Neural Basis of Eating Behaviour Flashcards
3 Forms of Energy
Delivered to body as: Lipids (fats) Amino acids (breakdown of proteins) Glucose (carbs) Stored in body as: Fats Glycogen Proteins
3 Phases of Energy Motabolism
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Fasting phase: unstored energy from previous meal has been used, energy is being withdrawn from reserves
Set-Point Theory
Hunger is a motivational drive to maintain homeostasis
This should lead to set-point of body weight
Animals behave in accordance with tissue needs
Set-Point 1: Glycotastic Short-Term Regulation
Eat
Blood glucose and insulin release increases
Insulin helps glucose enter cells for storage
Hunger decreases
Blood glucose and insulin level decrease
Campbell & Smith (1990) BGL
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
Strubbe & Stevens (1977) BGL
If expected meal is not serve then BGL returns to baseline
Rowland (1951) BGL
Insulin and glucose injections only have effect on eating if given in large quantities
Set-Point 2: Lipostatic Long-Term Regulation
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
Leptin (protein)
Released by fat cells and detected in the hypothalamus
Increase: enhanced satiety
Decrease: reduced satiety
Overweight people have high levels of leptin - sensitivity reduced
1950s Genetic Mutation in Mice
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
Lateral Hypothalamus and Hunger
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
Ventromedia Hypothalamus and Hunger
Ventromedial hypothalamic syndrome/lesion: hyperaphagia - over-eating
Daily food intake increases initially but plateaus overtime
Body weight increases until very high plateau
Interpretations of Hyperaphagia
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
Positive Incentive Theory
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
Factors Determining What We Eat
Learned taste preferences
Factors Determining When We Eat
Premeal hunger
Factors Determining How Much We Eat
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
Rolls & McCabe (2007) Chocolate Cravings
Chocolate cravers show more brain activity at the sight and taste of chocolate in the orbitofrontal cortex
Why is Obesity Increasing?
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
Individual Differences in Obesity
Larger energy intake: particularly large cephalic phase in response to the sight of food
Smaller energy output: slower basal metabolic rate, genetics
Pradar-Willis Syndrome
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
Obesity Treatment
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
5 Stages of a Typical Weight Loss Program
- Rapid weight losee
- Energy ‘leakage’ reduced, weight loss weight reduced
- Rate of intake matches reduced energy output - settling point achieved
- Diet terminated, rapid weight gain, low level of energy leakage
- Weight accumulates, incentive value of food declines, energy leakage rises, original settling point regained
Medical Treatment for Obesity
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
Anorexia Nervosa
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
Associative Learning in Anorexia
Strong negative association between eating and becoming fat
Aversive physiological effects of meals are enhanced in poeple that eat little (Brooks & Melnick, 1995)
Treatment for Anorexia
Therapy suggests small portions
Bulimia Nervosa
Increasing prevalence rates Often normal weight Binge eat/strict diets Purging behaviour e.g. vomiting, laxatives Comorbid with anxiety/depression/OCD
Increasing Appetite in Bulimia
Rats deprived of food 12 hours a day and have a very sweet sugar drink
Several weeks later: rats drinking level increased
