Biological Perspective of Eating

Hunger, Eating, and Health

• PSYC/NEUR 2P37, January 30, 2025

Learning Objectives

• Summarizes the digestion process and the three energy metabolism phases.
• Discusses hunger theories and influencing factors.
• Evaluates the concept of hypothalamic hunger and satiety centers.
• Explores obesity, its causes, and treatments.

Why We Eat

Biological Perspective:

• Eating provides energy for daily activities.
• Aids in rebuilding cells and producing hormones, chemicals, and enzymes.
• Ultimate purpose is to promote survival.

Social and Psychological Perspective:

• Eating serves as a means to socialize and celebrate.
• It helps form friendships and reaffirm relationships and commitments.
• Eating can be a response to stress.

Hunger and Satiety

• Hunger and satiety are two competing behavioral states.
• Hunger is the desire for food.
• Satiety is the sense of fullness or satisfaction.
• Complex mechanisms anticipate future requirements.

Source of Energy

Carbohydrates (Starches and Sugars):

• Broken down into glucose, fructose, and galactose (monosaccharides).
• Immediate energy source; body will burn glucose first.
• Excess glucose is stored in the liver and muscles.

Fats (Meats, Milk Products, Seeds/Grains):

• Broken down into fatty acids.
• Immediate energy source.
• Excess can be stored in fat tissue.

Proteins (Meats, Beans, Nuts, Seeds):

• Broken down into amino acids.
• May be converted to glucose, glycogen, or fat based on bodily needs.
• Used for body growth, repair, and energy.

Energy Metabolism

Cephalic Phase:

• Preparatory phase initiated by the sight, smell, or expectation of food.

Absorptive Phase:

• Nutrients from a meal meet immediate energy needs, with the excess stored.

Fasting Phase:

• Energy is withdrawn from reserves to meet immediate needs.

Hormonal Control of Energy Balance: Insulin & Glucagon

Insulin:

• Enables glucose to enter cells (excluding neurons).
• Promotes glucose use as an energy source.
• Stimulates glycogen, protein, and fat production. and storage

Glucagon:

• Stimulates glycogen breakdown.
• Encourages the release of free fatty acids from adipose tissue.
• Stimulates the conversion of free fatty acids into ketones.

Set Point Theory

• Hunger is a consequence of an energy deficit.
• Each individual has an optimal level of energy resources, named the set point.
• The body aims to return to this set point to maintain homeostasis.

What is Monitored

Glucostatic Theory:

• Glucose levels determine when we eat.

Lipostatic Theory:

• Fat stores determine how much we eat over the long term.
• Explains how body weight tends to be constant over time.
• It is used for long-term regulation.

Positive-Incentive Perspective

• Animals are driven to eat by the anticipated pleasure of eating.
• Eating enables taking advantage of good food when it's available.

Anticipated Pleasure:

• Expected pleasure is positive-incentive value (hedonic value).

Craving:

• Eating is initiated by craving.

Factors influencing hunger:

• Flavor, knowledge, time since last meal, the amount of food in the gut, and blood glucose levels.

Factors Determining What We Eat

Innate Preferences:

• Evolutionarily driven; with a natural preference for sweat and fatty foods (high-energy) and Salty food (sodium-rich).

Innately Avoided:

• bitter tastes, which are associated with toxins.

Learned Taste Preferences and Avoidance:

Learned Taste Preference:

• A glucose - Flavor B Water: rats prefer Flavor A after training

Learned Taste Avoidance:

• Flavor A - LiCl, Flavor B - Water: rats avoid Flavor A after training.

Social Transmission of Food Preference:

• Observer rats smell other rat's breath and then choose the food preference

Nutritional Content:

• Sodium deficiency induces the drive to consume salty foods.
• Animals have the ability which food will complete their diet.

Factors Determining When We Eat

• Mammals tend to eat many small meals throughout the day.
• Modern lifestyles have led to fewer, larger meals due to family and daily routines.

Premeal Hunger:

• Eating a meal stresses the body, moving it away from homeostasis.
• Meal signals evoke a cephalic phase.
• Insulin releases into the blood and decreases blood glucose.

Factors Determining How Much We Eat

Satiety Signals:

• Food in the gut and glucose in the blood. Plays a major role in how much is consumed.

Appetizer Effect:

• A small amount of food might increase hunger.

Serving Size:

• More food will get consumed with a larger serving.

Social Influences:

• Increased eatting within a group setting

Sensory-Specific Satiety:

• More tastes available at a cafeteria leads to more eating.
• As one type of food is consumed, the positive-incentive value decreases; a different offered food regenerates eating.

Functions of the Hypothalamus

• Regulation of food intake, body weight, electrolyte balance, body temperature, reproduction, sleep-wake cycle, and circadian rhythms.
• Influences behavior through links with the limbic system.
• Regulates endocrine function via the hypothalamic-pituitary system.

Appetite Control and Hypothalamus

• No single brain region controls the appetite but the hypothalamus is important for regulation of food intake, metabolic rate, and body weight.

Hypothalamic Hunger and Satiety Centers

• Dual-center hypothesis with two centers in the hypothalamus, but it turned out to be wrong:.
• Ventromedial hypothalamus (VMH) signaled satiety.
• Lateral hypothalamus (LH) signaled hunger.

Problems with Dual Centers Hypothesis

• Ventromedial hypothalamus (VMH) lesions cause animals to eat to excess and become obese, suggesting the VMH could be a satiety center.

  • Damage limited to the VMH does not consistently increase eating

• Lateral hypothalamus (LH) lesions cause aphagia, suggesting LH is a hunger center, but animals may also lose the desire to drink (adipsia) rather than just eat.

  • The aphagia may be due to a lack of responsiveness to sensory input, such as food and water.

Arcuate Nucleus of the Hypothalamus

• Contains neurons sensitive to hunger and satiety signals, including leptin, ghrelin, peptide. -YY3-36 (PYY3-36), and insulin.

Leptin:

• Discovered in mice with a mutation in the obese (ob) gene.
• The hormone helps regulate body weight, hunger, and fat storage.
• Produced by fat cells (adipocytes).

Ghrelin:

• Ghrelin is a hormone that increases appetite and food intake and is produced by endocrine cells in the stomach
• Levels rise during fasting and drop after a meal. However, obese subjects have lower baseline levels.

Peptide YY3-36 (PYY3-36):

• Produced by cells in the small and large intestine.
• Potent appetite suppressant.
• Lower than average levels are associated with obesity.

Integration of Hormonal Signals

• Involves two sets of neurons in the arcuate nucleus (NPY/AgRP and POMC/CART) that stimulate or inhibit appetite.

Obesity Kills!

• 7 common diseases due to obesity: Arthritis, Back Pain, Cancer, Infertility, Diabetes and Stroke and Heart Diseases

Obesity Stats

• In Canada, almost 2/3 of adults are overweight or obese, and 33% of children are overweight or obese. Obesity has tripped since 1980

Epidemic of obesity

• Evolution favored individuals thatPreferred high-calorie food, Ate to capacity, Stored as much energy as possible
• With recent modern lifestyle -Decline of home cooking Larger portions, junk food - Increased TV and internet Increased TV, internet, video games. Lack of physical activity

Body weight

Treatment of Obesity: Semaglutide

• Is a glucagon-like peptide-1 (GLP-1) analogue and stimulates insulin and inhibits glucagon
• Clinical trial results, in that is reduces blood glucose levels and reduces weight

Treatment of Obesity: Bariatric Surgery

• Indicated only for extreme obesity.
• Two common ones are gastric band and gastric bypass

Explore the primary biological purposes of eating, focusing on energy metabolism phases (absorptive, fasting). Learn about macronutrient breakdown, energy storage, and the influence of conscious decisions on energy output. Understand semaglutide's role in weight loss.