Biological, psychological and environmentaltriggers of eating behaviour:

Biopsychology of Obesity

Jason C.G. Halford Ph.D. C.Psychol. (Health)

Kissileff Laboratory, School of Psychology, University of Liverpool, Liverpool L69 7ZA

j.c.g.halford@liverpool.ac.uk

Liverpool Obesity Research Network (LORN): www.liv.ac.uk/obesity

Food and Appetite

Hunger, Satiety and Reward

The satiety cascade allows us to conceptualise the processes that start, sustain and terminate a meal, and those that suppress further consumption.

It also illustrates the structure of behaviour and the mechanisms underpinning appetite expression.

(Blundell circa 1984)

Triggering and terminating a mealThe Satiety Cascade

COMPONENTS OF APPETITE• Hunger

– The drive to consume, eliciting and sustaining a behavioural response (eating) to a biological need (but with a strong situational component)

• 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)

• Satiation

– Processes during a meal that generate the negative feedback leading to its termination (within-meal inhibition) (strengthened by meal volume and weakened by palatability)

• Satiety

– The end state of satisfaction. The further suppression of the drive to consume and post meal intake (between meal inhibition)

Finlayson after Halford (2008)

Inhibitory control

Satiety

Reward driven eating

Responsiveness to food cues

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

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

Regulatory control (satiety) and reward:

Dual System Model of CNS integration

Homeostasis:Negative Feedback

Hedonic Drive:Positive Feedback

BOOSTS

WEAKENS

Appetite

Eating Behaviour

Biological Regulation

Environmental

ENERGY INTAKE

Culture

Food Supply

Nutrition

SituationFat Stores(TONIC)

Satiety Signals(EPISODIC)

CNSHomeostatic

Regulation

HedonicSystems

Why is appetite important? Interaction between biology and environment in the control of energy intake in body weight

All Under Genetic

Influence

Blundell Cica 1993 modified by Finlayson

ENERGY BALANCE AND EATING BEHAVIOUR

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.

http://www.bis.gov.uk/assets/foresight/docs/obesity/17.pdf

Seven key domains:Food environment (production) (EI – population level)Food consumption (EI – individual level)Individual activity (EE)Activity Environment (EE - population)Societal influences (EI and EE population)Individual Psychology (EI and EE)Biology (EI and EE individual & population)

Around a core hub of energy balance

APPETITE CONTROL AND OBESITY

Behavioural phenomena associated with adiposity

Inadequate impact of ingestants

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

• Greater responsiveness to food cues

• Heightened hedonic responses to palatable food

• Experiences of uncontrolled hunger and greater disinhibition of eating behaviour

• Food ‘addiction’?

Individuals with Obesity end to demonstrate weaker regulatory control of eating behaviour.

Moreover, appetite regulation is more likely to be overwhelmed

by environmental cues to over-consume.

Endogenous PYY release:Lean Obese Differences in plasma levels pre and post lunch

Batterham et al., (2003) buffet lunch causes a significant and sustained increase in PYY secretion in

both the lean and obese. But basal (fasting) levels are lower in the obese and the response to the

lunch is weaker. Not explained by differences in intake between the two groups

FOOD CUES REACTIVITY, CRAVINGS AND OBESITY

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.

Greater reactivity to food cues associated with laboratory food intake in over weight individuals (Werthmann et al, 2011).

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 over weight individuals associated with food cue responsiveness (Werthamnn et al, 2011). i.e. initial orientation to food related cues.

Increased BMI is associated with more frequent craving, and craving for specific foods was associated with increased intake of them (Chao et al, 2014).

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

IMPACT OF DIETING AND ENERGY RESTRICTION

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 activities.

3. Serious difficulties in adhering to the diet when confronted with unlimited access to food.

FOOD CUE REACTIVITY, CRAVINGS IN DIETERS

FOOD CUE RESPONSIVENESS

Hunger predicts EEG response to (Nijs et al, 2008) and heightens perception of food cues (Piech et al, 2010)

Lower food cue reactivity predicts more successful weight loss in dieters (Murdaugh et al, 2012; see also Ouwehand & Papies, 2010).

CRAVINGS

Dieters experience stronger cravings that are harder to resist and typically for the foods being restricted (Massey & Hill, 2012).

Trait (not state) cravings discriminate between successful and unsuccessful dieters (Meule et al, 2012)

Therefore, cravings and FCR acts as a barrier to weight loss success.

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

Appetite 58 (3) 781-5, Meule et al (2012) Appetite 38 (1) 88-97,

Mann et al. Am Psychol 2007

Follow up range from 4 to 7 years

MAINTENANCE OF WEIGHT LOSS IS CHALLENGING

Wei

ght

chan

ge (

kg)

Mean change from baseline to end of diet (kg)

Mean change from baseline to follow-up (kg)

Anderson et al.

Fosteret al.

Graham et al.

Hensrudet al.

Jordanet al.

Krameret al.

Lantzet al.

Murphyet al.

Stalonaset al.

Waddenet al.

Walsh &Flynn

Wadden & Frey

Pekkarinen & Mustajoki

Stunkard & Penik

• 50 Overweight/obese.• 10 weeks weight loss (VLCD –

Optifast Nestle + veg. 500-550 kcal day).

• Appetite and postprandial hormone responses examined baseline, WK10 and WK62.

1. Significant weight loss (13.5kg)2. Led to reductions in leptin, PYY, CCK, insulin, amylin

and increase in ghrelin.3. Also increased subjective ratings of appetite*4. These different hormonal and appetite responses

persisted following weight regain.

Conclusion – Need to manage these changes

*Reductions in appetite noted in some studies of VLCDsE.g. Harvey et al 1993

THE OBESOGENIC ENVIRONMENT AND APPETITE CONTROL

PriceSize

Eating OccasionVariety

Preparation

Fixed meal - Hill, Magson & Blundell, (1984) 2 fixed meals containing foods varying in perceived pleasantness. Reported hunger levels higher before during and after, when offered pleasant food.

Ad-libitum Intake - Yeomans (1996)Pleasantness manipulated by altering the flavour of a pasta dish. Initial stimulation of Hunger and an increase in intake in the palatable condition.

Within meal measurement. Yeomans et al (1997)Palatable food caused an initial stimulation of hunger, and increased intake (accelerating it). NOTABLY – Fullness was delayed

Drewnowski (1998; 1999) palatable foods do not induce satiation

Effects Palatability on Intake and Appetite

(a). Number of Adverts Recognised.

0

2

4

6

8

10

lean

over

weigh

t

obes

e

Nu

mb

er

of

Ad

vert

s R

eco

gn

ised

Non-Food Adverts

Food Adverts

******

*** = p < 0.001

(b). Amount of Food Eaten After Presentation

of Adverts.

0

50

100

150

200

lean

over

weigh

t

obes

e

Am

ou

nt

Eate

n i

n G

ram

s (

g)

food eaten after non-

food adverts

food eaten after food

adverts

***

*

***

***

*** = p < 0.001

** = p < 0.01

* = p < 0.05

Effects of Food promotion on eating behaviour in children

(a). Number of Adverts Recognised.

0

2

4

6

8

10

lean

over

weigh

t

obes

e

Nu

mb

er

of

Ad

vert

s R

eco

gn

ised

Non-Food Adverts

Food Adverts

******

*** = p < 0.001

(b). Amount of Food Eaten After Presentation

of Adverts.

0

50

100

150

200

lean

over

weigh

t

obes

eA

mo

un

t E

ate

n i

n G

ram

s (

g)

food eaten after non-

food adverts

food eaten after food

adverts

***

*

***

***

*** = p < 0.001

** = p < 0.01

* = p < 0.05

Obese children recognised more food adverts than toy but all children responded to them by increasing gram intake and altering food choice

(including shifting to HFSS foods)

ACTIVE OVER CONSUMPTION

External cues and energy intakeIn lean, OW and OB children

Modified design Energy intake analysis

FA exposure increased intake in all children

However, the increased was greater in the obese children (155%) and the overweight children (101%) than the NW children (89%).

Weight status effects can be very obvious especially in older children

SUMMARY

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

Summary

1. 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 resit).

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

6. Appetite control is readily overwhelmed by the palatability of foods and / or food cues (e.g. adverts), an effect more pronounced in individuals with obesity.

Acknowledgements, Collaborators and Funding

The laboratory receives support from the BBSRC, MRC/NRPI, and EU Frame Work 7. These grants are focused on appetite control and weight management and funding within such schemes is dependent on the involvement various Universities, SMEs and Industry Partners.

The laboratory is a functional nutritional research facility and as such receives direct funding from the pharmaceutical, weight management, ingredients, and food industry for appetite research. Current research funders include American Beverage Association, Astra Zeneca, Bristol Meyers Squib and Unilever.

Companies engage the University in Consultancies related to weight management and appetite control (the generation of products that reduce hunger and increase satiety). The lab has advised Novo Nordisk, Optibioxand Orexigen on appetite control. No academic in the Laboratory takes any personally consultancy.

NO POLICY WORK IS SUPPORTED BY INDUSTRY AND NO WORK ON POLICY INVOLVES INDUSTRY

All work engaged on behalf of the University has to meet necessary institutional codes and standards. All research projects receive full independent review.

Human Ingestive Behaviour Laboratory

• Dr Joanne Harrold (academic – team lead)• Mrs Georgina Hughes (researcher)• Dr Una Masic (researcher)• Dr Emma Boyland (academic)• Mrs Nicola Williams (laboratory supervisor)• Dr Sonia Tucci (academic)• Prof Matt Field (associate academic)• Professor Tim Kirkham (academic)• Professor John Blundell (honorary academic)• Dr Graham Finlayson (honorary academic)• Dr Andrej Stancak (associate academic)• Ms Catherine Slevin (PhD Student)• Ms Vassiliki Sinopoulou (PhD Student)• Ms Sophia Komninou (PhD Student)• Ms Lauren McGale (PhD Student)• Ms Rosa Whalen (PhD Student)• Ms Bethan Mead (PhD Student)• Ms Jayne Pickering (PhD Student)