Eating and Eating Disorders C81BIO – Semester 2, Lecture 4 Dr. Mark Haselgrove.

Eating and Eating Disorders

C81BIO – Semester 2, Lecture 4

Dr. Mark Haselgrove

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

Sonya “The black widow” Thomas - 29 times world eating champion

Overview of the lecture

(1) EatingDigestion

(2) Theories of HungerSet points – description and analysisPositive incentive theory

(3) Eating FactorsWhat determines what we eatWhat determines when we eat

(4) Physiological ResearchVentromedial HypothalamusLateral HypothalamusThe stomach

(5) Obesity

Digestion

Theories of HungerSet point theory (Keesey & Powley, 1986)

Hunger a consequence of an energy deficit

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

As energy levels drop,hunger increases and a meal is initiated

Body seeks to return to this set point - Homeostasis

Theories of Hunger

(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

Problems with Set point theory

Theories of Hunger

(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 ….

Positive-incentive theory (e.g. Berridge, 2004)

What determines WHAT we eat?Learned taste preferences and aversions (e.g. Sclafani, 1990)

Flavour A → Glucose

Flavour B → Nothing

Flavour A vs. Flavour B

Training Test

Rats PREFER Flavour A

Flavour A → LiCl

Flavour B → Nothing

Flavour A vs. Flavour B

Training Test

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)

Almond + Salt

Banana + Sugar

Banana > Almond

Training TestInjection

Formalin

Nothing

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)

Buzzer & Light (CS) Food→Rats ate more food whenthe CS was subsequentlypresented

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 maintainedOver weight returned to following deprivation

Will not work for foodSensitive 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 PVNThis 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 caloriesto 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

- 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

- Incidence of obesity has doubled in the last 20 years in the US

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!

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