Neural Basis of Eating Behaviour

Question 1

3 Forms of Energy

Answer 1

Delivered to body as: 
Lipids (fats)
Amino acids (breakdown of proteins)
Glucose (carbs)
Stored in body as:
Fats
Glycogen
Proteins

Question 2

3 Phases of Energy Motabolism

Answer 2

Cephalic phase: preparatory phase
Absorptive phase: energy absorbed into blood
Fasting phase: unstored energy from previous meal has been used, energy is being withdrawn from reserves

Question 3

Set-Point Theory

Answer 3

Hunger is a motivational drive to maintain homeostasis
This should lead to set-point of body weight
Animals behave in accordance with tissue needs

Question 4

Set-Point 1: Glycotastic Short-Term Regulation

Answer 4

Eat
Blood glucose and insulin release increases
Insulin helps glucose enter cells for storage
Hunger decreases
Blood glucose and insulin level decrease

Question 5

Campbell & Smith (1990) BGL

Answer 5

Blood Glucose Levels (BGL)
Rats with free access to food and water had a BGL of 2%
Rats without free access had a BGL drop of 8% 10 minutes before expected meal

Question 6

Strubbe & Stevens (1977) BGL

Answer 6

If expected meal is not serve then BGL returns to baseline

Question 7

Rowland (1951) BGL

Answer 7

Insulin and glucose injections only have effect on eating if given in large quantities

Question 8

Set-Point 2: Lipostatic Long-Term Regulation

Answer 8

There is a set point of body fat - body fat in adults is relatively constant
Deviation from set-point results in compensatory adjustments in eating

Question 9

Leptin (protein)

Answer 9

Released by fat cells and detected in the hypothalamus
Increase: enhanced satiety
Decrease: reduced satiety
Overweight people have high levels of leptin - sensitivity reduced

Question 10

1950s Genetic Mutation in Mice

Answer 10

Morbidly obese mice with leptin deficiency
Leptin treatment worked on mice and humans with the genetic mutation
In normal humans treatment did not decrease body fat or eating

Question 11

Lateral Hypothalamus and Hunger

Answer 11

Lateral hypothalamic syndrome/lesion: aphagia - absence of eating, adipsia - absence of drinking
Motor disturbances and lack of responsiveness to sensory inputs
Lesioned rats partly recover when kept alive - tube fed

Question 12

Ventromedia Hypothalamus and Hunger

Answer 12

Ventromedial hypothalamic syndrome/lesion: hyperaphagia - over-eating
Daily food intake increases initially but plateaus overtime
Body weight increases until very high plateau

Question 13

Interpretations of Hyperaphagia

Answer 13

Initial interpretation: lesioned animals become obese because they overeat - no satiety
New interpretation: ingested calories are converted into fat at a high rate
Rat needs to eat more to ensure enough calories are in the blood for immediate energy requirements - more hunger

Question 14

Positive Incentive Theory

Answer 14

Driven by cravings
Take advantage of good food when available
Anticipation of eating - positive incentive value
Incentives dependent on various factors e.g. hunger levels, external environment
Acknowledges many factors influencing eating

Question 15

Factors Determining What We Eat

Answer 15

Learned taste preferences

Question 16

Factors Determining When We Eat

Answer 16

Premeal hunger

Question 17

Factors Determining How Much We Eat

Answer 17

Satiety signals: from gut and blood depend on volume and nutritional density of food
Rely on learned knowledge to stop eating - chewing/swallowing info
Sensory-specific satiety: (Rogers & Blundeu, 1980) rats with cafeteria diet increase caloric intake by 84% and weight by 49% - as you eat one food the positive incentive value for all food decreases but for this one particular it declines strongly

Question 18

Rolls & McCabe (2007) Chocolate Cravings

Answer 18

Chocolate cravers show more brain activity at the sight and taste of chocolate in the orbitofrontal cortex

Question 19

Why is Obesity Increasing?

Answer 19

Evolution: times of food shortage vs. endless variety of food available
Eating culture: 3 meals per day, food focus in social gatherings, salt/sugar added to foods, learned preference of high calorie foods

Question 20

Individual Differences in Obesity

Answer 20

Larger energy intake: particularly large cephalic phase in response to the sight of food
Smaller energy output: slower basal metabolic rate, genetics

Question 21

Pradar-Willis Syndrome

Answer 21

Insatiable hunger, slow metabolism, feeding difficulties at infancy, compulsiveness, tantrums, weak muscles
Genetic cause: chromosome 15 (from father)
If untreated: most people become extremely obese and die in early adulthood

Question 22

Obesity Treatment

Answer 22

Body weight regulation
Lifestyle changes: exercise, healthier food
Only 20% of people keep weight off for more than 2 years
If diet is maintained the body will stabilise at a new level - settling point

Question 23

5 Stages of a Typical Weight Loss Program

Answer 23

1. Rapid weight losee
2. Energy ‘leakage’ reduced, weight loss weight reduced
3. Rate of intake matches reduced energy output - settling point achieved
4. Diet terminated, rapid weight gain, low level of energy leakage
5. Weight accumulates, incentive value of food declines, energy leakage rises, original settling point regained

Question 24

Medical Treatment for Obesity

Answer 24

Sibutramine: 5HT and NA reuptake blocker, decreases meal size and binge eating
Oristat: prevents intestines absorbing fat. 50% users have atleast 5% weight loss 2 years later (Powell et al, 2007)
Surgical procedures

Question 25

Anorexia Nervosa

Answer 25

1-3% of all women
Higher classes, white and asian
16:1 female:male
15% below average body weight
Extreme dieting >2 years
Comorbid with OCD and depression
10% death rate, high suicide rate, high relapse rate
PIV of talking about food, PIV of taste is reduced

Question 26

Associative Learning in Anorexia

Answer 26

Strong negative association between eating and becoming fat

Aversive physiological effects of meals are enhanced in poeple that eat little (Brooks & Melnick, 1995)

Question 27

Treatment for Anorexia

Answer 27

Therapy suggests small portions

Question 28

Bulimia Nervosa

Answer 28

Increasing prevalence rates
Often normal weight
Binge eat/strict diets
Purging behaviour e.g. vomiting, laxatives
Comorbid with anxiety/depression/OCD

Question 29

Increasing Appetite in Bulimia

Answer 29

Rats deprived of food 12 hours a day and have a very sweet sugar drink
Several weeks later: rats drinking level increased