Week 7: Eating

Question 1

Hunger

Answer 1

Drive to consume food; aka appetite - motivating force

Question 2

Eating

Answer 2

Consumption of food - behavior

Question 3

Energy Metabolism

Answer 3

Process energy in food - metabolic

Question 4

Nutrients stored long-term

Answer 4

Glucose, carbs, proteins, fatty acids

Question 5

Role of glucose in the brain

Answer 5

Brain requires glucose to function. Brain takes 20% of all glucose consumed

Question 6

Basal/Resting Metabolic Rate (BMR/RMR)

Answer 6

Process of maintaining general function of the body. Uses 60-80% of the body’s energy

Question 7

Glucose storage

Answer 7

First: converted to glycogen and stored in the liver and muscles
After glycogen is full: converted to adipose/fat tissue

Question 8

Phases of Eating Behavior

Answer 8

Cephalic Phase
Absorptive phase
Fasting Phase

Question 9

Cephalic Phase

Answer 9

Relating to the head. Sensory input of food cues the autonomic nervous system. Involves vagus and cranial nerve

Question 10

Absorptive Phase

Answer 10

Break down food into nutrients to absorb into blood stream
Fills immediate energy needs, then stores extra
Increases insulin, decreases glucagon

Question 11

Fasting Phase

Answer 11

Any time you are not eating, using stored energy to meet demands
Over time insulin decreases and glucagon and ghrelin increase

Question 12

Glucostatic Theory

Answer 12

We eat to maintain glucose energy reserves

Question 13

Issues with Glucostatic Theory

Answer 13

Glucose rarely drops before meals
We eat beyond what is needed to maintain energy stores
Neuronal glucose levels don’t change (suggests no effects of blood glucose level)
Manipulating glucose levels does not affect hunger

Question 14

Lipostatic theory

Answer 14

Eating to maintain a constant body weight; suggests mechanisms exist to maintain body weight genetically or biologically

Question 15

Set point theory

Answer 15

OUTDATED
The body defends a certain weight; hard to deviate from a current weight
Relatively stable, set point will vary with time

Question 16

Issues with Lipostatic and Set Point theory

Answer 16

Relative stability isn’t explained; how can weight change over time
Not adaptive to stay at one weight, limits the energy store potential
We eat an insufficient amount to maintain weight

Question 17

Drive Reduction Theories

Answer 17

Theories that argue that behavior occurs to reduce a drive. Umbrella that covers glucostatic and lipostatic theories

Question 18

Rebound weight gain

Answer 18

Most weight that is lost is regained within 5 years

Question 19

Incentive value theory

Answer 19

Behavior occurs to gain a positive outcome
Explains cravings, does not explain behavior of consuming vitamins or minerals
Supported by preference for sweet, salty, and umami flavors and avoidance of bad flavors

Question 20

Reward circuit of food

Answer 20

Tongue -> Insula -> Amygdala -> Frontal Areas -> Striatum (reward and future behavior planning center)
Involves mesolimbic dopaminergic pathway (dopamine) - dopamine released when food is consumed, creating reward

Question 21

Critical parts of the Hypothalamus

Answer 21

Ventromedial (VHM)
Lateral (LH)
Paraventricular (PVH)
Arcuate (ARC)

Question 22

Ventromedial Hypothalamus (VMH) Function

Answer 22

Lesions increased eating and weight gain
Original theory: involved in fullness
New theory: involved in energy metabolism; controls fat storage

Question 23

Lateral Hypothalamus (LH) Function

Answer 23

Lesions increase weight loss, stimulation increases eating behavior
Intermediary sight that routes fibers important to eating

Question 24

PVH and ARC Nucleus function

Answer 24

Activation of POMC and AgRP Cells

Question 25

Pro-opiomelanocortin Cells (POMC)

Answer 25

Anorexigenic; involved in less hunger. Inhibits food intake, activated by leptin

Question 26

Agouti-related Peptide/Protein cells (AgRP)

Answer 26

Orexigenic; stimulate food intake Inhibited by insulin and leptin (during eating) Activated by Ghrelin (during fasting)

Question 27

Short-term satiety/fullness signals

Answer 27

CCK and GLP1 (Glucagon-like protein 1)

Question 28

Long-term satiety/fullness signals

Answer 28

Related to fat storage. Primarily insulin and Leptin

Question 29

Leptin

Answer 29

Secreted from fat stores. More fat -> more leptin -> less eating Affects neurons involved in metabolism and energy balance MORE POWERFUL than insulin

Question 30

Gene mutations affecting leptin

Answer 30

Associated with rapid weight gain and genetic obesity. Related to increase eating and less energy being spent/burned

Question 31

Leptin Resistance in Obesity

Answer 31

Increased fat over a long term can decrease effectiveness of leptin signaling More leptin, but it doesn't work

Question 32

Fullness cues from the stomach

Answer 32

More fullness leads to less hunger. Possibly the strongest cue for hunger

Question 33

Mouse study on stomach fullness

Answer 33

Method: surgically implanted second stomach and intestines into mouse. Stomach full of food and connected to bloodstream, but couldn't metabolize nutrients Findings: the more full the second stomach was, the less the mouse ate. Suggestions: Stomach fullness alone suppresses eating independent of nutrient fulfillment

Question 34

Settling Point Theory

Answer 34

Body defends a certain weight, but this point can change based on circumstance and the body will defend this new point

Question 35

Eating as a multisensory process

Answer 35

Disruption in sensory perception related to food can decreasing eating behavior. Likely due to both taste and smell passing through the orbitofrontal cortex Sensory processing areas involves leptin, insulin, and ghrelin

Question 36

Obesity

Answer 36

Affects 1 in 4 people; rate nearly tripled in past 40 years. Likely environmental component, but likely not a lack of exercise (activity doesn't burn as many calories as people think, and activity levels over time are relatively similar) Likely overabundance of food

Question 37

Obesity reward system

Answer 37

Those with obesity have decreased Dopamine receptor availability, decreased metabolism, and increased activity in food related brain areas. Suggests increase in the reward system as relating to food

Question 38

Drug treatments for obesity

Answer 38

Glucagon-like peptide 1, typically used in Ozempic. Targets GLP1 receptors. Might change reward circuit in general, suggested by side effects (change in food enjoyment, enjoyment of other activities, etc.)

Question 39

Anorexia nervosa

Answer 39

Most fatal eating disorder. Affects 1% of population, and 75-90% women. Defined as a refusal to eat to maintain weight or body image

Question 40

Traits associated with anorexia

Answer 40

Perfectionism, focus on appearance, body dysmorphia, brain development and hormonal factors (supported by age of onset)

Question 41

Risk factors associated with anorexia

Answer 41

Low reward of food, high anxiety of food, harm avoidance behaviors, high cognitive control lack of responses to food restriction

Question 42

Bulimia nervosa

Answer 42

Affects 1-3% of the population, majority women. Defined as repeated episodes of binge eating followed by purging to maintain body weight or image

Question 43

Myths of eating disorders (3)

Answer 43

1. Lifestyle choice - neuroanatomical and neurophysical components 2. Only affects high SES white women - can affect anybody 3. Just a phase - more extreme, often fatal, does not resolve independently

Question 44

Insulin

Answer 44

Decreases blood glucose level. Makes you feel full. Produced in the pancreas

Question 45

Glucagon

Answer 45

Increases blood glucose level. Produced in the pancreas. Opposes insulin. Facilitates energy storage

Question 46

Ghrelin

Answer 46

Makes you feel hungry. Produced in the stomach and hypothalamus