PSY290 - Lecture 7: Eating

hunger

hunger

the drive to consume food (thought or motivational force)

eating

the actual consumption of food (behavior)

energy metabolism

how we process the energy in the food (metabolic)

eating basic info

• food is a source of energy and we need energy to survive

• certain organs including the brain have especially high energy demands

• glucose is the main source of energy for the human brain

• the brain is only about ~2% of your body mass, but uses ~20% of your overall glucose intake

  • energy hog!

• sometimes eat more than necessary to store energy for the future

energy intake and utilization

• basal/resting metabolic rate (BMR/RMR)

  • high energy intake

• activity (exercise)

• thermogenesis (due to meals + other causes)

• we spend energy even if we are not doing anything

  • maintenance fee

energy storage over time

• most of us consume more energy than we need + end up storing it for the future

  • food scarcity in our past

• glucose is converted into glycogen in liver + muscles

  • only a certain amount stored at a time

• glucose + fatty acids converted to fat in adipose

  • no such limit

  • almost all excess energy will end up stored as fat

three phases of eating behavior

1. cephalic

2. absorptive

3. fasting

fasting basic definition

any period you are not eating

cephalic basic definition

immediately before and during the phase of eating

absorptive basic definition

digesting and absorbing the nutrients from the food

cephalic phase

• cephalic = “relating to the head”

• begins with sight, smell or expectation of food (cues)

  • the activation of a food related memory can trigger this phase

• prepares the body for food consumption by activating the autonomic nervous system

• involvement of Cranial Nerve X (vagus nerve)

cues for eating behavior

• many cues

• strong reaction to food cues predicts weight gain or disordered eating

• if you eat at the same time everyday, and it gets around that time you might start feeling hungry

absorptive phase

• nutrients are absorbed into blood stream

• absorbed nutrients are first consumed to meet immediate energy needs

• excess nutrients are stored as glycogen, proteins and fats for later use

  • short-term storage: glucose > glycogen in the liver

  • long-term storage: glucose + fatty acid > fats in the adipose tissue under the skin

• foods broken down into their useful fuels: carbs, fats, proteins

• as glucose in the blood plasma rises, there will changes in the levels of pancreatic hormones

  • insulin levels rise (affected in diabetes)

  • glucagon levels fall

  • hormones will spike after eating

  • after prolonged fasting periods, these processes flip

insulin

• glucose uptake from blood

• conversion of glucose + fatty acids to stored energy (glycogen + fat)

• lowers blood glucose

glucagon

• conversion of stored energy (glycogen + fat) to glucose + fatty acids

• increases blood glucose

fasting phase

• energy is taken from stores to meet needs

• insulin levels drop, Glucagon levels rise

• with prolonged fasting, the hormone gherlin is secreted by the stomach and increases hunger

• this fasting phase ends when the next meal begins

glucose

• an important energy source

• consuming foods with glucose causes changes in hormonal signalling

glucostatic theory

do we eat to maintain or energy reserves at a constant level (eg glucose in the blood)? no this theory is wrong

glucostatic theory problems

1. blood glucose levels rarely drop before eating

   1. if you measured levels of glucose and your times of eating there is rarely a relationship

2. you’ll eat well beyond the point where you correct a “blood glucose deficit”

3. through blood glucose levels in the body change w/eating, glucose levels for neurons do not

4. when we experimentally increase or decrease glucose levels, hunger is not significantly affected

set point (lipostatic) theory

• in most people, bodyweight changes slowly (if at all)

• bodyweight has a high heritability value (h² ~ 0.8) as does obesity (h² ~ 0.4-0.7)

  • many genes related to obesity are found in the nervous system (even though fat is stored elsewhere)

• what forces explain the tendency for bodyweight to resist change?

• do we perhaps eat to maintain our energy stores?

set point theory explanation

• the body ‘defends’ a certain weight

• many explanations

  • most likely involves changes in hunger (increases w/weight loss) and energy metabolism (decreases w/weight loss)

• difficult to have long term weight change

rebound weight gain

• caloric restriction (w/ dieting) in associated with an increase in the perceived pleasure of food and the amount of work done to obtain food

• most weight lost is regained within 5 years (> 80%)

set point theory problems

• some people (+ animals) gain weight consistently throughout their adult life

  • why would this happen if there was a drive to keep fat storage at a constant level?

• from an evolutionary perspective, maintaining a set bodyweight does not seem adaptive

  • why would we have a low limit on energy stores when food security is not guaranteed?

• there are many cases where there is insufficient eating to maintain weight

drive reduction theories

• homeostatic theory

• glucostatic and lipostatic theory

• in both theories, it is proposed:

  • deficits create motivational forces

  • motivational forces encourage behaviors (ie eating)

  • the behavior reduces the drive (once you eat, youll stop)

positive incentive value

• we eat because it is fun to eat (food is like a reward) not just because we desperately need energy from food at the current moment

• eating is joyful because we want to prevent forgetting to eat

• eating is guided by cravings, not just energy deficits

• consumption of nutrients activates the reward centres of the brain (eating is pleasurable)

  • strong innate preference for sweet, fatty, and salty foods

  • avoidance of bitter food (toxicity???)

  • problem: no mineral tastes/cravings

food as a reward

• tongue (taste)

• insula (recognition of taste)

• amygdala (emotion)

• frontal areas (cognitive value)

• striatum (reward and planning future behavior)

the reward system

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

  • signalling centrally involves the transmitter dopamine (DA)

• a critical part is the mesolimbic pathway

• pathway is implicated in the habit formation and impulse control disorders

wanting food

expectation + taste of food activates dopamine release in multiple reward-associated areas

neural mechanisms

• hypothalamus is critically important

• 4 hypothalamic nuclei will be discussed here:

  • ventromedial (VMH)

  • lateral (LH)

  • paraventricular (PVH)

  • arcuate (ARC)

• each may play a role in hunger and energy metabolism

role of the hypothalamus

• cells within hypothalamus will respond to hormones

• hormonal changes will effect hypothalamic cells

• partially the reason why there’s changes

ventromedial hypothalamus (VMH)

• lesion produces profound obesity

• originally, it was thought that the VMH played a role in terminating eating behavior

• newer data suggests that the VMH plays instead a role in energy metabolism (how energy is stored as fat)

• rat experiment

  • lesion in the VMH

  • increase in eating and weight gain

  • ate until it passed out, when it woke up it ate again

  • not just willpower, there is a biological factor

lateral hypothalamus (LH)

• with lesion to the LH, there is often weight loss

• maybe lesion will effect the feeling of hunger (not this simple but apart of the reason)

stimulating the LH

• with stimulation of the LH, we see increased eating

• light turns on, mouse eats

• light turns off, mouse stops eating

PVH and the arcuate nucleus

• paraventricular hypothalamic nucleus

• contrasting roles in energy intake + metabolism

AgRP neurons in the ARC

• these cells express agouti-related protein (an antagonist of melanocortin signalling) and other compounds

• stimulate food intake (orexigenic)

• respond to many signals

  • inhibited by both insulin and leptin

  • activated by ghrelin

• insulin increasing after you eat

anorexigenic

less eating (anorexia)

POMC neurons in the ARC

• express pro-opiomelanocortin (POMC) and release alpha-melanocyte stimulating hormone (alpha-MSH, agonist of melanocortin signalling)

• many POMC neurons inhibit food intake (anorexigenic)

• POMC neurons are activated by leptin

satiety signalling

• combination of short-term and long-term signals

• long-term (related to adiposity)

  • insulin

  • leptin

• short-term (related to satiety) from the gut

  • CCK

  • GLP1

satiety

sensation of fullness, associated with decrease levels of motivation to eat

leptin

• secreted from adipose + circulates in proportion to adipose stores

  • more fat, more leptin

  • less fat, less leptin

• affects neurons involved in energy balance

• leptin levels affect food intake and weight

  • leptin in the brain reduces food intake + weight

  • impaired leptin signalling increases food intake + weight

• on food intake, effects of leptin > effects of insulin

targets of leptin (rodent brain)

areas important for us today are the arcuate nucleus, ventromedial hypothalamus, lateral hypothalamus, and nucleus of the solitary tract

leptin gene mutations

• leptin gene mutations (in mice and humans) result in increased food intake and reduced energy expenditure

• variations can occur in human genes too

• result in strong motivation to eat

leptin resistance in obesity

• in obesity, leptin levels are higher (more white adipose tissue in obesity, white adipose tissue makes leptin)

• it is also suggested that leptin signalling is less effective in obesity (ie there is leptin resistance)

• changes in body weight over a period of time

satiety peptides from the stomach

• transplanted a 2nd stomach and intestine into a rat

• stomach 2 was joined to the rat’s blood vessels

• stomach 2 filled w/foods

• stomach 2 cannot absorb energy from this food (this occurs in intestine)

• as volume/density of food in stomach 2 increased, eating reduced

• reduced eating cannot be explained by the energy from the food in stomach 2

  • fullness of the stomach has physiological signals of their own that affect eating

• instead, reduced eating could be due to satiety signals from stomach 2 reaching the blood

modern perspective: settling point

• the point it defends can change

• move to a new body weight, and defend that weight

• by virtue of biological or environmental changes

food is a multi sensory experience

• sight, sound, smell and touch all influence our tendency to approach food (ie in the cephalic phase)

• sensory stimuli may modulate food intake and be modulated by the neural circuits controlling food intake

taste pathway

taste cells > bipolar neurons > cranial nerve (7, 9, 10) > brainstem structures > VPM thalamus > primary gustatory cortex (insula)

olfaction, food intake + weight

• role of olfaction (smell) in taste likely

• anosmia is linked w/ weight loss

  • parkinsons disease

• damage to ares involved in olfaction, such as the OFC, may have similar effects

  • patients with OFC lesions are ‘invariably slim’

anosmia

loss of sense of smell

regulating the sensory system

note how the chemical signals that regulate food intake (ghrelin, insulin and leptin) also regulate areas involved in sensory processing

obesity epidemic

• obesity is epidemic in developed countries

• affects 1 in 4 adult canadians

• though obesity is partly genetic increasing prevalence suggests environment matters

• relates to food availability

global obesity

1975 levels would be much lower, we have an abundance of food

activity levels not likely the problem

leisure-time activity levels have increased or stayed stable, more associated w/food and its availability rather than exercise

exercise alone does not work

• energy used by exercise is realtively low

• compensatory increase in eating is observed with exercise, as with dieting

• “you cannot outrun a bad diet”

• exercise is useful, but cannot be the sole treatment

reward system in obesity

• reduced dopamine receptor type 2 availability

• reduced glucose metabolism and increased activity in areas associated w/food salience

• food is a very different reward, food can be like an addiction

eating disorders

• anorexia nervosa (~ 1% of the population)

  • no appetite by nervousness

  • refusal to consume enough food to maintain weight

  • 75 - 90% affected are women

• bulimia nervosa (1-3% of the population)

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

  • also more common in women

• binge eating disorder

eating disorder myths

• MYTH: they are a ‘lifestyle choice’ that can be easily changed

  • TRUTH: eating disorders have neuroanatomical + neurophysiological correlates and are linked to genetic factors

• MYTH: they only affect young white women of high socioeconomic status (a ‘disease of affluency’

  • TRUTH: everyone can be affected including men, minorities and those of low socioeconomic status

• MYTH: they are a phase that will resolve easily, like dieting

  • TRUTH: eating disorders are more extreme than dieting and do not resolve independently, they can be fatal, they are among the most dangerous psychiatric disorders

  • not a choice, this is a disorder

traits associated with anorexia nervosa

• more common after a certain age

• societal changes affects this

• usually emerges AFTER puberty

• intervention is important

potential factors in anorexia nervosa

• reduced reward value of food and increased anxiety towards food

• lack of compensatory responses to food restriction

• harm avoidance (sensitivity to punishment, inflexible)

• increased cognitive control

• inability to accurately perceive and/or update body image

neural changes in anorexia nervosa

• in response to sweet tastes, there is lowered activation of the insula and anteroventral striatum

  • less taste reward?

• altered D2/D3 receptor expression in the caudate

  • correlated with harm avoidance

• neural systems responsible for representing body image may function differently

• treatment is associated with increased gray matter

  • most people do get better and some changes do reverse after treatment