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K1N334 > KIN334 Midterm > Flashcards

KIN334 Midterm Flashcards

1
Q

What are the 2 components of energy balance?

A

Energy intake and Energy expenditure

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2
Q

What are the 3 types of Energy Expenditure?

A

RMR (resting metabolic rate)
TEF (thermic effect of food)
EEA (energy expenditure of activity)

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3
Q

What is energy intake?

A

Macronutrients ingested/absorbed

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4
Q

What is the unit of energy for food?

A

Calorie

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5
Q

What is a kcal?

A

kg calorie – energy needed to increase the temperature of 1kg of water by 1˚C (1000 cal)

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6
Q

How do you measure energy intake?

A

Direct calorimeter: Burn food in the bomb calorimeter and see the increase in water temperature

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7
Q

What is the Atwood factor?

A

System that gives energy values to food.
o Estimate of available / metabolizable energy
o Energy value from heat of combustion (bomb calorimeter) corrected for energy losses in digestion, absorption and excretion

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8
Q

What is the Atwood factor for CHO?

A

4kcal/g

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9
Q

What is the Atwood factor for PRO?

A

4kcal/g

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10
Q

What is the Atwood factor for FAT?

A

9kcal/g

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11
Q

What is the Atwood factor for Ethanol?

A

7kcal/g

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12
Q

Which macronutrient has the lowest coefficient of digestibility?

A

Proteins

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13
Q

Why does protein have the lowest coefficient of digestibility?

A

15-19% of protein is nitrogen which doesn’t provide energy (~20%)

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14
Q

What is nitrogen excreted as?

A

Urea

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15
Q

What lowers energy availability (3)?

A
  • Protein: ~20% of protein is nitrogen, excreted as urea
  • Insoluble fibre: does not change inside the body, so the body cannot absorb it: 0 Kcals/g
  • Soluble fibre: is partially fermented (variable) provides some energy when broken down/absorbed
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16
Q

For %DV on food labels, what is considered low?

A

5% or less

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17
Q

For %DV on food labels, what is considered high?

A

20% or more

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18
Q

For the oxidative hierarchy, what is the order or macronutrients and how are they stored?

A

Alcohol - not stored
Carbs - glycogen
Protein - body protein
Fats - adipose tissue

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19
Q

What is the oxidative hierarchy?

A

An indicator of the fuel’s dominance within metabolic pathways

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20
Q

What is the oxidative hierarchy based on?

A

The body’s storage capacity for different substrates and their role in ensuring survival

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21
Q

What drives the oxidation of fat?

A

CHO metabolism

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21
Q

What drives the oxidation of fat?

A

CHO metabolism

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22
Q

What macronutrient is the primary source of energy for the brain?

A

CHO

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23
Q

Where are the glycogen stores in the body?

A

In the liver and muscle

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24
Q

What is the RER for CHO? FAT?

A

RER = 1.0 and 0.7

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25
Q

Which 2 types of energy intakes are tightly controlled?

A

CHO and PRO

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26
Q

Increased protein intake leads to?

A

Increased protein oxidation

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27
Q

How is dietary fat transported?

A

Plasma chylomicrons, with the FA’s found in TG’s cleared by adipose tissue (enzyme: LPL)

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28
Q

What is the obligatory requirement for fat oxidation?

A

Small

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29
Q

Increased fat in a meal does NOT mean

A

does not mean increased fat oxidization

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30
Q

What does alcohol suppress?

A

Other fuel oxidation

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31
Q

What macronutrient has no storage capacity?

A

Alcohol (toxin)

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32
Q

What macronutrient intake is tightly coupled with oxidation?

A

Alcohol

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33
Q

What is the oxidative hierarchy?

A

The hierarchy governing the order of fuel combustion:
Alcohol burned first because there is no storage capacity.
Excess consumption of protein or CHO results in an autoregulatory increase in their oxidation.
Fat oxidation is last.

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34
Q

From an energy expenditure perspective, does it matter if you absorb kcals from fat vs. CHO?

A

When in energy balance – NO!
* Fat oxidation is suppressed as CHO oxidation is increased.
* As CHO oxidation drops, fat oxidation will increase

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35
Q

What are the effects of absorbing kcals from fat vs. CHO in energy balance?

A

EE is similar, but RQ does change to reflect which macronutrients are being metabolised

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36
Q

Which macronutrient is driving fuel selection?

A

CHO

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37
Q

Where does excess fat go if not metabolized?

A

Storage in adipose tissue

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38
Q

From an energy expenditure (EE) perspective would it matter if you absorb kcals from fat vs. CHO?

A

In normal circumstance (balance), it would not have a meaningful direct impact total EE, but it could influence respiratory quotient.

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39
Q

Does the macronutrient source matter?

A

Yes! Storage of fat as body fat is very efficient! If it has the opportunity to store, it will!

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40
Q

What is the estimated efficiency of fat storage as new tissue?

A

0.96

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41
Q

How much of TDEE is Resting metabolic rate (RMR)

A

~60-75%
Low variability

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42
Q

How much of TDEE is Thermic effect of food (TEF) (aka “DIT”)

A

~10%

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43
Q

How much of TDEE is Energy expenditure for activity (EEA) [thermic effect of exercise (TEE) + Non exercise activity thermogenesis (NEAT)]

A

~15-30++ % of TDEE
Highly variable

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44
Q

What are 3 ways to estimate TDEE? Maybe 4th?

A
  1. Doubly Labeled Water
  2. Calorimetric Chamber (direct calorimeter)
  3. Measure TDEE by estimating components: (RMR, TEF, EEA)
  4. Free living? (Actigraphy, HR, METs, Questionnaires)
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45
Q

What is Doubly Labeled Water?

A

Water in which both the hydrogen and the oxygen have been partly or completely replaced (i.e. labeled) with an uncommon isotope of these elements for tracing purposes

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46
Q

What is the input and output of Doubly Labeled Water

A

Input: 2H2 18O Dose, food & water, atmospheric water vapor
Output: Water, water + CO2
18O elimination (water + CO2) - 2H2 elimination (water) = CO2 Production

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47
Q

What are the 2 ways hydrogen leaves the body?

A

Sweat and urine, but we only measure urine

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48
Q

How does Doubly Labeled Water work?

A

H2 18O (O18 + 2H) -> oxygen leaves the body in 2 ways:
- Water loss of O18 (sweat, urine)
- O18 appears in expired CO2.

2H2O (deuterium oxide)
- Water loss of 2H only

The difference in the two
reflects EE
- Measure urine within 4-6 hours
- Re-measure at intervals
- Up to 14 days
- Need to have a complete diet record
- Estimate RQ of the diet to estimate the amount of energy produced

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49
Q

What’s the difference between BMR and RMR?

A
  • BMR is taken in a darkened room upon waking after 8 hours of sleep, 12 hours of fasting (digestive system is inactive), and with the subject resting in a reclined position.
  • RMR is taken under less restricted conditions than BMR and do not require that the subject spend the night sleeping in the test facility prior to testing.
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50
Q

How do you measure RMR?

A
  • overnight fast (8-12 hr)
  • subject awake
  • controlled phase of menstrual cycle (higher in luteal)
  • abstinence from exercise (12 hr)
  • Resting in a supine position
  • Thermoneutral conditions
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51
Q

What is RMR and what are the 3 ways it is measured?

A

Energy needed to sustain basic life function while at rest
o Direct calorimetry (Heat production = metabolism)
o Indirect calorimetry (Analysis of expired gases)
o Prediction Formulas (estimate)

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52
Q

What is the conversion of lbs to kg?

A

Multiply by 2.2 (1kg = 2.2lbs)

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53
Q

What influence does body temperature have on BMR?

A

There is a 12% increase in BMR with every 1degree increase in body temperature

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54
Q

What is Thermogenesis made up of

A

Obligatory and facultative

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55
Q

What is Obligatory thermogenesis?

A

The energy required to digest, absorb and metabolize nutrients (ex. BMR)
It is independent of ambient temperature

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56
Q

When does facultative thermogenesis increase?

A

Colder temperatures

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57
Q

What is Facultative thermogenesis?

A

Activated only as a cold defense mechanism to maintain body temperature (increases MR).
* Extra heat produced on demand to maintain body temp.
* Shivering (skeletal muscle) (rapidly switched on and off by NS)
* Brown fat metabolism (contains mitochondria – produce energy)

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58
Q

What are the 2 effects of PA on RMR?

A
  1. Increased FFM means greater resting metabolism
  2. Due to the effect of EPOC it may be difficult to get a “true” estimate of RMR
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59
Q

What are the 6 organs that use RMR in order of most to least?

A

Heart, Kidney, Brain, Liver, Muscle, Adipose Tissue. First 4 are ~60%RMR, ~6%BW

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60
Q

For EPOC, how many kcals are burned for L of O2?

A

1L = 5kcal

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61
Q

What is diet-induced thermogenesis and how is it measured?

A

Energy needed to digest, absorb and store.
Indirect calorimetry or estimated from formulas.

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62
Q

What influences diet-induced thermogenesis to change?

A

Type of macronutrients – protein requires the most energy
Exercise

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63
Q

What effects does exercise have on diet-induced thermogenesis?

A

*magnitude of DIT proportional to energy and protein content (less food, less DIT)
*glycogen-depleting exercise may elevate DIT

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64
Q

What % of DIT is thought to be obligatory

A

50-75%
- CHO: DIT = 5-10% of Kcals ingested from CHO
- Fat: DIT = 3-5% of Kcals ingested from Fat
- Protein: DIT = 20-30% of Kcals ingested from Protein

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65
Q

What happens to DIT with age?

A

DIT lowers with age

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66
Q

What is the heat increment of CHO as body fat

A

0.20

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67
Q

What is the heat increment of CHO as glycogen

A

0.05

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68
Q

What does a β-adrenergic blockade do to RMR?

A

Decreases RMR ~12%

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69
Q

What is EEA?

A

Energy Expenditure for Activity
Energy needed for all activities (skeletal muscle)
* planned workouts
* spontaneous physical activity or NEAT

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70
Q

What does NEAT stand for and include?

A

Non exercise activity thermogenesis
Includes occupation, leisure, sitting, standing and ambulation.

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71
Q

What are 5 ways to estimate EEA?

A
  • Indirect calorimetry
  • Heart rate
  • Pedometers, accelerometers
  • Questionnaires (METs)
  • PAL (Ratio of TDEE:RMR)
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72
Q

What is the equation for EEA?

A

(METS × kg BW ) × (time (min) / 60 min)

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73
Q

1MET =

A

3.5 mLO2 / kg / min

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74
Q

Where did the MET come from and is it representative?

A

A 70kg, 40 year old male. Not representative! 3.5ml/kg/min is overestimated by 20%. Body comp accounted for ~60% variability. ~age 14

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75
Q

What is underestimated about the MET?

A

The energy cost of PA

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76
Q

What does EEA depend upon?

A

Frequency
Intensity
Time
Type

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77
Q

What are 3 other factors that effect EEA?

A

*Improved efficiency with training
*EPOC
*Exercise may affect NEAT?

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78
Q

What is NEAT?

A

The energy expended for everything that is not sleeping, eating, or sports/exercise-like activities

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79
Q

What activities does NEAT include?

A
  • Typing
  • Performing yard work
  • Walking at the office
  • Fidgeting
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80
Q

What are 7 ways to measure Activity Energy Expenditure (AEE)?

A

Indirect calorimetry
Heart rate monitoring
Accelerometry
Global Positioning System
Pedometry
Questionnaires
Observation

81
Q

If overfed 1000 calories a day, what would happen to fat mass?

A

Fat gain varied and was inversely related to the increase in total daily energy expenditure. NEAT causes the difference.

82
Q

Are we even in balance?

A

No. You are either too high (after eating) or too low (right before eating).

83
Q

How is the setpoint of balance achieved?

A
  • Feedback control systems designed to regulate a variable to match a specified target
  • The body has an internal control mechanism that regulates metabolism to maintain a certain level of body fat
  • Biological control – genes, hormones, etc.
  • Changing one side of the equation changes the other (Decrease EI, body decreases EE to maintain fat mass)
84
Q

How is the settling point of balance achieved?

A
  • Focused on environment and behaviour
  • No active feedback control of EI and EE.
  • Explain why overweight and obesity are more than problems of metabolism. Weight is related to the patterns of diet and PA that people “settle” into as habits based on the interaction of their genes, learning, and environmental cues to behavior.
85
Q

How is steady state balance achieved?

A
  • An increase in inflow = increase in outflow
  • Steady-state systems can resist continuous perturbations within a certain range.
  • Perturbations in EI or EE result in compensatory changes in these components
86
Q

What are passive compensatory changes?

A

Increase in energy expenditure with an increase in body size

87
Q

What are active compensation changes?

A

Changes in food intake after exercise.
- Occurs over the longer term – variability in weight loss with exercise interventions

88
Q

How is energy balance achieved through regulation?

A

Adding a float (sensor) to the system.
Negative feedback: sending information backwards to the input to close the “tap” or “intake” as the float rises
Positive feedback: using a rising float, the response is to turn up the outflow “tap” or “expenditure”

89
Q

Hoe does body weight generally change over time?

A

There is often a systematic increase in body weight fat with age

90
Q

What are 6 variables associated with body fat that may be regulated?

A
  1. body weight
  2. body fatness
  3. body temperature
  4. energy intake
  5. energy expenditure
  6. energy balance
91
Q

What is hedonics?

A

The pleasantness of food

92
Q

What are 3 emergency circuits?

A

Hypoglycemia, stress, inflammation

93
Q

What is one biological reason we eat or spend energy?

A

Homeostasis (maintaining balance/stability)

94
Q

Why is set point unlikely?

A
  • Doesn’t explain why the world’s set points have increased over the last 50 years (ie. Obesity epidemic)
  • Contradicted by studies showing that starvation and subsequent refeeding results in even higher body and fat mass.
95
Q

Why is settling point unlikely?

A

Doesn’t take into account biological regulation of weight control

96
Q

What are the 2 theories on food / weight regulation?

A

The set point and the settling point

97
Q

What are 3 ways we measure appetite?

A

Hunger, Satiation, Satiety

98
Q

What is hunger?

A

Sensations that promote food consumption. A multidimensional attribute with metabolic, sensory, and cognitive facets. (before a meal)

99
Q

What is satiation?

A

While eating a meal, hunger subsides with satiation, the sensations that govern meal size and duration become increasingly dominant…feelings of satiation will contribute to cessation of eating and begin a period of abstinence from eating (right after a meal)

100
Q

What is satiety?

A

Sensations that determine the intermeal period of fasting are termed satiety (in between meals)

101
Q

What is Orexigenic?

A

Having a stimulating effect on the appetite (eg. Ghrelin)

102
Q

What is Anorexigenic (anorectic)

A

Causing loss of appetite

103
Q

What is an Agonist (in Biochemistry)

A

A drug or other chemical that can combine with a receptor on a cell to produce a physiologic reaction typical of a naturally occurring substance.

104
Q

What is an Antagonist (in Biochemistry)

A

A chemical substance that interferes with the physiological action of another, especially by combining with and blocking its nerve receptor

105
Q

What are 4 ways to measure appetite that have limitations?

A
  1. Brain Imaging
  2. Biomarkers
  3. Food intake
  4. Questionnaires
106
Q

What is the most common way to measure appetite?

A

Visual analogue scales (VAS)

107
Q

What questions are on the Visual analogue scales (VAS)?

A
  • How hungry are you right now?
  • How strong is your desire to eat right now?
  • How much could you eat right now?
  • How full are you right now?
  • How strong is your desire to consume something sweet right now?
  • How strong is your desire to consume something savory right now?
  • How thirsty are you right now?
108
Q

What is the correlation between VAS and EI?

A

Weak/moderate

109
Q

How does the brain adapt to maintain fat stores?

A
  • Eating food inhibits the rewarding properties of food.
  • When you starve, the rewarding properties of food increase and satiety signals decrease.
110
Q

For Leptin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Obese protein gene proportional to fat mass
  • Synthesized/secreted from adipose tissue
  • Leads to decrease in food intake (anorexigenic) and weight loss
  • Causes loss of appetite (reduces EI)
111
Q

For Insulin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Peptide hormone
  • Secreted by the β-cells of the pancreas
  • Rises in response to glucose load
  • Insulin crosses blood brain barrier (BBB) and reduces appetite or increase EE
  • Less effective in obese or type 2
    diabetes (insulin-resistant)
112
Q

For Ghrelin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Peptide
  • Synthesized predominantly in stomach
  • Stimulates growth hormone (GH), levels rise with fasting and fall with feeding
  • Increases food intake (orexigenic)
113
Q

For Peptide YY (PYY):
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Peptide
  • Secreted from small and large bowel
  • Released after feeding and leads to reduced food intake
  • Anorexigenic (reduces EI)
114
Q

For Glucagon-like-peptide-1 (GLP-1):
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Peptide
  • Co-secreted with PYY in response to nutrients in the gut
  • Inhibits feeding
  • “incretin” = increase in the amount of insulin
    released with increased glucose levels (stimulates a decrease in glucose levels)
  • Enhances insulin secretion, suppresses glucagon (raises glucose concentrations) after a meal
115
Q

For Cholecystokinin (CCK):
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI

A
  • Hormone
  • Gut
  • Stimulates digestion of fat, secreted by the small intestine
  • May synergize leptin’s action (decrease food intake)
  • Inhibits feeding
116
Q

What happens with brain insulin injections vs peripheral insulin injections?

A

Brain insulin injections cause satiety and weight loss (ex. animal studies) but peripheral insulin injections (ex. humans with diabetes) can cause hunger and weight gain

117
Q

What is the history of Glucagon-like-peptide-1 (GLP-1)?

A
  • Originally approved for type 2 diabetes
  • Now approved for weight loss
  • slows gastric emptying
118
Q

What is energy availability?

A

The amount of dietary energy remaining after exercise, available for other physiological functions such as growth, muscle recovery and homeostasis.

119
Q

What is the EA (energy availability) equation?

A

dietary intake (kcal) - exercise energy expenditure (kcal)/ fat free mass (kg)

120
Q

Why is energy availability important in sport?

A

Sufficient energy availability and quality of nutrition are essential to support health and desired adaptations.

121
Q

What is considered low energy availability? Moderate energy availability? Adequate energy availability?

A

Low: 20kcal/kg/fm
Moderate: 30kcal/kg/fm
Adequate: 45kcal/kg/fm

122
Q

What are the performance consequences of LEA?

A

Decreased endurance performance, increased injury risk, decreased training response, impaired judgement, decreased coordination, irritability, decreased concentration, depression, decreased glycogen stores, decreased muscle strength

123
Q

What is LEA associated with?

A

The majority of consequences of relative energy deficiency in sport (RED-S), the Female Athlete Triad, and health / performance consequences.

124
Q

What are 3 risk factors for developing low energy availability?

A

Possible answers:
- participation in aesthetic, weight-making or endurance sports
- failure to increase calorie intake with increased or hard training loads
- attempts to lose weight when training loads are high
- restricted calorie intake due to physical impairments, gut tolerance, medical conditions
- excessive focus by coaches and other staff on weight and body fat as opposed to performance in sport
- presence of disordered eating behaviors, in athlete or training partners
- inadequate food availability
- diets very high in fiber and low in energy density

125
Q

What sports are at risk for LEA?

A
  • Sports where athletes aim for competition weight/weight class (Wrestling, Rowing)
  • Aesthetic Sports (Gymnastics, Figure skating)
  • Sports where food is excluded (Body building, Vegetarians)
126
Q

What is intentional low energy availability?

A

Restricting energy intake in the hope that becoming even leaner might improve performance

127
Q

What is adequate energy availability?

A

Continually adapting energy intake to match training load

128
Q

What is unintentional low energy availability?

A

Failing to increase energy intake to match a higher training load

129
Q

Can loosing weight increase performance?

A

To an extent, negative health outcomes can be masked by increased performance. Will only be masked for a certain amount of time

130
Q

What are the signs and symptoms of LEA?

A

Reduced training capacity
Repeated injury or illness
Delayed or prolonged recovery times
Change in mood state
Failure to lose weight
Reduced or low bone density
Reduced libido
Cessation or disruption in menstrual cycle
Excessive fatigue

131
Q

What is obesity?

A

Disease in which excess body fat has accumulated such that health may be adversely affected

132
Q

What risks are associated with obesity?

A
  • Diabetes
  • Hypertension
  • “Metabolic syndrome”
  • Others: Mental health, Osteoarthritis, Cancer
133
Q

What blood glucose level do you have to be at at any point of the day to be considered type 2 diabetes?

A

2hPG in a 75 g OGTT >= 11.1mmol/L

134
Q

What are the risk factors for type 2 diabetes?

A

Low PA
Aging
Genetics
Obesity (abdominal obesity)

135
Q

What % of the population has T2DM

A

5-10%

136
Q

What % of overweight / obese have T2DM

A

10-20%

137
Q

What is lipolysis

A

Breakdown of lipids

138
Q

How is excess fat in the liver a proposed explanation for the link between obesity and T2DM?

A

Increase gluconeogenesis, dyslipoproteinemia – abnormal levels of lipoproteins in blood

139
Q

How is excess fat in adipose tissue a proposed explanation for the link between obesity and T2DM?

A

Reduce antilipolytic effect of insulin – results in greater breakdown of fats to release FFAs

140
Q

How is excess fat in skeletal muscle a proposed explanation for the link between obesity and T2DM?

A

Insulin resistance, reduced glucose uptake, reduced oxidative potential

141
Q

How is excess fat in the pancreas a proposed explanation for the link between obesity and T2DM?

A

Hyperinsulinemia and potential beta-cell “failure”

142
Q

What blood pressure is considered hypertension?

A

Systolic BP (SBP) is ≥140 mmHg and/or
Diastolic BP (DBP) is ≥90 mmHg

143
Q

What % of people have hypertension? Obese people?

A

16%, 40%

144
Q

How can obese people reduce hypertension?

A

Weight loss and salt restriction

145
Q

What is primary vs. secondary hypertension?

A

Primary: High blood pressure with no obvious underlying cause = aging! (90-95%)
Secondary: Caused by other conditions affecting the kidneys, arteries or diseases (renal failure, pregnancy)

146
Q

What is Adiponectin?

A
  • Secreted “exclusively” by adipocytes
  • Inversely proportional to %body fat (more likely adipocyte size)
  • Weight (fat) loss increases adiponectin concentrations
147
Q

What effect does Adiponectin have?

A

Increased insulin sensitivity

148
Q

What are the different definitions of metabolic syndrome?

A

o IDF
o WHO
o EGIR
o NCEP
o American Heart Association/Updated NCEP

149
Q

What is metabolic syndrome AKA

A
  • Plurimetabolic syndrome, cardiometabolic syndrome
  • Syndrome X, Reaven’s Syndrome
  • Insulin resistance syndrome, CHAOS (Coronary artery disease, Hypertension, Atherosclerosis, Obesity, and Stroke)
150
Q

What is the cutpoint for elevated BP?

A

Systolic >= 130mmHg and/or diastolic >=85mmHg

151
Q

What is the cutpoint for elevated FPG?

A

> =5.6mmol/L

152
Q

How does cancer increase with obesity in men and women?

A

52% ↑ men
62% ↑ women

153
Q

What is Osteoarthritis? What is the number one preventable risk factor?

A

Obesity is the number one preventable risk factor.
- Found in the hands / fingers but it’s not just overloaded joints.
- Has inflammatory aspect: Cytokines (leptin, adiponectin, resist control local inflammatory processes)
- Associated with glucose / lipid disregulation
- Sedentary lifestyle impacts PA

154
Q

What are the biological mechanisms of obesity?

A
  • FFA
  • Ectopic fat
  • Insulin resistance
  • Adipocytes as endocrine cells (inflammation)
  • Inflammation
155
Q

What is Visceral fat?

A

“hidden” and stored deep in the belly around the organs (intestines & liver). Carries significant health risks.

156
Q

What is Abdominal obesity?

A

A condition where excessive visceral fat around the stomach has built up (apple shape / beer belly)

157
Q

What is Ectopic fat?

A

Excess adipose tissue that is not classically associated with adipose tissue storage (e.g., heart, kidney)
Increases the risk of cardiometabolic disease, but responds to exercise

158
Q

What is insulin resistance?

A

A physiological condition where the natural hormone insulin becomes less effective at lowering glucose

158
Q

What is insulin resistance?

A

A physiological condition where the natural hormone insulin becomes less effective at lowering glucose

159
Q

What are potential mechanisms of insulin resistance?

A
  • FFA, ectopic fat
  • Inflammation***
  • Adipokines (Cytokines produced by adipose tissue)
  • Adiponectin
160
Q

What is the relationship between sleep and BMI?

A

The less you sleep, the more BMI increases.
<7 hours sleep have a higher BMI.
A few studies show U shaped curve (higher BMI below 7hr and 9+)

161
Q

What is the relationship between sleep and food intake?

A

Sleep deprivation increases food intake

162
Q

What happens if you have a decrease in leptin?

A

You want to eat more

163
Q

What happens if you have an increase in ghrelin?

A

You want to eat more

164
Q

What is cortisol?

A
  • Is known as “the stress hormone”
  • Short term beneficial, long term not
  • Is the most potent glucocorticoid
  • Causes insulin resistance
165
Q

What is Cushing’s syndrome?

A

Excess cortisol of any cause

166
Q

What are 5 links / results between Cushing’s syndrome / metabolic syndrome?

A

Abdominal Obesity
Hypertension
Hyperglycemia
Insulin resistance
Dyslipidemia

167
Q

What was the response to chronic psychological stress and what was the overall effect?

A

~40% gain weight
~20% are weight stable
~40% lose weight
Overweight/obese tend to gain weight more often (More/less hungry during stressful period, but will increase sweets/savory foods and decrease fruits and vegetables)

168
Q

Even if the cortisol response is the same, why will weight change will be different?

A

There are responders and non-responders

169
Q

What is the acute effect of stress/cortisol on food intake?

A

On stress day, high reactors ate more calories after test. This explains why some people gain / loose weight when stressed.

170
Q

What are some food eating implications?

A
  • Restrained Eaters
  • Night eating syndrome
  • Binge eating syndrome
  • Emotional eating
  • Smoking and alcohol consumption
  • Implications for use of food/ PA diaries
171
Q

What is Assortative mating?

A

Lean individuals mate with lean individuals; individuals with obesity mate with individuals with obesity.

172
Q

What is Epigenetics?

A

How your genes express themselves

173
Q

What is 1kg in lbs?

A

2.2lbs

174
Q

What was the Quebec 100-day overfeeding experiment with twins?

A

12 pairs of twins were brought in for 100 days and were overfed 840 kcal a day. They gained ~8kg but it varied between twins due to NEAT.
FFM, RMR, Fasting insulin, and abdominal fat cell size increased. Muscle oxidative potential decreased.
BMR/RMR/metabolism/TEF didn’t change between the twins. NEAT accounted for the differences.

175
Q

What is NEAT? What does it represent?

A

Non exercise activity thermogenesis. - Metabolism that is not due to exercise (fidgeting, etc)

176
Q

What was the Quebec negative energy experiment with twins?

A

7 pairs of male twins were there for 117 days, and had an energy deficit of 58,000 kcals. There was a 30% drop in visceral fat. The twins had a closer correlation (less NEAT due to exercise).

177
Q

What genetic trait has direct transmission and a high effect size?

A

Mendelian disease

178
Q

What genetic trait is a gene that significantly affects a heritable characteristic >=5%?

A

Oligogenes

179
Q

What genetic trait is a gene that has a small effect on heritable characteristics (<5%) and has the most frequency?

A

Polygenes

180
Q

What are 5 genetic genes for obesity? What do they mean?

A
  1. Thriftiness (Body predisposed to taking all energy you get and storing it/not getting enough nutrients in the womb)
  2. Hyperphagia (eating a lot)
  3. Low lipid oxidation (body does not metabolize fat to same extent)
  4. Adipose tissue hyperplasia (predispose to increase in adipose tissue sites)
  5. Sedens (predisposing you to a sedentary lifestyle)
181
Q

What are Gene-Gene Interactions?

A

Expression of one gene affects expression of another gene. Seen at an individual level.

182
Q

What are Gene-Environment Interactions?

A

The interactions between genes and their environment that necessitate a cellular response. Usually seen at a population level.

183
Q

What is Epigenetics?

A

The Study of cellular mechanisms that
modify gene expression without changing the
underlying DNA sequence. Occur during a lifetime or passed on to next generation.

184
Q

What is the percentile cut off point for at risk for overweight in youth?

A

85th percentile

185
Q

What is the percentile cutoff for being overweight in youth?

A

95th percentile

186
Q

What happens if you are exposed to a famine in TM1 or TM2?

A

Increased risk of obesity at 19years - resetting appetite, metabolism, etc.

187
Q

What happens if you are exposed to a famine in TM3?

A

Lower rate of obesity at 19 years (usually laying down fat in TM3, doesn’t effect metabolism as much)

188
Q

What happens if you have early, excessive weight gain in early pregnancy?

A

May alter in utero environment to promote obesity. Linked to gestational diabetes, postpartum weight retention and childhood obesity

189
Q

What birthweight has a risk of being overweight?

A

> 4000g

190
Q

What pregnancy complications can you get?

A

GDM
Preeclampsia (high blood pressure)

191
Q

What effect does exercise have on pregnancy?

A

Lower rates of high birthweight

192
Q

What effect does smoking have on pregnancy?

A

Higher BMI in childhood

193
Q

What effect does breastfeeding have on pregnancy?

A

Associated with slightly lower BMI throughout life

194
Q

What are 12 ways to distinguish bad science?

A
  1. Sensationalized headlines
  2. Misinterpreted results
  3. Conflicts of interest
  4. Correlation and causation
  5. Unsupported conclusions
  6. Problems with sample size
  7. Unrepresentative samples used
  8. No control group used
  9. No blind testing used
  10. Selective reporting of data
  11. Unreplicable results
  12. Non-peer reviewed material
194
Q

What are 12 ways to distinguish bad science?

A
  1. Sensationalized headlines
  2. Misinterpreted results
  3. Conflicts of interest
  4. Correlation and causation
  5. Unsupported conclusions
  6. Problems with sample size
  7. Unrepresentative samples used
  8. No control group used
  9. No blind testing used
  10. Selective reporting of data
  11. Unreplicable results
  12. Non-peer reviewed material
195
Q

The coefficients of digestibility of CHO and fats are consistently over what?

A

90%

196
Q

Explain the chart linking obesity and T2D

A

AN increase in adipose tissue = and increase in FFA. This leads to an increase in gluconeogenesis in the liver (producing glucose from FFAs), and the increase in FFAs has a detrimental impact on insulin uptake by the liver. The increased glucose production leads to an increase in insulin production (hyperinsulinemia). The compensatory increase in insulin results in eventual B cell failure, which leads to hyperglycemia (T2D). The increased insulin resistance in skeletal muscle decreases the oxidative potential.

197
Q

How do increased adipocytes lead to inflammation?

A

Endothelial cells tell blood vessels to dilate, if there is inflammation, the endothelial cells won’t say to dilate and there will be the same amount of fluid going through constructed vessel. Increased stiffness in blood vessels which leads to CV disease. Exercise can help.

K1N334 (3 decks)

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