PSYC3410* - Chapter 12 : Hunger, Eating, Health

Appetitive Components

• Seeking out food

• Cost-benefit analysis

• Choosing an appropriate diet

Consummatory Components

• Behaviours involved in the consumption of food

3 sources of energy

Lipids from fats

Glucose from carbohydrates

Amino acids from proteins

Phases of energy metabolism

1. Cephalic Phase

   • first stage of digestion, increased salivation, hormone release etc.

2. Absorptive Phase

   • occurs after a meal when your body is digesting the food and absorbing the nutrients

3. Fasting Phase

Pancreatic Hormones

Insulin and Glucagon

Insulin

cephalic and absorptive phase

1. Promotes glucose use (cell uptake)

2. Energy conversions (to forms that can be stored)
   Lipids → fats
   Glucose → glycogen, fats
   Amino acids → proteins

3. Promotes storage (glycogen, fat,
   proteins)

Glucagon

Fasting Phase

1. Adipose tissue → free fatty acids (= body’s main fuel during fasting phase)
2. Fatty acids → ketones (used by muscles and brain)

Two theories of hunger and eating

• Set point theories

• Positive incentive perspectives

Set point theories

Glucostatic theory: the theory that blood glucose levels control hunger and food intake

Lipostatic theory: the theory that the body regulates fat stores by controlling hunger and metabolism to maintain a stable weight.

Weaknesses of set-point theories

• Evolutionary pressures not considered

• Fails to explain rising obesity rates

• Fails to explain diet induced changes

Positive incentive perspective

A theory that suggets that we eat not just because we need energy but because eating is enjoyable and rewarding. This theory explains why people sometimes overeat or choose tasty foods over nutritious ones.

Individual learning associated with eating

Conditioned preferences and aversions based on post-ingestion consequences

Social learning associated with eating

Eat what others eat, culturally differs in humans

Three reasons that it is hard to maintain a healthy diet?

1. Complex variety → leads to difficulty determining what is healthy

2. Food industry exploitation - unhealthy foods are made to taste good

3. Diet culture - emphasis on weight instead over nutrition

Factors influencing when we eat

Pre-meal hunger, environmental (sensory stimuli, social), physiological (biological clock, low glucose/fat levels)

Pre-meal hunger

A Conditioned response – Our body expects food at certain times, so it triggers hunger even if we don’t need energy.

Begins in cephalic phase

Satiety

The motivational state that makes us stop eating when
food is still available

Short-term satiety signals (factors)

Head, Gastric, Duodenum, Intestinal, Liver factors

Long-term satiety signals

Adipose tissue

Head factors

Taste, smell, and chewing help signal when to stop eating (learning-based)

Ghrelin

Hunger hormone – Increases appetite and encourages eating, also affects metabolism and growth hormones. Mostly produced by the stomach, levels rise before meals and drop after eating

Duodenal factors

The first part of the small intestine releases hormones, like CCK, to slow eating.

Cholecystokinin (CCK)

Communicates with the brain to reduce hunger and stop eating, helps you feel full

Serotonin’s role in satiety (rat experiment)

• reduced food attraction

• reduced amount of food consumed at meals

• stopped preferring fatty foods as much

Liver factors

The liver detects absorbed nutrients and signals the brain to reduce hunger

Adipose Tissue

Regulates body weight over time, not just meal-to-meal hunger, by releasing leptin, a hormone that tells the brain there’s enough stored energy, reducing hunger.

Vagus Nerve

Works with liver to trigger hunger when the body has low glucose or fat levels

Hyperphagia

Excessive eating, constantly feeling hungry

Ventromedial hypothalamus lesions (VMH syndrome)

Symptoms include:

Excessive eating or constantly feeling hungry.

The animal or person will choose tasty foods over less enjoyable ones.

Immediately after the lesion, there’s a very rapid weight gain.

Eventually, eating stabilizes at a higher level, and the new higher weight becomes the body’s new stable weight.

Lateral hypothalamus lesions (LH syndrome)

Symptoms include:

• Aphagia (cessation of eating)

• Adipsia (cessation of drinking)

Arcuate NPY neurons

NPY (Neuropeptide Y) and AgRP (Agouti-related peptide) are both feeding enhancers, increasing hunger and food intake

Arcuate POMC Neurons

Melanocortins (which activate the MC4 receptor) are feeding inhibitors, reducing hunger and food intake.

Prader-willi syndrome

A loss of function of specific genes on chromosome 15, those affected become constantly hungry, which often leads to obesity and type 2 diabetes

Melanocortins

Class of peptide hormones, that activate MC4 receptors in the brain. MC4 receptor mutations can lead to overeating and obesity by disrupting hunger signals

Treatments for obesity

serotonin (serotonin induces satiety, serotonin agonists), surgery (gastric bypass), semaglutide (ozempic)

semaglutide (ozempic)

Lowers blood glucose by stimulating insulin secretion, inhibiting glucagon secretion. In the brain, stimulates POMC neurons and inhibits NPY and AgRP

semaglutide (ozempic) side effects

GI upset, gallbladder function, increased heart rate, some concern
about negative effects on mood

Anorexia Nervosa

Extreme underconsumption of food, distorted body image, leads to severe health issues (kidneys, bones, heart), most frequent in women (1.4% incidence), extremely low recovery and 4% mortality

anorexia nervosa treatment (pinel’s view based on wood’s study)

Instead of large meals, anorexic patients should be fed frequently with small amounts to reduce stress and improve food tolerance.

orthorexia

Obsession with “healthy” or “clean” food
Gradual intensification of restriction with a prevalence of 4-8%. Symptoms include obsessive eating habits, anxiety, distorted body image, social isolation, and low self-esteem

orthorexia treatment

CBT, antidepressants (SSRIs)

bulimia nervosa

Reoccurring cycles of fasting, bingeing, purging. Health problems related to both malnutrition and damage from regurgitation/laxatives (Acid reflux, damage to teeth, esophagus etc.)

Incidence:
- 1.9% incidence in women, 0.6% in men
- 50% recovery rate, ~2% mortality
- Some heritability (28-83% based on twin studies)

Hypokalaemia

Disorder often caused by an excessive loss of potassium in your digestive tract due to vomiting, diarrhea or laxative use.

binge-eating disorder

Health problems related to resulting obesity/metabolic disease, as well as distress, shame, guilt, depression

Incidence

• 2.8% incidence in women, 1% in men

• High heritability (41-57% based on twin studies)

Insula

anorexia nervosa - LESS sensitive than normal

bulimia nervosa - MORE sensitive than normal

Anterior cingulate cortex

anorexia nervosa - LESS active in response to food

bulimia nervosa - MORE active in response to food

Dorsolateral prefrontal cortex

anorexia nervosa - MORE active in anticipation of food

bulimia nervosa - LESS active in anticipation of food