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PSYCH 202 Exam 4 > Hunger, Eating and Health > Flashcards

Hunger, Eating and Health Flashcards

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1
Q

The prevalence of eating disorders suggests that

A

mechanisms regulating eating are complex.

  • Over half of the adult population in the U.S. meets clinical criteria for obesity.
  • 3% of U.S. adolescents suffer from anorexia nervosa.
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2
Q

Diet must provide energy but also

A

nutrients (bricks and mortar) for growth, maintenance and repair of body structure (muscles, bones, etc).
Diet must provide:
- Nine essential amino acids (from the 20 in the body)
- A few fatty acids
- About 15 vitamins
- Several minerals

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3
Q

Available energy is used for

A
  • Processing newly ingested food = 8%
  • Basal metabolism (body heat, gland secretions, action potentials, etc) = 55%, depending on body weight
  • Active behavior = 12-13%
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4
Q

Purpose of eating is to provide the body with

A

molecular building blocks and energy.

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5
Q

Digestion

A

breaking down food and absorbing its constituents.

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6
Q

After digestion, energy is delivered to the body as

A

lipids (fats), amino acids (proteins), and glucose (carbohydrates: starches, sugar).

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7
Q

first step in digestion

A

Chewing breaks up food and mixes it with saliva.

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8
Q

second step in digestion

A

Saliva lubricates food and begins its digestion.

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9
Q

third step in digestion

A

Swallowing moves food and drink down the esophagus to the stomach.

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10
Q

fourth step in digestion

A

The primary function of the stomach is to serve as a storage reservoir. The hydrochloric acid in the stomach breaks food down into small particles and pepsin begins the process of breaking down protein molecules into amino acids.

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11
Q

fifth step in digestion

A

The stomach gradually empties its contents through the pyloric sphincter into the duodenum, the upper portion of the intestine where most of the absorption takes place.

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12
Q

sixth step in digestion

A

Digestive enzymes in the duodenum, many of them from the gall bladder and pancreas, break down protein molecules to amino acids, and starch and complex sugar molecules to simple sugars. Simple sugars and amino acids readily pass through the duodenum wall into the bloodstream and are carried to the liver.

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13
Q

seventh step in digestion

A

Fats are emulsified (broken into droplets) by bile, which is manufactured in the liver and stored in the gall bladder until it is released into the duodenum. Emulsified fat cannot pass through the duodenum wall and is carried by small ducts in the duodenum wall into the lymphatic system.

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14
Q

eighth step in digestion

A

Most of the remaining water and electrolytes are absorbed from the waste in the large intestine, and the remainder is ejected from the anus.

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15
Q

energy stored as

A

fats, glycogen and proteins.

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16
Q

fats are the

A

most efficient for energy storage.

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17
Q

one gram of fat stores

A

twice as much energy as one gram of glycogen.

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18
Q

fat does not attract and hold as much

A

as glycogen.

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19
Q

glycogen

A

Glycogen, a polymer of glucose, referred as animal starch, made primarily in the liver and muscles.
If all fat calories were stored as glycogen, one would weight about 600 pounds (275 Kg).

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20
Q

energy metabolism

A

Chemical changes that make energy available for use.

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21
Q

cephalic phase (1st phase of energy metabolism)

A

preparation for eating (seeing, smelling food).

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22
Q

absorptive phase (2nd phase of energy metabolism)

A

food absorbed meets immediate energy needs.

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23
Q

fasting phase (3rd phase of energy metabolism)

A

Withdrawing energy from reserves, weight loss. Ends with next cephalic phase. Insulin is low, so glucose cannot be used by cells in the body, but brain cells do not need insulin to use glucose, so glucose is reserved for the brain.

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24
Q

three phases of energy metabolism controlled by two pancreatic hormones

A

insulin and glucagon

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25
Q

insulin

A

high during cephalic and absorptive phases (low during fasting phase). produced by beta cells.

  • triggers glucose use as fuel by body cells.
  • triggers conversion of bloodborne glucose into fats and glycogen, and aa to proteins.
  • triggers energy storage in adipose cells, liver, and muscles.
  • the storage of fats, glycogen, and proteins.
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26
Q

glucagon

A

high during fasting phase (low in other two phases). produced by alpha cells.

  • release of free fatty acids from adipose tissue to be used for energy.
  • Triggers transformation of stored energy to usable fuel: fat to free fatty acids and then ketones, which are used by muscles.
  • low levels of insulin trigger protein to glucose (gluconeogenesis).
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27
Q

the set-point assumption

A

Motivation to eat (hunger) comes from an energy deficit; we eat to maintain an energy set point. Eating regulation works like a thermostat, a negative feedback system – turns on when energy is needed, off when set point is reached.

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28
Q

glucostatic theories

A

there is a glucostat and a set point for blood glucose level. Short term regulation. glucose would interact with glucoreceptors.

  • The primary stimulus for hunger is a decrease in the level of blood glucose below its set point.
  • The primary stimulus for satiety is an increase in the level of blood glucose above its set point.
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29
Q

lipostatic theories

A

there is set point for body fat. Long term regulation. Would explain why short-term diets do not work.

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30
Q

Gold thioglucose (neurotoxin) damaged the

A

damaged the Ventromedial Hypothalamus, VMH (Satiety center), animals became fat (hyperphagia). It was observed that weight gain had a dynamic phase and a static phase, in which the new body weight was defended. The weight at the static phase was the one that is maintained and defended by the body.

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31
Q

lesions of the lateral hypothalamus (LH, feeding center)

A

produce aphagia (no eating) and adipsia (no drinking water). Stimulation of the LH caused eating behavior.

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32
Q

Problems with Set-Point Theories of Hunger and Eating

A
  • Epidemic of eating disorders.
  • Early ancestors needed to store body fat.
  • Eating is not always motivated by energy deficits (Thanksgiving!).
  • Do not account for the influence of external factors on eating and hunger.
  • Reductions in blood glucose or body fat do not reliably induce eating.
  • Caloric restriction has beneficial effects.
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33
Q

positive-incentive perspective

A

We are drawn to eat by the anticipated pleasure of eating – we have evolved to crave food. Multiple factors interact to determine the positive-incentive value of eating (e.g., flavor, social factors, etc). Accounts for the impact of external factors on eating behavior.

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34
Q

Addition of saccharin, a sweetener,

A

causes rats to eat more rat chow.

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35
Q

Adding bitter-tasting quinine has

A

the opposite effect (tonic water uses quinine).

36
Q

Factors That Determine What We Eat

A
  • Tastes preferred:
    Sweet and fatty foods – high energy
    Salty – sodium-rich
  • Tastes avoided:
    Bitter tastes – often associated with toxins
    Learned taste aversions:
    Ingestion followed by illness (often one trial learning)
  • Learned preferences:
    Smell of mother’s milk or food smelled in other rats’ breath
    When deficient in vitamins and minerals (sodium): craving for foods with vitamins and salt
37
Q

Factors That Influence When We Eat

A

Cultural norms, schedules, routines: We tend to get hungry at mealtime. Pavlovian conditioning of hunger demonstrated experimentally (sound plus food).

38
Q

[when we eat] As mealtime approaches, the body enters the

A

cephalic phase leading to a decrease in blood glucose. Hunger caused by expectation of food, not by energy deficit.

39
Q

We need about 2500 Calories/day

A

One Calorie: amount of energy (heat) needed to raise the temperature of 1 liter of water by 1 degree C (Celsius).

40
Q

Rats increase eating if caloric content

A

is reduced, up to a point. Stomach distention inhibits eating.

41
Q

Appetizer effect

A

small amounts of food may increase hunger. Elicit cephalic-phase response.

42
Q

social influences influence how much we eat

A

Eating increases when eating with others.

43
Q

Sensory-specific satiety influences how much we eat

A

eat more with a cafeteria diet. satiety is largely taste-specific, except rice, bread, potatoes, sweets and salads.

44
Q

Satiety signals are related to the

A

volume and nutritive density (calories per unit of volume) of the food.

45
Q

We use 2500 Calories/day

A

= energy to heat 25 lt (6.5 gallons) of water from 0 to 100 C (boiling point) = 100 cups of tea.

46
Q

Taste-specific satiety may have adaptive value:

A

promotes a varied diet. Encourage to take advantage during periods of abundance.

47
Q

sham eating

A

Amount we eat is influenced by previous experience with a particular food’s postingestive effects, not by the immediate effect of the food on the body. Cut end of esophagus is tied off and swallowed food falls to the ground. However, the amounts of sham food were much larger from the start for foods the rats had not experienced before.

48
Q

Blood glucose drops prior to a meal as

A

preparation to eat – not a cue to eat. The drop in glucose levels is most likely due to the release of insulin in the cephalic phase, rather than to energy deficiency. If meals are not served, glucose levels goes back up.

49
Q

Must decrease blood glucose by

A

50% to trigger feeding.

50
Q

Reduced blood glucose may contribute to hunger, but

A

changes in blood glucose do not prevent hunger or satiety.

51
Q

Cannon and Washburn (1912)

A

Studies suggested stomach contractions led to “pangs of hunger”, and distension led to satiety. But hunger is still experienced without a stomach… blood borne satiety signals?

  • However, cutting the nervous connection of the stomach did not change the ingestive behavior.
  • Also, ablation of the stomach did not prevent the feelings of hunger and satiety, although the patients ate more frequent and smaller meals.
52
Q

transplantation of an extra stomach and length of intestine

A

Food maintained in the transplanted stomach was able to decrease eating in proportion to its caloric content and volume. Evidence for blood borne satiety chemicals released by the stomach. Transplant had blood supply but no innervation. No food is absorbed by stomach.

53
Q

Food interacts with receptors in the gastrointestinal tract causing

A

the release of peptides into the blood.

54
Q

Several gut peptides bind to receptors in the brain and reduce food intake:

A

cholecystokinin (CCK), bombesin, glucacon, somatostatin, alpha-melanocyte-stimulating hormone.

55
Q

Other peptides, produced in the hypothalamus, increase appetite (hunger peptides):

A

neuropeptide Y, galanin, orexin-A, ghrelin.

56
Q

Peptides, Polypeptides, and Proteins have how many amino acids

A

Peptides: less than 10 aa. Polypeptides, 10 -100 aa. Proteins, more than 100 aa.

57
Q

Serotonin agonists

A

consistently reduce food intake in rats. Even intake of palatable food is affected. Reduces amount eaten per meal. Preferences shift away from fatty foods. Similar effects seen in humans. Serotonin agonists: fenfluramine, fluoxetine (Prozac). Unfortunately, there is risk of heart disease.
- seem to increase short-term satiety signals during a meal. These agonists reduce: the urge to eat high-calorie food, the consumption of fats, the size of meals, the number of between-meal snacks, bingeing.

58
Q

Serotonin

A

is a monoamine neurotransmitter, it is an indolamine: synthetized form triptophan. Induces satiety in rats.

59
Q

Approximately 90% of the human body’s total serotonin is located in the

A

enterochromaffin cells in the alimentary canal (gut), where it is used to regulate intestinal movements. The remainder is synthesized in serotonergic neurons of the CNS, where it has various functions. These include the regulation of mood, appetite, and sleep. Serotonin also has some cognitive functions, including memory and learning. Modulation of serotonin at synapses is thought to be a major action of several classes of pharmacological antidepressants.

60
Q

Settling-Points in Weight Control

A

Body weight drifts around a natural settling point – “the level at which the various factors that influence body weight achieve an equilibrium.” There is no set point being defended. Leaky-barrel model.

61
Q

1st stage of a typical weight-loss program

A

weight loss occurs rapidly at beginning of diet.

62
Q

2nd stage of a typical weight-loss program

A

as weight declines, the amount of energy leakage is automatically reduced and this reduces the rate of weight loss.

63
Q

3rd stage of a typical weight-loss program

A

gradually reduced rate of intake is matched by the reduced energy output and a new stable settling point is achieved.

64
Q

4th stage of a typical weight-loss program

A

when the diet is terminated, weight gain is rapid because of the high incentive value of food and the low level of energy leakage.

65
Q

5th stage of a typical weight-loss program

A

as weight accumulates, the incentive value of food gradually decreases and the energy leakage increases until the original settling point is regained.

66
Q

leptin

A

a negative feedback fat signal (satiety signal). Peptide hormone released by fat cells. Leptin receptors found in the brain.

67
Q

ob/ob mice are

A

are three times normal weight. Homozygous for a mutant gene ob (1950). Lack leptin. Eat more, and store fat more efficiently than controls.

68
Q

Human leptin research

A

However, most obese humans have high leptin levels. Leptin injections help the few ob/ob humans. Useful in replacement therapy in lipectomy.

69
Q

insulin (negative feedback fat signal)

A

Brain levels of insulin are positively correlated with levels of body fat (especially visceral fat). Receptors of insulin were found in the brain. Brain infusions of insulin in rats reduced eating and body weight, but insulin-deficient individuals are not obese, unlike leptin-deficient ones.

70
Q

insulin-deficient individuals are not necessarily fat

A

despite hyperphagia, they remain slim because they cannot convert food to fat without insulin and most of the excess calories are excreted.

71
Q

Why Do Some People Become Obese and Some Not?: energy input differences

A

Craving for high-calorie foods (advertising). Cultural, environmental factors (farms vs. city). Large cephalic-phase response to sight and smell of food.

72
Q

Why Do Some People Become Obese and Some Not?: energy output differences

A

Exercise: walking 3 miles = 150 Cal = 1candy bar. NEAT (nonexercise activity thermogenesis). Many genes linked to obesity: difficult to sort out.

73
Q

Anorexia

A

voluntary self-starvation; self perception as being fat. About 2.5% of population, mostly women. Fatal in 10% of patients.

74
Q

Bulimia

A

cycles of bingeing and purging, without extreme weight loss. Associated with obsessive-compulsive disorder and depression. can be associated with acid reflux, loss of vitamins, minerals, electrolytes, and dehydration.

75
Q

Energy is stored as:

A
  • fats in adipose tissue (85%).
  • proteins in muscle (14.5%).
  • glycogen in muscle and liver (0.5%).
76
Q

In the 1940s and 1950s, it was proposed that food components would go from the

A

gut to the brain through the blood stream and provide information (feed back) about energy supply: it would produce satiety if supply is large, and hunger if energy supply is small. several possibilities could provide feedback: lipids, amino acids, and glucose.

77
Q

Later it was proposed that it was not the level of blood-glucose which was regulated but the

A

level of glucose utilization. This explain cases of hyperphagia (overeating) associated with high levels of blood-glucose, as in patients with diabetes mellitus. in these patients, the pancreas does not produce enough insulin, which is needed for glucose to enter most cells in the body and be utilized.

78
Q

The Dual-Center Set-Point model

A

A theory of eating behavior based on the satiety center (VMH), the hunger center (LH), and the glucose and body fat set points was very popular in the 1940s and 1950s.

79
Q

In rats, when the caloric content of food is reduced (mixing food with nonnutritive material), rats

A

increased their intake so as to maintain their caloric intake at normal levels! However, if caloric content was reduced beyond 50%, rats lost weight.
Several conclusions come from this experiment:
1. Somehow, rats monitor their caloric intake.
2. A decrease in caloric intake produces a compensatory increase in eating.
3. Stomach distention inhibits the consumption of large volumes of food.

80
Q

New evidence shows that bilateral VMH lesions increase

A

blood insulin levels, which increases lipogenesis (production of body fat) and decreases lipolysis (the breakdown of body fats into molecules that can be utilized for energy production). Thus, to have calories in the blood that are readily available for immediate energy use, the rats must keep eating.

81
Q

Some of the effects of VMH lesions can be attributed to

A

lesions of neighboring structures, such as the ventral noradrenergic bundle and the paraventricular nucleus. Lesions of these structures produce effects similar to those produced by VMH lesions.

82
Q

In the case of the LH, it has been observed that lesions of the LH not only produce aphagia and adipsia, but also other effects including:

A
  • motor disturbances
  • general lack of responsiveness to sensory stimuli.
    These observations indicate that the LH is not dedicated solely to feeding regulation.
83
Q

calorie-restriction experiments indicate that

A

reducing food intake below normal consumption levels has beneficial effects, including increased life span, better immune responses, and lower incidence of cancer.

84
Q

leaky barrel model

A

1) Water entering represents the amount of food available.
2) Water pressure at the nozzle represents the incentive value of the food.
3) Amount of water entering the barrel is analogous to the amount of consumed energy.
4) Water level is analogous to level of body fat.
5) Water leaking is analogous to the amount of energy being expended.
6) Weight of the barrel is analogous to the strength of the satiety signal.
If one overeats, more leakage occurs and a new level is reached which is not too far from the initial equilibrium level. If intake is reduced, less leakage occurs and again a new settling point is achieved, not too far from the first.

85
Q

Permanent changes in body weight require

A

permanent changes in factors that influence energy intake and output.

PSYCH 202 Exam 4 (3 decks)

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