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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 Digestion (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 Digestion 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 presented 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 eating 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 = Hunger 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 satiety Obesity - 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 Leptin - 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 Obesity 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) Reading 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! Email: Mark.Haselgrove@nottingham.ac.uk
"Eating and Eating Disorders"