Ch. 12- Hunger, Eating and Health Flashcards
1
Q
What are the three forms of energy resulting from digestion?
A
lipids (fats), amino acids (proteins) and glucose (sugar)
2
Q
3 form the body store energy in between meals?
A
Stored in three forms: fats, proteins, and glycogen
- most is stored as fats, a little is stored as protein and glycogen
3
Q
Why is fat primarily used for energy?
A
because one gram of fat can store twice as much energy as a gram of glycogen
- glycogen holds a lot of water so we would weight a lot
4
Q
What are the three phases of energy metabolism?
A
Cephalic, absorptive, fasting
5
Q
Explain the cephalic phase
A
- preparatory phase
- begins with sight, smell, or thought of food
- ends when food is absorbed into the bloodstream
- insulin lowers the levels of glucose in anticipation of the impeding influx
6
Q
Explain the absorptive phase
A
- period during which the energy is absorbed in the bloodstream meeting the body’s immediate energy needs
7
Q
Explain the fasting phase
A
- period during which all of the energy from the previous meal has been used and the body starts to use stored energy to meet immediate needs
- ends when the cephalic phase begins
- high levels of glucagon and low levels of insulin
8
Q
The flow of energy between phases is controlled by what hormones
A
pancreatic hormones insulin and glucagon
9
Q
Describe 3 functions of insulin
A
- Promotes the use of glucose as the primary energy source
- Promotes the conversion of blood-borne fuels to forms that can be stored
- Promotes the storage of glycogen in the liver, fat in adipose tissue and protein in muscles
10
Q
Explain the role of insulin during the cephalic phase
A
insulin lowers the levels of glucose in anticipation of impending influx
11
Q
Explain the role of insulin during absorptive phase
A
insulin minimizes the increasing levels of bloodborne fuels by utilizing and storing them
12
Q
Explain the role insulin during the fasting phase
A
Low levels of insulin increases glucagon
- glucose has a hard time entering cells and therefore stops being the primary fuel source
- low levels of insulin promotes conversion of glucagon and protein to glucose (gluconeogenesis)
13
Q
What is the set point assumption
A
The theory that ppl think hunger is attributed to the presence of an energy deficit (deviating from set level)
- after a meal, persons energy is assumed to be at their set point, as energy is being used it falls and once it is low enough, the person is motivated to eat
- negative feedback system
14
Q
What are the 3 components of the set point assumption
A
- set point mechanism (defines set point), detector mechanism (detects deviations from set point), effector mechanism (acts to eliminate deviations from set point)
15
Q
What is the glucostatic theory
A
- eating is regulated by a system designed to maintain blood glucose set point
- We become hungry when our blood glucose levels drop below set point and we become satiated when eating returns or levels to normal
- This makes sense because glucose is the brains primary source of energy
- Thought to determine meal initiation
16
Q
What is the lipostatic theory
A
- Every person has a set point for body fat, and deviations from this set point produce adjustments in the level of eating that return levels of body fat to their set points
- Support from this theory comes from the fact that most adults stay the same weight
- Thought to determine long term regulation
17
Q
What are 3 problems with the set point theories
A
- Inconsistent with basic eating related evolutionary pressures: in order to survive, they had to eat a lot when it was available which makes it hard to view a set point theory as plausible
- Reductions in blood glucose or the magnitude needed to reliably induce eating do not occur naturally, and high levels of fat deposits at the time of eating are associated with increased rather than decreased hunger
- Fail to recognize the important factors like taste, learning and social influences
18
Q
What is the positive incentive perspective on hunger and eating?
A
- We are driven to eat because of the anticipated pleasure instead of internal energy deficits
-We have evolved to crave food (not just bc we need it) - The degree of hunger you feel at any time depends on the interaction of all the factors that influence the positive incentive value of eating
○ Flavour of the food, type/quantity of food, what the effects are, when you last ate, whether other ppl are eating, your glucose levels etc. - This theory doesn’t single out one factor as the determinant of hunger
19
Q
What are two factors that determine what we eat?
A
- Learned taste preferences and aversions:
○ Learn to prefer tastes that are followed by an infusion of calories
○ Learn what to eat from ppl around us- Learning to eat vitamins and minerals:
○ When we are deficient in sodium, we crave salty foods
○ When animals are deficient in another vitamin, they have to learn to craze the effects of the vitamin (they need to want to eat the diet that makes them feel healthy)○ Harris rat study:
Thiamine deficient rats were offered two new diets, one with thiamine and one without and all learned to eat the complete one and ignored the deficient one
But, when they were offered 10 new diets, only one contained the thiamin and a few developed the preference for the complete diet
- Learning to eat vitamins and minerals:
20
Q
What are two factors that determine when we eat?
A
Premeal hunger:
- Woods: the key to understanding hunger is to appreciate that eating meals stresses the body
○ Before a meal, energy reserves are in reasonable homeostasis, but as a meal is consumed there is a disrupting influx of fuels into the bloodstream
○ To combat this, the body enters into the cephalic stage to soften the impact and releases insulin and reducing glucose
○ Mealtime hunger is caused by the expectation of food (and the preparation) and not by an energy deficit
Pavlovian conditioning of hunger
- Weingarten confirmed from rats that hunger is caused by expectation of food and not an energy deficit
- Found that rats would eat at the time the buzzer was presented even if they had just had a meal
21
Q
List the major factors that influence how much we eat
A
Satiety signals, sham eating, appetizer effect, serving size, social influences, sensory specific satiety
22
Q
Describe satiety signals
A
- Food in the gut and glucose entering the blood can induce satiety signals inhibiting consumption
- These signals depend on the volume and nutritive density of the food
23
Q
Describe sham eating
A
- Indicates that satiety signals from the gut or blood are not necessary to terminate a meal
- In experiments testing this, food is chewed and swallowed by passes out of the body through a tube
- Because this theoretically adds no energy for the body, set point theories predict that all sham eaten meals should be huge but this is not the case
- Instead this indicates that satiety is a function of previous experience, not the current increases in the body energy resources
24
Q
Describe appetizer effect
A
- Small amounts of food consumed before the meal increases hunger rather than reduces it
- Consumption of small amounts of food is particularly effective in eliciting cephalic phase responses
25
Describe serving size
- The larger the serving, the more we tend to eat
26
Describe social influences and satiety
- Satiety also depends on if we are eating alone or with others
- We consumes more when eating with others
27
Describe sensory specific satiety
- Number of tastes available has a major effect on satiety
- As you eat one food, the positive incentive value of all food declines slightly, but the positive incentive value of that particular food plummets and you become satiated on that food, but if another food is offered you will being eating it again
28
Describe Rolls findings on sensory specific satiety
- Human volunteers rated the palatability of 8 foods and ate a meal of one of them, after the meal they were asked to rate the palatability of the 8 foods again,
○ Ratings of the food they just ate declined way more than the other 7 foods
Rolls suggests that sensory specific satiety has 2 main effects:
- Brief effects influencing the selection of food within a single meal
- Relatively enduring effects influencing the selection of foods from meal to meal
- Rice, potatoes, bread and sweets are immune to sensory specific satiety
29
Describe Booths findings on sensory specific satiety
Asked volunteers to rate the momentary pleasure produced by the flavour, the smell, the sight, or thought of various foods after consuming a large high caloric liquid meal
○ Decrease in the palatability of foods of the same flavour as was consumed, this was followed by a decrease in the palatability of all substances about 30 mins later
○ Signals from taste receptors produce immediate decline in positive incentive value of similar tastes and that signals associated with the post ingestive consequences of eating produce a decrease in the incentive value of all foods
30
What is the relationship between blood glucose levels and hunger and satiety?
- Glucose does not decline gradually, instead it occurs suddenly before eating begins
- Eliminating the premeal drop in glucose does not eliminate the meal
- If expected meal is not served, blood glucose will return to previous level
- Glucose levels in extracellular fluid stay relatively constant, even when blood glucose levels in the circulation drop
31
Describe the myth of hypothalamic hunger and satiety
- Satiety was thought to be controlled by ventromedial hypothalamus (VMH)
- And hunger by lateral hypothalamus (LH)
- In the 1940s it was discovered that lesions to the VMH produced hyperphagia (over eating) and extreme obesity in rats
○ Two phases:
Dynamic: begins as soon as the subject regains consciousness after operation and is characterized by over eating and rapid weight gain for several weeks
Static phase: consumption gradually declines to a level just sufficient to maintain the rats new weight
- Anand and Brobeck reported that lesions to the LH produce aphagia (cessation of eating leading to death)
- Teitelbaum and Epstein discovered 2 important features of LH syndrome:
○ Aphagia was accompanied by adipsia (cessation of drinking)
○ LH lesioned rats partially recover
32
Recent research on the role of the hypothalamic nuclei in hunger and satiety
- evidence suggests that certain distinct cell population within the hypothalamus can influence hunger and satiety
- certain neurons in the paraventricular nucleus of the hypothalamus act as nutrient sensors that can influence feeding and satiety
- neuronal populations in the arcuate nucleus of the hypothalamus have been shown to influence the metabolism of energy resources (consumed food)
33
Explain Cannon and Washburn's study on the role of the gastrointestinal tract in satiety
- Washburn swallowed an empty balloon tied to the end of a thin tube
- Cannon pumped air into the balloon and connected the end of the tube to a water filled glass so that Washburns stomach contractions produced an increase in the level of the water at the other end of the U-tube
- led to the theory that hunger is the feeling of contractions caused by an empty stomach whereas satiety is the feeling of stomach distention
34
Explain other studies related to GI tract and eating
Koopmans extra stomach:
- transplanted an extra stomach and intestines into rats then joined the major arteries of implants to the recipients circulatory system
- found that food injected into the transplanted stomach and kept there by a noose decreased eating in both caloric and volume content
- this tells us that there has to be some chemical released from the stomach in response to the caloric value or volume of food
35
Describe the discovery of the role of hypothalamic circuits, peptides and the gut in food consumption and metabolism
- After they discovered that the stomach releases chemical signals to the brain, they found that these chemicals were peptides (short chains of amino acids that function like hormones/neurotransmitters)
36
How does food cause release of peptides?
- ingested food interacts with receptors in the GI tract which causes the release of peptides into the bloodstream
37
Functions of peptides
- Function as satiety signals
- bind to receptors in the brain (especially in the hypothalamus areas responsible for energy metabolism)
- Some produce metabolic changes that reduce food intake (satiety peptides)
38
Relationship of CCK (cholecytostokinin) and rats
- when injected into rat, they ate smaller meals
- satiety peptide
- induces nausea in humans
39
Widely studied hunger peptides
- neuropeptide Y
- orexin-A
- ghrelin
- galanin
40
What is the role of serotonin in satiety?
3 major properties:
- caused rats to resits powerful attraction of highly palatable cafeteria diets
- reduced the amount of food consumed during each meal rather than reducing the number of meals
- was associated with a shift in food preferences away from fatty foods
41
Why is serotonin useful in combating obesity
- reduce hunger and eating
42
What is Prader-Willi Syndrome
- insatiable hunger, little to non satiety, slow metabolism
- acts as though they are starving
- weak muscles, small hands and feet, impulsivity
- if untreated they become obese, and usually die from diabetes or heart disease
43
Etiology of Prader Willi syndrome
- accidental chromosomal replication
- accident of reproduction that deletes or disrupts a section of chromosome 15 coming from the father
44
What are three things that challenge fundamental aspects of set point theories of body weight regulation?
Variability of bodyweight: set point mechanism should make it virtually impossible for an adult to gain or lose large amounts of weight but this is not the reality (overeating)
Set points and health: free feeding levels of consumption are unhealthy, reductions in calorie intake have improved health and longevity
Regulation of body weight by changes in the efficiency of energy utilization: as a persons level of body fat declines, that person starts to use energy resources more efficiently which limits further weight loss
45
What is diet induced thermogenesis
- the mechanism by which the body adjusts to the efficiency of energy utilization in response to its levels of body fat
- increases in the level of body fat increases body temperature, which require additional energy to maintain and decreases in the level of body fat have opposite effects
46
What is basal metabolic rate
- the rate at which energy is utilized to maintain bodily processes when resting
47
What is the settling point model in weight control?
- states that body weight tends to drift around a natural settling point (the level at which various factors that influence body weight achieve an equilibrium)
- as body fat increases, changes occur that tend to limit further increases until a balance is achieved between all factors that encourage weight gain and all those that discourage it
- body weight remains stable as long as there are no long term changes in the factors that influence it
- A neurons resting potential is a well known settling point
48
Why is the settling point model called the leaky barrel model
- amount of water entering hose is the food available
- water pressure is the positive incentive value of the food
- amount of water entering is the amount of energy consumed
- water level in the barrel is the level of body fat
- amount of water leaking from the barrel is the energy being expended
- the weight of the barrel on the hose is the strength of the satiety signal
49
Why do some ppl gain weight from overeating while others do not
Differences in energy expenditure:
- difference in exercise
- differences in basal metabolic rate
- non exercise activity thermogenesis (fidgeting and maintenance of posture and muscle tone)
Differences in gut microbiome:
- microbes can influence neurodevelopment, blood barrier, etc.
- mice colonized with microbes from the twins with high body fat levels gained more weight and had greater amounts of body fat compared to those with microbes from the learn co twins
Genetic and epigenetic factors
- single gene mutation have been linked to pathological conditions that involve excessive weight gain
50
Why are weight loss programs often ineffetive?
settler model says: most of the lost weight is regained once the dieter stops the program and the original conditions are reestablished
- key to permanent weight loss is permanent lifestyle change
51
Describe the discovery of leptin
- in 1950, a genetic mutation occurred in the mouse colony at Jackson Lab
- the mutant mice were homozygous for the gene ob and had high levels of body fat
- these mice are called ob/ob mice
- they eat more than control mice, convert calories to fat more efficiently and use calories more efficiently
- this gene is expressed only in fat cells and characterized the protein it normally encodes (leptin)
- ob/ob mice lack leptin (which was thought to decrease appetite and increase fat metabolism)
52
Findings that support insulin as a negative feedback signal in the regulation of body fat
- receptors for insulin were found in the brain
- brain levels of insulin were found to be positively correlated with body fat levels
- genetically modified mice that have lower levels of brain insulin also display higher levels of fat
- humans with high levels of fat have lower levels of insulin in their brains
53
Leptin levels are more closely correlated with ___ fat whereas insulin levels are correlated with ___fat
subcutaneous (under the skin) , visceral (around internal organs)
54
Distribution of leptin and insulin
- in the arcuate nucleus
- on neurons that release neuropeptide Y (gut hinger peptide) and melanocortins (includes gut satiety peptide)
55
Two treatments for overeating and high body fat
Serotonergic agonists:
- increase short term satiety signals
- reduce the urge to eat high calorie food, size of meals etc.
Gastric bypass:
- surgical treatment short circuiting the normal path of food through the digestive tract so absorption is reduced resulting in weight loss
56
Symptoms of anorexia nervosa
- underconsumption disorder
- eat so little they experience severe weight loss
- they often perceive themselves as fat (skewed representation)
- high rate of death and suicide
57
Symptoms of bulimia nervosa
- periods of not eating interrupted by binge eating followed by purging (efforts to eliminate what was consumed)
- may be overweight or underweight
58
Explain how anorexia and bulimia are related
- both begin with an obsession with body weight and slimness and extreme efforts to lose weight
- both try to lose weight by restriction or dieting
- those with bulimia are less able to control eating and enter into binge-starve cycle
- distorted body images
59
How does the positive incentive affect anorexia
- suggests that the decline in eating results from a corresponding decline in the positive incentive value of food
