Required Readings - Midterm Flashcards

1
Q

Average weight loss maintained after 4.5 years upon completing a weight loss program?

A

3 kgs

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2
Q

Define successful weight loss (According to the study: defence of body weight)

A

Intentionally losing at least 10% of initial weight and keeping it off for at least one year

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3
Q

Where is the homeostatic regulation of body weight regulated?

A

The arucuate (ARC) nucleus Hypothalamus - involved in the control of food intake.

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4
Q

What protects us from weight loss? Is it the same for weight gain?

A

Regulation of signals from the hypothalamus - not as vigorously regulated for weight gain (easier to gain weight)

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5
Q

What does the evolutionary protection of weight loss mean?

A

It is difficult to lose weight

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6
Q

What two neuro-peptides within the ARC responsible for stimulating food intake?

A

1) Neuropeptide Y

2) Agouti-related peptide

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7
Q

What neuro-peptide within the ARC is responsible to suppress food intake?

A

POMC

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8
Q

Anorexigenic neuropeptides from the pancreas?

A
  • Amylin
  • Insulin
  • PP
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9
Q

Anorexigenic neuropeptides from the adipocytes?

A

Leptin

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10
Q

Anorexigenic neuropeptides from the GI tract?

A

CCK
GLP-1
PYY

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11
Q

What is the reward circuit?

A

Hedonic pathway

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12
Q

What is the hedonic pathway? Can it override the homeostatic system?

A

Relates to the sight, smell and taste of food along with emotional and social factors. Can override homeostatic system, causing us to gain weight

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13
Q

Name the physiological adaptations to diet-induced weight loss (EFTC)

A
  • Decr. Energy expenditure
  • Decr. Fat oxidation
  • Decr, thyroid homrones
  • Incr. cortisol
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14
Q

What does EFTC favour

A

Increase in energy storage

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15
Q

Name the physiological changes to diet-induced weight loss (PAIL-GG-A)

A
  • decr. PPY
  • decr. Amylin
  • decr. Insulin
  • decr. Leptin
  • incr. GIP
  • incr. Grehlin
  • incr. Appetite
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16
Q

What doe PAIL-GG-A favour?

A

Work together to increased food intake

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17
Q

What physiological factor may reduce food intake after diet-induced weight-loss?

A

An increase in pancreatic polypeptide

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18
Q

Diet-induced weight loss of 10% of BW leads to a reduction in TEE by ___ due to changes in body mass and composition.

A

15%

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19
Q

Weight stable formerly obese patients have lower fasting / 24 hour rates of ___ oxidation

A

fat

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20
Q

What does a lower rate of fat oxidation cause?

A

May lead to a positive fat balance and negative carbohydrate balance

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21
Q

Low fat oxidation (burning carbohydrate instead of fat) is associated with what?

A

Weight gain

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22
Q

How can we increase fat oxidation rate?

A

Exercise, which may cause slow-twitch muscle fibres to derive more energy from fat, compared to fast-twitch which rely on glycogen stores.

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23
Q

Obesity is associated with a resting ____ overactivity

A

sympathetic nervous system

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24
Q

What does overactive SNS cause?

A

down-regulation/desensitization to adrenoreceptors

-impair EE, TEF and fat oxidation

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25
Q

___ hormones play an important role in energy expenditure

A

Thyroid

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26
Q

Increase is TSH increase/decrease REE

A

Increase

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27
Q

How does diet-induced weight loss impact thyroid hormones?

A

Energy restriction suppresses the hypothalamic-pituitary axis, impairing secretions of thyroid hormones.

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28
Q

Following reduction of food intake, higher amounts of ___ is secreted

A

Cortisol

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29
Q

Wha are the effects of increased cortisol?

A
  • Suppression of cortisol
  • Weight gain
  • Central adiposity
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30
Q

How does leptin decease food intake?

A

Reduces expression of AgRP and NPY (orexigenic) and stimulates POMC (anorexigenic)

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31
Q

Leptin secretion is proportional to ___

A

fat mass

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32
Q

Leptin administered to people at baseline weight had ___ effect on BW and appetite

A

little

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33
Q

Leptin administered to people during an energy deficit ___ appetite

A

decreases

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34
Q

In weight-stable, weight-reduced subjects, leptin “replacement” to pre-weight loss levels___ many fo the adaptive physiological changes to diet-induced weight-loss.

A

reverses

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35
Q

What neuropeptides INCREASE during diet-induced weight loss and INCREASE food intake?

A

Grehlin

GIP

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36
Q

What neuropeptides INCREASE during diet-induced weight loss and DECREASE food intake?

A

Pancreatic Polypeptide (PP)

37
Q

What neuropeptides DECREASE during weight loss and INCREASE food intake?

A
PYY
CCK
Insulin
Amylin
Leptin
38
Q

What neuropeptides normally suppress food intake, but when decreased themselves, will increase food intake?

A
PYY
CCK
Insulin 
Amylin 
Leptin
39
Q

The neuropeptides work together to achieve what (3)

A

increasing hunger
reducing satiety
promoting energy storage

40
Q

Besides hormonal changes, what else has been reported to increase after diet-induced weight loss?

A

Appetite and perceived rewarding properties of food.

41
Q

There may be reduced activity in the _______ which may indicate an increased responsiveness to food reward with decreased control of food intake

A

hypothalamic areas involved in the emotional control of food intake

42
Q

In the National Weight Control Registry, what ere the key behaviours common to the patients successful in maintaining weight loss? (5)

A
  • Low-cal, low-fat diet with minimal variation
  • Eating breakfast everyday
  • Frequent self-monitoring
  • Regular exercise
  • Limit TV
43
Q

Does bariatric surgery cause the same physiological changed as diet-induced weight loss?

A

Yes, for LAGB

No, for RYGB (appetite suppression)

44
Q

Besides physiological adaptations, name other difficulties in weight-maintenance after loss

A

-Surrounded by food
-Environment not conducive to PA
“obesogenic environment”
-Gut flora may also contribute (maybe)

45
Q

What are some medications that may counteract the appetite-increasing effects after diet-induced weight loss?

A
  • Lorcaserin
  • Qsymia
  • GLP-1 (clinical-trials)
  • Contrave (clinical trials)
46
Q

What can also counteract the appetite-increasing effects after diet-induced weight losss?

A

Administration of leptin at pre-weight loss levels BUT may cause altered metabolism

47
Q

What treatment may have a synergistic effect?

A

Administration of amylin and leptin

48
Q

Why was the amylin and leptin treatment discontinued?

A

Safety concerns (biological perturbations)

49
Q

Define starvation

A

Total cessation of food (caloric) intake and survival on endogenously stored substrates.

50
Q

What are fatty-acid using tissues?

A

Heart, skeletal muscle, liver and kidney

51
Q

Explain why the greatest importance of a TG (as stored in humans) is NOT it’s high-calorie content but it’s hydrophobic nature.

A

While TGs store lots of energy, they are able to congregate into adipose tissue WITHOUT water, protein and electrolytes. It is an efficient form of storage, and yields 6-8 g/kcal.

52
Q

Why is carbohydrate stores as glycogen a poor energy source?

A

When we take into account the water, it only yields about 1 kcal/g

53
Q

Explain why the development of the brain and our mobility within human evolution contradicts

A

Our brain runs almost exclusively on glucose, but the most efficient way to store energy (and go for longer periods without eating, allowing us to move from place to place) is triglycerides in adipose tissue.

54
Q

Adipose tissue could supply ___ of calories for BEE

A

2 months

55
Q

What is critical for the transition between the fed and the starved state?

A

Amount of muscle protein that provides calories

56
Q

Glycogen in muscle and liver provides energy for how long?

A

1 day

57
Q

When is glycogen life-saving?

A

During acute stress for anaerobic-glycolysis (readily available glucose to fight the stressor)

58
Q

If only the basal energy is being expended, how are all calories being lost?

A

To heat (~1kcal/min)

59
Q

What consumes 1/5th of basal calories?

A

The brain

60
Q

Explain how people can survive amputation

A

Severance of peripheral system will redirect blood flow to head, heart and lungs

61
Q

What ONE substance can cross the BBB?

A

Glucose

62
Q

With prolonged hypoglycemia, the brain has ____ access to blood glucose

A

easier

63
Q

Explain the hyperglycaemic, life-saving effect that is caused by the release of epi/norepi (fight/flight)

A

Stimulate glycogen breakdown in the liver, increase catecholamines and increase glucagon release. All increase blood glucose levels. After a while, gluconeogenesis may increase and could last longer if stress is prolonged.

64
Q

2-3 days of starvation, what fuel is predominant?

A

Glucose from muscle protein, lactate and pyruvate may also be used.

65
Q

When do blood levels of ketone bodies start to increase, when do they decrease?

A

Within the first week of starvation.

Only decrease if glucose is reintroduce, or fat stores exhausted (death)

66
Q

When is muscle protein spared? What does this mean?

A

About 2 weeks after starvation, this means that fat oxidation is favoured and gluconeogenesis is no longer favoured.

67
Q

How does IOM define successful long-term weight loss?

A

a 5% reduction in initial body weight that is maintained for at least one year

68
Q

What were the most important factors that influenced the selection of goal weights?

A

Appearance and physical comfort …

NOT medical conditions

69
Q

Provide some examples of high fat, low-CHO and high protein diets

A
  • Atkins new diet revolution
  • Protein power
  • Life without bread
70
Q

Provide some examples of moderate fat, high CHO and moderate protein diets

A
  • USDA food guide
  • DASH diet
  • Weight Watchers
71
Q

Provide some examples of Low-fat, very-low fat, high-CHO and moderate protein diets

A
  • Dr. Dean Ornish
  • Eat More, Weigh LEss
  • Pritikin Program
72
Q

Diets containing ~1400-1500 kcal result in weight-loss regardless of _____

A

macronutrient composition

73
Q

Explain why the macronutrient composition does not matter in terms of weight loss

A

If someone eats a high-fat, high-protein, low CHO diet since eating high-fat and protein foods is self-limiting. High-CHO and low/very-low diets will eat high volume of vegetables that are low in caloric density

74
Q

Weight loss is NOT the same as what?

A

Weight maintenance

75
Q

What is the major determinant of weight loss?

A

Caloric balance INDEPENDENT of macronutrient composition (Category A evidence)

76
Q

Free-living overweight individuals who self select high-fat, low-CHO diets consume fewer calories and lose weight (T/F)

A

True (Category C evidence)

77
Q

What diet yielded the strongest evidence in terms of weight loss?

A

Overweight individuals consuming moderate fat, balanced nutrient reduction diets lose weight because they consume fewer calories.

78
Q

What is the optimal diet for weight loss?

A

One that maximizes loss of body fat and minimizes loss of lean body mass.

79
Q

Does macronutrient composition influence maximizing the loss of body fat or minimizing the loss of lean body mass?

A

No

80
Q

What happens in high-fat ketogenic diets?

A

Rapid weight loss due to water loss, in the end same weight loss as calorie reduced mixed diet.

81
Q

Name some limitations of high-fat, low CHO diets

A

High in sat fat, cholesterol

Low in vitamin A, E, thiamin, B6, folate, magnesium, potassium, iron dietary fibre

82
Q

Name some limitations of low-fat, high-CHO diets

A

Low in vitamins E, B12 and zinc since fat and meat intake low

83
Q

What decreases with body weight?

A

Blood lipid levels
Insulin
Plasma leptin
Blood pressure

84
Q

TGs typically increase with CHO intake. What CHO will NOT lead to hypertriglyceridemia?

A

High-fibre foods, such as vegetables and legumes

85
Q

How is intake regulated meal-to-meal

A

mostly hedonic factors

86
Q

How is long-term weight regulated?

A

Hormonal signals from endocrine pancreas and adipose tissue (insulin, leptin)

87
Q

What do subjects of low-fat diets complain of?

A

Too much (volume) of food to consume

88
Q

Moderate-fat, balanced nutrient reduction diets do what?

A
  • Reduce LDL
  • Normalice HDL
  • Normalize Plasma TGs
89
Q

Dietary compliance is likely to be a function of ___ than ____

A

psychological issues

macronutrient composition