Hunger, Eating, and Health

Biopsychology: Hunger, Eating, and Health

Chapter 12 Summary and Notes

Learning Objectives

  • 12.1 Summarize the process of digestion and explain how energy is stored in the body.

  • 12.2 Explain the three phases of energy metabolism.

  • 12.3 Describe the set-point assumption and explain glucostatic and lipostatic set-point theories of hunger and eating. Outline three problems with set-point theories.

  • 12.4 Describe the positive-incentive perspective on hunger and eating.

  • 12.5 Describe at least two factors that determine what we eat.

  • 12.6 Describe at least two factors that influence when we eat.

  • 12.7 Describe major factors that influence how much we eat.

  • 12.8 Explain the relationship between blood glucose levels and hunger/satiety.

  • 12.9 Describe the evolution of research on hypothalamic nuclei in hunger and satiety.

  • 12.10 Describe the gastrointestinal tract's role in satiety.

  • 12.11 Describe the discovery of the role of hypothalamic circuits, peptides, and the gut in food consumption/metabolism.

  • 12.12 Describe the role of serotonin in satiety.

  • 12.13 Describe the symptoms and etiology of Prader-Willi syndrome.

  • 12.14 Evaluate evidence for set-point assumptions about body weight and eating.

  • 12.15 Compare and evaluate set-point vs. settling-point models of body-weight regulation.

  • 12.16 Explain concerns surrounding the overeating epidemic.

  • 12.17 Describe the evolutionary perspective on the overeating epidemic.

  • 12.18 Explain why some gain weight from overeating while others do not.

  • 12.19 Explain why weight-loss programs are often ineffective.

  • 12.20 Explain how leptin and insulin serve as feedback signals for body fat regulation.

  • 12.21 Describe two treatments for overeating/high body-fat levels.

  • 12.22 Describe symptoms of anorexia nervosa and bulimia nervosa.

  • 12.23 Explain how anorexia and bulimia are related.

  • 12.24 Explain why starving individuals with anorexia do not appear as hungry.

  • 12.25 Explain how anorexia may result from conditioned taste aversions.

Digestion and Energy Storage

  • Digestion Process:

    • Involves breaking down food into absorbable components.

  • Gut Microbiome:

    • Consists of bacteria and organisms aiding food breakdown.

  • Forms of Energy: (3)

    • Lipids: Fatty acids used as major fuel source.

    • Amino Acids: Building blocks of proteins.

    • Glucose: Main carbohydrate energy source.

  • Energy Storage Forms: (3)

    • Fats: Preferred storage, highly efficient.

    • Glycogen: Carbohydrate storage in liver and muscle.

    • Protein: Ample storage but less efficient for energy.

Energy Metabolism Phases

  • Three Phases:

    • Cephalic Phase:

    • Anticipation of food; preparatory changes in the body.

    • Absorptive Phase:

    • Nutrients are absorbed into the bloodstream.

    • Fasting Phase:

    • Body utilizes stored energy.

  • Hormones:

    • Insulin: Facilitates glucose uptake and energy storage.

    • Glucagon: Promotes release of energy stores.

Set-Point Assumption

  • Concept of Set-Point:

    • Body maintains weight around a specific set-point.

  • Glucostatic Set-Point Theory:

    • Suggests hunger is triggered by low blood glucose.

  • Lipostatic Set-Point Theory:

    • Suggests hunger is triggered by low fat stores.

  • Weaknesses of Set-Point Theories:

    • Inability to explain eating disorders.

    • Not consistently supported by evolutionary evidence.

    • Fails to account for taste, learning, and social factors influencing eating behavior.

Positive-Incentive Perspective

  • Developed to address set-point shortcomings.

  • Focus on Anticipated Pleasure:

  • Factors influencing hunger:

    • Preferred tastes

    • Past experiences with food

    • Time elapsed since last meal

    • Social contexts or others eating

Factors Influencing Eating

  • What We Eat:

    • Preference for sweet and salty flavors.

    • Aversion to bitterness.

    • Conditioned taste aversions/preferences.

    • Cravings linked to nutrient deficiencies.

  • When We Eat:

    • Availability of food influences frequency and size of meals (i.e., humans have fewer large meals vs. animals' smaller frequent meals).

    • Stress factors may trigger or discourage eating patterns.

  • How Much We Eat:

    • Satiety Signals:

    • Volume of food and nutritive density impact satiety.

    • Research on Sham Eating: Phenomenon where eating without caloric consumption affects meal size.

    • Appetizer Effect: A small pre-meal intake increases subsequent meal size.

    • Influence of Serving Size and Social Context:

    • Group norms and variety in offerings encourage larger intakes.

Blood Glucose Levels and Hunger

  • Mixed research; initial drops in blood glucose are not directly correlated with hunger or meal consumption.

  • Blood glucose levels return to baseline even without food consumption, suggesting other mechanisms at play in hunger and satiety.

Hypothalamic Nuclei and Hunger

  • Lesion Studies:

    • Ventromedial hypothalamus (VMH) lesions linked to hyperphagia (excessive eating).

    • Lateral hypothalamus (LH) lesions lead to aphagia (lack of eating) and adipsia (lack of drinking).

  • The hypothesis has evolved: VMH damage often coincided with other significant neural disruptions.

Role of the Gastrointestinal Tract

  • Early Research:

    • Cannon and Washburn's balloon study measured stomach contractions linked to hunger.

  • Animals without stomachs adjust eating but only consume what’s necessary for maintenance.

Hypothalamic Circuits and Peptides

  • Peptides Linked to Satiety:

    • Cholecystokinin (CCK), Glucagon, Bombesin, Somatostatin, etc.

  • Peptides Linked to Appetite:

    • Neuropeptide Y, Ghrelin, Orexin-A, etc.

Serotonin and Appetite Regulation

  • Serotonin Role:

    • Agonists can lower food intake; preferable to develop side effect-free options.

Prader-Willi Syndrome

  • Overview:

    • Genetic condition (chromosomal replication error on chromosome 15).

    • Symptoms:

    • Insatiable hunger leading to obesity.

    • Slow metabolism, weak muscle tone.

    • Challenges in early feeding, behavioral issues, including compulsivity and skin picking.

  • Potentially fatal if untreated.

Evaluation of Set-Point Assumptions

  • Traditional theories cannot explain vast weight fluctuations.

  • Research indicates body regulates fat levels through metabolic adjustments rather than solely through intake modifications.

Settling-Point Models

  • Body weight adjusts to balancing food intake and energy expenditure, staying relatively stable unless external factors create long-term weight changes.

  • Leaky-Barrel Model: Describes the settling-point model and incorporates feedback mechanisms.

Overeating Epidemic Insights

  • Societal Factors:

    • Rise in fast-food culture promoting high calorie intake.

    • Evolutionary factors favoring caloric efficiency.

    • Social norms dictate meal times and quantities.

  • Demographic Concerns:

    • Growing anxiety over increasing rates of obesity among older individuals and younger generations.

Ineffectiveness of Weight-Loss Programs

  • Commonality of reverting to previous lifestyle choices post-program hampers long-term success.

  • Acknowledgment that exercise alone contributes marginally to caloric expenditure relative to dietary intake.

Leptin and Body Fat Regulation

  • Leptin:

    • Hormone secreted by adipose tissue; relates inversely to food intake.

    • Critically linked to body fat measures.

  • Insulin:

    • Levels correlate with body fat, contributes to appetite regulation.

Treatments for Overeating

  • Treatment options include:

    • Use of serotonin agonists.

    • Surgical interventions such as gastric bypass or adjustable gastric banding.

    • Importance of lifestyle modifications beyond surgical solutions.

Anorexia and Bulimia Nervosa

  • Anorexia Nervosa:

    • Characterized by severe restriction and significant weight loss; high mortality due to health complications (4% mortality rate).

  • Bulimia Nervosa:

    • Involves cycles of binge eating followed by purging; similar mortality rate (4%).

  • Interrelation of Disorders:

    • Both conditions often present with distorted body images and comorbidities such as OCD and depression.

Positive Incentives in Anorexia

  • Positive-incentive model suggests that individuals with anorexia have low motivation to eat due to high cognitive fixation on food without positive appetitive responses.

Hypothesis for Anorexia and Meal Consumption

  • Proposal that calorie infusion disrupts homeostasis; individuals with anorexia exhibit amplified negative responses to food intake, akin to conditioning from traumatic dietary experiences (e.g., camps).

  • Treatment possibilities could include small, manageable portions of food to mitigate aversive responses.