Hunger Flashcards
Introduction - Hunger
Eating drives survival, carried out by every mammal.
Energy delivered to body by lipids, amino acids and glucose. Energy stored by fats, glycogen and proteins.
Two main theories
- Set-point theory: Hunger is the response to an energy deficit. Eating allows energy levels to return to normal. Popular view.
- Positive incentive theory: People drawn to the pleasure of eating. Anticipation and presence of food produces feeling of hunger. Hunger depends on many factors.
Explain the phases of energy metabolism
Process of making energy available for use.
Cephalic Phase
- Begins with sight, smell or thought of food.
- Ends when food starts to be absorbed into bloodstream
- High levels of insulin, low levels of glucagon
Absorptive Phase
- Energy absorbed into the bloodstream from the meal meets bodys energy needs.
- High levels of insulin, low levels of glucagon
Fasting Phase
- Unstored energy from previous meal has been used
- Body withdraws energy from reserves to meet immediate energy requirements
- Ends with start of next cepahlic phase
- Glucagon levels high. Insulin levels low. Glucose stops being main fuel, saving glucose for brain.
- High levels of glucagon promotes conversion of fats to free fatty acids to use as bodys primary fuel and stimuluates the conversion of free fatty acids to ketones used by muscles as a source of energy during fasting phase.
What are the problems with set-point theory?
- Doesn’t make sense from an evolutionary perspective. Used to be inconsistent access to food so would eat when available
- Doesn’t consider taste, learning, social influences. Able to think of food and feel hungry.
What do the different theories say about when and how much we eat?
Set Point Theory
- Know when we are full because signals from what we have just eaten return to a pre-defined energy requirement
Positive-Incentive
- Stop eating when eating no longer pleasureable
Woods and Ramsay (2000) - Strong unpleasant feelings before eating are the body preparing for expected homeostastic-disturbing meal. Expectation of food, not energy deficit.
How does satiety influence how much we eat
- Motivational state which stops us eating when food still available. Signals depend on volume and calories.
Discuss the role of blood glucose in hunger
Campfield and Smith (1990)
- Rats given free access to food and water. Blood glucose monitored.
- 10 mins before meal, levels dropped by 8%. If denied eating, levels normalise
- Initating eating controls glucose levels
Evaluate the concept of hypothalamic hunger
Suggested that eating behaviour controlled by 2 regions of hypothalamus
Ventromedial Hypothalamus
- Lesions cause excessive eating
- Two phases. Dynamic Phase - After surgery, eat excessively and gain weight. Static phase: Food intake reduces to sufficient level to maintain stable level of obesity
- Maintains new body weight.
Lateral Hypothalamus
- Lesions stop eating and drinking (aphagia)
- Need tube to be kept alive
- Feeding centre
- Conclusion that hyptholamus has distinct feeding and satiety regions is wrong.
- Lesions to ventromedial hypothalmus increase blood conc of insulin suggesting it plays a role in regulating hormones.
- Show by rats eating more to fuel increased conversion of glucose to fat caused by insulin levels.
Discuss the role of the gastrointensional tract in hunger and satiety
Cannon and Washburn (1912)
- Swallowed balloon
- Hunger is the feeling of contractions caused by empty stomach.
- Satiety feeling of stomach distension
- This idea cirtiqued bc ppl with removed stomachs still feel hungry
Koopmans (1981)
- Rats implanted 2nd stomach attached to circulatory system, but not NS
- Food injected into stomach decreased eating
- Stomach had no nerves. Satiety signals reaching brain through blood.
Peptides released by stomach. Short chains of amino acids which act as hormones.
- Food interacts with receptors in gastorinestinal tract and releases petides
- Gibbs, Young and Smith (1973) - Injected peptides into hungry rats. Ate small meals
- Provide brain with info on quantity and nature of food.
- Hypothalmus where peptides bind to receptors
Evaluate set-point and settling-point models of body weight regulation
Challenging Set Point
- Variability of body weight - Should make it hard to gain large amounts of weight, however this does happen.
- Health - Free feeding is unhealthy. Those on island of Okinawa eat less and have lower levels of mortality.
Settling Point Model
- Flexible
- Body wright drifts around a natural setting point and stable as long as no long-term change in factors that influence it. If change, impact limited by negative feedback.
- As body fat inc, changes happen which limit further increases until balance achieved between all factors that encourage weight gain and those that discourage it.
- More consistent with data
- Simpler model with fewer assumptions
Discuss the role of genes on obesity
Set-point theory
- Might be specific genes which determine how body will metabolise and store energy
Leptin
- Peptide hormone which allows us to maintain stable fat levels
- Coleman (1979) - Rats which were homozygous for gene ob were obese. Lack hormone that inhibits fat production.
- Friedman (1979) - Cloned gene. Ob mice lack leptin.
- Treatment - Humans had higher levels compared to mice. Did not reduce obesity. Different in rats and humans,
Describe the study of Weindruch et al. (1986) in hunger
- Food deprived rats
- Reductions in food improved health
- Lowest intake showed least health effects
- Fasting can improve health
Discuss Matheson et al. (2012) and hunger
- Association between health lifestyle habits and mortality across diff weight levels
- Those with 0 healthy habits more likely to have higher BMI
How does sham eating influence how much we eat?
- Satiety signals from gut/blood not necessary to terminate meal.
- Study where food chewed, but goes out by a tube before digesion.
- Food consumption influenced by experience rather than energy.
How does the sensory specficness of food influence how much we eat?
- Rogers and Blundell (1980) - Group 1 or rats ate normal food freely. Group 2 had bread and chocolate along with normal meal. Group 2 consumed 84% more calories and gained 49% inc in body weight. Overeat when there is a variery of food. Satiety is sensory specific
- As eat one food, the positive incentive value of all declines
- Rolls et al. (1981) - Rate pleasantness of food and then given one of foods to eat until good then rate again. Ratings for food just had declined. Need nutrients from all food.
- Booth (1981) - Rate pleasatness of food after eating large meal. Decrease in pleasure and 30 mins after eating, reduced apetite.
How do social factors and the appetizer effect influence how much we eat?
Appetizer Effect
- Small amounts of food can increase hunger rather than reduce
- Effective in eliciting cephalic-phase responses
Social Influence
- Eat more when with others
