Appetite Flashcards
(46 cards)
1
Q
Homeostasis
A
The ability to maintain a relatively stable internal state.
2
Q
metabolism
A
The process by which your body converts what you eat and drink into energy
3
Q
hunger
A
The drive to consume, elicits a behavioural response (eating) to a biological need.
4
Q
satiation
A
Processes during a meal that generate negative feedback leading to its termination (within-meal inhibition).
5
Q
satiety
A
The end state of satisfaction. The further suppression of the drive to consume and post-meal intake (between-meal inhibition).
6
Q
peripheral appetite control
A
Includes motor functions of the stomach (e.g. rate of emptying) and release of peptides and hormones from the gut and fat tissue.
7
Q
central appetite control
A
Brain and central nervous system.
8
Q
homeostasis and energy balance
A
- Negative feedback systems:
- Feedback from changes in one direction elicit compensatory changes in the opposite direction.
- Act to maintain homeostasis – a stable environment.
- Energy balance (EB):
- Energy intake (EI) minus energy expenditure (EE).
- In an ideal homeostatic energy system an organisms energy intake should equal energy expenditure.
9
Q
homeostatic control of energy
A
- A biological need to maintain the body’s energy stores.
- Depletion of energy stores → drive to eat.
- Repletion of energy stores → negative feedback signals to terminate eating.
Co-ordinated by the hypothalamus.
10
Q
asymmetry of homeostatic control
A
- Defends well against energy deficit. However, defence against energy excess is weaker.
- → More sensitive to under-eating than over-eating.
- → We can gain weight more than easily than losing weight.
“Eat more” command is dominant over the “Stop eating” command.
11
Q
what starts a meal
A
- Ghrelin: A peptide hormone released by the stomach when energy levels are low
Prior to meals ghrelin levels begin to arise
12
Q
what ends a meal
A
Gastric Distension- A potent satiety signal that terminates intake and promotes initial post-meal satiety.
13
Q
the gut food and hormones
A
- CCK (Cholecystokinin)
- GLP-1 (Glucagon-like peptide-1)
- Duodenal Brake- CCK’s response to fat in the duodenum.
- Decreases rate of gastric emptying
- Satiation and early satiety
- Further down the small intestine…
- Ileal Brake- GLP-1 responds to fat.
Post-meal satiation and reduced hunger at the next meal
14
Q
long term control- leptin
A
- Produced by adipose tissue (the body’s fat stores) when ‘full’.
- Lots of our energy is stored as fats- evolutionary advantage
- Reduces food intake.
- Long term (“tonic”) signal.
Mice with genetic obesity (ob/ob) cannot produce leptin because they are born without required gene code.
15
Q
evidence for weaker regulatory control in people with obesity
A
- Weaker gastric distention (Geliebter, 1988).
- Blunted satiety hormone response to eating (PYY, GLP-1) (Lean & Malkova, 2016).
- Rare cases of human obesity where leptin cannot be produced due to gene defect.
- However, most people with obesity people do not possess a leptin deficiency. In fact, they produce excess leptin
→ leptin insensitivity or leptin resistance?
16
Q
new drug treatments- fulness
A
- Semaglutide (Wegovy) is a GLP-1 receptor agonist.
- Works by supressing appetite and increasing feelings of fullness.
Associated with sustained, clinically relevant reductions in body weight.
17
Q
central nervous system appetite control
A
- CNS regions receive signals from the body (e.g. gut, liver).
- Receptors within the CNS also detect circulating levels of nutrients.
- Substances, such as glucose, can cross the blood-brain barrier.
Specific neuronal populations recognise and integrate multiple energy-relevant signals and act in a network to determine energy intake and expenditure.
18
Q
CNS structures involved in appetite regulation- lower
A
- Vagal Nerve
- Afferent fibres from gastrointestinal tract and liver → brainstem
- Brainstem (Hind Brain)
- Relays afferent vagal signals associated with eating to the hypothalamus. Key sites are:
- Nucleus Tractus Solitarius - NTS.
- Area Postrema - AP (adjacent to NTS).
19
Q
CNS structures involved in appetite regulation- higher
A
- CNS structures involved in appetite regulation- higher
- Hypothalamus
- Key hypothalamic sites:
- Arcuate Nucleus (ARC)
- Ventro-Medial Hypothalamus (VMH).
- Lateral Hypothalamus (LH).
Paraventricular Nucleus (PVN).
20
Q
CNS structures involved in appetite regulation- neuronal populations
A
- The ARC contains functionally discrete populations of neurones:
- The ARC has extensive reciprocal connections with other hypothalamic regions including the PVN, VMH, and LH.
- These regions receive afferent information via the NTS/AP.
- CNS mechanisms: satiety
- 5-HT (Serotonin):
- A key CNS satiety signal in the short-term (“episodic”) regulation of food intake.
- 5-HT drugs are successfully used as appetite suppressants to treat obesity.
- The 5-HT drug Lorcaserin was hailed by the media as a “magic bullet” (but caution needed)
21
Q
reward motivated eating
A
- Eating for pleasure
- Eating to feel better
- Cues associated with the intake of tasty foods (e.g. the sight and smell of food) acquire strong motivational properties and become highly wanted
22
Q
is dopamine the pleasure neurotransmitter?
A
- The Anhedonia theory (Wise, 1982):
- Dopamine mediates pleasure, based on observation of rat behaviour:
- Disruption of brain dopamine systems lead to failure to eat or drink.
- Dopamine receptor antagonists reduce working for food.
Argued that apparent loss of motivation to eat is due to loss of reward – or hedonic consequences – that are normally mediated by dopamine.
23
Q
why the anhedonia theory is wrong
A
- Dopamine blockade prevents animals from attending to food, and working to obtain it – but this reflects motor incapacity not motivational deficit.
- Stimulating dopamine activity can increase responding for food – but doesn’t increase how much is eaten!
Critical experiments show that dopamine is not required for the experience of pleasure from eating.
24
Q
Berridges theory of food reward
A
- Food reward contains distinguishable psychological components that are controlled by separate neurobiological systems.
- Key distinction is between processes associated with affective vs. motivational consequences of consuming food.
→ Core processes of Liking and Wanting.
25
liking vs wanting
- Liking represents the pleasure or affective aspect of food. Liking may activate, but does not require, wanting.
Wanting is the motivational component – also known as “incentive salience”2. Wanting without liking adds the compulsive element to eating.
26
dopamine is not required for liking
- Chemical lesions of brain dopamine systems using 6-hydroxydopamine (6-OHDA)
* Aphagia (rejection of food)
* Adipsia (absence of thirst)
* but NORMAL taste reactivity
Hedonic evaluation of food (“liking”) is therefore independent of dopamine.
27
dopamine and incentive salience
- So, if dopamine is not the ‘pleasure neurotransmitter’, what does it do?
- Dopamine does play a role in:
* Recognizing motivationally important stimuli.
* Energizing of goal-directed behaviour.
* Learning of associations between psychological state/experience, environmental stimuli and behaviour.
* Effort.
Dopamine thus serves alerting and activating functions related to wanting.
28
what mediates liking
- Natural opioid (opiate-like) chemicals occur in the brain.
- Morphine (opioid agonist) increases food intake.
- Opioid antagonist drugs reduce food intake.
* Naloxone reduced hedonic preference for sweet, high-fat foods in humans (Drewnowski et al. 1992, Physiology & Behavior, 51, 371-9).
Evidence for a specific role for opioids in liking (but not wanting).
29
obesity and food liking
- Little evidence that individuals with obesity experience greater food liking
Individuals with obesity work harder to obtain food
30
cue reactivity
- Learned associations between food cues (e.g. the sight and smell of food) and the rewarding consequences of eating.
- These cues elicit conditioned responses such as:
* Increased desire and craving for food.
* Attentional bias.
* Physiological changes (e.g. increased salivation)
Food-seeking behaviours.
31
craving
- Food craving - an intense desire which is directed towards a particular food, drink or taste (Hill, 2007, Proceedings of the Nutrition Society, 66, 277-285).
Top ten most “problematic foods”: (Schulte et al., 2016, PLoS ONE 10(2): e0117959).
32
what is happening in our brains when we crave chocolate?
* Chocolate cravers vs non-cravers
* Sight and flavour of chocolate, plus their combination
* fMRI
Greater activation in medial OFC and ventral striatum in cravers
33
cue reactivity and obesity
- Exposure to sight and smell of pizza increased desire to eat and salivary response in participants who were overweight relative to participants who were healthy weight (Ferriday & Brunstrom, 2011, International Journal of Obesity, 35(1), 142-149).
- → increased motivation to consume food.
People with obesity showed a greater attentional bias to food images, but only when they were satiated (Castellanos et al., 2009, International Journal of Obesity, 33(9), 1063-1073).
34
neural evidence for differences in cue reactivity by weight status
- Rothemund et al. (2007), NeuroImage, 37, 410-421.
- fMRI study - responses to pictures of high-calorie foods, low-calorie foods, eating-related utensils and neutral images, following abstinence from eating for at least 1.5 h.
- Women with obesity (BMI > 30) - greater activation to high-calorie foods vs. neutral images in the caudate/putamen (reward/motivation), anterior insula (taste, interception, emotion), hippocampus (memory) and parietal cortex (spatial attention).
In relation to control group of women who were lean (BMI 19–24)
35
cognitive control of appetite
- Without higher level control/executive control, we would be slaves to our reward system.
- But we do not always respond to the presence of food cues by initiating eating. Some individuals are very successful at controlling their food intake.
An appetitive response to a tasty food may be inhibited if the individual has a long-term goal for health (for empirical support see Yokum & Stice, 2013, International Journal of Obesity, 37(12), 1565-1570).
36
cognitive control of appetite and the brain
- Involvement of ventromedial-prefrontal cortex (vmPFC) and network that includes dorsolateral prefrontal cortex (dlPFC).
- Obesity is characterized by lower gray matter volume in brain areas important for executive control.
Genetic vulnerability to higher body weight is expressed in brain areas important for cognitive function
37
cognitive control increases during satiation
- Thomas et al (2015):
- 16 healthy participants were scanned on 2 separate test days, before and after eating a meal to satiation or after not eating for 4 h.
- Satiation reduced activity in reward-related brain regions.
- Satiation increased activity in the dorsolateral prefrontal cortex (dlPFC),
→ “top down” cognitive influence on satiation.
38
memory for recent eating- the case of patient RH
- R.H. had bilateral damage to the medial temporal lobes which resulted in severe amnesia.
- He was able to eat multiple meals:
* Ate three meals in a short space of time. Rejected a fourth meal because his “stomach as a little tight”.
* R.H was unable to remember his recent eating and continued to eat as a result.
A large number of studies with neurologically intact participants indicate that memories about recent eating episodes are an important determinant of food intake (Higgs, 2005, Physiology & Behavior, 85, 67-72).
39
peripheral appetite signals
- Stomach distension - stretch receptors transmit signals via the vagus (afferents) to the hypothalamus.
Signals satiation and inhibits food intake.
40
balloon belly (Geliebter, 1988)
- N = 8 (4 with obesity, 4 lean).
- Within-subjects design (6 conditions). Small, standardised breakfast, ingestion of ‘gastric balloon’:
* 0mL inflation
* 100mL
* 200mL
* 400mL
* 800mL
* 800mL inflation followed by immediate deflation
- Dependent variable: Intake of liquid meal
Balloon was passed orally into the stomach of four lean and four participants with obesity before they ingested a liquid lunch meal. The balloon was filled with 0, 200, 400, 600, and 800 ml of water in a random sequence on different days. The balloon was kept inflated during ingestion then deflated and removed. Food intake was significantly reduced (p<0.01) by a balloon volume of ⩾400 ml
41
Geliebter 1988- differences in stomach capacity by body weight
- Inflation of balloon in 100mL steps.
- Participants rated their discomfort as 1 to 10.
- Larger stomach capacity in participants with obesity (relative to participants who were lean).
- In the second study, another balloon was inserted into the stomach of these subjects to estimate stomach capacity. The balloon was gradually filled at the rate of 100 ml/min with 30 sec pauses. The subjects rated their discomfort as 1 to 10, from no discomfort to extreme discomfort. A rating of 10 was the main index for stomach capacity.
-
Critical analysis
- Study isolated effects of stomach distension on appetite, independent of metabolic effect of nutrient ingestion.
- Strengths included within-subjects design and standardisation of appetite at baseline.
* BUT weight-related differences in gastric capacity, metabolic needs, habitual meal size, mean that standardisation might not have been as effective for group comparisons (Study 2)
- Also…
- Small sample size.
- Naturalistic eating conditions?
Practical implications
- Intragastric balloon as a (temporary) therapeutic device to treat obesity.
* Patient experience
- But potential for serious adverse events, and questionable efficacy compared to other treatment options (Tate & Geliebter, 2017, Advances in Therapy, 34, 1859-1875).
42
Milkshakes and fake saliva- Burger & Slice, 2013
- How to measure neural activity in response to food consumption?
- Practical challenge: eating in the scanner – chocolate milkshake
- Control stimulus? Tasteless solution designed to mimic taste of saliva
- N = 155 healthy-weight adolescents, standardised appetite.
- Measured neural activity in response to anticipated intake and during intake:
* Attentional regions (visual and medial prefrontal cortices).
* Reward regions (striatum).
* Gustatory and oral somatosensory regions (e.g., anterior insula, postcentral gyrus, opercula).
- 2-week energy intake estimated (doubly labelled water).
- Energy intake correlated with increased activity in anticipation of palatable food in:
* Visual cortex (visual processing and attention).
* Frontal operculum (gustatory [taste] cortex).
- No association energy intake and BOLD responses during consumption of palatable food.
-
Critical analysis
- Provides novel evidence on the associations between brain reward and habitual energy intake (not ‘fat mass’ driving effects as in previous studies of participants with or without obesity).
- Objective measure of energy intake.
- But cross-sectional and observational research:
* Experimental manipulation of energy intake (i.e., change energy intake to examine changes in BOLD signals) necessary to disentangle direction of causality.
Practical implications
- Strengthening cognitive control / inhibition of cue reactivity and reward:
* Computerised tasks training inhibition of automatic motivations toward palatable foods as a potential adjunct to weight loss programs (Lawrence et al., 2015, Appetite, 85, 91-103).
43
the never ending soup bowl- Brunstrom et al., 2012
- Between-subjects design (N = 100).
- 2 (perceived soup volume) x 2 (ingested soup volume).
- Hunger rated immediately after, and +1, 2, 3 hours.
Critical analysis
- Study isolated effects of perceived intake (cognitive influence on satiety) from actual intake
- But…
- No measure of actual food intake.
- Episodic memory manipulation confounded with:
* Pre-meal expectations? Disappointment vs satisfaction with portion.
* Eating rate? Eat faster when perceived smaller portion à weaker satiety response (Wilkinson et al. (2016). PLoS One, 11(2), e0147603).
Practical implications
- Attentive eating versus distracted eating – impact on meal memory and potential to influence later intake:
* Review of evidence (Robinson et al. (2013) American Journal of Clinical Nutrition, 97(4), 728-742).
- Attentive eating advice via a phone app to supplement to weight loss program:
* Robinson et al. (2013). BMC Public Health, 13, 639.
44
manipulating eating rate
- Specific verbal instructions “chew 15 / 40 times per mouthful”
* Impact on satiety hormones (Zhu et al. (2013). British Journal of Nutrition, 110(2), 384-390).
- Instructions + facilitate with spoon size (Andrade et al (2008). Journal of the American Dietetic Association, 108(7), 1186-1191).
Measure pace and provide real time feedback to increase/decrease speed (Zandian et al.(2012). BMC Public Health, 12, 1-8).
45
universal eating monitor
- Allows covert monitoring of intake (and eating rate) during meal using concealed scales underneath food tray
(Kissileff et al. (1980). American Journal of Physiology, 238(1), R14-R22).
46
manipulation of oral cavity size
Reduce oral cavity size to reduce bite size and eating rate:
McGee et al. (2012). Obesity, 20(1), 126-133.
A potential intervention- (another example of University of Liverpool research!)
Summary
