Week 7: Eating Flashcards
Eating
Hunger
Drive to consume food; aka appetite - motivating force
Eating
Consumption of food - behavior
Energy Metabolism
Process energy in food - metabolic
Nutrients stored long-term
Glucose, carbs, proteins, fatty acids
Role of glucose in the brain
Brain requires glucose to function. Brain takes 20% of all glucose consumed
Basal/Resting Metabolic Rate (BMR/RMR)
Process of maintaining general function of the body. Uses 60-80% of the body’s energy
Glucose storage
First: converted to glycogen and stored in the liver and muscles
After glycogen is full: converted to adipose/fat tissue
Phases of Eating Behavior
Cephalic Phase
Absorptive phase
Fasting Phase
Cephalic Phase
Relating to the head. Sensory input of food cues the autonomic nervous system. Involves vagus and cranial nerve
Absorptive Phase
Break down food into nutrients to absorb into blood stream
Fills immediate energy needs, then stores extra
Increases insulin, decreases glucagon
Fasting Phase
Any time you are not eating, using stored energy to meet demands
Over time insulin decreases and glucagon and ghrelin increase
Glucostatic Theory
We eat to maintain glucose energy reserves
Issues with Glucostatic Theory
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
Lipostatic theory
Eating to maintain a constant body weight; suggests mechanisms exist to maintain body weight genetically or biologically
Set point theory
OUTDATED
The body defends a certain weight; hard to deviate from a current weight
Relatively stable, set point will vary with time
Issues with Lipostatic and Set Point theory
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
Drive Reduction Theories
Theories that argue that behavior occurs to reduce a drive. Umbrella that covers glucostatic and lipostatic theories
Rebound weight gain
Most weight that is lost is regained within 5 years
Incentive value theory
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
Reward circuit of food
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
Critical parts of the Hypothalamus
Ventromedial (VHM)
Lateral (LH)
Paraventricular (PVH)
Arcuate (ARC)
Ventromedial Hypothalamus (VMH) Function
Lesions increased eating and weight gain
Original theory: involved in fullness
New theory: involved in energy metabolism; controls fat storage
Lateral Hypothalamus (LH) Function
Lesions increase weight loss, stimulation increases eating behavior
Intermediary sight that routes fibers important to eating
PVH and ARC Nucleus function
Activation of POMC and AgRP Cells
Pro-opiomelanocortin Cells (POMC)
Anorexigenic; involved in less hunger. Inhibits food intake, activated by leptin
Agouti-related Peptide/Protein cells (AgRP)
Orexigenic; stimulate food intake
Inhibited by insulin and leptin (during eating)
Activated by Ghrelin (during fasting)
Short-term satiety/fullness signals
CCK and GLP1 (Glucagon-like protein 1)
Long-term satiety/fullness signals
Related to fat storage. Primarily insulin and Leptin
Leptin
Secreted from fat stores. More fat -> more leptin -> less eating
Affects neurons involved in metabolism and energy balance
MORE POWERFUL than insulin
Gene mutations affecting leptin
Associated with rapid weight gain and genetic obesity. Related to increase eating and less energy being spent/burned
Leptin Resistance in Obesity
Increased fat over a long term can decrease effectiveness of leptin signaling
More leptin, but it doesn’t work
Fullness cues from the stomach
More fullness leads to less hunger. Possibly the strongest cue for hunger
Mouse study on stomach fullness
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
Settling Point Theory
Body defends a certain weight, but this point can change based on circumstance and the body will defend this new point
Eating as a multisensory process
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
Obesity
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
Obesity reward system
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
Drug treatments for obesity
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.)
Anorexia nervosa
Most fatal eating disorder. Affects 1% of population, and 75-90% women. Defined as a refusal to eat to maintain weight or body image
Traits associated with anorexia
Perfectionism, focus on appearance, body dysmorphia, brain development and hormonal factors (supported by age of onset)
Risk factors associated with anorexia
Low reward of food, high anxiety of food, harm avoidance behaviors, high cognitive control lack of responses to food restriction
Bulimia nervosa
Affects 1-3% of the population, majority women. Defined as repeated episodes of binge eating followed by purging to maintain body weight or image
Myths of eating disorders (3)
- Lifestyle choice - neuroanatomical and neurophysical components
- Only affects high SES white women - can affect anybody
- Just a phase - more extreme, often fatal, does not resolve independently
Insulin
Decreases blood glucose level. Makes you feel full. Produced in the pancreas
Glucagon
Increases blood glucose level. Produced in the pancreas. Opposes insulin. Facilitates energy storage
Ghrelin
Makes you feel hungry. Produced in the stomach and hypothalamus
