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PSY290: Behavioral Neuroscience > Week 7: Eating > Flashcards

Week 7: Eating Flashcards

Eating

1
Q

Hunger

A

Drive to consume food; aka appetite - motivating force

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2
Q

Eating

A

Consumption of food - behavior

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3
Q

Energy Metabolism

A

Process energy in food - metabolic

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4
Q

Nutrients stored long-term

A

Glucose, carbs, proteins, fatty acids

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5
Q

Role of glucose in the brain

A

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

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6
Q

Basal/Resting Metabolic Rate (BMR/RMR)

A

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

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7
Q

Glucose storage

A

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

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8
Q

Phases of Eating Behavior

A

Cephalic Phase
Absorptive phase
Fasting Phase

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9
Q

Cephalic Phase

A

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

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10
Q

Absorptive Phase

A

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

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11
Q

Fasting Phase

A

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

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12
Q

Glucostatic Theory

A

We eat to maintain glucose energy reserves

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13
Q

Issues with Glucostatic Theory

A

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

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14
Q

Lipostatic theory

A

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

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15
Q

Set point theory

A

OUTDATED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

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16
Q

Issues with Lipostatic and Set Point theory

A

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

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17
Q

Drive Reduction Theories

A

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

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18
Q

Rebound weight gain

A

Most weight that is lost is regained within 5 years

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19
Q

Incentive value theory

A

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

20
Q

Reward circuit of food

A

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

21
Q

Critical parts of the Hypothalamus

A

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

22
Q

Ventromedial Hypothalamus (VMH) Function

A

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

23
Q

Lateral Hypothalamus (LH) Function

A

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

24
Q

PVH and ARC Nucleus function

A

Activation of POMC and AgRP Cells

25
Q

Pro-opiomelanocortin Cells (POMC)

A

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

26
Q

Agouti-related Peptide/Protein cells (AgRP)

A

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

27
Q

Short-term satiety/fullness signals

A

CCK and GLP1 (Glucagon-like protein 1)

28
Q

Long-term satiety/fullness signals

A

Related to fat storage. Primarily insulin and Leptin

29
Q

Leptin

A

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

30
Q

Gene mutations affecting leptin

A

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

31
Q

Leptin Resistance in Obesity

A

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

32
Q

Fullness cues from the stomach

A

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

33
Q

Mouse study on stomach fullness

A

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

34
Q

Settling Point Theory

A

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

35
Q

Eating as a multisensory process

A

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

36
Q

Obesity

A

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

37
Q

Obesity reward system

A

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

38
Q

Drug treatments for obesity

A

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.)

39
Q

Anorexia nervosa

A

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

40
Q

Traits associated with anorexia

A

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

41
Q

Risk factors associated with anorexia

A

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

42
Q

Bulimia nervosa

A

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

43
Q

Myths of eating disorders (3)

A
  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
44
Q

Insulin

A

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

45
Q

Glucagon

A

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

46
Q

Ghrelin

A

Makes you feel hungry. Produced in the stomach and hypothalamus

PSY290: Behavioral Neuroscience (10 decks)

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