Feeding Behaviour: Appetitive and Consummatory

Feeding Behaviour

• Feeding behavior involves a range of behaviors, not just ingestion.

Feeding Components: Appetitive vs. Consummatory

• Feeding includes appetitive components like seeking food and consummatory components, which involve food consumption.

Appetitive Components of Feeding: Seeking Food

• Seeking out food, also known as foraging, includes detection and identification of food, approaching food, latency to eat, and handling.

Appetitive Components of Feeding: Cost-Benefit Analysis

• Cost-benefit analysis in feeding considers dangers, predators, competitors, trade-offs with other behaviors, hedonic value, prior history/experience, and the suitability of consumption.

Appetitive Components of Feeding: Choosing an Appropriate Diet

• Choosing an appropriate diet means the type of food that meets nutritional needs, such as macro- and micronutrients.

Why We Eat

• Eating supplies the body with energy for survival, involving digestion to break down food into constituent elements for absorption.
• The three sources of energy are lipids from fats, glucose from carbohydrates, and amino acids from proteins.

Forms of Energy Storage

• The three forms of energy storage are body fat, glycogen, and muscle protein.
• Body fat is the most efficient of the body's energy stores.
• Glycogen, found in the liver and muscles, is the most utilized form.
• Muscle protein is the least utilized as an energy store.

Steps in Digestion

• Chewing breaks food up and mixes it with saliva.
• The saliva lubricates the food and begins digestion.
• Swallowing moves food down the esophagus and into the stomach.
• The stomach stores food, and hydrochloric acid breaks food down into smaller particles.
• Pepsin starts breaking protein molecules down into amino acids.
• The stomach empties its contents gradually into the duodenum where most absorption takes place.
• Digestive enzymes in the duodenum, largely from the gallbladder and pancreas, break up molecules into amino acids and simple sugars.
• Simple sugars and amino acids pass through the duodenum wall into the bloodstream, and are transported to the liver.
• Bile, which is manufactured in the liver and stored in the gallbladder, emulsifies fats.
• Emulsified fats are carried by small ducts in the duodenum wall into the lymphatic system.
• Most of the remaining water and electrolytes are absorbed from the waste in the large intestine.
• What's left of the waste is ejected from the anus.
• The Gut (GI) bacteria, viruses, and fungi makeup the microbiome.

Phases of Energy Metabolism

• Energy metabolism phases include the cephalic, absorptive, and fasting phases, all controlled by two pancreatic hormones.
• Insulin (beta-cells)
• Glucagon (alpha-cells)

Pancreatic Hormones: Insulin vs. Glucagon

• Insulin, released during the cephalic and absorptive phases, promotes glucose use and energy conversions to forms that can be stored.
• Insulin also promotes the storage of glycogen, fat, and proteins.
• Glucagon, released during the fasting phase, facilitates the conversion of adipose tissue into free fatty acids.
• Glucose and gluconeogenesis are released when insulin level is low.
• Fatty acids are turned into ketones, which are used by muscles and the brain.

Set-Point Theories: Components

• Set-point theories include set-point, detector, and effector mechanisms.
• Negative feedback systems are used to maintain homeostasis and a stable internal environment.

Set-Point Theories: Glucostatic vs. Lipostatic

• Glucostatic theory involves the short-term regulation of eating.
• Lipostatic theory involves the long-term regulation of eating.

Weaknesses of Set-Point Theories

• Evolutionary pressures are not considered.
• Major predictions are not confirmed.
• Taste, learning, social factors, or reward mechanisms are not incorporated.

Positive Incentive Perspective

• There are no internal energy deficits.
• It involves the anticipated pleasure of eating or positive-incentive, hedonic, value.
• Multiple factors affect the positive incentive value of food, including flavor, previous experience, social context, time since the last meal, and blood glucose.

Set-Point Theories vs. Positive Incentive Perspective

• Physiological motivators can override behavioral motivators.
• Behavioral motivators can override physiological motivators.

Factors Influencing Eating: What, When, How Much

• Factors that influence diet selection, preferences, and aversions are both innate and learned.
• Factors that influence the initiation of a meal to occur are pre-meal hunger, environmental, and physiological cues.
• Factors that influence when a meal ends are previous experience, psychological factors, sensory-specific satiety, and satiety signals.

Innate Factors Influencing What We Eat

• Species-specific preferences and aversions include sweet, fat, salty, bitter, and sour.
• In 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

• Individual learning conditions preferences and aversions are based on post-ingestion consequences of eating.
• Social learning, such as eating what others eat, can determine preferences at weaning, adulthood.
• Rats and mice prefer food they've smelled on others' breath
• Humans are often culturally defined.

What to Eat: Innate vs. Learned Factors

• Seeking salty foods when deficient is an innate preference in order to obtain sodium.
• Seeking foods containing vitamins and minerals depends on associative learning.
• Rats fed a thiamine (B1)-deficient diet get sick, develop an aversion for it, and learn to prefer a diet that makes them recover from the deficiency.

Why We Go Wrong

• The variety of complex foods make it hard to make associations
• The food industry exploits innate preferences.
• Diet culture promotes weight over nutrition.

Factors Influencing When We Eat

• Most mammals tend to eat small meals (snacks) each day, especially if they have ready access to food.
• Rodents eat many small meals but also show two peaks of high feeding per day.
• Humans tend to eat a few bigger meals a day. pre-meal hunger.

Factors Influencing When We Eat: Premeal Hunger

• Premeal hunger can be a conditioned response rather than from an energy deficit.
• Woods' theory is that a meal acts as a stressor that disrupts homeostasis.
• Premeal hunger is a stress coping response when starting the cephalic phase
• Premeal hunger creates insulin release, increases glucose consumption, and causes imbalanced Homeostasis

Factors Influencing When We Eat: Environmental & Physiological

• Environmental factors include sensory stimuli, food-related stimuli (conditioned), time of day, and others' behavior.
• Physiological factors include glucoprivic hunger, lipoprivic hunger, and biological clock.

Factors Influencing When We Eat: Physiological Hunger Signals

• Hunger can be stimulated by hypoglycemia, Glucoprivation, and Glucoprivic Hunger, Low lipids/fatty acids, Lipoprivation and Lipoprivic Hunger.
• A Brain contains two sets of glucoprivation-sensitive detectors.
• The Liver also contains glucoprivation and lipoprivation-sensitive detectors.

Factors Influencing How Much We Eat: Satiety

• Satiety is when we stop eating but food is still available.
• Satiety signals are the act of eating itself, previous experiences, short-term or long-term.
• Short term includes gastrointestinal tract to brain.
• Long term includes body weight and adipose tissue to brain.

Factors Influencing How Much We Eat: Short-Term Satiety Signals

• Short-term satiety signals:
  • Head factors (eating & learning)
  • Gastric, duodenum, intestinal and Liver factors.
• Long-term satiety signals include adipose tissue.

Factors Influencing How Much We Eat: Head Factors, Glucose, etc.

• It comes from eyes, nose, tongue, and throat, and is mostly learned.
• Premeal decline in blood glucose does not cause hunger, but the intention to start eating does triggers a decline in blood glucose. Blood glucose levels in the brain remain relatively constant.

Factors Influencing How Much We Eat: Psychological Factors

• Eating more based on the serving size vs eating a tasty appetizer and social eating behaviors.

Factors Influencing How Much We Eat: Sensory-Specific Satiety

• Rats offered a cafeteria diet ate 84% more than normal rodent chow.
• Reduced incentive comes from taste signals due to consumption.
• Postingestive consequences of eating reduce the incentive value of all tastes eventually
• Varies diets with evolutionarily adaptive value and eating more in times of abundance

Short Term Satiety Signals: Gastric Factors

• Volume from Cannon & Washburn (1912)
• Nutritive density of food in Rats with a pyloric cuff as well as rats with an additional stomach

Short Term Satiety Signals: Cannon and Washburn (1912)

• Washburn swallowed a balloon with a thin tube to pump air and test stomach contractions by measuring fluctuations on a U-Tube
• He noted that sensations of hunger was linked to stomach contractions and an empty stomach

Short Term Satiety Signals: Nutritive Density vs Pyloric Cuff

• Testing nutritive density with a pyloric cuff revealed that nutritive content matters more than volume per se
• Testing with additional stomach transplants can be an indicator of blood factor

Short Term Satiety Signals: Ghrelin

• Ghrelin is a gastric factor and feeding enhancing factor
• It affects metabolism, growth hormone and produced by the stomach
• Ghrelin levels rise just before eating and decline after a meal.

Short Term Satiety Signals: Intestinal Factors

• Cholecystokinin (CCK):
• Peptide YY (PYY):
  • It interrupts eating in proportion to calories
• Neurotransmitters (e.g., serotonin)

Short Term Satiety Signals: Cholecystokinin (CCK) from the Duodenum

• Synthesized by endocrine cells in the duodenum and released into the brain and gall bladder
• Actions in the brain are controlled by (CCK-A and CCK-B) two receptors which then decreases food intake, as well as induce food aversions and learned satiety

Short Term Satiety Signals: Neurotransmitters

• Serotonin(5-hydroxytryptophan/5-HT) plays a role in satiety. 5-HT administered to rodents
• reduced food attraction, reduced amount of food consumed and no preference for fatty foods In humans: similar effects and ADHD medications reduce eating

Short Term Satiety Signals: Liver Factor

• Post-absorption signals via vagus nerve
• Infusion of glucose or fructose to intestines have reduced feeding _ Fructose and Glucose are metabolized in liver to reduce feeding behavior

Long Term Satiety Signals: Adipose Tissue

• Long term signals → Body weight regulation
• Factors released by body fat (adipose tissue) → Leptin

Summary: Hunger and Satiety

• The liver and vagus nerve control Glucopivic/Lipoprivic hunger during initiation of eating
• Glucodetectors in the brain as well as grelin in the stomach also control hunger
• Satiety/Inhibition is due to volume in the stomach and Duodenum CCK, Intestine PYY, and Leptin in the adipose tissue

Early Studies of Hunger and the Brain

• Brainstem: Fairly normal eating is shown in decerebrated rats
• Hypothalamus: feeding and satiety centres come from old lesion and stimulation studies
• Lateral hypothalamus (LH) is used as a feeding centre
• Ventromedial hypothalamus (VMH) as satiety centre

Ventromedial Hypothalamus Lesions

• The VMH can cause VMH syndrome
• The phases are Hyperphagia (excessive eating and finickiness for palatable food)
• Dynamic phase is the early part of the VMH syndrome, characterized by excessive eating and rapid weight gain.
• Static phase when eating stabilizes and gets stable

Lateral Hypothalamus Lesions.

• LH causes the syndrome aphagia and andipsia, along with motor distribution

Updated Role of the Hypothalamus Summary

Lateral Hypothalamic Nuclei

• It Enhances feeding by triggering Melanin Hormone (MCH)

Paraventricular Hypothalamic Nucleus

• Inhibits feeding with MC4-R.

Arcuate Hypothalamic Nucleus

• NPY neurons enhance eating using Neuropeptide and Agouti-related Peptide
• POMC neurons inhibit eating using Melanocortins

Role of Hypothalamic Nuclei in Hunger and Eating: Summary

• In summary of the nuclei: Arc NPY enhancer, Arc POMC inhibitor, Lat enhancer, PVN inhibitor

Effects of Food Restriction

• There is Evidence suggesting enhancement of health and longevity in food restricted humans and animals
• Humans show 20-38% food restriction along with chronic caloric restriction and intermittent fasting
• Mice show that less than 65% food that is less than free fed leads to chronic caloric restriction and intermittent Fasting

Regulation of Body Composition: Energy Consumption

• Its not just how much we eat rather, energy usage
• Daily energy includes Basal metabolic rate, Diet induced thermogenesis, and physical activity

New food restriction:

• Weight metabolism that increased life with better immunity with (i. Di Francesco et al., 2024; Duregon et al., 2023; Fontana et al., 2010; Mitchell et al., 2019)
• Intermittent fasting is sufficient for helping.
• Process of intracellular autophagy by which fasting increases.

Regulation of Body Composition: Changes in the Efficiency of Energy Use

• A decrease in bodyfat leads to more efficient fat usage
• An increase in bodyfat leads to less efficient fat usage
• Adjustments in diet is the reason that weightgain are better in its early phase

Body Composition Regulation: Settling-Points Theory

• A loose homeostasis that includes feedback mechanisms to to limit impact through changes, not just regulation
• Long term changes body various factors

Disorders of Feeding and Metabolism

• Include Anorexia, Bulimia and Binge Eating disorders as well as obesity, which is not a mental disorder

Human Obesity

• Is when excessive tissue with a negative affect

• Physiology helps with optimal eating such as the times where you store energy

Behavioral Factor Obesity Diet and cultural problems

• Stress and environment. Can effect advertising
• Large portions increase and cause globalization

Binge Eating Disorder Distraction and increase of fast food

Genetic factors affect hormones increase of obesity

• MC, and insulin Treatments that affect are leptin

Genetic Disorder affect leptin:

• Treatment can cause obesity.

Genetic effect people:

• Eating and stimulating hormones Food and taste

Anorexia disorder affect:

• Taste and other bodies cause a version Affects eating with food

Stop or reduce to stop the problems

• Anorexia disorders is stop the problem Treatments such as (CCK, and insulin)
• Treatment can cause to stop obesity if affected.