proving an effect on appetite challenges and · pdf fileproving an effect on appetite –...
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Proving an effect on appetite – challenges and pitfalls
Jason C.G. Halford Ph.D. C.Psychol. (Health)
Chair of Biological Psychology ad Health Behaviour
Kissileff Laboratory, Department of Experimental Psychology,
University of Liverpool, Liverpool L69 7ZA
Liverpool Obesity Research Network (LORN): www.liv.ac.uk/obesity
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
Eating Behaviour
Biological Regulation
Environmental
ENERGY INTAKE
Culture
Food Supply
Nutrition
Situation Fat Stores (TONIC)
Satiety Signals (EPISODIC)
CNS Homeostatic
Regulation
Hedonic Systems
Interaction between biology and environment in the control of appetite and energy intake
All Under Genetic
Influence
Blundell Cica 1993 modified by Finlayson
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 aberrant behaviour?
Less control of ingestion
• Greater responsiveness to food cues (in sated state).
• Heightened hedonic responses to palatable food.
• Experiences of uncontrolled hunger and greater disinhibition of eating behaviour.
• Food ‘addiction’?
The obese tend to demonstrate weaker regulatory control of eating behaviour.
Moreover, in the obese appetite regulation is more likely to be
overwhelmed by environmental cues to over-consume.
Halford et al (2010) Nature Rev, Endocrin. 6: 255-269
Weak inhibitory feedback with weight gain
Appetite
Eating Behaviour
Biological Regulation
Environmental
Passive & Active Over-consumption
Culture and Societal Practices
Food Environment
Branding and promotion
Food Formulation
Portion Size
Nutrition information and Knowledge
Energy Density
Palatability & Attractiveness
Drive To Eat
Food Choice
Fat Stores (TONIC)
Satiety Signals (EPISODIC)
CNS Homeostatic
Regulation
Hedonic Systems
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
Interaction between biology and environment in the control of appetite and energy intake in obesity
Blundell Cica 1993 adapted by Finlayson
Impact of Weight Management on Appetite
Energy restriction and the psychology of deprivation.
Deprivation, restriction and weight regain
Weight loss through dieting is a difficult endeavour;
1) Physiological consequences of energy restriction
and
2) Psychological consequences of perceived deprivation
undermine individual attempts to lose weight.
Obsession with food , increased response to food cues, cravings, loss of concentration and dysphoric mood all contribute to failure in dieting (Polivy et al., 2005; Hill 2007; Hawks et al., 2008).
Hunger is a barrier
• Increased caloric intake is a normal consequence of caloric restriction and weight loss.
• Deprivation increases reinforcing value of food (Epstein et al 2003).
• Fasting increases brain reward system response specifically to high calorie foods (Goldstone et al., 2009).
• Hunger significantly predicts weight regain (Pasman et al., 1999).
• 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 VLCDs E.g. Harvey et al 1993
Effects of caloric restriction and weight loss on human appetite (Franklin et al, 1948; Keys, 1950)
The Minnesota Semi-Starvation Experiment: 24 weeks half normal intake (equivalent to VLCD) to reduce body weight by 25%:
During:
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.
After:
• Loss of control over appetite demonstrated by the majority of the participants during re-feeding.
Although these were lean individuals at outset – by and large their experiences were similar to those
dieting for WL including the obese
Appetite
Satiation and Satiety
Importance of Satiation
• Verbal reports on processes bringing a meal to an end indicate that two major reasons to stop eating are:
1. ‘fullness’
2. ‘boredom with taste’
• With a single food it is more likely that boredom of taste becomes involved.
• With composite dishes/meals fullness may be more important in ending the meal.
• Satiation is important because it determines meal size.
• No strong relationship between eating frequency and body weight.
• Meal size may be the key factor in the over consumption of energy.
• Some evidence for this in studies of the obese and weight gainers.
Range of appetite and /or weight control products
Herbal
• Green tea, saponins and other teas (oolong & black) extracts (various catechins – EGCG, EGC, ECG & EC) and green coffee beans
• Caffeine based and ephedrine like products
• Saffron extract, gallic acid, hydroxycitric acid, chinese willow, platycodi radix, K. scoparia, A. turbinata, bitter orange, gingseng, nicotine, khat, C. fimbriata, C. forskohlii.
• Blends such as YGD Zotrim (Natures Remedies), pharmacy own brands (e.g. Boots) and Adios
• Capsaicin
Fibre as a medical devices and fat absorption blockers
• Appesat (Goldshield) or Obesimed
• ObX, Lipobind, Chitosan
Fibre as food ingredient / supplement
• Viscose fibres (traditional bulking gums)
• Alginates (gelling polymers and gastric viscosity)
• Non-viscose highly fermentable fibres (inulins, FOS etc.)
• Insoluble fibres
• Resistant starches
Fats
• Olebra – fabuless TM oat and palm oil (DSM)
• Korean Pine nut oil pinnothin (Lipid Nutrition)
• CLA products from Congis and Lipid Nutrition
Proteins supplement
• Whey, soy and casein
Protein fibre supplement
• Mycoprotein (Quorn).
Gut peptide boosters
Protease inhibitor – Slendester (Kemin)
Protein fibre manipulations
• Shape / Vitalinea (Danone)
• Special K sustain (Kellogg’s)
• Quaker oats (US)
• Slimfast (Unilever)
• Supermarket own brands (Tesco’s)
Pharma crossover
• Alli (GSK) & Hoodia P57 (Phytopharm)
0
100
200
300
400
500
600
700
800
900
1000
Lunch Supper Lunch&Supper
Gra
ms
Time
Gram Intake on Study Day
Placebo
Product
0
200
400
600
800
1000
1200
1400
1600
1800
2000
Lunch Supper Lunch&Supper
kcal
Time
Kcal Intake on Study Day
Placebo
Product
Effects of a commercial CM3 Alginate weight control product 24hr INTAKE STUDY Within subjects, double-blinded, placebo-controlled 24 hour intake study (n=17). CM3 Alginate –3 capsules given prior to fixed load breakfast, ad libitum lunch and evening meal as per manufacturers instructions. No significant effect on gram or kcal intake at lunch or evening meal. No significant suppression of hunger or increase in fullness in product condition – in fact some evidence of an increase in appetite.
Appetite Control and Weight Management
Proof of principle from CNS pharmacotherapy?
104
88
90
92
94
96
98
100
102
8 10 12 14 16 18 20 22 24 0 2 4 6
Sibutramine weight loss and weight maintenance (STORM)
Placebo + Diet & Exercise Sibutramine + Diet & Exercise
Adapted from James WPT, Lancet 2000;356:2119-25
Month
Run-in phase#
#All patients received
sibutramine
10 mg for 6 months
-4.7 kg
-10.2 kg
STUDY 1. Double-blind, randomized, placebo-controlled trial,
57 (39 women) overweight and obese (BMI 27–45 kg/m2) given 10mg twice daily lorcaserin (n=29) for 56d.
2. From d8, a diet and exercise plan targeting a 600 kcal/d deficit.
After 7d of weight maintenance, 1. EI was significantly reduced with lorcaserin but not
placebo. After 56d, lorcaserin resulted in significantly: 1. Larger reductions in body weight (lorcaserin, 3.8 ±
0.4 kg; placebo, 2.2 ± 0.5 kg; P 0.01), 2. EI (lorcaserin, 470 ± 87 kcal; placebo, 205 ± 91 kcal;
P .05), and appetite ratings than in placebo
GLP-1, GLP-2 & Exendin-4 (Exenatide - Byetta)
Study Participants Affect on Appetite
Flint et al. 1998 20 lean men GLP-1 (50 pmol kg/hr)
↓intake 12%. Pre-meal ↓ hunger & prospective consumption, ↑ fullness & satisfaction
Naslund et al. 1999 8 obese men, GLP-1 (0.75 pmol kg min)
Overall reduction of intake of 21%. Significant reduction in hunger.
Gutzwiller et al. 1999
16 lean men (0, 0.375, 0.75, and 1.5 pmol/kg/min)
Dose depended reduction in intake (max 31%). Reduction in pre-meal appetite (hunger and fullness) at highest dose.
Gutzwiller et al. 1999 12 T2D
GLP-1 (1.5 pmol·kg21·min21)
Significant decreases in hunger and increases in fullness pre-meal. 27% reduction in ad libitum intake.
Long et al. 1999 10 non obese men GLP-1 infusion (1.2 pmol/kg per min)
No significant effects on pre-meal appetite or ad-libitum intake.
Flint et al. 2001 18 obese men GLP-1 (45 pmol kg FFM)
Significant reductions in hunger and prospective consumption but not other pre-meal rating or on ad libitum intake.
Schmidt et al., 2003 8 lean (5♂,3♀) GLP-2
(0.75 and 2.25 pmol kg min)
No effect of GLP-2 on appetite.
Gutzwiller et al. 2004
24 lean men GLP-1 (0.9 pmol kg min ) CCK-33 (0.2pmol kg min)
Combination produced significant effects on pre-meal hunger and intake.
Naslund et al. 2004
19 obese 5 days subcutaneous injections of GLP-1
Overall 15% reduction in meal intake.
Degan et al. 2006 Lean males, GLP-1 iv or sc with preloads of water or protein
GLP-1 significantly reduced caloric intake, an effect enhances by the protein preload. Effects accompany by changes in hunger and satiety.
Edwards et al. 2001 8 lean (7♂,1♀) Exendin-4 (0.05 pmol kg min)
19% reduction in meal intake. Effects on appetite unclear.
Appetite
Appetite control, methodology, and substantiating health claims for appetite
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)
Hormones produced by gut and pancreas in response to differing nutrients
STOMACH
Release of Ghrelin
the hunger hormone
suppressed by
carbohydrate
DUODENUM
(Proximal SI)
Cholecystokinin
(CCK) released in
response to protein
and free fatty acids
(duodenal brake)
ILEUM (Distal SI)
GLP-1 released in
response to
carbohydrate and
fats and influenced by
fibres
(Ileal brake)
COLON
Peptide Y (PYY)
released in response
to carbohydrate and
fat and influenced by
fibres.
PANCREAS
Pancreatic
Polypeptide -PP and
Amylin stimulated
by carbohydrate
Measuring Appetite: The Preload study design
• Common experimental technique used to study the short-term regulation of satiety and / or subsequent food intake.
Design features
• Within-subject repeated measures design and whenever possible, double-blind conditions.
• Precisely prepared food(s) matched for taste, appearance and other organoleptic properties.
• Vary in energy and/or macronutrient composition.
Measures
• Effects of the preload on spontaneous food intake are measured through test meal(s).
• Subjective measures of appetite are taken prior to, and at predetermined time intervals after the preload and test meal.
• Respective roles of post-ingestive / pre-absorptive and post-absorptive mechanisms in the regulation of food intake can be separated and assessed (i.e. levels of Ghrelin, CCK, GLP-1 and PPY).
Blundell et al (2010) Obesity Rev 11: 251=270
Preload and Test Meal Issues
• Lack of standardisation (energy content, energy density, macronutrient composition, physical state, weight/volume, sensory and cognitive characteristics) produces highly variable outcomes.
• Outcome - size of next meal (grams / kcal) or time taken to eat next (seconds)? Both valid but intake generally used.
• Timing of preload test meal interval can vary. Rationale not always given on the basis of mechanism or pretesting pilot.
• Nature of the test meal i.e.
– Buffet (variety delays satiation? High hedonic value of certain foods causes overconsumption).
– Single food (monotony brings a meal to early end? No measure of food choice or macronutrient selection).
• Covert vs overt – covert manipulation controlled to isolate physiological effects but underestimate cognitive components of compensation in real world.
• Duration – can a single occasion predict enduring effects across a day (compensation) and during repeated dosing?
9.00am: Fixed load breakfast (pre and post breakfast VAS). 10am, 11am, 12pm: VAS measures.
1.00pm: Ad libitum lunch (pre and post lunch VAS).
2pm. 3pm, 4pm: VAS.
5pm: Ad libitum dinner (pre and post VAS). Preload can be given within or at breakfast or at any
time up to the first test meal. However, timing should be informed by 1) supposed
mechanism and 2) pilot data
Study protocol with second ad libitum meal to determine compensation across the study day
Self-report scales in common use
Specific self-report scales in common use
address, for example:
– feelings of hunger, fullness, satiety;
– prospective consumption (anticipated quantity that would or could be eaten);
– desire to eat (or for a snack or meal);
– urge to eat;
– thoughts of food;
– somatic sensations (e.g. emptiness or fullness of stomach);
– desire for something sweet/savoury;
– thirst;
– nausea, gastrointestinal malaise or other side effects
Four basic scales recommended
History of widespread and consistent
use and acceptance over several
decades in many different countries
and laboratories, with different test
stimuli and subject groups.
1. Hunger
2. Fullness
3. Desire to Eating
4. Prospective Consumption
VAS measures and Mean Appetite Score
How hungry do you feel at this moment?
Not at all
hungry Extremely
hungry
60mm
Appetite
Score
VAS Hunger + VAS Desire to Eat +
VAS Prospective Consumption + (100 – VAS fullness)
= 4
Anderson, G. H., (2002). American Journal of Clinical
Nutrition, 76, 1023–1030.
PILOT timings and dose combinations
Increasing fibre (top left) and increasing protein
(top right) increased fullness.
At the highest dose of fibre (20g/l), all doses of
protein (10g/l, 15 g/l and 21g/l) appeared to
decrease fullness.
Additive effects are hard to achieve and ingredients can unexpectedly block each other’s activities
SOUP PRELOAD STUDY
5 soups containing 50 g maltodextrin,
whole-grain (Hi Maze whole-grain), high-amylose (Hi-
Maze 260 National Starch), or regular cornstarch or no
added starch.
Ad libitum FI was measured at 30 min (experiment 1)
or 120 min (experiment 2).
EI reduced by maltodextrin (86% RDS, 12% RS) (P
<0.05) at 30 min.
EI reduced by whole-grain (24% RDS, 66% RS), high-
amylose corn (40% RDS, 48% RS) & regular corn (27%
RDS, 39% RS) starch (P<0.0001) at 120 min.
NEED A SUBSTANTIVE PRE-LOAD TEST MEAL
INTERVAL TO OBSERVE EFFECTS
Am J Clin Nutr doi: 10.3945/ajcn.2009.28443
Kcal intake at ad-libitum lunch
-
8.0
%
-
5.3
%
-
3.0
%
0
100
200
300
400
500
600
700
800
900
1000
Control Fibre Snack A (weight
matched)
Fibre Snack A (energy
matched)
Fibre Snack B (weight
matched)
Fibre Snack B (energy
matched)
Inta
ke a
t ad
lib
itu
m lu
nch
on
ly (
kcal
)
Kcal intake across the study day
(Three ad-libitum meals; lunch, dinner, snack box)
-
4.7
%
-
8.6
%
-
4.3
%
-
6.8
% 2000
2100
2200
2300
2400
2500
2600
2700
2800
Control Fibre Snack A (weight
matched)
Fibre Snack A (energy
matched)
Fibre Snack B (weight
matched)
Fibre Snack B (energy
matched)
Tota
l in
take
in k
cal (
lun
ch, d
inn
er,
sn
ack
bo
x &
sn
ack)
*
**
Measuring Over Multiple meals with multiple doses
Dried Fruit (prunes or raisins)
Snack based study
Single preload single test meal?
Single preload and test meal designs may be inadequate
12 WK WEIGHT LOSS STUDY
Healthy adults BMI > 25 receive 21 g
oligofructose (Raftilose P95) a day or a
placebo (maltodextrin) for 12 wk.
Reduction in body weight of 1.03kg
with oligofructose whereas weight gain
in placebo of 0.45kg (PSWL =1.45kg
P=0.01) and reduction in fat mass (in
trunk).
Reduction in AUC Ghrelin, increase in
AUC PYY, and reduction in self
reported intake (3d diary) but no effect
on appetite ratings.
NEED TO DOSE FOR PROLONGED
PERIOD TO OBSERVE EFFECTS
Appetite Control and Weight Management
Substantiating health claims for weight management.
Sc
Company Dossier
1. Food 2. Health Relationship
3. Wording of Claim
EU Member state compilation and translation in
some member states
European Union further organisation claims
for EFSA final approval based on EFSA
recommendation
EFSA Nutrition, Dietary products and Allergies (NDA) panel remaining translation and
grouping
Claims/Sub-Working Groups 1: Gut/Immune 2: Cardio, Antioxidants 3: Bone, Dental, Connective Tissue 4: Weight, Satiety, Physical Performance
Tetens (Chair) De Graaf, Hansen, Harrold, Kristensen & Sjodin (Working Group Experts) Asp, Blundell & Riccardi (Ad-Hoc Experts)
5: Mental, Nervous System 6: Botanical
SC
RE
EN
ING
PR
OC
ES
S
Incom
ple
te
or Q
uerie
s
Cla
rifica
tion
s
or Q
uerie
s
?
Nutrient
profiling?
Appetite
1. Must result in changes in energy intake (if this is claimed physiological effect rather that decreased body weight).
2. Must be sustained across day – no compensation.
3. Must be enduring – observable e.g. up to four weeks during dosing.
4. Biomarkers useful for proof-of-concept but not necessary for efficacy.
5. Appetite ratings must be assessed using VAS.
Appetite
1. Considered only in context of decreased body weight - intake no longer as important but body weight is (most claims to date focus on intake – and are negative)?
2. Must be sustained (12 weeks) with continuous consumption of food to exclude adaptation through compensatory mechanisms – must have body weight change to make any communication on appetite (how many claims have actually been reviewed with body weight)?
3. Biomarkers may support behavioural assessment
4. Behavioural assessment (appetite ratings) must be assessed using VAS.
Blundell (2010) Nat. Rev. Endocrin 6: 53-55 Halford & Harrold (2012) Proc Nut Soc 71: 350-362
EFSA Journal 10 (2) 2604
‘Claims on changes in appetite ratings have been made in the context of body weight. In this context evidence for a sustained effect on appetite ratings and body weight with continuous
consumption of the food, should be provided’
Weight Management
1. Weight loss must be observed for at least 12 weeks with continuous consumption of food.
2. Weight regain prevention much be observed for 24 weeks after weight loss.
3. Changes in body fat not strictly required if study duration is appropriate but can be performed on subsample as supporting evidence (measures of body composition: MRI/DXA not waist circumference or bio-impedance).
Weight Management
1. Weight loss must be observed for at least 12 weeks with continuous consumption of food and be sufficient large not to be attributed to loss of water or lean mass.
2. Weight regain prevention much be observed for 24 weeks after weight loss.
3. Changes in appetite ratings, energy intake, energy expenditure or fat oxidation considered in support of mechanism to achieve weight reduction (if sustained effect) – appetite can be used as supporting evidence.
Halford & Harrold (2012) Proc Nut Soc 71:350-362
‘Changes in energy intake etc have been proposed in the context of claims related to the reduction of body weight.
Evidence for a sustained effect of any of these variables with continuous consumption of the food may be considered in support of mechanism by which the food may exert the claimed (BW) effect’
Protein
• Generic claim on proteins and energy intake/body weight rejected. – Study designs did not allow conclusions on whether effects
observed were owing to dietary protein per se or to the concomitant modification of carbohydrate and fat intakes.
• Soy Protein: cause and effect relationship between soy protein and the maintenance of a normal body weight rejected. – Only study that allowed conclusions to be drawn showed no effect
on body weight when compared to other protein sources.
• Whey protein: maintenance of a normal body weight was rejected. – Failure to provide references from which conclusions could be
drawn for the scientific substantiation of the effect.
Fibres
• Generic fibre-based claims for appetite and weight management rejected.
– Ingredients category was diverse and “the food constituent, dietary fibre, is not sufficiently characterised in relation to the claimed effects considered in the opinions”.
• Beta-glucans - no studies testing the sustainability of an effect on appetite ratings
and subsequent energy intake were submitted.
• Inulin-type fructans and Xanthan gum not sufficiently characterised to substantiate an effect on satiety.
• Guar gum - no controlled studies assessing effects on appetite ratings and subsequent energy intake were presented.
• Partially hydrolysed guar gum (PHGG) - studies presented showed no effects on appetite ratings leading to a reduction in energy intake when the energy content of the test meal was taken into account .
WEIGHT MAINTAINANCE STUDY 6-week weight loss period (2.1 MJ/day) followed by 18 weeks weight maintenance with test (Olibra) or placebo yoghurt. Fifty overweight women.
1. No significant weight regain in Olibra treated condition (1.1 ± 3.4 kg) but the placebo group did gain weight (3.0 ± 3.1 kg, P < 0.001).
2. But no significant difference in WL between placebo and Olibra condition
Summary and concluding remarks
Summary - proving an effect on appetite in weight management.
Does it affect satiation? Compared to appropriate comparator:
1. Are meal size and duration
reduced?
2. Is there a reduced energy intake at meal?
3. Does this produce a meaningful effect on within-meal appetite levels and prevent compensation?
4. Does this result in useful and durable changes in day to day experience of appetite control and meal intake likely to lead to weight control?
Does it strengthen satiety?
Compared to appropriate comparator:
1. Does it reduce hunger or increase fullness?
2. Does it delay the time of the next meal?
3. Is appetite between meals controlled (e.g. snacking)?
4. Does this result in useful day to day and durable changes in appetite control and caloric intake which aid weight management?
Does the product aid appetite control and combat the psychology of deprivation produced by chronic energy restriction?
Role of Energy Intake?
• Not now a proxy for the health benefit of appetite suppression (body weight control).
• Now another measure of enduring effects on appetite.
• Can be included along with VAS.
• Enduring changes in VAS and / or change in food intake now accepted as evidence of mechanism of action.
• HOWEVER, this now has to be in the context of weight management.
• In correct population.
• Adequate sample size and study duration.
• With approved validated outcome measures for health benefits or their proxies.
• Uses food constituent that is the subject of the claim.
• Independent and peer reviewed trials.
Appropriate Evidence Base: Trial Choice and other matters
Specific and General points for Appetite Studies
Public and Private Strengths and synergies
CROs
• Size and capacities.
• Extensive experience of conducting trials for various industrial partners.
• Substantial participant pools.
• Comprehensive accompanying services.
Lack discipline specific expertise.
‘Off the shelf’ protocols.
Universities
• Specialist experience.
• Inherent understanding of the science.
• Credibility within the field.
• Bespoke study designs based on understand of key methodological and mechanistic aspects.
Small capacity and lack flexibility
(discipline specific).
Poor insight into the commercial environment
(regulatory and market concerns).
Concluding Considerations: Where are we?
1. Many experience great difficulty controlling eating behaviour; appetite regulation likely to be overwhelmed by environmental cues to over-consume.
2. Dieting is difficult - the psychological consequences of energy restriction, particularly perceived deprivation, undermine attempts to lose weight.
3. Is a satiety-based approach to weight management viable? Pharmaceutical interventions suggest yes...
4. Nutritional approaches target same biopsychological system BUT because they act on distinct mechanisms, rather than sites of integration, the timing of the next eating occasion can be critical to their effectiveness.
5. Regulatory requirements for appetite health claims on foods now stress weight management over the modulation of energy intake - weight loss or weight regain prevention are now endpoints.
6. Few foods or ingredients have produced effects on body weight in appropriately designed large scale trials. HOWEVER, a multi-product strategy may validate a satiety-based approach.
Acknowledgements, Collaborators and Funding
The laboratory has received support from:
• Coca-Cola • California Prune Board • BBSRC-Case • Danone • EU Frame Work 7 • GlaxoSmithKline • Goldshield • Lipid Nutrition • Kellogg’s • Kemin Health Care • Medical Research Council / NPRI • National Starch • Natures Remedies • NovoNordisk • Nutraveris • Sanofi • Prosidion OSI • Weight Watchers
Human Ingestive Behaviour Laboratory
• Dr Joanne Harrold (academic – team lead)
• Mrs Georgina Hughes (researcher)
• Dr Emma Boyland (academic)
• Dr Leanne Breslin (researcher)
• Dr Rory McGill (researcher)
• Ms Jennifer Walsh (researcher)
• Dr Simon Child (researcher)
• Mrs Nicola Williams (laboratory supervisor)
• Dr Sonia Tucci (academic)
• Dr 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)