Hunger

14
Hunger

description

Hunger. Do Now. Identify correlations between hunger and other ideas/feelings/motivations. Hypothalamus. Hypothalamus. Hunger Drive. Two areas of the hypothalamus, the lateral and ventromedial areas, play a central role in the hunger drive. Hypothalamus. Hypothalamus. Lateral Area. - PowerPoint PPT Presentation

Transcript of Hunger

Page 1: Hunger

Hunger

Page 2: Hunger

Do Now

• Identify correlations between hunger and other ideas/feelings/motivations

Page 3: Hunger

Hunger Drive

• Two areas of the hypothalamus, the lateral and ventromedial areas, play a central role in the hunger drive

Hypothalamus

Hypothalamus

Page 4: Hunger

Lateral Area• Electrical lesions to tract of

axons connecting brainstem, hypothalamus and basal ganglia cause a loss of all goal-directed behavior

• Stimulation causes drives in response to available incentives

• However, chemical lesions to specific cell bodies reduce hunger drive, but do not abolish it - most other drives appear normal– What does this suggest?

Hypothalamus

Hypothalamus

Page 5: Hunger

Ventromedial Area• Lesions alter digestive

and metabolic processes

• Food is converted into fat rather than energy molecules, causing animal to eat much more than normal and gain weight

Hypothalamus

Hypothalamus

Page 6: Hunger

Hunger Drive• Other stimuli that act on the brain to increase or decrease hunger include– satiety signals from the

stomach– signals indicating the

amount of food molecules in the blood

– leptin, a hormone indicating the amount of fat in the body

– the appetizer effect

Page 7: Hunger

Homeostasis

• Homeostatis and negative feedback governs hunger– Homeostasis: maintaining state: Thermostat– Need sufficient calories

• Activation based on anticipation• Why hungry?

– Nutrients: basic components of structural integrity (proteins and amino acids stored)– Calories: energy for metabolic processes (glucose, glycogen and fat)

Page 8: Hunger

Hungry Hungry Hormones• Hormone systems work as feedback loop to turn on/off food

seeking or digesting behavior• Insulin: Motivate to seek food when low

– Glucose in system leads to insulin release and tells body to stop seeking food

– High: about to eat or eating– Cues (sight/smell) elevate glucose– Converts glucose to glycogen for storage

• Leptin: released by fat when enough NRG is present (safety valve)

– Injection: eat less• Mutated mice receive no negative feedback =

overweight– Increasing leptin does not solve obesity as it decreases

hunger only up to a certain level• PYY: released form intestines when food is present

– Systematic injection: stop eating• Lower presence of PYY in blood for obese people than

thin. Thin people show a significant increase in PYY after eating compared to obese people.

• Neuropeptide Y: digestive behavior– Produced by hypothalamus– Leptin suppress NPY

Page 9: Hunger

Research on Weight Regulation and Dieting

• No consistent personality trait differences found between obese and non-obese people (e.g., willpower, anxiety)

• Dieters and obese are more likely to eat in response to stress than non-dieters

• Family environment of little importance in determining body weight - genetics plays a large role

• Number of fat-storage cells is a major determinant of body weight

• Settling point (set point) - cluster of genetic and environmental factors cause a person’s weight to settle within a given range

Page 10: Hunger

Research on Weight Regulation and Dieting

• Fat cells are determined by genetics and food intake• They increase with weight gain, but merely shrink with

weight loss - may stimulate hunger • Weight loss causes a decline in basal metabolism

Fat cells

Normal

diet

High-fat

diet

Return to

normal diet

Page 11: Hunger

Peripheral Cues for Eating (and Stopping)

- Full vs. empty stomach- Nutrient level of stomach contents- Glucose levels- Sensory-specific satiety

- Can feel satiated on one type of food but then there is renewed interest in a different type of food

- All of these factors cause signals in specific area of brain (Stellar’s Dual-Center Hypothesis):

• Lateral Hypothalamus (LH) - Hunger Center (“on switch”) • Ventromedial Hypothalamus (VMH) -Satiety Center (“off

switch”)

Page 12: Hunger

Nisbett (1968) - External hypothesis• Subjects arrive hungry

• IV-weight of subject (overweight vs. normal)• IV-quantity of visible food (1 vs. 3 sandwiches)

• Task: Fill out questionnaires• DV-number of sandwiches consumed

• Hypothesis: If overweight people more sensitive to external cues, sight of more food should lead obese to eat more, whereas normal weight people will eat same amount regardless of how much in sight

Page 13: Hunger

ResultsInteraction Effect

– Quantity of visible food had no effect on the eating behavior of normal weight subjects but for overweight it did. Overweight subjects ate more when more food was visible

11.21.41.61.8

22.22.42.62.8

3

1 sand 3 sand

Sandwiches eaten

ObeseNormal

Page 14: Hunger

Psychology and Dieting

• Rapid loss of weight means rapid return• Shifting to eating healthier food is more effective

than eating less• Apply sensory-specific satiety to each a variety of

different healthy foods• Eat meals slowly as it takes 15 minutes for Leptin

and PYY to start reaching the brain• Find activities for exercise that you are internally

motivated to perform