16. Eating & Appetite

Digestion: The Basics

  • Chewing mixes food with saliva, initiating digestion.
  • Swallowing moves food to the stomach.
  • Stomach stores food; hydrochloric acid and pepsin break it down.
  • Contents empty into the duodenum for absorption.
  • Enzymes break down proteins and sugars.
  • Fats are emulsified by bile.
  • Remaining water is absorbed in the large intestine.

Theories of Hunger

Set Point Theory (Keesey & Powley, 1986)

  • Hunger arises from energy deficit; body aims for optimal energy level (set point).
  • Homeostasis: body seeks to maintain this set point.
  • Problems:
    • Evolutionarily unlikely due to inconsistent resources.
    • Not supported by evidence (glucose reduction needed is substantial).
    • Ignores environmental factors like learning and social factors.

Positive Incentive Theory (Berridge, 2004)

  • Eating driven by expected pleasure (positive-incentive value).
  • Craving initiates eating, enabling food advantage.
  • Influenced by flavor, learning, time since last meal, and glucose levels.

Eating Factors: What do we Eat?

  • Learned taste preferences and aversions (e.g., Sclafani, 1990).
  • Socially acquired food preferences (e.g., Galef, 1995).
  • Learning to eat vitamins and minerals; associating salt with flavors (Fudim, 1978).
  • Example: Harris et al., (1933) - Vitamin B1 depleted rats chose a complete diet but effect weakened with more choices.

Eating Factors: When do we Eat?

  • Pre-meal hunger (Woods, 1991): body prepares for homeostasis disruption.
    • Signals (time, smells) evoke cephalic phase; insulin released, lowering blood glucose.
  • Conditioned hunger in rats (Weingarten, 1983): Buzzer & Light (CS) → Food; rats ate more when CS presented.

Physiological Research: The Hypothalamus

Ventromedial Hypothalamus (VMH)

  • Satiety center; inhibits eating.
  • Hetherington & Ranson (1940): VMH lesions = hyperphagia (overeating & obesity).
    • VMH syndrome: Dynamic phase (excessive eating), static phase (weight maintained).
    • VMH Syndrome rats won't work for food, sensitive to unpalatable foods.

Lateral Hypothalamus (LH)

  • Feeding center.
  • Anand & Brobeck (1951): Lesion = aphagia (cessation of eating).
    • LH syndrome (Teitelbaum & Epstein, 1962): Aphagia often with adipsia; recovery possible with tube feeding.

Problems with Hypothalamus Theory:

  • VMH lesions damaged PVN, causing hyperphagia & obesity.
  • Hypothalamus regulates metabolism, not just eating.
  • VMH lesions increase blood insulin → ↑ lipogenesis, ↓ lipolysis.
  • LH lesions produce motor disturbances and lack of responsiveness.

Physiological Research: The Stomach

  • Cannon & Washburn (1912): Contractions linked to hunger but stomach not necessary.
  • Koopmans (1981): Transplanted stomach; food injection ↓ eating, satiety signal via blood flow.

Physiological Research: Peptides

  • Short amino acid chains acting as hormones/neurotransmitters.
  • Released into bloodstream upon food ingestion; can cross blood-brain barrier.

Choleystokinin (CCK)

  • Gibbs, Young & Smith (1973): Satiety peptide; injection in rats reduced eating.
  • Mosher et al., (1998): CCK may induce nausea or flavor aversion.

Leptin

  • Discovered via genetic mutation in mice; low leptin = increased eating & fat conversion.
  • Seeley & Woods (2003): Leptin receptors in brain; injections reduce eating & weight in obese mice.
  • Human trials: leptin ineffective for most obese individuals.
  • Successful treatment: girl with no leptin (Farooqi et al., 1999) showed weight loss with leptin therapy.