Eating and Eating Disorders by fjwuxn

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									C81BIO – Semester 2, Lecture 4
Eating and Eating Disorders
Dr. Mark Haselgrove
Sonya “The black widow” Thomas - 29 times world eating champion

Cheesecakes 11 pounds of downtown Atlantic cheesecake in 9 minutes

Chicken nuggets: 80 chicken nuggets in 5 minutes

Chicken wings: 173 chicken wings in 12 minutes

Eggs: 65 hard boiled eggs in 6 minutes and 40 seconds

Fruitcakes: 4 pounds, 14 1/4 ounces of Wegman's Fruitcake in 10 minutes

Hamburgers: 7 burgers (3/4 pound) "Thickburgers" in 10 minutes

Hot dogs: 37 hot dogs in 12 minutes

Lobster: 44 lobsters totalling 11.3 pounds of lobster meat in 12 minutes
Overview of the lecture
   (1) Eating

   (2) Theories of Hunger
          Set points – description and analysis
          Positive incentive theory

  (3) Eating Factors
          What determines what we eat
          What determines when we eat

   (4) Physiological Research
          Ventromedial Hypothalamus
          Lateral Hypothalamus
          The stomach

   (5) Obesity
Theories of Hunger
Set point theory (Keesey & Powley, 1986)

 Hunger a consequence of an energy deficit

 Each individual has an optimal level of energy resources – set point

 Body seeks to return to this set point - Homeostasis

                                                            As energy levels drop,
                                                            hunger increases
                                                            and a meal is initiated
Theories of Hunger
Problems with Set point theory

 (1) Evolutionarily unlikely
     - Need to cope with inconsistent resources in the environment
     - Not a system that just responds to energy deficits

 (2) Not supported by evidence
     - Reductions in blood glucose needed to start a meal are substantial
     - Drinking a high calorie drink prior to meal time does not stop the meal
       (Lowe, 1993 - beliefs about the content of the drink has more of an effect)

 (3) Ignorance of environmental factors
     - Effects of learning, preference and social factors.
     - Thought experiment
Theories of Hunger
Positive-incentive theory (e.g. Berridge, 2004)

 (1) Anticipation
      - Animals driven to eat by the expected pleasure of eating
      - Expected pleasure = positive-incentive value

 (2) Craving
     - Eating (and the perception of hunger) is initiated by craving
     - Enables you to take advantage of good food (when its available)

 (3) Multiple factors:
     - Flavour of the food
     - Knowledge about the food (learning)
     - Time since last meal, amount of food in gut, blood glucose levels ….
What determines WHAT we eat?
Learned taste preferences and aversions (e.g. Sclafani, 1990)

             Training                   Test

      Flavour A → Glucose
                                   Flavour A vs. Flavour B
      Flavour B → Nothing
                                                Rats PREFER Flavour A

             Training                   Test

      Flavour A → LiCl
                                  Flavour A vs. Flavour B
      Flavour B → Nothing
                                               Rats AVOID Flavour A

 Food preferences can be socially acquired too (Galef, 1995)
What determines WHAT we eat?
Learning to eat vitamins and minerals

 Associating salt with flavours (Fudim, 1978)

             Training           Injection         Test

           Almond + Salt         Nothing    Banana > Almond

           Banana + Sugar       Formalin    Banana < Almond

 So why do people have such a poor diet?

 Harris et al (1933): Thyamine (Vitamin B1) depleted rats

          Learned to chose a complete diet and avoid a thyamine deplete diet
          Effect weakened when there was a choice between 10 different diets
What determines WHEN we eat?
Collier (1986) Most mammals will eat many small meals throughout the day

   - What initiates a meal?

  (1) Pre-meal hunger (Woods, 1991)

   - Eating a meal stresses the body: influx of fuel moves it away from homeostasis

   - Signals for a meal (e.g. time of day, smells) evokes a cephalic phase
        Insulin released into blood: ↓ blood glucose

   - Thus, hunger isn’t a cry for energy → body preparing for homeostasis disruption

  (2) Conditioned hunger in rats (Weingarten, 1983)

                                           Rats ate more food when
    Buzzer & Light (CS) →     Food         the CS was subsequently
Physiological Research
 The Hypothalamus

                     -   Ventralmedial – A satiety centre
                     - Hetherington & Ranson (1940)
                     - Lesion = hyperphagia (overeating & obesity)

                     - VMH syndrome :
                     (1) Dynamic phase:
                          excessive eating, weight gain
                     (2) Static phase:
                         Body weight maintained
                         Over weight returned to following deprivation

                         Will not work for food
                         Sensitive to unpalatable foods (finicky)
Physiological Research
 The Hypothalamus

                     -   Lateral - A feeding centre
                     - Anand & Brobeck (1951)
                     - Lesion = aphagia (cessation of eating)
                     - Lateral Hypothalamus = feeding centre

                     - LH syndrome (Teitelbaum & Epstein, 1962) :

                     (1) Aphagia accompanied by adipsia
                          (cessation of drinking)
                     (2) Recovery is possible –
                             (i) tube feeding
                             (ii) milk soaked cookies
                             (iii) dry food pellets
Physiological Research
 The Hypothalamus

                    - BUT the theory crumbled….
                    (1) VMH lesions in fact damaged the PVN
                        This region produces hyperphagia & Obesity

                    (2) Hypothalamus regulates metabolism not

                         VMH lesions: increases blood insulin →

                              (i) ↑ lipogenesis (production of fat)
                              (ii) ↓lipolysis (breakdown of body fat)

                    Thus the rats must consume more calories
                    to meet demand.

                    (3) LH lesions produce a variety of motor
                        disturbances, and lack of responsiveness
Physiological Research
 The Stomach

                         - Cannon & Washburn (1912)

                         Contractions caused by empty stomach =

                         But, patients without stomachs still get hungry

                         - Gibbs, Young & Smith (1973)

                         -    Cholecystokinin (CCK) – a peptide
                             (chemicals released by the gut to the brain)

                         - Injected into the rat = ate smaller meals

                         - Now, many peptides are known to induce
 - Incidence of obesity has doubled in the last 20 years in the US

 - Haslam et al., (2006) In the US, a third of all babies born in 2000
   will suffer from diabetes

 - 10% of these will develop life threatening conditions in early adulthood

 -   Spontaneous genetic mutation in a
     mouse colony
 -   Ate more, converted calories to fat
     more efficiently
 -   Mice lacked the peptide leptin

 - Negative feedback signal to ↓
   appetite & enable fat metabolism
 Leptin (Continued…)

 - Seeley & Woods (2003): leptin receptors found in the mouse brain
                           Injections of leptin in ob/ob mice: ↓eating, ↓ weight

 - Some success in treating human obesity:

 The case of the girl with no leptin

 The patient was of normal weight at birth, but her weight soon began to increase at an excessive rate. She
     demanded food continuously and was disruptive when denied food. As a result of her extreme obesity,
     deformities of her legs developed, and surgery was required.

 She was 9 when she was referred for treatment. At this point she weighed 94.4 kilos (15 stone) and her
     weight was still increasing at an alarming rate. She was found to possess the ob/ob gene, and had no
     detectable leptin. Thus leptin therapy was commenced

 The leptin therapy immediately curtailed the weight gain. She began to eat less, and she lost weight
     steadily over a year – a total of 36 pounds, almost all in the form of fat. There were no obvious side
     effects. (Farooqi et al., 1999)

Pinel, J. P.J. (2008) Biopsychology, Pearson. Chapter 12

Carlson, N. R. (2007) Physiology of Behavior, Allyn & Bacon. Chapter 12

Kalat, J. W. (2007) Biological Psychology, Thompson. Chapter 10

 Next Time: Sex!


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