratings
of appetite and daily energy intakes were measured. No
significant differences were seen in appetite ratings, but
energy intakes were significantly higher (by 20%) on the
higher-energy density than on the lower-energy density
diets. When energy density was matched, the fat content
of the diets did not affect energy intake, indicating that
it was the energy density and not the fat content that
influenced satiety (Bell & Rolls 2001).
Saltzman et al. (1997) conducted a study with seven
twin pairs, investigating the effects on energy intake of a
high-fat vs. a low-fat diet eaten ad libitum over 11 days.
The two diets were matched for energy density, and no
significant differences were detected in energy intakes
between the two diets (Saltzman et al. 1997)
When high-fat diets are compared with lower-fat diets
in the longer term, it has been found that subjects
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
consume less energy and lose more weight on low fat
diets, without any restriction on the amount of food
eaten (Glueck et al. 1982; Lissner et al. 1987; Kendall
et al. 1991). Glueck et al. took a number of daily appe-
tite ratings and found no significant differences between
the high-fat and low-fat conditions. Lissner et al. and
Kendall et al. did not measure appetite. These studies
suggest that humans do not detect a reduction in energy
when the fat content of the diet is reduced and thus do
not compensate by eating more. However, although pal-
atability of the high-fat and low-fat diets was matched
in these studies, energy density would have been lower
in the low-fat condition, so it is not possible to conclude
whether it was the reduction in the fat content of the
diet specifically or the lower energy density of the low-
fat diets that led to the reduction in energy intake. As
mentioned in section 4.1, Raben et al. (2003) found
that, when energy density was kept constant, varying
the macronutrient content of meals did not affect satiety.
The effect of energy density on satiety is discussed
further in section 4.8.
Overall, it appears that when energy density is con-
trolled, fat does not have a lesser effect on satiety than
other macronutrients do. However, for free-living
people whose conditions are not controlled, high-fat
foods and diets will often also have a higher energy
density than high-carbohydrate or protein foods. So, in
practice, fat content and energy density are closely
linked. The palatability of high-fat foods/diets is also a
factor that could contribute to their over-consumption.
The chain length of fatty acids in a triaclyglyceride
(fat) affects how they are absorbed and processed by the
body (French 2004), and this and their degree of unsat-
uration (e.g. MUFA vs. PUFA) have also been suggested
to influence satiety. However, where effects have been
shown, they have generally been small or occur only on
extreme diets (Stubbs & Harbron 1996; van Wymelbeke
et al. 1998; French et al. 2000; Lawton et al. 2000;
Krotkiewski 2001) and some studies have failed to dem-
onstrate an effect (Kamphuis et al. 2001; Kovacs et al.
2001; Bendixen et al. 2002; Alfenas & Mattes 2003;
Flint et al. 2003; MacIntosh et al. 2003).
4.6 Liquids and satiety
Trends in sugar-sweetened soft drink consumption have
increased alongside increases in obesity prevalence, par-
ticularly in the US, leading to a speculation that these
drinks may be partly responsible for the obesity epi-
demic (Malik et al. 2006). It has been suggested that
caloric soft drinks could lead to excess energy consump-
tion because energy from liquids fails to trigger satiety
© 2009 The Author

compared with equivalent energy intakes from solid
food (Mattes 2006). Drewnowski and Bellisle (2007)
reviewed the literature on liquid energy and weight gain
and found that studies comparing the effects of equiva-
lent amounts of liquid or solid energy on satiety have
yielded inconsistent results and do not consistently
support the hypothesis that liquid calories go undetected
by appetite control systems. However, they emphasised
that the consumption patterns of caloric soft drinks (i.e.
consumption when thirsty and with meals rather than as
a source of fuel when hungry) and their relatively low
cost might be more important in determining their rela-
tionship with excess energy consumption and obesity
than their physiological consequences (Drewnowski &
Bellisle 2007).
Sugar-sweetened drinks have been the focus of much
research, but it is also important to consider drinks
containing protein or fibre, which may have greater
effects on satiety, although there are few studies on these
to date.
With regard to drinks containing protein, 1% milk
(3.4 g protein/100g) did not exert a stronger effect on
satiety than orange juice (0.5 g protein/100 g) or cola
(zero protein content) (DellaValle et al. 2004). However,
a yogurt drink containing 17.1 g of protein was found
to be more satiating than a dairy fruit drink containing
2.6 g of protein, or a fruit drink that contained no
protein (all were matched for energy and volume)
(Tsuchiya et al. 2006), indicating that there may need to
be a threshold amount of protein present to have a
significant effect on satiety. With regard to fibre in
drinks, fibre added to a beverage increased its viscosity
and produced higher satiety ratings (Mattes &
Rothacker 2001), and addition of a fruit puree to a
drink has been found to increase the drink’s satiating
power (Haber et al. 1977).
In addition to the effects of drinks on satiety, the effect
of liquid foods (in particular, soup) has also been inves-
tigated. Rolls et al. (1990) compared the effects of three
energy-matched preloads – tomato soup, melon and
cheese with crackers – on subsequent energy intake.
Soup was the most effective at reducing subsequent
energy intake. Although the cheese with crackers had a
higher energy density, the melon and tomato soup were
matched for energy density. Therefore, soup appears to
have some additional satiating qualities (Rolls et al.
1990).
Mattes (2005) tested the effect of soups on appetite
ratings and energy intake with energy-matched preloads
of comparable solid foods (chicken soup vs. chicken
breast, peanut soup vs. roasted peanuts and apple soup
vs. whole apples) and a beverage (apple juice). Appetite
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Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 151
ratings were comparable for the solid and liquid foods,
all of which were rated more satiating than the apple
juice. However, energy intakes tended to be lower after
the soups than after the solid foods. Thus, soups appear
to have a particularly satiating effect, which may be due
in part to their lower energy density. It has also been
suggested that cognitive factors are important in the
satiating effect of soups. The fact that soups are seen as
part of a meal and consumed in response to hunger,
compared with drinks, which are consumed to address
thirst or to accompany food, may have important impli-
cations for the effect of soups on satiety and energy
intake (Mattes 2005).
Overall, there is inconsistent evidence to suggest that
energy from liquids is less satiating than energy from
solids. However, the mode of consumption and the per-
spective a person has on the function of the liquid (i.e. as
a food or as a drink) may modulate the effect that
liquids have on eating behaviour.
4.7 Alcohol and satiety
Raben et al. (2003) compared the effects of protein,
carbohydrate, fat and alcohol on satiety and subsequent
energy intake. The energy density of the meals was
matched, and no differences were seen in appetite
ratings or in energy intakes at the following meal
(Raben et al. 2003). This suggests that, under controlled
conditions, alcohol can stimulate satiety and reduce
energy intake in a similar way to the other macronutri-
ents. However, when alcohol is tested in a more realistic
context (i.e. alcohol or a non-alcoholic control given as
a drink before or with a meal), it does not reduce
energy intake and indeed appears to stimulate appetite
(Westerterp-Plantenga & Verwegen 1999; Hetherington
et al. 2001; Yeomans & Phillips 2002). These effects
occur fairly rapidly after alcohol consumption and so
are likely to be a result of the pharmacological rather
than metabolic effects of alcohol (Yeomans 2004).
The mechanisms by which alcohol could increase
energy intake are not clear. Yeomans (2004) suggests
that alcohol could act both by enhancing the hedonic
(pleasurable) effects of food and by inhibiting satiation.
In those who consciously restrain their eating, alcohol
could have a disinhibiting effect, although it appears
that the belief that alcohol has been consumed, rather
than actual consumption of alcohol, mediates this effect
(Yeomans 2004). Overall, lack of satiety and the stimu-
lation of appetite after alcohol consumption may lead to
passive over-consumption of energy. For more informa-
tion on the effects of alcohol on energy intake, see Foster
and Marriot (2006).
152 B. Benelam
4.8 Energy density and satiety
Energy density is the amount of energy in a given weight
of food or drink (kJ/g, kcal/g). A number of studies have
shown that, when subjects are allowed free access to a
range of foods, they will consistently consume a similar
weight of food each day, rather than a constant amount
of energy (Rolls 2000). This means that the lower the
energy content of the foods eaten (i.e. the less energy
dense they are), the lower overall energy intake will be
and vice versa.
The primary determinants of energy density are water
and fat, and foods with the lowest energy density are
those with the most water and least fat. Conversely,
high-energy dense foods are typically high in fat and low
in water. Fibre can also help reduce energy density
(Drewnowski 1998). It is important to note that energy
density tends to be proportional to palatability, which
itself affects satiety (see section 5.1), and therefore it is
important for studies investigating the effects of energy
density to control for palatability (Drewnowski 1998).
Investigating the effects of energy density on satiation
(i.e. how much energy is consumed in one sitting), Bell
et al. (1998) tested the quantity of foods with high-,
medium- or low-energy density that female subjects con-
sumed over two days, using a crossover design, so that
subjects tried all three dishes on separate occasions. The
dishes were matched for fat content and palatability,
and energy density was reduced by adding vegetables.
The subjects ate a similar weight of the meal in each case,
which resulted in a 30% reduction in energy intake from
the meal with the low- vs. high-energy density, without
any differences in ratings of hunger or fullness (Bell et al.
1998). This study showed that higher-energy density
foods were less satiating, but did not provide further
information about satiety or subsequent energy intake.
Rolls et al. (1998) tested the effects of energy density
on satiety using a milk-based preload, which was diluted
with varying amounts of water to change the energy
density. The energy and nutrient contents of the pre-
loads were the same, but the volume increased to
decrease energy density. The preloads were followed by
an ad libitum lunch and then dinner. Energy intake at
lunch was reduced by 18% after the lowest, compared
with the highest energy dense preload, and this reduc-
tion in energy was not compensated for by an increase in
energy intake at dinner (Rolls et al. 1998). As these
studies had reduced energy density by adding water, this
group also tested the effect of drinking water with a
meal compared with incorporating it into the meal itself.
Water added to the meal (chicken soup compared with
a casserole with less added water) increased satiety and
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
reduced subsequent energy intake. However, the equiva-
lent amount of water served as a drink with the meal did
not have the same effect (Rolls et al. 1999).
Incorporating air into a food to increase its volume
without increasing energy content has also been found
to increase satiety in a study by Rolls et al. (2000).
Subjects consumed yogurt-based milkshakes that had
been whipped up to increase their volume by incorpo-
rating air. The milkshakes contained the same amounts
of energy and were of relatively high, medium or low
volume. Energy intake after the milkshakes was 12%
lower following the one with the highest compared with
the lowest volume, and satiety was increased by both the
high- and medium-volume milkshakes compared with
the one with the lowest volume (Rolls et al. 2000).
Although this study did not strictly alter the energy
density in kJ/g, as the weight of the milkshakes was
unchanged by the addition of air, simply increasing the
volume of the drink without any additional energy led
to a reduction in subsequent energy intake.
A number of studies have shown that covertly altering
the energy density of foods results in significant differ-
ences in energy intake. Stubbs et al. (1995a) gave sub-
jects a HF, medium-fat or low-fat diet for 7 days. Energy
density varied in proportion to the fat content of the
diet. Subjects consumed significantly more energy on the
HF diet, without any concurrent increase in satiety; in
fact, there were no differences in appetite ratings
between the diet conditions (Stubbs et al. 1995a). These
findings were confirmed in a follow-up study that tested
the same diets over a two-week period (Stubbs et al.
1995b).
Covert manipulation of a high-carbohydrate, low-fat
ad libitum diet to be of high- or low-energy density was
investigated over a 14-day period (Stubbs et al. 1998a).
Subjects consumed significantly less energy and lost
more bodyweight on the low-energy density diet than on
the high-energy density diet, but were also significantly
hungrier. In a further study by the same group, varying
the energy density of medium-fat diets, energy density
increased energy intake without altering appetite ratings
(Stubbs et al. 1998b).
Leahy et al. (2008a) looked at the effect of reducing
the energy density of a dish served at lunch on energy
intake in children aged between 2 and 5 years. Higher-
and lower-energy density versions were served along
with other side dishes, and children were allowed to eat
ad libitum. The lower-energy density version led to a
decrease in energy intake from both the dish itself and
the lunch overall (Leahy et al. 2008a). This finding was
confirmed by a further study that also tested changes in
portion size. For both portion sizes, reduction in energy
© 2009 The Author

density reduced energy intake from the dish and the
lunch. As the energy density was reduced by adding
vegetables, this also led to an increase in the children’s
vegetable intake (Leahy et al. 2008b). The effect of
reducing energy density on children’s energy intakes was
then tested for breakfast, lunch and snacks over two
days. It was found that children consumed a consistent
weight of food over the two days, so that energy intake
was reduced when energy density was lower (Leahy
et al. 2008b). Although appetite measures were not
taken in these studies, the amount the children could eat
was not restricted, and, if it is assumed that they ate to
fullness, this would mean that the lower-energy density
foods were no less satiating than the higher-energy
density versions.
When eating patterns and bodyweight are assessed in
the longer term, energy density also appears to affect
energy intake and bodyweight. Greene et al. (2006)
followed up people who had participated in a weight
management programme approximately two years
previously, which promoted the consumption of low-
energy dense foods to determine which dietary pattern
aided weight maintenance. All subjects ate a similar
amount of food, but those who maintained their body-
weight ate a lower-energy dense diet overall and ate
smaller portions of high-energy dense food than those
who put on weight (Greene et al. 2006). No data were
collected on satiety, but, again, if it is assumed that
subjects ate until they were full rather than restraining
their consumption, this suggests that satiety was not
reduced by the lower-energy density diet.
A year-long trial compared two weight-loss diets, one
where subjects were counselled to reduce fat intake (RF)
and the other where they were counselled to reduce fat
and to increase consumption of water-rich foods, par-
ticularly fruits and vegetables (RF + FV), reducing the
energy density of the diet to a greater extent. Both
groups were told to eat ad libitum within these recom-
mendations. Both groups reduced their fat intake to a
similar extent, but those on the RF+FV diet had a lower-
energy density, consumed a larger weight of food and
reported being less hungry than the RF group. Both
groups lost weight, but the RF+FV group lost signifi-
cantly more that the RF group (Ello-Martin et al. 2007).
A six-month intervention trial tested the effects of
different levels of dietary advice, resulting in a reduction
in energy density of the diet and weight loss. When
subjects were categorised according to the reduction in
energy density resulting from the intervention, it was
found that both modest and large reductions in energy
density were associated with weight loss (Ledikwe et al.
2007).
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 153
Saquib et al. (2008) looked at the effects of long-term
reductions in energy density on bodyweight in a large
group of overweight female breast cancer survivors
over a four-year period. The intervention group
members were counselled to lower their dietary energy
density by reducing fat and increasing fruit, vegetable
and fibre consumption and were given telephone
support, cooking classes and newsletters to promote
dietary change. The control group was given printed
materials with US dietary guidelines and sent newslet-
ters with health and nutrition information. The inter-
vention group had a small but significant weight loss at
one year. However, although the intervention group
maintained a diet of lower-energy density compared
with the control group, no differences in energy intake
or weight loss were seen between the groups after four
years. No information was collected on the effects of the
diets on appetite (Saquib et al. 2008). Thus, it is not
clear whether the apparent satiating effect of low-energy
density diets in the short-term can help to maintain
weight loss in the long-term, and further long-term
studies are needed to investigate this.
A number of epidemiological studies (some cross-
sectional and others prospective) have looked at
whether there is an association between the energy
density of the diet in different populations and body-
weight or weight gain. In cross-sectional studies, higher
dietary energy density was found to be an independent
predictor of obesity (Mendoza et al. 2007) and a risk
factor for higher BMI or greater waist circumference
(Howarth et al. 2006; Murakami et al. 2007).
In an eight-year prospective study of women (the
Nurse’s Health Study), increases in dietary energy density
were associated with greater weight gain (Bes-Rastrolo
et al. 2008) and, in another US study, lower energy
density diets appeared to moderate weight gain (Savage
et al. 2008). A cohort study of children in the UK found
that higher energy density at 7, but not 5 years old was a
risk factor for excess adiposity at 9 years old (Johnsone
et al. 2008). McCaffrey et al. (2008) assessed the rela-
tionship between the energy density of children’s diets at
6–8 years and change in adiposity to adolescence. Five
different methods to assess energy density were used, but
results from none of these methods were related to
measures of body fatness in adolescence (McCaffrey
et al. 2008). So there is a relatively (but not completely)
consistent relationship between dietary energy density
and weight gain or higher bodyweight. These studies did
not collect any information on satiety, and, in free-living
subjects who can eat as much as they like, increased
satiety on a low-energy density diet could be a factor in
the apparent reduction in energy intake. Overall, the
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energy density of foods and drinks appears to have a
major impact on satiety and this may be more important
than macronutrient composition in terms of enhancing
satiety and helping to reduce the risk of weight gain.
5. The effect of external factors on
satiation and satiety
Despite the internal mechanisms that exist to control
appetite, most people know from experience that, in
certain circumstances, people eat when they are sated
and refrain from eating when hungry. Therefore, there
are external factors that may affect or act independently
of our responsiveness to internal signals of satiation and
satiety that are important to take into account. Some of
these are discussed in this section.
5.1 Palatability
Palatability refers to the pleasurable experience when
consuming food. It is somewhat difficult to define, as it
is not an inherent characteristic of a food, but a person’s
evaluation of his or her experience of eating food under
particular circumstances (Yeomans 1998). Palatability is
generally measured by using one of the rating scales
described in section 3. Palatable stimuli act on hedonic
pathways in the brain, stimulating a positive emotional
response and increasing the drive to consume more
(Berthoud 2007).
Increasing the palatability of food by, for example,
adding fat, increases appetite, meal size, meal duration
and eating rate (Yeomans 1998). Hence, if composition
is not controlled, the most palatable foods tend to be
the least satiating and the least palatable foods the most
satiating (Drewnowski 1998). However, there is a
strong relationship between palatability and energy
density, in that higher-energy dense foods tend to be the
most palatable and vice versa (Drewnowski 1998),
perhaps reflecting innate preferences for energy-rich
foods (Berthoud 2007). However, the relationship
between energy density and palatability is not fixed, and
the association between the two can be (experimentally)
manipulated by altering the taste and appearance of
foods while keeping energy density constant.
A study by Bobroff and Kissileff (1986) found that
adding cumin to yoghurt reduced palatability and
intake. Yeomans et al. (1997) added oregano to a
tomato sauce served with pasta, which made the dish

Key points
• Studying the effects of specific variables within a food or drink, without affecting others, is inherently difficult,
and, when considering the results from studies on the effects of foods and drinks on satiety, it is important to
consider any confounding factors that could have had an effect.
• Energy from protein seems to have a greater effect on satiety than the other macronutrients.
• The effect of sugars on satiety has been investigated, and although they can stimulate satiety and reduce
subsequent energy intake, this compensatory reduction in energy consumption may not be complete.
• Although it has been suggested that low-GI foods are more satiating than high-GI foods, current evidence shows
that, when other factors such as fibre content are controlled, GI does not have a significant effect on satiety.
• Fat invokes a satiety response, but, in typical food compositions, it is associated with high energy density and
palatability, so that it is readily over-consumed, leading to higher energy intakes.
• Some types of fibre can promote satiety, but this is highly dependent on the dose and especially on the type of
fibre. Viscous fibres, such as petin, or novel gelling fibres, usually alginates, appear to be the most satiating.
• There has been debate surrounding whether intense sweeteners increase, decrease or have no effect on satiety,
which is complicated by the different foods or drinks that contain intense sweeteners and the different types of
sweetener used. Overall, evidence suggests that intense sweeteners do not increase or decrease satiety, although the
reduction in energy intake associated with their use is not compensated for by a subsequent increase in energy
intake.
• Energy from drinks has been suggested to be less satiating than that from solid foods. However, evidence to
support this is conflicting. Studies using soups, which tend to be highly satiating, indicate that observed effects are
not directly related to liquid vs. solid composition.
• Alcohol appears to stimulate appetite in the short-term and may lead to passive over-consumption of energy
• Energy density is important in the satiety response and may be more important than macronutrient content.
Lower-energy density foods appear to be more satiating than higher-energy density foods.

© 2009 The Author

Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173

more palatable, and compared this with the same sauce
without oregano, which was rated as bland. Hunger
increased in the early stages of eating the dish with
oregano and then declined, while it fell throughout con-
sumption of the dish without the herb added. Subjects
also ate more quickly when given the more palatable
dish (Yeomans et al. 1997).
De Graaf et al. (1999) investigated the effects of
reducing the palatability of a soup on satiation and
satiety by adding increasing amounts of citric acid. Pal-
atability was found to be inversely related to the amount
of citric acid in the soup. Satiation was measured by
allowing subjects to eat the soup ad libitum, and satiety
was measured by giving a fixed amount and then mea-
suring appetite. When the soup was offered ad libitum,
the amounts consumed were inversely related to the
palatability. No effect was seen on appetite ratings after
the standard portions of soup, indicating that, in this
case, palatability affected satiation but not satiety (De
Graaf et al. 1999).
Poortvliet et al. (2007) attempted to dissociate the
inverse relationship between palatability and satiety by
designing a healthy meal that was both palatable and
satiating and comparing this with a palatable control
meal that was more energy dense. The healthy meal was
high in fibre and protein and low in energy density, and,
as energy was kept constant across the two meals, the
serving size for the healthy meal was greater than the
control (400 g vs. 185 g). Hunger, prospective consump-
tion (how much subjects thought they could eat) and
desire to eat were significantly reduced by the healthy
meal compared with the control, and subsequent energy
intake from a dessert after the meal was significantly
lower (Poortvliet et al. 2007). Thus, although palatable
energy dense foods have been shown to increase energy
intake and reduce satiety, it appears to be possible to
design lower energy density foods and diets that are
both palatable and satiating.
It should be noted that, although the ‘liking’ of pal-
atable foods may be important, the motivation to eat or
the ‘wanting’ of foods should also be considered. These
two factors may occur together, but evidence suggests
that they may also operate separately (Mela 2006) and
that, in the real world, ‘wanting’ may be more impor-
tant than ‘liking’ (Castro & Plunkett 2000).
5.2 Variety
A number of studies have shown that the greater the
choice of foods offered at a single eating occasion, the
more people will eat (see Rolls 1984). This effect
appears to be mediated by a phenomenon known as
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 155
sensory-specific satiety (SSS), whereby the desire to eat
a food that has already been tasted is significantly
reduced compared with one that has not. This was
initially demonstrated by allowing subjects to taste and
rate the palatability of small portions of 8 or 9 foods,
then offering an ad libitum meal containing one of
these foods. After the meal, the foods that had been
rated initially were then rated again, and the palatabil-
ity of the food eaten at the test meal was found to have
significantly decreased compared with the ones that
had not (Rolls 1984). Hetherington et al. (1989) com-
pared the palatability ratings of the foods after the test
meal 2, 20, 40 and 60 minutes later and found that the
decrease observed in the tasted vs. the non-tasted foods
was most pronounced at 2 minutes after consumption.
For the most palatable food, the palatability recovered
somewhat after 60 minutes (Hetherington et al.
1989). The rapid nature of this response suggests that
SSS occurs because of the sensory properties of food,
rather than effects associated with digestion and
absorption.
There also appear to be age-related differences in SSS.
Rolls and McDermott (1991) tested SSS responses in
adolescents, young adults, older adults and elderly sub-
jects and found that the response was most pronounced
in the adolescent subjects and decreased with age, with
the elderly group showing the lowest response (Rolls &
McDermott 1991).
It is not clear whether consuming an increased variety
of foods in the longer term would lead to increased
energy consumption, but it has been shown that consum-
ing some foods (e.g. meat, shellfish) repeatedly for a
period of time reduces their acceptance, although, for
staple foods like bread and highly palatable items like
desserts, this does not appear to be the case (Rolls 1984).
Overall, it appears that restricting the variety of foods
eaten can stimulate satiety via SSS, and, conversely,
increasing the variety of foods available could stimulate
energy intake by avoiding SSS.
5.3 Portion size
In the US, portion sizes of many foods have been
increasing since the 1970s (Young & Nestle 2002).
There does not appear to have been a consistent increase
or decrease in portion sizes in the UK, and, although the
variety of portion sizes available has increased, standard
portion sizes appear to have remained relatively con-
stant (FSA 2008). If the amount eaten was determined
only by internal satiation and satiety mechanisms, the
portion sizes of foods served should not affect energy
intake. However, it appears that, when presented with a
156 B. Benelam
larger portion, most people will consume more food
(Ello-Martin et al. 2005).
Very young children are a notable exception to this
pattern. When children 3 years old and younger were
served increasing portions of macaroni and cheese, their
energy intake remained constant. However, when the
same portions were served to 5-year-old children, they
significantly increased their energy intake as the portion
sizes became larger (Rolls et al. 2000). This effect was
also seen in 4-year-olds, who ate 25% more when they
were served a portion double the size appropriate for
their age (Fisher et al. 2003).
A number of experiments have tested the effect of
increasing portion sizes on adults’ energy intake in the
short-term. These have used a number of different foods,
including macaroni and cheese, sandwiches, crisps,
pasta, salad and drinks, and consistently found that
increasing the portion size leads to an increased energy
intake. The effects on satiety vary, with two studies
finding that satiety increased with bigger portion sizes,
while the others found no differences in appetite ratings
between larger and smaller portions sizes, despite a sig-
nificant increase in energy intake when consuming the
larger portion size (Rolls et al. 2002, 2004a, 2004b;
Diliberti et al. 2004; Kral et al. 2004; Flood et al. 2006).
Further studies have investigated this effect over a
longer period to assess whether increased energy intake
from larger portion sizes is compensated for by a sub-
sequent reduction in energy intake. Studies conducted
over 2 days, 11 days and 2 months found that subjects
continued to eat more for the period of the study when
portion sizes were larger than when they were smaller,
without reducing energy intakes to compensate for the
additional energy consumed (Rolls et al. 2006, 2007;
Jeffery et al. 2007).
Generally, greater portion size appears to increase
energy intake. Some studies have found that this also
increases satiety, while others have found no difference.
So it appears that the ability of internal appetite controls
to detect extra energy intake is limited, especially
because no compensatory reduction in energy intake is
typically observed. The fact that people eat more when
given larger portion sizes also indicates that, for many
people, the presence of food acts as a stimulus for (con-
tinued) consumption and that, within the time frame of
a meal, this positive stimulation can be more powerful
than the physiological signals that inhibit eating. It is
interesting to note that very young children (<3 years)
eat a consistent amount, regardless of portion size, and
it may be that, at this age, children are more sensitive to
internal signals of satiety (Rolls et al. 2000). There is
some evidence that parental behaviour, such as pressur-
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
ing children to finish their food, may have a negative
effect on children’s ability to control their energy intake
(Savage et al. 2007).
It should also be noted that, within the studies men-
tioned above, there was an inter-individual variation in
the response to portion size, and it is likely that indi-
viduals vary in their sensitivity to the effects of portion
size on energy intake.
5.4 Sleep
Epidemiological studies have linked a chronic lack of
sleep to obesity (Magee et al. 2008), and it has been
suggested that restricted sleep has an impact on the
appetite hormones leptin and ghrelin (Knutson 2007).
As outlined in section 2.2.1, ghrelin, the so-called
‘hunger hormone’ secreted from the gut, appears to
stimulate appetite and is suppressed after eating. Leptin
is primarily produced by the adipose tissue in propor-
tion to fat stores. A fall in leptin stimulates appetite,
while an increase has an inhibitory effect (see section
2.2.2). Both hormones operate according to a circadian
rhythm whereby they reach a peak level during sleep
(Yildiz et al. 2004). Sleep restriction has been found to
reduce leptin and increase ghrelin levels and to increase
appetite (Spiegel et al. 2004). The association between
reduced sleep and a reduction in leptin and increase in
ghrelin was also observed in the Wisconsin Sleep Cohort
study, although, in this case, no measures of appetite
were taken (Taheri et al. 2004). The importance of these
findings requires further study, as there may be other
aspects of short sleep duration, apart from its potential
effect on appetite, that could increase the risk of obesity,
for example, having more time available to eat, reduc-
tions in physical activity when tired, or more unhealthy
food choices (Knutson 2007).
5.5 Physical activity
Physical activity generally affects the body by increasing
fitness, changing body composition by increasing lean
body mass and increasing energy expenditure (see Miles
2007). The effects of physical activity on appetite and
satiety have been investigated. For example, a number of
studies have tested the effects of an acute bout of physi-
cal activity on appetite. These studies have consistently
found that, even when large energy deficits are induced,
this does not result in a compensatory increase in hunger
and energy intake (see Blundell et al. 2003). This con-
trasts with studies that have induced negative energy
balance by reducing energy intake, resulting in increased
appetite and energy intake (Lawton et al. 1993; Green
© 2009 The Author

et al. 1994; Delargy et al. 1995; Hubert et al. 1998).
Intense physical activity actually appears to suppress
hunger for short periods (Thompson et al. 1988;
Kissileff et al. 1990; King et al. 1994, 1996; Westerterp-
Plantenga et al. 1997). This phenomenon, known as
physical activity-induced anorexia, is not seen in
moderate- or low-intensity physical activity and may be
a result of the redistribution of blood flow away from the
gut to the muscles (Blundell et al. 2003).
The effects of a physical activity-induced energy deficit
in the longer-term (over a number of weeks) have been
investigated in lean men and women, and it appears that
subjects can tolerate this energy deficit without a com-
pensatory increase in energy intake for approximately
two weeks. After this, energy intake begins to increase,
but, initially, compensation is incomplete, accounting for
approximately 30% of the deficit on average after 16
days. There were inter-individual differences in how
much subjects adjusted their energy intake to account for
increases in physical activity, and it is not clear what the
reasons for this were (Wyebrow et al. 2008).
Lim and Lee (1994) investigated the impact of five
months of military training, while eating ad libitum.
They found that lean body mass remained constant,
but body fat was reduced progressively throughout the
training. Consequently, subjects who were initially
fatter lost most weight, while those who were initially
lean maintained their bodyweight (Lim & Lee 1994).
As the function of stored fat is to supply the body with
energy when demands are not met by energy intakes
and/or the need for physical activity is high, it may be
that excess adipose tissue buffers the effect of an
energy deficit and that a compensatory increase in
energy intake occurs when lean body mass is threatened
(Blundell et al. 2003). The evidence from intervention
studies using physical activity to promote weight loss or
prevent weight gain is mixed. Thus, physical activity-
induced negative energy balance may be reduced over
time until the individual compensates completely for the
additional energy expenditure. However, there may also
be issues with compliance in these studies (see Miles
2007).
Stubbs et al. (2004) investigated the effects of a reduc-
tion in physical activity by imposing a sedentary routine
on lean men for nine days and comparing their energy
intakes and appetite ratings with those when they had a
moderately active routine. The reduction in physical
activity caused a significant reduction in energy expen-
diture compared with the active routine, but this did not
lead to reductions in appetite or energy intake, resulting
in positive energy balance and weight gain on the sed-
entary regime (Stubbs et al. 2004).
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 157
Thus, it appears that satiety pathways may not always
detect changes in energy balance caused by physical
activity. This is the case both when physical activity is
increased, which can lead to substantial energy deficits
without corresponding reductions in satiety and
increases in energy intake, and when it is reduced, where
the reduction in energy expenditure does not appear to
increase satiety or reduce energy intake. Although large
energy deficits due to physical activity cannot be main-
tained in the long-term, physical activity can aid short-
term weight control and help maintain a healthy weight.
5.6 Television viewing and other distractions
Some studies have reported that children (Bellissimo
et al. 2007; Temple et al. 2007; Manios et al. 2008),
adolescents (Van den Bulck & Van Mierlo 2004) and
adults (Stroebele & de Castro 2004) increase their
energy intake when eating while watching television,
compared with eating undistracted.
Some of these studies monitored appetite as well as
energy intake. Bellissimo et al. (2007) monitored the
appetite ratings and energy intakes at lunch of boys
between 9 and 14 years old, with and without watching
television. They also tested the ability of the boys to
compensate for a glucose-containing preload at the
subsequent lunch, again, with and without television
watching. Watching television significantly increased the
boys’ energy intake at lunch. When not watching tele-
vision, the boys reduced their energy intake at lunch to
compensate for the glucose preload, but did not do this
as effectively when watching television at lunch time.
No significant differences were seen in appetite ratings,
despite the differences in energy intake. The authors
concluded that television viewing had made the boys
less sensitive to internal signals of satiation and satiety
(Bellissimo et al. 2007).
Temple et al. (2007) looked at the effect of watching
television on children’s motivation to eat and their
energy intake. Firstly, children were given a computer-
based task that had to be completed to earn portions of
food. The group that watched television while doing this
spent more time doing the tasks and ate more food than
the control group who were not watching television.
The second experiment measured the effect on energy
intake of a continuous segment of television, which was
compared with showing repeated short segments and to
no television. The group that watched a continuous
segment of television consumed more energy and spent
longer eating than the other groups. Based on these
results, the authors suggested that television increased
motivation to eat and that the attention needed to watch
158 B. Benelam
a continuous television programme distracted children
from their habitual eating patterns (Temple et al.
2007).
In a review of cognitive influences on eating behav-
iour, Higgs (2008) concluded that the memory of a
previous meal reduces subsequent snack intake and that,
if the formation of this memory is disrupted, subsequent
energy intake is increased. This effect can be seen in
amnesiacs who eat multiple meals because they do not
remember the previous eating occasion (Higgs 2008).
In a subsequent study, Higgs et al. (2009) found that
watching television while eating reduced the vividness of
the memory of the meal, compared with a eating a meal
without distraction. Snack intake after the meal with
television was higher than that without, suggesting that
the disruption of the memory of the meal increased
energy intake (Higgs et al. 2009). It is possible that this
effect could apply to any form of distraction that affects
the memory of eating.
The idea that distractions while eating can influence
energy intake was explored by Bellisle and Dalix
(2001) in women who cognitively restrain their eating
(the effect of dietary restraint is discussed in section
3.3.2). They tested the effects of four conditions on
women’s energy intake: eating alone, eating alone
while listening to a recording that encouraged them to
pay attention to their food, eating alone while listening
to a recorded detective story, and eating in a group.
The first two conditions were considered as non-
distracting and the second two as distracting. In both
the ‘distracting’ conditions, the women consumed more
energy than in the ‘non-distracting’ conditions, but
this was not reflected in differences in appetite ratings
(Bellisle & Dalix 2001). The results from this study
may reflect a loss of cognitive restraint in these women
when distracted, or that distraction inhibited the effects
of internal signals of satiation and satiety. Listening to
music while eating has also been shown to increase
energy intake compared with eating without music
(Stroebele & de Castro 2006).
Overall, there is some evidence that distractions when
eating (commonly television) can make people less sen-
sitive to internal appetite controls and lead to increased
energy intake. The relationship between television
viewing and weight gain is complex, as watching tele-
vision introduces more sedentary time as well as the
opportunity to eat more (Crawford et al. 1999).
However, a recent review suggests that part of the asso-
ciation that appears to exist between obesity and time
spent watching television may be mediated by increased
consumption of food and drink while watching televi-
sion (Cleland et al. 2008).
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
5.7 Social situations
It has been shown that, typically, people eat significantly
more (on average 44%) when with other people than
they do alone (De Castro & De Castro 1989). In addi-
tion, the satiating power of these meals per unit of
energy is lower in those eaten in a group than those
eaten alone. In fact, there appears to be a direct rela-
tionship between the number of people present at a meal
and the amount that the diners eat, so that the more
people present at a meal, the more energy is consumed
(De Castro & De Castro 1989). This may be because, in
the presence of people eating large amounts, others will
imitate this and consume more. It has also been sug-
gested that the emotional effect of eating with others
stimulates energy intake, that social interactions while
eating might facilitate disinhibition (i.e. relaxing any
cognitive restraint when eating) and finally, that eating
in groups might simply mean that people will eat for
longer and thus eat more (De Castro 1994; Feunekes
et al. 1995).
De Castro (1994) looked at the effect of different
dining companions on energy intake: spouses, family,
friends, co-workers and others. In all cases, meals eaten
with other people were larger and longer in duration
than those eaten alone. However, there were some dif-
ferences depending on the eating companions. Meals
eaten with spouses and family were larger and eaten
faster than those with other companions, while meals
eaten with friends were also larger but of longer dura-
tion. The author suggested that, in general, the social
interaction of eating with others prolongs meal times,
thus increasing energy intake. Eating with family and
friends may have increased this effect by relaxing diners
and allowing disinhibition of restraint, making energy
intake even greater (De Castro 1994).
Kristensen et al. (2002) performed a qualitative study
in Denmark that investigated 20 people’s perceptions of
‘proper satiety’ in different social situations, in order to
gather information on the social contexts and cultural
norms surrounding satiety. There was a variation in the
subjects’ preferences regarding satiety. Some preferred
a light feeling of satiety, as experienced when eating
vegetables, and associated being full after high-fat foods
with feeling sluggish and lethargic; while others pre-
ferred the feeling of being really full and felt unsatisfied
without this. Many subjects reported enjoying eating to
excess with friends, and enjoyed the feeling of being
sated and lazy but said that they avoided this with those
who they did not know well. Conversely, those who
described themselves as having a weight problem tended
to limit their intake when eating with others and were
© 2009 The Author
 Satiation, satiety and their effects on eating behaviour 159

Key points
• Palatability tends to reduce satiation and satiety and leads to increased energy intake. Palatable foods are often
energy dense, which may drive this relationship, but the relationship can also be manipulated by using different
ingredients and flavours.
• Offering a variety of foods seems to decrease satiety and increase energy intake within a meal. ‘Sensory-specific
satiety’ describes the process of reduced palatability and increased satiety for a particular food when it is consumed
repeatedly, and it is this process that drives increased consumption if alternative foods are offered.
• Most people consume more energy when offered larger portions of food, and satiety does not appear to be
increased after this greater energy intake.
• Children younger than four years do not consume more when given a larger portion size, which may be a result
of a greater sensitivity to internal satiation and satiety signals.
• Lack of sleep has been associated with increased bodyweight. Some studies have shown that sleep deprivation
affects hunger and satiety signals in a way that would be expected to reduce satiety, but this requires further
investigation.
• In the short-term, large energy deficits can be induced by physical activity, without a corresponding reduction in
satiety. However, this cannot be maintained indefinitely, and the negative energy balance is gradually compensated
for by an increase in energy intake over the longer-term. Nevertheless, there are inter-individual differences in the
extent to which the energy deficit is compensated for.
• People tend to eat more and be less responsive to satiety signals when distracted by television or other means,
and television watching has been associated with an increased risk of obesity. This association is complicated by
the sedentary nature of television watching, which could also contribute to obesity risk.
• When eating with others, people consume significantly more energy than when eating alone. This may be the
result of a number of factors, such as longer duration of eating and to a relaxation of dietary restraint.

more likely to eat in excess when alone. Female subjects
reported feelings of guilt surrounding excessive eating
and the subsequent feelings of satiety, whereas males
generally did not. Many subjects felt the need to control
food intake, with the aim of limiting satiety, if at work or
working at home, in order to be more alert, and meals in
this context were viewed as more functional than plea-
surable. However, meals eaten in one’s spare time were
enjoyed more, and it was seen as more acceptable to eat
more and to feel more sated after eating (Kristensen et al.
2002). Although this study must be viewed in context of
its location and small size, it highlights the fact that, as
well as internal mechanisms of satiation and satiety,
there will be expectations about satiety that can change
according to the social context of the situation, and these
will also influence eating behaviour.
6. Satiation, satiety and weight control
Levels of obesity in the UK have tripled since the 1980s
(National Audit Office 2001), and this trend is predicted
to increase so it is estimated that over half of UK adults
will be obese by 2050 (Foresight 2007). This rapid
increase suggests that it is environmental rather than
genetic changes that have lead to the increased risk of
weight gain. However, within this current ‘obesogenic’
environment, certain individuals appear to be at greater
risk of developing obesity than others. The reasons for
this are complex and involve physiological, psychologi-
cal and environmental factors (Foresight 2007). Appe-
tite control, including the development of satiation and
satiety, is one of the variables that are important to
consider in weight management.
This section evaluates some of the factors that may
affect either the development of satiation and satiety or
an individuals’ responsiveness to these internal signals,
and how these may modulate the risk of obesity. There
are a number of levels at which differences in satiation
and satiety could increase the risk of obesity. Genetic
differences, for example, may impact on components of
satiation and satiety signalling pathways. There may
also be physiological differences in the way that satia-
tion and satiety develop or are linked into reward and
learning systems that influence eating behaviour. Behav-
ioural, neurological and psychological factors may also
affect how much internal appetite signals control energy
intake compared with the hedonic experience of eating
or external influences on energy intake.

© 2009 The Author

Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
160 B. Benelam
6.1 Obesity genes and satiety
In relatively rare cases, obesity may be linked to a single
mutation in a gene that renders its product non-
functional. All obesity genes that have been character-
ised appear to cause obesity by disrupting satiety
(O’Rahilly & Farooqi 2008). For example, mutations in
the leptin gene cause extreme over-eating and obesity in
early childhood. This can be dramatically reversed by
administration of leptin (Gibson et al. 2004). Mutations
in the melanocortin 4 receptor (MC4R) gene are the
most common mutation linked to human obesity
(Farooqi et al. 2003). As outlined in section 2.3.1,
MC4R is expressed in appetite centres in the brain and
conveys signals of satiety, resulting in a reduction in
energy intake. Humans have two copies of every gene,
and mutation of both copies of the MC4R gene results
in over-eating and severe obesity. If only one copy of the
gene is affected, these symptoms are still present but are
less severe (Farooqi et al. 2003).
Gene mutations, such as those described above,
account for a very small proportion of cases of human
obesity. However, it has been estimated that a person’s
genetic profile may account for 45% to 75% of their
variation in BMI (Farooqi & O’Rahilly 2007), indicat-
ing that, within the current ‘obesogenic’ environment,
genetic profile affects an individual’s risk of obesity.
Although all humans have the same set of genes, varia-
tions known as polymorphisms give rise to interindi-
vidual differences between people. Polymorphisms in
over 100 genes have been linked to obesity (Rankinen
et al. 2005) and, although their contribution to increas-
ing or decreasing the risk of obesity is relatively small, it
is possible that they are part of a phenotype (the physi-
cal expression of a genetic profile) that increases the
likelihood of weight gain.
Many genes that have been linked to obesity are
involved in the control of appetite, and a recent update of
15 new genetic locations linked with BMI found that
the roles of all of the proteins the genes code for could be
traced to appetite centres in the hypothalamus (Hofker &
Wijmenga 2009). One example is the FTO gene, of which
certain polymorphisms were found to increase or
decrease the risk of obesity (Frayling et al. 2007). Poly-
morphisms in the FTO gene that increase the risk of
obesity have recently been linked with increased energy
intake in adults (Haupt et al. 2008) and children (Cecil
et al. 2008; Wardle et al. 2009). Wardle et al. suggested
that the low risk form of the FTO gene was protective
against this increased energy intake by promoting
responsiveness to internal signals of satiety (Wardle et al.
2009). Thus, overall, the evidence strongly implies that
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
the genetic profile can influence the risk of obesity via
components of appetite control systems and pathways
involved in hedonic responsiveness.
6.2 Physiological differences in satiation and satiety
responses in obese people
In addition to genetic differences that may influence
appetite, there may also be differences in the physiologi-
cal signals of satiation and satiety that influence risk of
obesity.
As discussed in section 2.1.1, gastric distension is
involved in satiation. Some studies have found that
obese subjects have greater gastric capacities (Geliebter
1988; Kim et al. 2001), which could result in a greater
energy intake before gastric distension-stimulated
satiation occurs. However, this may be related to binge
eating and not strictly to obesity itself, and, although
the likelihood of binge eating increases with the degree
of obesity, the gastric capacity of normal weight
bulimic patients has been found to be larger than that
of some obese subjects (Geliebter & Hashim 2001).
The gastric capacity of obese subjects can be reduced
after weight loss, and it is possible that this could help
restore a stronger satiation response (Geliebter et al.
1996).
There may also be differences in satiety signalling
in obese people. Ghrelin increases hunger and is sup-
pressed after energy intake (see section 2.2.1). Ghrelin
levels are significantly lower in obese than in lean sub-
jects (English et al. 2002). In addition, the post-prandial
suppression of ghrelin that occurs in lean subjects is not
observed in obese people. This may be because levels
of ghrelin have already been maximally suppressed
because of excess fat storage (English et al. 2002). Mor-
bidly obese subjects appear to have an altered pattern of
hunger without the pre-prandial rise and post-prandial
fall in hunger seen in lean individuals. However, it has
been found that normal hunger profiles can be restored
in these morbidly obese subjects by administering exog-
enous ghrelin (Huda et al. 2009). Although suppression
of ghrelin in obesity may be an adaptive response to
excess energy storage, any effects on reducing hunger do
not appear to be reflected in reductions in energy intake
and bodyweight. Indeed, it has been suggested that
disruption of hunger may result in continuous ‘grazing’
rather than defined meals (Huda et al. 2009).
Gut hormones that signal satiety are also altered in
the obese. Release of PYY, which is secreted from the
gut after feeding and induces satiety (see section 2.2.1),
is lower in obese than in lean subjects (Batterham et al.
2003a), and this is associated with reduced satiety (le
© 2009 The Author

Roux et al. 2006). Although a lack of PYY could poten-
tially contribute to an increased risk of obesity, it is
also possible that obesity itself causes a reduction in
PYY release. Release of GLP-1, another gut hormone
involved in satiety (section 2.2.1), has also been found
to be attenuated in the obese (Ranganath et al. 1996).
When GLP-1 release was compared in lean, obese and
obese subjects who had significantly reduced their body-
weight, the obese subjects who had reduced their body-
weight released GLP-1 at a level between that of the lean
and obese subjects (Verdich et al. 2001). This indicates
that weight loss improves GLP-1 secretion and that
impaired GLP-1 secretion may be a consequence of
weight gain.
PYY and GLP-1 are raised significantly after gastric
bypass surgery to treat obesity because of the drastic
change in the structure of the gut, and it is thought that
this contributes to the weight loss seen after surgery (le
Roux et al. 2007). In addition, a number of gut hor-
mones are being tested in clinical trials as obesity treat-
ments (Field et al. 2008). Therefore, changes in gut
hormones that have been implicated in increasing the
risk of obesity may also be useful in treating it.
Thus, some aspects of the physiological induction of
satiety appear to be altered in obese people. As these are
only parts of the complex physiological control of appe-
tite, it is difficult to determine how much they may be
involved in increasing the risk of weight gain or inhib-
iting weight loss. However, they may be important when
considering the relationship between satiation, satiety
and obesity.
6.3 Behavioural differences in the response to
satiation and satiety in obesity
Previous sections in this chapter have outlined genetic
and physiological differences that may affect satiation
and satiety and thus bodyweight. There may also be
behavioural differences that affect an individual’s
responsiveness to internal signals of satiation and
satiety.
The way people eat may encourage excess energy
intake and weight gain. For example, a number of studies
have found associations between bodyweight and the
speed of eating (Barkeling et al. 1992; Sasaki et al. 2003;
Otsuka et al. 2006; Maruyama et al. 2008). Laessle et al.
(2007) studied the eating behaviour of lean and obese
individuals and found that obese subjects ate faster, took
bigger spoonfuls and had a greater overall energy intake
than lean subjects. Differences in the rate of eating may
encourage excess energy intake before internal signals of
satiation can take effect, predisposing those with faster
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 161
eating rates to positive energy balance and weight gain.
Equally, as obese people have greater energy require-
ments, it is possible that faster eating is related to con-
suming larger meals in order to maintain energy balance
and is a consequence, rather than a cause, of obesity.
High consumption of high-fat foods is a risk factor
for obesity (e.g. Bray et al. 2004). An interesting link
between preference for fat and behaviour has been
described by Blundell et al. (2005). When characterising
obese subjects with habitually high-fat diets (not all
those with a habitually high proportion of fat in the diet
were obese), it was found that their eating behaviour
seemed to predispose them to weight gain. Their satiety
response to fatty meals was weaker, and satiety did not
reduce their preference for fatty foods. They also had
greater hedonic responses to palatable foods and to
eating in general, and reported greater feelings of hunger
and were more prone to disinhibition (the loss of control
over eating) (Blundell et al. 2005). This cluster of
behavioural characteristics appears to predispose these
individuals to gain weight in the current ‘obesogenic’
environment.
With regard to food preferences, it should be noted
that this concept can be divided into two components:
‘liking’ and ‘wanting’. These describe the difference
between enjoying the taste of a food (liking) and the
desire to consume it (wanting), and it is possible for
these to operate separately. The relationship between
obesity and increased ‘liking’ of foods is not consistent,
and it has been suggested that it is an increased moti-
vation to eat (wanting), not necessarily accompanied
by an increased liking of foods, that could predispose
individuals to obesity (Mela 2006).
Another aspect of research into the relationship
between eating behaviour and weight control is the
‘externality theory’ of obesity, which suggests that sus-
ceptibility to external cues such as time, presence of
food and situation is greater in the obese (Schachter
1968). However, the relationship between the external
environment, eating behaviour and obesity is complex
and difficult to measure, and results from studies inves-
tigating this have been inconsistent (Mela 1996). It has
been suggested that susceptibility to over-consuming
palatable foods is the external factor that most consis-
tently accounts for differences between lean and obese
subjects (Spitzer & Rodin 1981). This susceptibility to
external influences may mean that internal signals of
satiation and satiety have less impact on energy intake in
obese individuals.
Carnell and Wardle (2008) investigated the effect of
responsiveness to internal satiety signals and to external
food cues on BMI and waist circumference in 2- to
162 B. Benelam

3-year-old and 8- to 11-year-old children. In both age
groups, lower satiety responsiveness and higher food
cue responsiveness were associated with greater BMI
and waist circumference (Carnell & Wardle 2008). The
authors highlighted the fact that it is important to dis-
tinguish whether low satiety responsiveness and suscep-
tibility to external food cues operate separately or are,
in effect, two sides of the same coin. In this study, these
two factors were correlated but also contributed inde-
pendently to predicting adiposity, suggesting that they
are related but separate (Carnell & Wardle 2008).
Further studies to determine the mechanisms behind
these phenomena are needed in order to disentangle this
relationship.
In addition to the possibility that susceptibility to
external cues may influence eating behaviour, it is also
possible that variations in a person’s sensitivity to the
internal hedonic response to foods may also play a role.
The role of ‘sensitivity to reward’ (STR), (i.e. the capac-
ity to experience pleasure) has been investigated with
regards to the risk of weight gain. There are two pos-
sible routes by which STR could affect energy intake
and risk of obesity. Heightened STR could stimulate
excess consumption of palatable foods because of their
increased reward value. Alternatively, reduced STR
could increase consumption of palatable food in order
to gain an optimal level of hedonic stimulation
(Finlayson et al. 2007). There is some evidence that both
may be involved in increasing the risk of obesity.
Franken and Muris (2005) found a direct relationship
between STR and BMI. However, Davis et al. (2004)
measured STR in lean, overweight and obese subjects
and found a U-shaped relationship, with overweight
subjects having greater STR than both lean and obese
subjects (Davis et al. 2004). The possibility of a lower
capacity to experience reward in obese people has also
been observed in brain-imaging studies. The dopamine
D2 receptor, which is involved in hedonic pathways in
the brain, has been found to be decreased in obese
compared with lean subjects, in proportion to BMI
(Wang et al. 2001). Thus, it appears that the relation-
ship between STR and obesity is complex. It has been
suggested that hedonically driven over-consumption of
palatable foods may eventually lead to down-regulation
of the dopamine system in the brain, leading to a reduc-
tion in the capacity to experience reward from food.
This would mean that high STR could be a risk factor
for weight gain but not necessarily a characteristic of
obese people (Blundell & Finlayson 2004).
Overall, it is emerging that variations in eating behav-
iour may be particularly important in determining the
risk of obesity. Within the current environment, which
is replete with food cues, it may be a person’s overall
sensitivity to positive stimuli to eat, rather than single
specific defects in internal signals of satiation and
satiety, that play the most important role in weight gain.
7. Conclusions
Satiation, satiety and their effects on eating behaviour
are important when considering energy intake, particu-
larly with regard to weight control and obesity.
Satiation and satiety are typically measured by using
a combination of energy intake and self-reported
appetite ratings, and there are many factors that can
potentially confound these measurements. For these
confounders to be controlled, studies are generally per-
formed in a laboratory setting and are relatively short-
term (i.e. 6–12 hours per test condition). It is much
more difficult to get reliable data about satiation and

Key points
• Satiation and satiety are important in controlling energy intake and, therefore, should be taken into account
when considering weight control and the risk of obesity.
• The majority of obesity genes that have been characterised affect the risk of obesity via effects on appetite
control. In rare cases, single-gene mutations can cause severe obesity, but more commonly, there appear to be
particular genetic profiles that affect the risk of obesity within the current ‘obesogenic’ environment.
• There are some physiological differences in the development of satiation and satiety that have been observed in
obese people, including increased gastric capacity and differences in the production of gut hormones. However, it
is not clear whether these are a cause or effect of obesity.
• Differences in eating behaviour affect an individual’s responsiveness to internal signals of satiety, and these may
predispose certain people to excessive energy intake and obesity.
• Knowledge about the relationship between satiation, satiety and eating behaviour may help when designing
strategies to reduce or prevent obesity in the future.

© 2009 The Author

Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173

satiety in the longer term, outside a laboratory setting,
because of problems in obtaining accurate self-
reported dietary intake data. This raises issues as to
how far laboratory data can be extrapolated to free-
living people.
Energy density appears to be the major dietary factor
influencing satiation and satiety, and there is a substan-
tial body of evidence to suggest that low-energy density
foods and diets promote satiation and satiety and may
help to control weight. For this to be of benefit to people
who wish to prevent weight gain or lose weight, prac-
tical guidance is needed on how to reduce dietary energy
density. There are a variety of ways to reduce the energy
density of the diet, for example, eating only small por-
tions of fatty foods, increasing the water content of
dishes, eating more fruit and vegetables and choosing
higher-fibre foods. This could provide the flexibility to
make this approach acceptable to consumers who want
to control their weight.
However, regardless of how effective a dietary
manipulation might be in enhancing satiation and
satiety, the fact remains that people do not always
respond well to these internal signals. Free-living indi-
viduals often eat when sated and sometimes refrain from
eating when hungry. Therefore, an understanding of the
factors other than satiation and satiety that affect eating
behaviour, is essential. Evidence is emerging that inter-
individual variations in sensitivity to internal appetite
signals and responsiveness to the influence of external
eating cues may underlie the differences in susceptibility
to obesity that are seen in the current environment.
It is clear from the increasing worldwide prevalence of
obesity that internal signals of satiation and satiety are
not sufficient to restrain energy intake in many indivi-
duals. Systems to control energy balance in the body
evolved under conditions where energy intake was
directly related to energy expenditure and where the
storage of excess energy as fat could enable humans to
survive periods when food was not abundant. However,
the current environment in much of the world, where
food is plentiful and accessible and physical activity is
largely unnecessary, means that, in susceptible people,
these homeostatic controls are simply overwhelmed by
positive stimuli to eat.
Fundamental changes in our environment and behav-
iour are needed to halt and reverse current trends in
obesity prevalence. Knowledge about the effects of
satiation and satiety on eating behaviour and how these
are manipulated can contribute to reversal of current
trends, provided that this knowledge is translated into
practical advice that helps people control their energy
intake and achieve a healthy bodyweight.
© 2009 The Author
Journal compilation © 2009 British Nutrition Foundation Nutrition Bulletin, 34, 126–173
Satiation, satiety and their effects on eating behaviour 163
Acknowledgements
The Foundation wishes to thank the members of the
Foundation’s Scientific Advisory and Industrial Scien-
tists Committees who have helped to shape the contents
of this Briefing Paper, and Professor John Blundell,
Professor Barbara Livingstone and Dr David Mela who
reviewed the paper. The Foundation also wishes to
thank Kellogg’s for their financial support in writing the
Briefing Paper.
Conflict of interest
The Foundation has received financial support from
Kellogg’s in the production of this Briefing Paper.
However, the views expressed are independent and
Kellogg’s have not been involved in writing or shaping
the contents of this paper.
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