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Psych neural eating
Psych neural mechanisms in controlling eating behaviour
| Question | Answer |
|---|---|
| Who was Cannon and what was his theory? | One of the first to investigate this topic, believed that we stopped feeling hungry when our stomachs are physically full... so he shoved a balloon down his colleagues throat! YUCK |
| What was Lashley's theory? | An area of the brain was responsible for eating behaviour. Kept dissecting rat brains until he took out hypothalamus and rats were no longer motivated to get food. |
| What is the hunger centre? | Lateral hypothalamus (LH) |
| What is the satiety centre? | Ventromedial hypothalamus (VMH) |
| What do you call the failure to eat when hungry and overeating? | Aphagia and hyperphagia |
| What was Mayer's theory? | It isn't blood sugar that trigger LH (or else why do diabetics with high blood sugar get hungry?) It's the glucose IN THE CELLS - BGL change depending on your normal food pattern, regardless if you actually eat meal or not |
| What is the dual feeding system? | Lateral hypothalamus makes you eat, ventromedial hypothalamus tells you to stop eating |
| What is the problem with Cannon's theory? | Hugely reductionist. Some patients who have had their stomach removed still report feelings of hunger. Also, he shoved a balloon down someone's throat. HE'S INSANE. |
| What was Stanley's theory? | Neuropeptide Y (NPY) causes you to eat. Repeated injections of NPY in rats caused obesity in just a few days |
| Name two hormones that supposedly control eating behaviour and how they affect it | Leptin and ghrelin. When ghrelin is high, you are hungry (lots of gremlins eating all your food). When leptin is low, you are hungry (Leptin is Low) |
| 3 forms energy is delivered to the body in | Lipids (fats), glucose (carbohydrates), amino acids (proteins) |
| 3 forms energy is stored in the body in | Fat, glycogen, protein (muscle). Mostly fat, a little muscle, a tiny glycogen |
| 3 phases of food homeostasis | 1) Cephalic phase (hungry). 2) Absorptive phase (eating). 3) Fasting phase (not hungry) |
| What happens in them? | 1) Insulin high, glucose low 2) Uses some glucose from food, converts left-overs into glycogen and fat 3) Glucose high, insulin low. Slowly draws on glycogen to sustain energy |
| Set-point theory | Homeostasis/drive-reduction basis. Leads to a set-point of body weight. Explains eating behaviours but ignores learning, social factors, etc. and eating disorders |
| Glycostatic regulation (set-point 1) | Short-term regulation. Insulin converts glucose into glycogen. When no more glucose, insulin down, glucose up. When sufficient loss of glycogen, hunger starts. Too much insulin, hungry quicker BUT blood glucose levels only small role? |
| Ghrelin regulation | Short-term. Travels in the blood to hypothalamus where it acts, higher quantities when time for hunger |
| Lipostatic regulation (set-point 2) | Long-term. Leptin is a protein released by fat cells. Lose a lot of weight, less fat cells. Hypothalamus notices lack of leptin and encourages eating to keep body weight of adults relatively constant |
| Ventromedial hypothalamus debate | Satiety centre or change in metabolic rate? VMH -> more insulin -> more converted to fat (fatter) and energy locked up in glycogen so need more food quicker (fatter) |
| Consequence of VMH lesion | "Settling point", altered set-point body weight |
| Positive Incentive Theory | We aren't just motivated to eat to reduce drives. We are actually drawn to it by the anticipated pleasure of eating. Explains how ppl with memory impairments will keep eating even if they shouldn't be hungry based on ghrelin, etc. |
| Positive Incentive Theory - brain | Same as rewards in motivation theories, mesolimbic dopamine pathway |
| Possible incentives | Learned behaviours (e.g. sick after shrimp, dislike shrimp) // Choose healthy foods |
| Rolls & McCabe | Chocolate Craving Study. Different fMRI results to chocolate-related stimuli in cravers than non-cravers (both for pics and choc in mouth) - brain bits linked to addiction |
| How much do we eat? | Stop eating due to satiety signals (BGL, nutritional density of meals -> learned knowledge) or sham eating // Eat more if larger plate // Eat more in social situations (or less) |
| Sham eating | Acting as though you are eating - even if food doesn't get to stomach - decreases hunger. Works better with familiar food (know right amount) |
| Sensory-specific satiety | You don't want to eat pasta every day for a week. When you have more variety of foods, you become fatter |
| Body Weight Regulation Theories | Like set-point theory but not just homeostasis - explains obesity and anorexia |
| Leaky-barrel model | Amount of water in = amount leaking out. Barrel resting on hose = strength of satiety signal. Go on diet: less water in, still leaking out BUT less weight on hose so want to eat more. One factor changes and rest change with it until new equilibrium |
| Leaky-barrel advantages | Explains enduring changes to body-weight. Explains why weight is put back on so quickly after dieting. Integrates changes in basal metabolic rate |
| Obesity reasons | Eating culture (3 meals a day, variety of food so less sen-spec satiety, salt/sugar added for flavour). Evolutionary - had to shore up fat for warmth/energy reserves but now bountiful food |
| Leptin and obesity | Ob mice - fat. Ob gene controls leptin production. Overweight child w/ no leptin. Both cured with treatment of artificial leptin BUT can't use leptin as weight loss in normal humans (fat ppl tend to have high leptin) |
| Anorexia and Positive Incentive Theory | Thin = praise = incentive. Incentive for interacting with food, not just for eating it |
Created by:
Georgia11
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