Appetite regulation

Dr. Carl Roberts

Carl.roberts@liverpool.ac.uk

APPETITE EXPRESSION

Human eating is a complex and varied

behaviour

This can be broadly categorised as

psychological experiences, peripheral physiological signals and central neural

processes

Defining concepts in appetite (Psychological experiences)

Hunger

• The drive to consume, eliciting and sustaining a behavioural response (feeding) in

response to a biological need.

Satiation

• Processes during a meal that generate negative feedback leading to its termination

(within-meal inhibition).

Satiety

• The end state of satisfaction. The further suppression of the drive to consume and post

meal intake (between-meal inhibition).

Peripheral physiological signals

to the CNS

Controlling energy balance demands

extensive coordination from the CNS. The

brain integrates numerous signals in order

to determine the energy requirement of

the body and to modify the experience

of hunger and initiate the relevant

behavioural actions in response to this.

Short term appetite regulation Satiety-related hormones

.

.

.

.

.

Vagal

afferents to

the brain

• Post-ingestive signals are generated by nutrients in the

gastrointestinal tract (hormone release from stomach,

intestine, & colon)

• Hormones (satiety-related peptides) signal the brain via

the vagal nerve connection from periphery to

brainstem or act directly via Blood-Brain Barrier

• Some signals exert their effects during the meal and

others after the meal

• Some signals are stimulatory (ghrelin) but most are

inhibitory (CCK, GLP-1)

• Some signals are nutrient-specific (greater release to

fat, CHO, protein or fibre)

Long term appetite regulation Insulin and Leptin

NPY AgRP POMC CART

+ -

inhibit stimulate

Increase EIDecrease EE

Decrease EIIncrease EE

hypothalamus

Arcuate Nucleus

(ARC)

• Insulin secreted by the pancreas and leptin

secreted by adipocytes in proportion to fat

mass

• Both act on receptors in the hypothalamus

(ARC) that inhibit neurons that promote EI and

excite neurons that reduce EI

• Tonic signals modulate how responsive the brain

is to satiety signals from food

• Elevated levels of insulin and leptin associated

with obesity cause downregulation of

hypothalamic receptors and resistance

NPY = Neuropeptide Y

AgRP = Agouti Related Peptide

POMC = Proopiomelanocortin

CART = Cocaine and Amphetamine Regulated Transcript

Central psychological

influences: Hedonics

Physiological models of food intake give relatively little

attention to psychological influences such as the

enjoyment and pleasure of eating. Which can be termed

FOOD HEDONICS.

Hedonic eating – food is rewarding

• Whilst there is an impressive neural system designed to achieve energy homeostasis – Given obesity prevalence it is clear that these signals are unable to prevent development of obesity in modern environment.

• Palatability and pleasure are arguably THE MOST powerful motivators of food intake – the rewarding nature of food easily overrides homeostatic control of appetite.

• Food reward drives eating in the absence of hunger

• We have evolved efficient motivational mechanisms that direct us toward food sources (wanting), encourage overconsumption (liking) and permit storage of excess energy (fat) as a protection against food shortage.

• The prevalence of obesity is an indication of the efficiency of these hedonic processes in governing eating motivation.

• Wanting– The hedonic motivation to consume a specific food, manifesting explicitly (craving) or implicitly

(incentive salience)

• Liking– The sensory pleasure elicited by contact with food contributing to the hedonic motivation to

consume (wanting)

Finlayson after Halford (2008)

Defining concepts in appetite: hedonic and motivational factors (Psychological experiences)

Neurobiology of desire• Opioid receptor agonists increase liking

• Specific sites in the nucleus accumbens are sensitive to the intake inducing actions of opioids and opiates

• Eating palatable food causes opioid release in these same regions

• Cannabinoids enhance wanting and liking• Like THC, endocannabinoids (anandamide, 2-arachidonoylglycerol, noladin ether) increase food

intake.

• Cannabinoids enhance food palatability.

• Consumption of palatable food linked to increased brain endocannabinoid activity.

NEUROTRANSMITTER SYSTEMS MODULATING FOOD INTAKE /

ENERGY EXPENDITURE CENTRALLYSerotonergic

Noradrenergic

Endocannabinoid

CART

Dopaminergic

NPY

Melanocortin

Histamine

INHIBIT NUTRIENT ABSORPTION

Gastrointestinal

lipase inhibitors

MODIFY PERIPHERAL METABOLISM

Lipolysis

Inhibit lipogenesis

Increase muscle energy utilisation

GASTROINTESTINAL FUNCTION AND APPETITE

Ghrelin

CCK

PYY

GLP-1 analogues

DPPIV inhibitors

Amylin analogue

Targets for weight control and treatment of obesity

Lau (2007) from Finer and Abbott Pharmaceuticals 2006

Role of Behaviour in Weight Control: The Energy Balance Equation

Intake Expenditure

Hunger & Satiety

Hedonics

Nutrient Absorption

Metabolic Rate

Thermogenesis

Activity

Energy intake has

a strong

behavioural

component

Energy

expenditure has a

behavioural

component

Behaviour has a critical role in the

aetiology of weight gain, contributing both

to excessive energy intake and

inadequate energy expenditure.

What kind of difficulties related to hedonics do you routinely see in those seeking treatment?

EATING BEHAVIOUR AND

OBESITY

Individuals with obesity tend to demonstrate

weaker regulatory control of eating behaviour.

Moreover, appetite regulation is more likely to be

overwhelmed by environmental cues to over-consume

Behavioural phenomena associated with obesity = susceptible behavioural phenotype

Inadequate impact of ingestants (Satiety)

• Often increases in eating rate and a failure to develop normal satiation during the course of a meal

• After consumption demonstrate weakened satiety responsiveness

• Physiological weakness – cause and / or consequence of abnormal behaviour?

Less control of ingestion

• Experiences of uncontrolled hunger a

• Greater disinhibition of eating behaviour

Hedonic Eating (reward)

• Greater responsiveness to food cues

• Heightened hedonic responses to palatable food

• Eating for pleasure

Individuals with obesity tend to demonstrate weaker regulatory control of eating behaviour. Moreover, appetite regulation is more likely to be overwhelmed by environmental cues to over-consume

Individuals with obesity have a biological vulnerability for weight gain which is manifested in eating behaviours that lead to overconsumption.

FOOD CUE REACTIVITY• Individuals with obesity are more reactive to food cues (Castellanos et al,

2009) i.e. their attention is more easily grabbed and held by these cues.

• When hungry, these effects become more potent “attention grabbing”, an effect more pronounced in overweight/obese participants (Nijs et al, 2010).

CRAVINGS• High BMI correlates with cravings while dieting (Delahanty et al, 2002).• Subjective cravings in overweight individuals associated with food cue

responsiveness (Werthamnn et al, 2011). • Increased BMI is associated with more frequent craving, and craving for

specific foods was associated with increased intake of them (Chao et al, 2014).

Food cues reactivity, cravings and obesity

Castellanos, E. H., (2009). IJO 33(9), 1063–1073, Werthmann, J.(2011). Health Psychology 30(5), 561–9. Nijs, I. (2010).. Appetite, 54(2), 243–54.,Delahanty et al (2002) Diabetes Care 25 (11): 1991-8, Chao et al (2014) 15, 478-82

Regulatory control (satiety) and reward:

Dual System Model of CNS integration Hedonic Drive:

Positive Feedback

Appetite regulation involves a complex interplay between satiety, reward and inhibitory control

Direct: ad libitum intake, eating rate, caloric compensation. Self-report: Appetite ratings, expected satiety, perceived hunger, satiety quotient. Neurophysiological markers: insula and hypothalamus. Physiological makers: Ghrelin, GLP-1 and PYY,

metabolic factors, energy balance.

Direct: Food Choice, macronutrient intake, implicit & explicit liking and wanting, visual probe, eye tracking.Self-report: palatability, taste, pleasure, expected palatability, food preference, cravings,. Neurophysiological markers: activation and connectivity mesolimbic DA system

Direct: Cue specific inhibitory control task. Self report: Power of food, external eating, mindful eating.Neurophysiological markers: anterior cingulate and dorsolateral PFC

DIETING AND ENERGY

RESTRICTION

Psychology of Deprivation and

Physiological Consequences of Energy

Deficit

The Challenge of DietingPsychology of Deprivation and Physiological

Consequences of Energy Deficit.

Obsession with food, increased response to food cues, cravings, loss of concentration and dysphoric mood all contribute to failure in dieting

Energy restriction and weight loss reduce satiety hormone levels – so change may outlast the diet

Hunger is a barrier to and a consequence of dieting

1. Increase in preoccupation with food 2. Relentless thoughts of food and eating inhibited

concentration on usual daily activities3. Serious difficulties adhering with diet when

confronted with unlimited access to food

Food cue responsiveness

• Hunger predicts EEG response to1 and heightens perception of food cues.2

• Lower food cue reactivity predicts more successful weight loss in dieters.3,4

Cravings

• Dieters experience stronger cravings that are harder to resist and typically for the foods being restricted.5

• Trait (not state) cravings discriminate between successful and unsuccessful dieters.6

Therefore, FCR and cravings act as barriers to weight loss success

Food cue reactivity, cravings in dieters

1. Nijs et al (2008) Eating Behaviors 9, 462-70; 2. Piech et al (2010) Appetite 54; 579-82;3. Murdaugh et al, (2012) Neuroimage 59(3); 2709-21; 4. Ouwehand & Papies (2010) Appetite 55; 55-60;

5. Massey and Hill (2012) Appetite 58 (3) 781-5; 6. Meule et al (2012) Appetite 38 (1) 88-97,

Hunger

Food Cue Responsiveness

Inhibitory Control

Executive Function

Coping &Self Regulation

Mood

Incr

ease

sU

nd

erm

ined

Dep

lete

d

Low mood leads to food-related coping

strategies

Impaired executive function

+ less effort in controlling behaviour

Diet

• Dieting increases hunger and

food cue responsiveness,

undermining inhibitory control

and other executive functions

and in turn, the ability to cope

and maintain the diet (self-

regulation)

• Dieting has negative effects

on mood which reduces self-

regulation of controlling

behaviour and reintroduce

food-related coping strategies

• Negative mood reduces

inhibitory control and other

executive functions producing

a cycle whereby ability to

control behaviour and self-

regulation is undermined

-

+

-

Interaction between biology and environment in the control of appetite and energy intake in obesity

Blundell Cica 1993 adapted by Finlayson

Weak inhibitory feedback with

weight gain

Appetite

Eating Behaviour

Biological Regulation

Environmental

Passive & ActiveOver-consumption

Culture and SocietalPractices

Food Environment

Branding and promotion

Food Formulation

Portion Size

Nutrition information and Knowledge

Energy Density

Palatability

Drive To Eat

Food Choice

Fat Stores(TONIC)

Satiety Signals(EPISODIC)

CNSHomeostatic

Regulation

HedonicSystems

Weaker effect of energy intake on wanting

Foo

d P

rod

uctio

n an

d A

vailability

Snacking, eating out / alone

Cheap, ready prepared, easy available

Steadily increasing

HFSS (High Fat, Sugar, Salt)

Labelling and education

Extensive and poorly controlled

Implicit processing

Hedonic Hunger

Weaker inhibitorycontrol

Summary1. Eating behaviour is influenced by the regulatory (satiation and satiety) and hedonic (liking and wanting) components

of appetite

2. The former is driven by signals generated by ingestion (largely but not exclusively physiological), the latter by palatability of foods and the wider food environment.

3. The concept of energy balance fails to capture the difficulty of lasting behaviour change especially in an obesogenic environment.

4. Individuals with obesity tend to demonstrate weaker regulatory control and increased responsiveness to the food environment. This will weaken inhibitory control (the ability to resist).

5. Dieting also tends to weaken regulatory control and increase responsive to the food environment (irrespective of weight status)

6. Individuals with obesity have a biological vulnerability which is intensified by dieting, that makes long lasting behaviour change very difficult. Individual weight management plans require patient input to tailor interventions to individual needs