Lecture 18 - Eating and Appetite Flashcards
(26 cards)
What are the basics of digestion
30 ft long muscular tube
(Detailed diagram in notes)
What is the set point theory of hunger?
Keesey and Powley (1966)
Hunger is a consequence of an energy deficit
Each individual has an optimal level of energy resources = set point
Bodies inherently seek to return to this set point (homeostasis)
As energy levels drop, hunger increases and a meal is initiated
How is the fact it is evolutionarily unlikely a problem with the set point theory?
Need to cope with inconsistent resources in the environment e.g. if animals only ate when hungry, they probably wouldn’t survive a harsh winter
Not a system that just responds to energy deficits
How is the fact it is not supported by evidence a problem with set point theory?
Reductions in blood glucose needed to start a meal are substantial
Drinking a high calorie drink prior to meal time does not stop the meal
Beliefs about the content of the drink has more of an effect (Lowe, 1993) e.g. a drink of full fat coke/beer won’t stop a meal
How is ignorance of environmental factors a problem with set point theory?
Effects of learning, preference and social factors
Thinking about food can initiate cravings without a drop in energy/glucose (further disputes SPT)
Who came up with the positive incentive theory of hunger?
Berridge (2004)
What is anticipation in the positive incentive theory?
Animals driven to eat by the expected pleasure of eating
Expected pleasure = positive-incentive value
What is craving in the positive incentive theory?
Eating (and the perception of hunger) is initiated by craving
This may be for something specific
Enables you to take advantage of good food (when its available)
What are multiple factors in the positive incentive theory?
Flavour of the food
Knowledge about the food (learning)
Time since last meal, amount of food in gut, blood glucose levels…
What determines what we eat?
Learned taste preferences/aversions and social
What did Sclafani et al. (2011) show about learned taste preference?
In training, flavour A is paired with glucose and flavour B is paired with nothing
At test, rats prefer flavour A even though the flavours are no longer mixed with glucose
They’ll still prefer flavour A even though it has no nutritional value
What did Scalfani et al. (2011) show about conditioned taste aversion?
During training, flavour A is paired with LiCl and flavour B is paired with nothing
At test, rats avoid flavour A because LiCl causes the rats to feel sick (although at test it is a neutral flavour)
How is what we eat determined socially?
Food preferences can also be socially acquired (e.g. Galef, 1995)
Animals will prefer a certain type of food if they’ve seen other animals eating it (clear evolutionary advantage e.g. poison/death)
How do we learn to eat vitamins and minerals?
We can learn to eat food associated with specific vitamins and minerals
Associating salt with flavours (Fudim, 1978):
Training: rats can feely eat both mixtures (almond + salt and banana + sugar)
Stage 2: injection of formalin (prompts a salt craving) vs. control (nothing)
Test: control = prefer banana (previously paired with sugar (tasty). Formalin = prefer almond (previously paired with salt)
Formalin induces a salt craving in the rats
Demonstrates that animals can learn an association between neutral flavours and minerals even when they don’t need them
So why do some people have such a poor diet?
Harris et al. (1933) = Thyamine (vitamin B1) depleted rats learned to choose a complete diet and avoid a thyamine deplete diet
Effect weakened when there was a choice between 10 different diets (humans have a wide range of choice in terms of foods and flavours)
What determines when we eat?
Collier (1986) – most mammals will eat many small meals throughout the day
How does pre-meal hunger initiate a meal?
Pre-meal hunger (Woods, 1991)
Eating a meal stresses the body: influx of fuel moves it away from homeostasis
Signals for a meal (e.g. time of day, smells) evokes a cephalic phase (insulin is released into the blood, lowering blood glucose)
External stimuli such as time of day or specific smells can prompt a drop in blood glucose (i.e. not set point theory)
Hunger isn’t a cry for energy, it is the body preparing for homeostasis disruption
How does conditioned hunger in rats show what determines when we eat?
Conditioned hunger in rats (Weingarten, 1983)
Buzzer & Light (CS) -> food (rats ate more food when the CS was subsequently presented). Ate more when buzzer and light were turned on
How is the ventralmedial hypothalamus involved in eating and appetite?
A satiety centre (inhibits eating)
Hetherington and Ranson (1940) = VMH lesions lead to hyperphagia (overeating and obesity)
VMH syndrome:
1) Dynamic phase = excessive eating, weight gain
2) Static phase = body weight maintained, overweight state returns following diet
VMH syndrome rats will not work for food. Sensitive to unpalatable foods (finicky)
How is the lateral hypothalamus involved in eating and appetite?
A feeding centre
Anand and Brobeck (1951) = lesion leads to aphagia (cessation of eating)
LH syndrome (Teitelabum & Epstein, 1962):
1) Aphagia if often accompanied by adipsia (cessation of drinking)
2) Recovery is possible e.g. tube feeding, milk soaked cookies, dry food pellets
How did the theory about the hypothalamus’ role crumble?
(1) VMH lesions damaged the PVN (region produces hyperphagia and obesity – not the hypothalamus)
(2) Hypothalamus regulates metabolism, not eating
VMH lesions = increased blood insulin:
Increases lipogenesis (production of fat)
Decreases lipolysis (breakdown of fat)
Thus, rats must consume more calories to meet demand (not being able to breakdown their own body fat and use it means they need to keep eating for energy instead of relying on stores)
(3) LH lesions produce a variety of motor disturbances, and lack of responsiveness
What did Cannon and Washburn (1912) show about the role of the stomach in hunger?
Cannon the physiologist, Washburn the participant (could swallow a balloon)
Tube down oesophagus which inflated the balloon to be the size of the stomach and contained a small quantity of water. When stomach contracts, water moves and moves cork which marks graph paper with contractions
Contractions caused by empty stomach correlated with hunger
But, patients without stomachs still get hungry
Stomach is not necessary for hunger
What did Koopmans (1981) show about the role of the stomach?
Transplanted an extra stomach & length of intestine into rats. Joined the major arteries & veins
Food injected into the stomach (& held there) ↓ eating
Weird…transplanted stomach had no functioning nerves
Satiety signal must have reached the brain through blood flow (can’t have been nutrients (not absorbed by the stomach))
Still don’t have an airtight comprehension of what stomach does
What are peptides?
Short chains of amino acids (can function as either a hormone, or a neurotransmitter)
Ingested food stimulates receptors in the gastrointestinal tract to release these into the bloodstream (these can pass through the blood-brain barrier)
Gibbs et al. (1973) = satiety peptide
Injected peptide (CCK) into the gut of hungry rats and rats ate less food because CCK may induce illness (supporting a flavour aversion)
Food A -> LiCl = aversion to food A
Food A -> CCK = learn aversion (Mosher et al., 1998). Peptide makes you feel satiated by sense of bleugh
