Week 9-Appetite

Question 1

What’s the process of digestion?

Answer 1

■ The process of breaking down food and absorbing its constituents into the body.
– Food has not been consumed until it has been digested.

Question 2

How is energy delivered and stored following digestion?

Answer 2

■ Following digestion, energy is delivered to the body as:
-Lipids (from fats)
-Amino acids (from proteins)
-Glucose (from carbohydrates)
■ The body uses energy continuously, but it must also store energy as:
-Fats, Proteins, Glycogen
■ Most of the body’s energy reserves are stored as fat.
■ Glycogen is stored in the liver and muscles and is readily converted to glucose – the body’s main usable source of energy.

Question 3

What is energy metabolism and its 3 phases?

Answer 3

Energy Metabolism=(chemical changes which make energy available for use)

1.Cephalic Phase – Preparation to eat
2.Absorptive Phase – Energy from the meal is absorbed into bloodstream to meet body’s immediate energy needs (excess energy is stored).
3.Fasting Phase – Unstored energy from the meal has been used. Energy is withdrawn from stores to meet body’s immediate needs.

Question 4

What hormones control energy metabolism?

Answer 4

Insulin and Glucagon

Question 5

What is insulin?

Answer 5

Released by the pancreas during cephalic and absorptive phases. Three main functions:
1. Promotes glucose use as the body’s primary energy source.
2. Promotes conversion of bloodborne energy to glycogen, fat and proteins.
3. Promotes energy storage in liver, adipose (fat) tissue, and muscles. Insufficient insulin production causes diabetes.

Question 6

What happens if insulin levels are low during the fasting phase?

Answer 6

-Glucose stops being the body’s primary fuel and is saved for the brain.
-Low levels of insulin promote conversion of glycogen and protein to glucose.

Question 7

What’s glucagon?

Answer 7

Released by the pancreas during the fasting phase.
Main function is to trigger conversion of stored energy to usable fuel by:
■ Promoting release of free fatty acids from adipose tissue and their use as body’s primary fuel.
■ Stimulating conversion of free fatty acids to ketones (used as energy source by muscles).

Question 8

What’s energy balance?

Answer 8

■ Homeostasis = a stable environment.
■ Energy intake (EI) minus energy expenditure (EE). In an ideal homeostatic energy system an organisms energy intake should equal energy expenditure.
■ Homeostatic eating = eating behaviour that functions to produce an equilibrium (energy balance - EB).

Question 9

What are negative feedback systems?

Answer 9

-Feedback from changes in one direction elicit compensatory changes in the opposite direction.
-Negative feedback system act to maintain homeostasis.

Question 10

What is the set-point assumption?

Answer 10

Set point = the body’s energy resources are maintained at optimal level.
* After eating, energy resources are close to the set point.
* Energy resources decline as the body uses energy to fuel physiological processes.
* Energy resources fall far enough below the set point → hunger and eating.
* Eating continues until energy level returns to set point → satiety.

Question 11

What are the Glucostatic and Lipostatic Set-Point Theories? Mayer (1955)

Answer 11

Glucostatic theory: Eating is regulated by a system designed to maintain a blood glucose “set-point”.
↓ in blood glucose significantly below set-point – HUNGER
↑ in blood glucose as a result of eating and return to set-point – SATIETY

Lipostatic theory: There is a set-point for body fat. Deviations from this set-point produce compensatory adjustments in eating that return levels of body fat to set-point.

Glucostatic theory - short-term regulation (i.e. meal initiation and termination)
Lipostatic theory - long-term regulation.
Dominant perspective in the 1950s, but now known to be overly simplistic.

Question 12

How have we moved beyond the set-point assumption?

Answer 12

■ The regulation of food intake is far more complicated than a matter of simple energy balance.
■ The body needs a balanced diet of macronutrients and micronutrients i.e. a number of homeostatic sub-systems to be satisfied.

Question 13

What are the problems with the set-point assumption?

Answer 13

• Humans and animals are not normally driven to eat by internal energy deficits.
• Instead, the anticipated pleasure or incentive (reward) value of eating is critical.
• Environmental cues associated with food reward can trigger the desire to eat.
• Food’s incentive value is shaped by emotional, cognitive and environmental factors.

Question 14

What’s Sensory-specific satiety (“the dessert effect”)

Answer 14

■ The decline in the pleasantness of a food as it is eaten relative to an uneaten food.
■ An adaptive mechanism.
■ Makes it easy for us to over-eat when there is a lot of variety

Question 15

What’s the “Appetizer Effect”?

Answer 15

Consumption of a palatable food produces a small increase in hunger early in the meal, relative to a bland food and a food with overly strong flavour.

Question 16

What’s “hedonic” hunger? (Lowe & Butryn, 2007)

Answer 16

• Human food consumption which is driven by pleasure, not by the need for calories.
• People experience thoughts, feelings and urges to consume food in the absence of energy deficit (homeostatic hunger).
• Exacerbated in modern food environments.
• Areas of the brain which mediate hedonic eating are distinct from areas which mediate homeostatic eating.
• Restrained eating/dieting involves eating less than wanted.

Question 17

What’s The Junk Food Experiment? Results

Answer 17

■ After 3 weeks of eating only junk food, Peter’s brain responses to food pictures resembled those of a person with severe obesity.
■ An artificial experiment BUT blood pressure also increased and sleep apnoea worsened (in the absence of big changes in weight).
■ Highlights the negative metabolic consequences of foods high in salt, fat and sugar.

Question 18

What environmental factors are associated with obesity in children?

Answer 18

■ Systematic review of evidence on the influence of the food environment on child obesity.
■ Strongest impact was found for (1) availability of sugar-sweetened beverages, (2) large portion sizes, and (3) food promotion and advertising.
■ Reduction to these three elements likely to hold promise in obesity prevention among children.

Question 19

What’s Leptin – the obesity gene?

Answer 19

■ Mice who were homozygous for the ob
gene (ob/ob) develop severe obesity.
■ Ob/ob mice ate more than control mice.
Also converted calories to fat more efficiently.
■ Blood from thin mice reduced body weight of obese mice.
■ Ob/ob mice did not have a key blood factor called leptin because they were born without required gene code.

Question 20

What’s Congenital Leptin deficiency? (Farooqi et al., 2001)

Answer 20

■ Rare condition in humans where, due to a single gene defect, leptin cannot be produced.
■ Children demonstrate excessive weight gain and appetite.
■ Administration of recombinant leptin completely reverses this condition
■ BUT, most obese people do not possess a leptin deficiency. In fact, they produce excess leptin.
■ It has been suggested that they display leptin insensitivity or leptin resistance.

Question 21

Is obesity nature or nurture? (Llewellyn, C., 2018).

Answer 21

■ Body weight is highly heritable. – Twin and family studies indicate 47–90% heritability.
■ Many common genetic variants [single nucleotide polymorphisms (SNPs)] have been identified, which collectively explain ∼ 3% of the variation in BMI.
■ Genetic risk of obesity is thought to operates via the neurobiology controlling appetite
regulation:
– Manifests as the tendency to overeat when prompted by environmental food cues and the opportunity to eat.

Question 22

What are “Thrifty genes”?

Answer 22

■ During most of human evolution, food was often scarce and came at a high cost of physical activity.
■ The capacity to consume large meals and easily store energy as fat would have ensured survival.

Question 23

What’s the “Thrifty gene” hypothesis? (Neel, 1962)

Answer 23

– Genes that promote storage of energy as fat during periods when food was abundant.
– During famines, individuals with the ‘‘thrifty’’ genotype would have a survival advantage.
– But these same genes are counter-productive in modern “feast” environments