Psyc*3410- Intro to Hunger and Satiety

feeding behaviour

involves a range of behaviours, not just ingestion

Feeding compromises two sets of components

Appetite components

- seeking out food

- cost-benefit analysis

- choosing an appropriate diet

Consummatory Components

- behaviours involved in the consumption of food

Seeking out food (foraging)

- detection and identification of food

- approaching food

-latency to eat

- handling

Cost-benefit analysis

- dangers, predators, competitors

- trade-off with other behaviours

- hedonic value

- prior history/ experience

- suitability of food for consumption

Choosing an appropriate diet

- the type of food meets nutritional needs

- macro/micro nutrients

Why do we eat?

We eat to supply our body with energy for survival

Digestion: food > constituent elements > absorption

3 Sources of energy

1. Lipids from fats

2. Glucose from carbs

3. Amino acids from protiens

3 Forms of energy storage

1. Body fat

- most of the body's energy stores, very efficient

2. Glycogen

- the most utilized; in the liver/muscles

3. Muscle protein

- less utilized as energy store

Phases of energy metabolism

1. Cephalic phase

2. Absorptive phase

3. Fasting phase

All the phases of metabolism are under the control of two pancreatic hormones released from the islets of Langerhans:

1. insulin (beta-cells)

2. glucagon (alpha-cell)

Insulin

cephalic and absorptive phases

1. promotes glucose use (cell uptake)

2. Energy conversions (to forms that can be stored)

- Lipids to fats

- glucose to glycogen, fats

- amino acids to proteins

3. promotes storage (glycogen, fat, proteins)

Theories of hunger and eating

1. set- point theory

2. positive incentive perspective

3 components of set point theories

1. set point mechanisms

2. detector mechanisms

3. effector mechanisms

2 main set point theories

1. Glucostatic theory: short term regulation of eating

2. Lipostatic theory: long-term regulation of eating

Set point theories

Negative feedback system

maintains homeostasis (a stable internal environment)

Weaknesses of Set-point theories

1. Evolutionary pressures not considered

- food supply traditionally not constant or predictable

- need to prevent energy deficits (e.g. energy storage), not respond to them

2. Major predictions not confirmed

- feeding not very sensitive to body fat or caloric status

- blood glucose drops as preparation (anticipation) of feeding and returns whether meal taken or not

> people with high body fat do not eat less than thin people

> high calorie drink before meal does not reduce consumption

> BUT, the idea that premeal drink is high in calories does reduce eating...

3. Do no incorporate taste, learning, social factors or reward mechanisms

Positive Incentive Perspective

No internal energy deficits

The anticipated pleasure of eating

Positive-incentive (hedonic) value: the anticipated pleasure of a behaviour (e.g. eating, sex...)

Examples of multiple factors that affect the positive incentive value of food

- intrinsic (e.g. flavour)

- previous experience (e.g. learning)

- social context

- time since last meal

- blood glucose

Set-point theories vs. positive incentive perspective

the two theories interact:

Physiological motivators can override behavioural motivators

- eg not being able to finish something because youre so full

Behavioural motivators can override physiological motivators

- eg snacks in front of the TV after dinner

-eg eating in a group

Factors Influencing Eating

What: diet selection, preferences, and aversions

1. innate

2. learned

When: what initiates a meal

1. Pre-meal hunger

2. Environmental cues

3. Physiological cues

How much: what ends a meal

1. Previous experience/act of eating

2. Psychological/behavioural factors

3. Sensory-specific satiety

4. Satiety signals

Innate factors influencing what we eat

Species-specific preferences and aversions: sweet, fat, salty, bitter, sour

Humans:

Sweet/fat foods = high energy

Salty foods = high sodium

Bitter foods = can be toxic

Sour foods = can have gone bad

Learned factors influencing What we eat

1. individual learning: conditional preferences and aversions

- based on post-ingestion consequences of eating

2. social learning: eat what others eat

- In utero, during lactation can determine preferences at weaning, in adults

- rats and mice prefer food they've smelled on others' breath

- human similar--> often culturally defined

What to eat: innate vs. learned factors

Sodium: distinctive flavour (salty); seeking when deficient mostly innate

Vitamins and other minerals:

- No distinctive flavour-> seeking foods containing these substances depends on learning

- Associative learning about flavours paired with the post-ingestive consequences of foods

- Example: rats fed a thiamine (B1)- deficient diet

1. get sick

2. develop an aversion for the low-thiamine diet

3. learn to prefer a diet that makes them recover from the deficiency

Where do we go wrong? Why are there so many people who do not eat a correct diet?

1. Variety of food is too complex -> hard to make associations

2. Food industry exploits innate preferences

- often, food low in nutrients is made to taste good (salt, fat, sugar)

3. Diet culture and emphasis of weight over nutrition

When do most mammals eat?

Most mammals eat small meals each day if they have ready access to a continuous supply of food. However...

In labs rats eat many small meals but also show peaks of high feeding per day

Humans tend to eat a few bigger meals per day

Those who do have regular meals experience premeal hunger

Woods Premeal hunger theory

Not necessarily caused by a pre-meal energy deficit -> a conditioned response

Woods' theory: meal as stressor; disrupts homeostasis

- premeal hunger= stress coping (conditioned compensatory response)

- begins in the cephalic phase of eating

> Insulin release

> Increased glucose consumption

> homeostasis is imbalanced

What Factors influence when we eat

Environmental

- sensory stimuli from food (sight smell)

- food-related stimuli (conditioned)

- time of day

- others' behaviour- social

Physiological

- glucoprovic hunger

- lipoprivic hunger

- biological clock

Physiological Hunger Signals + the detectors

Hunger stimulated by:

- hypoglycemia > glucoprivation > glucoprivic hunger

- low lipids/ fatty acids > lipoprivation > lipoprivic hunger

Two sets of detectors:

1. Brain > glucoprivation sensitive

- brainstem: maybe area postrema or nucleus of the solitary tract

2. liver > glucoprivation and lipoprivation sensitive

- vagus nerve

Factors influencing how much we eat

Satiety: the motivational state that makes us stop eating when food is still available

Satiety signals

- the act of eating?

- previous experiences with the food (learning)

- short term -> stop a meal: gastrointestinal tract -> brain

- long term -> body weight: adipose tissue -> brain

Factors Influencing How Much We Eat: Glucose

Is it all about blood glucose levels?

Evidence does not support the glucostatic interpretation: premeal decline in blood glucose does not cause hunger

Evidence suggests that the intention to start eating triggers a decline in blood glucose

- blood glucose levels decline suddenly before eating

- eliminating blood glucose decline does not stop eating

- if a meal is not serves, blood glucose levels will rise again

- blood glucose levels in the brain remain relatively constant

Long vs short-term Satiety Signals

Short-term Satiety Signals

1. Head factors (eating and learning)

2. Gastric factors

3. Duodenum factors

4. Intestinal factors

5. Liver factors

Long term Satiety Signals

- Adipose tissue

Head factors

Eyes, nose, tongue, throat

most learned through previous experience and/or the act of eating

- sham feeding studies

Psychological/Behavioural Factors for how much we eat

Serving size: the bigger the portion, the more we eat

Appetizer effect: eating a tasty appetizer increases hunger, rather than decreasing it

Social influences: laboratory rats substantially more when feeding in a group (social facilitation)

Sensory-specific satiety (Type of rat food experiment)

Cafeteria diet vs. rodent chow in a rat study: rates ate up to 84% more when offered a cafeteria diet vs. normal rodent chow

Sensory-specific satiety

- taste signals form a food reduce its own incentive value much more than that of other foods/tastes

- postingestive consequences of eating reduce the incentive value of all tastes eventually

Sensory-specific satiety has evolutionary adaptive value

-varied diet

- eat more in times of abundance

Cannon and Washburn

1. Washburn swallowed a balloon and a thin tube connected to a water filled glass U-tube

2. Cannon pumped air into the balloon

3. Washburn's stomach contractions produced an increase in water level in the U-tube

4. Washburn reported a pang of hunger each time a large stomach contraction was recorded

- hunger is the feeling of contractions caused by an empty stomach

Short Term Satiety Signals: Gastric Factors

Volume:

-cannon and washburn

Nutritive density of food

- rats with a pyloric cuff: nutritive content matters more than volume

- rats with an additional stomach: induction of satiety is a blood factor (signals sent to blood)

Short Term Satiety Signals: Nutritive Density of Food

Rats with pyloric cuff

- prevents stomach emptying

- rats that receive an additional infusion of saline still eat the same (not fooled by the low nutritive volume)

- nutritive content matters more than volume

Rats with transplanted stomach

- filling of the additional stomach (with no innervations and no nutrient absorption) still induces satiety

- a blood factor

Short Term Satiety Signals: Ghrelin

Gastric factor: Ghrelin

1. A feeding enhancing hormone

2. Also affects metabolism, growth hormones, etc.

3. Produced and released by the stomach (small amounts also by the small intestine, pancreas and brain)

4. Blood levels rise just before eating and decline after a meal

Short Term Satiety Signals: Intestinal & duodenal Factors

Duodenal factors

- cholecystokinin (CCK)

Intestinal factos

- peptide YY (PYY)

> interrupts a meal

> released in proportion to calories

- neurotransmitters (serotonin)

Cholecystokinin (CCK) from the Duodenum

- synthesiezed by endocrine cells in the duodenum

- gallbladder contraction

- pancreatic enzyme secretion

- pancreatic hormone secretion (insulin, glucagon)

- inhibits stomach emptying

- signals to the brain

Actions in the brain through two receptors (CCK-A and CCK-B)

- decreases food intake and induces food aversions

- endogenous satiety signal? Part of leaned satiety response?

Short Term Satiety Signals: Neurotransmitters

Serotonin plays a role in satiety

5-HT administered to rodents

- reduced food attraction

- reduced amount of food consumed at meals

- stopped preferring fatty foods as much

In humans

- similar effects in human experiments

- ADHD medication reduce eating

Short Term Satiety Signals: Liver Factors

Liver factors

- post-absorption signals via vagus nerve

Studies with portal vein infusions

- Infustion of glucose or fructose -> reduced feeding

-Fructose is metabolized mostly in the liver -> the liver causes the reduction in feeding

Long Term Satiety Signals: Adipose Tissue

Long term signals -> body weight regulation

- e.g. studies with force-fed rats

Factors released by body fat (adipose tissue) -> Leptin

Hunger and Satiety: Summary

Initiation of eating

1. Liver and vagus nerve: glucoprivic and lipoprivic hunger

2. Brain: glucodetectors

3. Stomach: ghrelin

Inhibition of eating

4. Stomach volume

5. Duodenum: CCK (cholecystokinin)

6. Intestine: PYY (peptide YY)

7. Adipose tissue: leptin