PSY290 - Eating

hunger

drive to consume food (motivational force)

eating

actual consumption of food (behavior)

energy metabolism

how we process the energy in food (metabolic)

glucose

simple carbohydrate/ sugar serving as the main source of energy for the human brain (20% of intake goes to the brain)

how is energy utilized?

• by basal/resting metabolic rate

• activity

• thermogenesis

short term energy storage

conversion of glucose to glycogen in liver and muscles

long term energy storage

glucose and fatty acids conversion to fat in adipose tissue

what are the 3 phases of eating behavior?

• cephalic

• absorptive

• fasting

cephalic phase

sight smell and expectation of food serving as cues to prepare the body for food consumption by activating the autonomic nervous sytem

what nerve is involved in the cephalic phase?

the cranial nerve x (vagus nerve)

absorptive phase

nutrients like glucose are absorbed into the bloodstream to meet immediate energy needs

what happens to excess nutrients

they are stored as glycogen, proteins and fats for later use

what are the useful fuels?

carbohydrates, fats and proteins

what happens when glucose in the blood plasma rises?

insulin levels rise and glucagon levels fall

insulin

lowers blood glucose converting glucose and fatty acids to glycogen and fat for storage

glucagon

increases blood glucose converting glycogen and fat to glucose and fatty acids for use in the body

fasting phase

energy is taken from stores to meet needs so insulin levels drop and glucagon levels rise

ghrelin

secreted by the stomach and increases hunger the longer fasting occurs

what are the issues regarding glucostatic theory?

• blood glucose levels rarely drop before eating

• you eat well beyond the point correcting blood glucose deficit

• blood glucose levels in the body change with eating but glucose levels for neurons dont

• increasing or decreasing levels doesnt really affect hunger

glucostatic theory

eating to maintain energy reserves at a constant level

set point theory

there is a set body weight your body is trying to defend/achieve, biological process will promote weight gain or loss if you are off your set point

what is associated with an increase in the perceived pleasure of food and the amount of work done to obtain food?

caloric restriction

what are the issues associate with set point theory?

• some people gain weight consistently through life

• maintained a set weight is not adaptive in evolution

• there are cases where insufficient eating is used to promote weight maintenance

drive reduction theories

glucostatic and lipostatic theory

what makes a drive reduction theory?

• deficits create motivational forces

• motivational forces encourage behaviors

• the behavior reduces the drive

positive incentive value

we eat because its pleasurable not just because we desperately need energy from food in the moment

• consumption activates the reward centers of the brain

how is reward center activation explained?

• we will gravitate towards sweet, fatty and salty food cause they taste good and avoid bitter food cause they seem harmful

taste

tongue

recognition of taste

insula

emotion

amygdala

cognitive value

frontal areas

reward and planning future behavior

striatum

what is the critical part of the reward system?

the mesolimbic system

the reward system

group of interconnected neural structures implicated in the attribution of reward to stimuli

• implicated in habit formation and impulse control disorders

what transmitter does reward center signaling involve?

Dopamine

what activates the release of dopamine?

expectation and taste of food

Hypothalamic nuclei

• ventromedial hypothalamus

• lateral hypothalamus

• paraventricular hypothalamus

• arcuate

ventromedial hypothalamus

though the be involved in terminating eating behavior but recent suggestions that it plays a role in energy metabolism and fat storage

lateral hypothalamus

stimulating it increases eating and its lesion leads to weight loss

anorexigenic neurons and hormones

POMC neurons and leptin

orexigenic neurons and hormones

AgRP, NPY,GABA and Ghrelin

neurons in the arcuate

AgRP and POMC

AgRP

agouti related protein that is an antagonist of melanocortin signaling and other compounds

orexigenic

stimulate food intake by activated ghrelin and inhibiting insulin and leptin

POMC neurons

express pro-opiomelanocortin and release a-melanocyte stimulation hormone which is the agonist of melanocortin signaling

anorexigenic

inhibit food intake by POMC neurons that are activated by leptin

long term satiety signaling

insulin and leptin

short term satiety signaling

CCK and GLP1

how do leptin levels affect food intake and weight

it reduces it

leptin

secreted from adipose tissue and circulates in proportion to adipose stores so the more fat there is the more leptin there is

• affects neurons involved in energy balance

nucleus of the solitary tract

part of the taste pathway

what happens when leptin stops working?

results in increased food intake and reduced energy expenditure

what is the effect of leptin resistance in obesity?

leptin levels are higher and signaling is less effective in obesity

what is the modern perspective on hunger?

settling point, set point can change on the basis of many changes in your life

what modulates food intake?

sensory stimuli in the cephalic stage and neural circuits involved in food intake

primary gustatory cortex

insula

secondary gustatory cortex

in the orbitofrontal cortex involved in olfaction

what is anosmia?

loss of sense of smell

• linked to weight loss

how many people are affected by obesity?

1 in 4 adult canadians

how is obesity acquired?

partly genetic but increased prevalence suggest involvement in environmental factors

• activity levels are not the problem and that cant be the only treatment

how is the reward system affected in obesity?

reduced DR2 availability, reduced glucose metabolism and increased activity in areas associated with food salience

anorexia

no appetite by nervousness, refusal to consume enough food to maintain weight (75-90% of the 1% of the population affected are women)

bulimia nervosa

recurrent episodes of binge eating followed by inappropriate behaviors like vomiting to reduce weight gain

• more common in women

eating disorder myths

• lifestyle choice that can be easily changed

• only affect young white women of high socioeconomic status

• phase that will resolve easily like dieting

traits associated with anorexia nervosa

• perfectionism

• negative emotion

• drive for thinness

• increased interoceptive awareness

• OCD

potential factors in anorexia nervosa

• reduce reward value of food and increased anxiety towards food

• lack of compensatory responses to food restriction

• harm avoidance

• increased cognitive control

• inability to accurately perceive body image

neural changes

• lowered activation in the insula and anteroventral striatum in response to sweetness

• altered D2/D3 receptor expression in the caudate

• neural systems associated with body image function differently

• treatment associated with increased gray matter