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Psych370 > module 4 > Flashcards

module 4 Flashcards

1
Q

how many calories does the avg American consume per day?

how many times required is this?

A

3800, 2x

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2
Q

what percentage of the US population is overweight or obese?

A

68

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3
Q

what is the lifetime prevalence of individuals in the US with anorexia or bulimia

A

1.2

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4
Q

what is the common assumption about the trigger for eating?

A

when the bodies energy sources fall below a set point

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5
Q

Describe the case of the “man who forgot not to eat”

A

RH was offered 4 meals at 15 minute intervals, ate the first three no problem, didn’t eat the fourth, then after a few minutes went for a walk to get more

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6
Q

what is the primary purpose of hunger?

what is the primary purpose of eating?

A
  1. to increase probability of eating

2. to supply the body with molecular building blocks

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7
Q

define digestion

A

gastrointenstinal process of breaking down food and absorbing its constituents into the body

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8
Q

what is the gut biome, and what is its main function?

A

the bacteria and other organisms living within our gastrointestinal tract.
to breakdown food as it passes through the tract

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9
Q

what are the three forms of stored energy in the body, and why are they necc?

A
  1. fats, glycogen and proteins

2. bc the body continuously uses energy but does not continuously absorb it

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10
Q

what is the bodies preferred storage system?

why? as related to glycogen (2)?

A

fats

  1. store around 2x as much energy per gram as glyc
  2. does nt hold a lot of water (if we stored mostly as glycogen, we would be fuckin heavy)
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11
Q

what are the three phases of energy metabolism

A
  1. cephalic phase
  2. absorptive
  3. fasting
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12
Q

describe the cephalic phase of enrg meta

A
  • prepratory phase, begins with the perception of food and ends with the food beginning to be absorbed
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13
Q

describe the absorptive phase of enrg meta

A
  • energy absorbed from a meal is meeting to bodies immediate energy needs
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14
Q

describe the fasting phase of enrg meta

A

all of the unstirred enrg from the previous meal has been used, and the body is now using enrg from its reserves
- ends at the beginning of the next cephalic

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15
Q

what does the process of energy metabolism look like in those who are gaining weight rapidly?

A

cut out the fasting phase, straight from cephalic to absorption

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16
Q

what are the two hormones that control the stages f energy metabolism?
where are they secreted?

A
  1. insulin
  2. glucagon
    - - pancreas
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17
Q

during which phases does the body release insulin > glucagon?

A

cephalic and absorptive

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18
Q

what are the three main functions of insulin?

A
  1. promotes the use of glucose as the primary energy source
  2. promotes the conversion f blood borne fuels into forms that can be stored (glucose to glycogen, fat, a acids to proteins)
  3. promotes the storage of glycogen in the liver and muscle, and fat in the adipose tissue, and proteins in the muscle
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19
Q

what is the general role of insulin in the cephalic phase

A

lower levels of blood borne fuels (specifically glucose) in preparation for the impending influx

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20
Q

what is the general role of insulin in the absorptive phase

A

minimize the increasing levels of bloodborne fuels by utilizing and storing them

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21
Q

during which phase of enrg meta does the body secrete glucagon > insulin?

A

the fasting phase

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22
Q

`what do low levels of insulin cause?

what is the major secondary effect off this, and why?

A

glucose build up in blood, specifically because it has trouble entering most cells
saves glucose for the brain, bc neurons dont need it to intake glucose

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23
Q

what is a secondary effect of low insulin levels?

A

promote the conversion of glycogen and protein into glucose, called gluconeogenesis

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24
Q

what do high levels of glucagon promote?

what happens to brain cells if the second effect is maintained over time?

A
  1. release of free fatty acids from adipose tissue, along with their use as the bodies primary source of fuel
  2. conversion of these free fatty acids to ketones, used by muscles as a source of energy during the fasting phase
    - if the body goes a long time without food, tho, the brain will also used ketones which further preserves the stores f glucose
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25
Q

define the set-point assumption

A

the belief that hunger (as motivation to eat) is always a response to an energy deficit (energy set point)

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26
Q

what occurs after a meal according to the set-point assumption?
what ends a meal?

A

energy resources are assumed to be near their set point, decline after
- eat until satiated (no longer hungry) which is believed to correspond to arriving at the set point

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27
Q

what are the three components of all set point systems

A
  1. set point mechanism
  2. detector mechanism
    3, effector mechansim
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28
Q

what is the set point mechanism?

A

that by which the body defines a set point

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29
Q

what is the detector mechanism

A

that which detects deviations from the set point

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30
Q

what is the effector mechanism

A

that which acts to eliminate any deviations from the set point

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31
Q

what are all set point systems defined as? explain

A

negative feedback systems - feedback from changes in one direction elicit compensatory effects in the opposite direction

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32
Q

why are negative feedback systems common in mammals?

A

act to maintain homeostasis (stable internal environment) which is critical to survival

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33
Q

why were set point systems assumed to be necessary prior to the discover of adult brain plasticity?
what did this discovery do to the underlying logic of the set point system?

A

since the brain couldn’t change, energy resources had to be very regulated
made it seem less necessary

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34
Q

define the glucostatic theory

what is the primary piece of evidence

A

set-point offshoot that argued blood glucose is the set point measure,
- glucose is our brains primary fuel

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35
Q

define the lipostatic theory

what is the primary piece of evidence?

A

set-point offshoot that argued that each person has a set body fat percentage, deviations from which alter eating requirements so as to level out back to the set point
- adults weights stay fairly fixed

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36
Q

what is the relationship between the glucosattic and lipostatic theories?

A

complementary

  • glucostatic accounted for meal initiation and termination
  • lipostatic accounted for long term regulation
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37
Q

what are the three main problems with the set-point theory? evidence?
1 - (1)
2 - (3)
3 - (phenomenological 1)

A
  1. the evolutionary account - our ancestors main problem was inconsistency of food sources - doesn’t make sense that our hunger system is designed only to respond to immediate requirement, rather than future potential requirements (long term storage)
  2. major predictions just dont work - large reductions in glucose or body fat in lab animals that produce eating behaviours are never present to a similar magnitude in nature. lots of people have enough fat to survive for awhile, but eat anyways, and if we give ppl high calorie drinks before a meal they will still eat!
  3. fail to recognize the importance of influences such as taste, learning and social influences.
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38
Q

what is the positive-incentive theory of hunger and why did it arise/

A

bc of the failure to account for several hunger phenomena (the problems with set-point theories)
- postulates that hunger and eating are promoted by the positive-incentive value of eating, ie that we know it will make us feel good

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39
Q

is the positive-incentive theory of hunger one theory?

A

no, it is several that are considered the positive incentive perspective

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40
Q

according to the positive incentive theory of hunger, what is eating similar to?

A

sex - we engage in these behaviours because we crave them

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41
Q

what its he evolutionary explanation for the positive incentive theory of hunger?

A

unexpected food shortages have made us love to eat when there is good food around

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42
Q

what influences the degree of hunger at any given moment according to the positive incentive perspective?
what are some of these? (6)

A

the interaction of all the factors that influence the reward value of eating.

  1. flavour of food
  2. learned of effects of the food
  3. time since last feeding
  4. type and quantity of food in the gut
  5. whether or not there are other ppl around
  6. blood glucose levels
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43
Q

what is a major benefit of the positive incentive perspective?

A

doesn’t single out any one factor - there are lots

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44
Q

why are energy deficits not included among the list of factors that determine when/what/how much we eat?

A

because in our current situation (food-replete societies) we never encounter deficits of sufficient magnitude to actually stimulate hunger

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45
Q

why do humans prefer sweet, fatty and salty flavours?

A

sweet and fatty - typical of high energy foods rich in vitamins and minerals
salty - sodium rich

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46
Q

why do humans not like bitter tastes

A

denote foods rich in toxins

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47
Q

are human taste preferences universal?

A

no way jose

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48
Q

what are the two main ways humans and other animals learn what to enjoy

A
  1. prefer tastes that come with calorie influx, hate those hat make them sick
  2. conspecificis - species or culturally specific taste preferences that are learned socially
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49
Q

what are some examples of rats conspecific learning of food preferences

A
  1. like what is similar to tastes in mothers milk

2. like what they smell on the breath of other rats

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50
Q

what are the two ways animals learn to enjoy foods that contain necc. vitamins and minerals?

A
  1. sodium - deficiencies result in the craving of sodium rich food
  2. other - learn to like the effects of foods that contain the minerals, since they have no taste
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51
Q

Give an example of animals learning to enjoy foods rich in a mineral/ vitamin despite there not being any taste to it?

A

rats raised on a thiamine (B1) deficient diet will prefer a diet that has high B1 levels in it to one that is deficient bc of the positive health effects

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52
Q

what are the two main reasons that humans have so many vitamin and mineral deficiencies despite our ability to learn too prefer their health effects?

A
  1. lack of nutrients in market goods - companies produce tasty shit that isn’t any good bc it makes moe money
  2. variety of possible diets - if rats w B1 deficiency are offered 10 new dietary options, not a lot learn to prefer the thiamine one bc they cannot associate
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53
Q

what is a major difference between eating frequency in most mammals and humans

A

mammals prefer small snack sized meals throughout the day when there is ample resources, but humans (particularly those in large family groups) eat a few big meals

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54
Q

what is the association between typical meal time and hunger

A

we get hungry when we usually eat, and our negative symptoms of hunger are experienced when we miss such a meal

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55
Q

what is Wood’s position on premeal hunger

A

learning that a meal time approaches causes the body to enter is cephalic phase, releases insulin into the blood (decreases glucose)
thus, premeal hunger is the bodies preparation for the massive influx of nutrients prior to meal time, and the resulting homeostatic changes

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56
Q

describe the Weingarten study that supported Wood’s position on premeal hunger

A

pavlovian conditioning in rats - irregular feeding intervals began by a tone
when food is continuously present, the sheer presence of the tone caused them to eat, even if they had just finished

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57
Q

what is the motivational state that determines when we should stop eating

A

satiety

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58
Q

what induces satiety signals? what do their magnitudes depend on?

A

food in the gut, glucose entering the blood

- volume and nutritive density (calories per unit volume)

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59
Q

describe the findings on lab rats that demonstrate the importance and limitations of nutritive density

A

rats fed one baseline of consumption, then change nutritional density
- can adjust to preserve body weight until the density is reduced by more than 50% (lose weight) or major changes to palatability

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60
Q

what is the sham eating paradigm

A

artificially changing physiology to project food not into the stomach but just out of the body

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61
Q

what doe sham eating studies find?

what does this indicate about satiety?

A

contrary to the set point theory (meals should be huge if there is no change in energy), the first meal is the same as usually, but then they begin to increase slowly over time
- that it is a function of experience and learning

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62
Q

what is the appetizer theory, and what does it indicate about the set-point theory?
why does it work?

A
  1. small bites of food increase hunger, not the other way around
  2. buuulshit, this makes no sense under that view
  3. probs bc small amounts of food activate the cephalic phase response and prepare the body for calorie influx
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63
Q

how does serve size influence consumption

A

larger the serving, the more we eat

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64
Q

how do social factors influence consumption

A

we eat more in the presence of others, which is the same in rats

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65
Q

what is the effect of the cafeteria diet and what does this indicate? (2)

A
  1. cafeteria diets (lots of different tastes) increase caloric intake in rats by up to 84 percent, and body weight by up to 50 after 120 days
    a) number of different tastes has a major effect on serving size
    b) set pint theory is bs
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66
Q

what is the major conclusion fo the lab. results of the cafeteria diet?

A

satiety is very much sensory specific
- when we eat a lot of food a), our positive incentive for food a plummets, but for b and c it only goes down a bit, so if we can switch from a to b or c we are happy to. do so

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67
Q

describe the rolls study on sensory-specific satiety

A
  • human volunteers asked to rate the palatability of 8 foods
  • then ate a meal of one of them
  • after the meal, asked to rerate the 8 foods
  • rating of the meal they had eaten had declined way more than the other 7
  • when offered a surprise second meal, ate most of it UNLESS it was the same type of food
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68
Q

explain the Booth study on sensory-specific satiety

A
  • volunteers to rate the pleasure prod. by flavour, smell sight or thought of foods at times after consuming a large, high calorie high carb liquid meal
  • immediate sen. specific decrease in the palatability of foods of similar flavour to the original meal right after consumption
  • decrease in all palatability 30 minutes later
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69
Q

what is the general conclusion of the Booth study on sensory-specific satiety (2)

A
  • signals from tase receptors produce an immediate decline in positive incentive value of similar tastes
  • signals associated with the post ingestive consequences of eating produce a general decrease in palatability of all food
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70
Q

what did rolls suggest the two effects of sensory specific satiety are

A
  1. relatively brief effects that influence the selection of foods within a single meal
  2. relatively long term effects that influence of the selection of foods between meals
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71
Q

are the long term effects of sensory specific satiety universal among foods?

A

nope, rice, bread, potatoes, sweets, green salads can be mucked all the time with no palatability decline.

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72
Q

what are the two adaptive consequences of sensory specific satiety?

A
  1. encourages consuming a varied diet

2. encourages animals with access to a large variety of foods to eat a lot to preserve it in storage for less good times

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73
Q

explain the campfield and smith study on glucose levels during eating rituals, and the conclusions the study draws

A

measured blood glucose levels in rats housed with free access to food and water

  • blood glucose rarely ever changed more than about 2%
  • but dropped 8% before meals
  • not glucose decrease then hunger, but desire to feed then glucose decrease
74
Q

what are the four relevant observations of the campfield and smith study on glucose levels (4)

A
  1. time course of blood glucose does not reflect the glucose set point theory - decline occurs rapidly right before eating, not at a stable rate
  2. eliminating premeal drop in blood glucose does not stop one from eating
  3. if an expected meal is not served, bg goes back to normal levels
  4. glucose levels in the extracellular fluid surrounding the CNS stay fairly constant, even when levels drop in general
75
Q

what were the two brain areas that were thought to control eating behaviours in rats in the 1950s?
was this right?

A
  1. ventromedial hypothalamus
  2. lateral hypothalamus
    noooooope
76
Q

what did bilateral electrolytic lesions to the ventromedial hypothalamus cause? what do we call this?

A

hyrerphagia - excessive eating and extreme obesity

VMH syndrome

77
Q

what are the two phases f VMH syndrome

A
  1. dynamic phase - starts as soon as the patient wakes up, characterized by several weeks of a lot of eating and weight gain
  2. static phase - eating declines to a level that maintains as stable degree of obesity
78
Q

what is the most important feature of the static phase of VMH syndrome

A

the animal will always maintain its new weight - if its starved until weight loss, it will regain he weight, and if force fed to a new weight, it will lose it

79
Q

describe the Anand and Brobeck findings surrounding the LH feeding centre

A

bilateral electrolytic lesions to the lateral hypothalamus produce aphagia (complete cessation of eating)
works even in those with VMH lesions
- concluded this is a feeding centre

80
Q

describe the Teitelbaum and Epstein findings surrounding the LH feeding centre (2)

A
  1. the aphasia was accompanied by adipsia - complete stoppage of drinking too
  2. partially recover if kept alive by tube feeding
    - first begin to eat wet, palatable foods, and eventually dry food pellets if water is also available
81
Q

what is the piece of evidence that caused a reinterpretation of the VMH syndrome (in terms of body fat production)
explain this mechanism

A
  1. primary role of the hypothalamus is the regulation of energy metabolism,. not the regulation of eating
    - overeat because they become obese, not the other way around
    - increase blood insulin levels (as caused by VMH lesions), increases lipogenesis (prod of body fat) and decreases lipolysis (breaking of body fat)
    - so nutrients are converted to fat so fast they have to keep eating to ensure they have enough calories in their blood
82
Q

What are the other brain regions that produce the same symptoms as VMH dmg
explain

A

many effects of VMH lesions are not attributable to dmg to that area

  • large fibre bundle Called the ventral noradrenergic bundle runs through it and is always damaged when it is
  • these fibres project from the nearby paraventricular nuclei of the hypothalamus
  • bilateral lesions to either the bundle or thhe paraventricular nuclei cause hyrerphagia just like VMH lesions
83
Q

what is the main evidence that refuted the LH feeding centre interpretation?

A

there are more general sensorimotor disturbances that follow lesions to this structure, mostly a general lack of responsiveness to sensory input

84
Q

what are the two pieces of evidence that support hunger motivation localization (3 on 2)

A
  1. certain neurons in the paraventricular nucleus of the hypothalamus act as nutrient sensors (can influence hunger)
  2. a few neuronal populations in the arcuate nucleus uf the hypthal either 1. control metabolism of adipose tissue, 2. reduce feeding or 3. increase feeding
85
Q

explain the Washburn and cannon study on the balloon

A

inserted a balloon, pangs of hunger when they recorded a large stomach contraction - thought that hunger was the result of stomach contractions when it was empty

86
Q

what findings shit on the Washburn and cannon study

A

patients with surgically removed stomachs, esophagus hooked directed to the duodenum (first area of the small intestine) continued to report hunger and satiety, and maintained. weight by eating more, smaller meals

87
Q

explain the Koopmans study on satiety signals from the GI tract
- what are two main conclusions

A

transplanted an extra stomach and intestine into rats and joined the major arteries to ie
food injecting into the transplanted stomach and held there w a noose around the pyloric sphincter decreased eating in proportion to both caloric content and volume
1. new organs had no nerve fibres - had to be signalling the brain through blood
2. since food is not absorbed in the stomach, this blood borne chemical could not be a nutrient, must be some chemical released in response to the presence of food \

88
Q

what is the molecular structure of the chemicals released by the stomach that signal satiety

A

peptides

89
Q

explain the Gibbs, Hund and Smith study on chemical satiety signals in rats
what hypothesis did this lead to?

A 
injected cholecystokinin (a peptide) into hungry rats - ate smaller meals 
- circulating peptides tell the brain how much and nature of food in the GI tract
90
Q

what is some of the support for the existence and role of peptides in hunger? (2)

A
  • several gut peptides have been shown to bind to receptors in the brain (hypothalamus regions involved in meabolism)
  • dozen have been reported to reduce food intake (satiety peptides)
91
Q

what possibility concerning satiety peptides did researchers have to rule out?

A

that the peptides effects were not the result of illness

92
Q

which peptide has been shown to induce illness?

what are its effects in rats and humans, respectively?

A

CCK

  • in rats after they eat a novel substance induces conditioned taste aversin
  • in humans - nausea
93
Q

Why does CCK still qualify as a satiety peptide despite its illness inducing effects?

A

it still reduces appetite/eating at doses much lower than those necc t produce its illness

94
Q

where are hunger peptides synthesized?

A

in the brain, particularly the hypthalamus

95
Q

what are the 4 most widely studied hunger peptides?

A
  1. Neuropeptide Y
  2. Galanin
  3. Orexin-A
  4. Ghrelin
96
Q

what are the two effects fo the discover of hunger and satiety peptides?

A
  1. the vast number of them tell us that the NS responds to a lot of different signals when controlling for hunger
  2. relationship to the hypothalamus has renewed interest in its role in hunger and eating behaviours
97
Q

why supported the renewed interest in the hypthal in hunger and eating

A

discover that microinjections of gut peptides into some sites off the hyp that can really mess w hunger

98
Q

what is the general conclusion from the novel research on gut peptides and the hypohalamus

A

the hypthal circuits are only a part of a two pronged comm system between the Brian and gut

99
Q

what is a neurotransmitter that plays a major role in hunger and eating

A

seratonin

100
Q

what are the 3 main effects of serotonin induced satiety

A
  1. caused rats to resists the desire for cafeteria diets
  2. decreased the ammt of food consumed during each meal, rather than the number fo meals
  3. associated w a shift away from preference in fats foods
101
Q

what do we now believe about the utility of serotonin agonists in obesity?
give 3 examples of such drugs

A

they can maybe help decrease it

  1. fenfluramine
  2. dexfenfluaramine
  3. fluoxetine
102
Q

what is Prader-Willi syndrome

A

results from an accident of chromosomal replication

  • insatiable hunger
  • little or no satiety
  • very slow metabolism
  • muscle weakness, small hands and feet, feeding problems in infancy, tantrums, compulsivity and skin picking
103
Q

what ooccurs to most patients with Prader Willy if left untreated

A

obesity, heart disease r other related disorders, sometimes even dying from gorging too much so that their stomach splits open

104
Q

what is the precise genetic cause of prader will

A

an accident of reproduction that deletes or disrupts a section of chromosome 15 from the dad

105
Q

are obese people who are otherwise metabolically healthy safe from health risks?

A

nope

106
Q

is obesity only risky for the obese person?

A

no, obese women are at a higher risk of having kids with health problems

107
Q

where is the concern surrounding obesity greatest?

A

in the coming generations (like mine)

108
Q

what are the estimated statistics pertaining to diabetes and life threatening conditions for those born in 2000

A

1/3 of those in the sates will dev diabetes

10% with have related life threatening conditions

109
Q

what are the four characteristics of an evolutionary fit individual prior to civilizations?

A
  1. high calorie food preferences
  2. ate to capacity when food was avail.
  3. stored excess calories as body fat
  4. used their caloric stores efficiently
    - otherwise, wouldn’t survive the winers
110
Q

What are some f the cultural practices that promote consumption? (5)

A
  1. eat 3 meals per day, regardless f hunger
  2. food is the focus fo social gatherings
  3. meals should be served in courses of progressively increasing palatability
  4. salt, sweet, fats should be added t food to improve their flavour
  5. tendency to make unhealthy eating choices is passed on to kids
111
Q

what are the two main kinds f individual differences that result in some ppl getting obese while others do nt

A
  1. diffs in energy output

2. diffs in energy input

112
Q

what are three common reasons why some folks eat a lot

A
  1. strong preferences for calorie rich fods
  2. raised in families or cultures that promote over eating
  3. massive cephalic response to the sight or smell off foodos
113
Q

what are 3 individual differences outside of exercise that can cause some people too expend more energy
what’s the third?

A
  1. basal metabolic rate

2. diet induced thermogenesis

114
Q

what is a main strength of set point theories

A

account for body weight regulation

115
Q

what are the three lines of evidence that really give set point theories a hard time in terms of body weight

A
  1. shouldn’t let people change their weight a lot - bu they do (obesity epidemic, etc)
  2. suggest that the bodies desires are the best indicator of when and what to eat - very bad juju
  3. body weight is regulated by changes to efficiency of energy utilization
116
Q

what are the two pieces of evidence that ad libitum levels of consumption are unhealthy?

A
  1. Non-experimental studies - those who eat less calories (Okanaway), even if up to 40% less than suggested by health norms, are at 59%, 69% and 59% decreased risk of stroke, cancer, hearth disease respectively. up to 4x higher rates of making it past 100
  2. Experimental studies - rats on calorie-resprtricted diets fair better to the degree that they eat less - live 67% longer, lowest incidence of cancer, best immune responses, can be beneficial even in later life, supported in humans
117
Q

what are the two neurological conditions that have sown to be slowed by dietary restrictions

A
  1. epileptics - reduced seizure susceptibilioty

2. improves memory in the elderly

118
Q

what modulates body fat levels over and above caloric intake?

A

the bodies controlling how efficiently it uses its energy - as we lose body fat, we become more efficient, and it is hard to loose more and vice versa

119
Q

explain the Rothwell and Stock study that demonstrates the bodies ability to modulate energy use efficiency

A

created obese rats by maintaining them on a caf diet, found that resting energy levels in these dudes was 45% higher than in other rats

120
Q

describe diet induced thermogenesis

A

the mechanism by which the body adjusts the efficiency of its energy uses
- increased fat caused increased body temp, which requires more energy to maintain and vice versa

121
Q

describe basal metabolic rate

A

the rate at which energy is utilized to maintain bodily processes while at rest

122
Q

are those who have excellent basal metabolic rates and poor diet induced thermogenesis (ie, can loose weight quickly all the time) safe from the effect fo over eating

A

Nope, they can still get fucked even without obesity

123
Q

what is a more flexible version of the set point model (explain)

A

the settling point model, body weight tends to drift around a natural settling point, ie the level at which the various factors that influence body weight achieve an equillibrium
- as body fat levels increase, changes occur that limit further increase until a balance is achieved between all factors that encourange and discourage weight gain

124
Q

what are the two main implications of the settling point model

A
  1. body weight doesn’t change unless there are long term changes to the factors that influence it
  2. if changes do occur, they are limited by negative feedback, although this doesn’t return it to a set point, just limits changes in the same direction
125
Q

what is a functional analogue to the settling point model

A

a neurons resting potential

126
Q

describe the leaky barre model

A

1,. amount of water entering the hose is analogous to the ammt of food available

  1. water pressure at the nozzle is analogous to the positive incentive value of the food
  2. water in is food in
  3. water level in the barrel is fat
  4. amount of water leaking out is energy expenditure
  5. weight of the barrel on the hose is the strength of the satiety signal
127
Q

what are the main benefits of the settling point model fo the set point one

A
  1. more consistent with the data

2. when the two make the same prediction, the settling one does so more parsimoniously

128
Q

why is the settling point model useful to bio psychologists (2)

A
  1. better understand and predict changes to body weight in situations
  2. indicates the kinds of physiological mechanisms that mediate these changes
129
Q

what is NEAT

A

non-excerisize activity thermogenesis - the energy used by actives such as fidgeting or etc - doesn’t acct for much

130
Q

what is the proportion of gut microbes to body cells

A

10-1

131
Q

what are three things that the gut microbes can influence outside of food

A

neurodev, the blood-brain barrier and myelination of some CNS axons

132
Q

explain the Ridaura and colleagues study on the influence of gut microbiomes on body fat

A

two groups of rats, one that was obese one that was not, injected a third and fourth group with the microbiomes of each respectively, those that got the fat biomes were fatter

133
Q

how many human chromosome loci have been linked to obesity

what do many of these seem to influence

A

100

the degree to which obesity can influence gut microbiomes

134
Q

are there any single gene mutations that cause obesity

A

yes

135
Q

are there transgenerational epigenetic effects that can predispose generations to obesity

A

yes

136
Q

what is the only way to actually keep fat off

A

permanent lifestyle changes

137
Q

why is exercise not an effective weight loss strategy (3)

A
  1. only a small percentage of energy expenditure - most is just used to keep us alive
  2. efficient bodies - dont burn many calories
  3. ppl tend to think they can muck after exercise, which is bs
138
Q

is fat just a passive storehouse of energy? why or why not

A

no, because it actively releases the peptide hormone leptin

139
Q

what are ob/ob mice

4 symptoms

A

homozygous for the gene ob, which caused them all to be morbidly obese,

  • up to 3x heavier than ur avg mouse
  • eat more than controls
  • convert calories to fat better
  • use their calories more efficiently
140
Q

what did Coleman hypothesize about ob/ob mice

A

that they lack a hormone that normally inhibits fat production and maintenance

141
Q

where is the ob gene expressed, and what does it code for?

A

fat cells only, LEPTIN

142
Q

what did the discovery tat ob/ob mice lack leptin cause in terms of a hypothesize

A

leptin is a negative feedback signal normally released from fat stores to decrease appetite and increase fat metabolism
- maybe able to reverse obesity if administered to humans

143
Q

what hormone did woods et al think served a negative feedback role in body fat

A

insulin

144
Q

how can insulin provide negative feedback signals over long term periods if it fluctuates between meals?

A

doesn’t pen. the blood brain barrier so well, so it might work fine there

145
Q

what are the tree findings that support the conclusion that insulin serves as a negative feedback signal in the regulation of body fat?

A
  1. brain levels of insulin were psotiviely correlated with body fat levels (Seeley)
  2. receptors for insulin found in brain (Baura)
  3. Infusions of insulin into the brains of lab animals reduce eating and body weight
146
Q

why are there two negative feedback signals for body fat levels?
what do they code for specifically

A
  1. insulin codes for visceral fat whereas leptin codes for subcutaneous fats babyyyy
147
Q

which of the two types of fat is more dangerous to the human? is it more common in the mens or the women’s section?

A

VISCERAL, mens ocs

148
Q

where are the majority of receptors fro insulin and leptin located (general structure and specific sub structure)

A

in the hypothalamus, specifically the arcuate nucleus

149
Q

where are leptin and insulin receptors the arcuate nucleus predominant?

A

on two neuron classes

  1. those that release neuropeptide Y
  2. those that release melanocortins
150
Q

what is a melanocortin

A

a class of peptides that includes the gut satiety peptide alpha melanocyte-stimulating hormone

151
Q

why has attention to the arcuate nucleus of the hypothalamus focussed non the melanocortin system

A

injections of alpha melanocyte stimulating hormone have been shown to suppress eating, promote weight loss

152
Q

is the melanocortin system super important in weight loss?

A

No, elimination of leptin receptors in this system only produces a little bit of weight gain

153
Q

what were the two problems with using leptin in human patients to stop obesity

A
  1. unlike mice, have high leptin levels (obese ppl that is)

2. injections of leptin didn’t reduce eating or body fat

154
Q

when is leptin effective in treating obesity

A
  • few ppl have low leptin levels, but those who do it seems to work on a lot
155
Q

what are two common treatments for obesity

A

seratonergic agonists and gastric surgery

156
Q

what are the proposed mechanisms of seratongergic agonists in anti fat meds
what is the difference between these and leptin/insulin

A

increase short term satiety signals associated with the consumption of a mealtime
the others are long term

157
Q

what have serotonergic antagonists have been shown to influence (6)

A
  1. urge to eat high cal food stuffs
  2. consumption of fats
  3. subjective intensity fo hunger
  4. size of meals
  5. number of between meal snacks
  6. bingeing
158
Q

what are the long term effects of seratonergic antagonists (why were they removed from the market?)

A

bc they give heart disease for people!

159
Q

What is the only approved seratonergic antagonist for use and why?

A
  • lorcaserin, has a more favourable side effect profile, modest effects on obesity
160
Q

what is a gastric bypass?

A

surgical treatment for extreme obesity that involves short-circuiting the normal path of food through the digestive tract so its absorption is reduced

161
Q

what is an alternate procedure to gastric bypass

A

adjustable gastric band procedure - surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it circumference of the band can be adjusted by injecting saline into the band through a port that is implanted on the skin

162
Q

what is an advantage of the adjustable gastric band procedure over gastric bypass

A

the band is removable

163
Q

are the surgical obesity procedures effective? which is more than the other? which is more dangerous? does the patient need to change their habits

A

yes, gastric bypass, gastric bypass, yessir gotta eat better

164
Q

describe anorexia nervosa

A

disorder of under consumption, eat so little there is health threatening weight loss

  • body dysmorphia
  • 4% morality rate
  • high suicide rates
165
Q

describe Bulimia nervosa

A

periods of starvation allowed by bingeing, then purging

  • may be obese or of normal weight
  • mortality rate is 4%
166
Q

are all people with bulimia underweight?

A

nooooope nope nope! can be normal or obese

167
Q

what do we call bulimics that are underweight

A

binge-eating/purging anorexia

168
Q

why is it important to distinguish bulimia from anorexia as a physician

A

starvation has different effects that bingeing-purging behaviours

169
Q

what are symptoms associated with anorexia (5)

A
  1. reduced metabolism
  2. bradycardia - slow heart rate
  3. hypotension - low bp
  4. hypothermia - low body temp
  5. anemia - decificeny of red blood cells
170
Q

what are symptoms associated with bulimia (5)

A
  1. irritation and inflammation of the esophagus
  2. vitamin/mineral deficiencies
  3. electrolyte imbalance
  4. dehydration
  5. acid reflux
171
Q

How o scientists view the relationship between bulimia and anorexia

A

variations of the same disorder, both begin with an obsession about body image, extreme efforts to loose weight (strict dieting)

172
Q

according to the scientists view, what is the main difference between anorexia and bulimia?

A

people w bulimia are less capable of controlling their appetites and enter into their cycles as a result

173
Q

what are the three main similarities between those with anorexia and bulimia

A
  1. disorder body image
  2. many patients straddle the two diagnoses; flip flop between the two or not hyper specific to either
  3. highly correlated with OCD and depression
174
Q

what does the positive incentive perspective suggest about anorexia and bulimia/

A

decline in eating in these disorders is the result of a decline in positive incentive value of food

175
Q

why doest he positive incentive value of food get little attention in those with anorexia

A

they seem to display substantial interest in food - they talk about it a lot, cook it for others and think about it
- however, this is positive incentive for INTERACTING with food, not EATING it

176
Q

how does the positive incentive value of those with anorexia compare to controls
- why does this underestimate its importance in the disorder?

A
  • generally lower

- compared to normal weight controls, rather than those who are starving to a similar degree

177
Q

what do we find when we compare the positive incentive value of food in those with anorexia to those who are starving and of the same weight

A

Much much lower - starving people LOVE food

178
Q

Why does the adaptive massive increase in the positive-incentive value of eating that occurs in victims of starvation not occur in those starving due to anorexia?

A

Woods and colleagues studies on the aversive physiological effects of meals

  • homeostatic balance is disturbed by the influx of calories
  • this disturbance may be way worse in deprived individuals
  • referring evidence - people can die if given food that they have been deprived of
179
Q

why do those with anorexia not experience an increase of the positive incentive value of eating like that in others who are starving?

A

could be meals - could produce taste aversions

- shouldn’t be encouraged to eat, should be fed or infused with small amounts of food intermittently throughout the day

180
Q

explain the findings of the blackburn study on feeding meals to starving individuals

A

can cause anorexia

Psych370 (37 decks)

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