KIN334 Midterm Flashcards
(200 cards)
1
Q
What are the 2 components of energy balance?
A
Energy intake and Energy expenditure
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)
3
Q
What is energy intake?
A
Macronutrients ingested/absorbed
4
Q
What is the unit of energy for food?
A
Calorie
5
Q
What is a kcal?
A
kg calorie – energy needed to increase the temperature of 1kg of water by 1˚C (1000 cal)
6
Q
How do you measure energy intake?
A
Direct calorimeter: Burn food in the bomb calorimeter and see the increase in water temperature
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
8
Q
What is the Atwood factor for CHO?
A
4kcal/g
9
Q
What is the Atwood factor for PRO?
A
4kcal/g
10
Q
What is the Atwood factor for FAT?
A
9kcal/g
11
Q
What is the Atwood factor for Ethanol?
A
7kcal/g
12
Q
Which macronutrient has the lowest coefficient of digestibility?
A
Proteins
13
Q
Why does protein have the lowest coefficient of digestibility?
A
15-19% of protein is nitrogen which doesn’t provide energy (~20%)
14
Q
What is nitrogen excreted as?
A
Urea
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
16
Q
For %DV on food labels, what is considered low?
A
5% or less
17
Q
For %DV on food labels, what is considered high?
A
20% or more
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
19
Q
What is the oxidative hierarchy?
A
An indicator of the fuel’s dominance within metabolic pathways
20
Q
What is the oxidative hierarchy based on?
A
The body’s storage capacity for different substrates and their role in ensuring survival
21
Q
What drives the oxidation of fat?
A
CHO metabolism
21
Q
What drives the oxidation of fat?
A
CHO metabolism
22
Q
What macronutrient is the primary source of energy for the brain?
A
CHO
23
Q
Where are the glycogen stores in the body?
A
In the liver and muscle
24
What is the RER for CHO? FAT?
RER = 1.0 and 0.7
25
Which 2 types of energy intakes are tightly controlled?
CHO and PRO
26
Increased protein intake leads to?
Increased protein oxidation
27
How is dietary fat transported?
Plasma chylomicrons, with the FA’s found in TG’s cleared by adipose tissue (enzyme: LPL)
28
What is the obligatory requirement for fat oxidation?
Small
29
Increased fat in a meal does NOT mean
does not mean increased fat oxidization
30
What does alcohol suppress?
Other fuel oxidation
31
What macronutrient has no storage capacity?
Alcohol (toxin)
32
What macronutrient intake is tightly coupled with oxidation?
Alcohol
33
What is the oxidative hierarchy?
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.
34
From an energy expenditure perspective, does it matter if you absorb kcals from fat vs. CHO?
When in energy balance – NO!
* Fat oxidation is suppressed as CHO oxidation is increased.
* As CHO oxidation drops, fat oxidation will increase
35
What are the effects of absorbing kcals from fat vs. CHO in energy balance?
EE is similar, but RQ does change to reflect which macronutrients are being metabolised
36
Which macronutrient is driving fuel selection?
CHO
37
Where does excess fat go if not metabolized?
Storage in adipose tissue
38
From an energy expenditure (EE) perspective would it matter if you absorb kcals from fat vs. CHO?
In normal circumstance (balance), it would not have a meaningful direct impact total EE, but it could influence respiratory quotient.
39
Does the macronutrient source matter?
Yes! Storage of fat as body fat is very efficient! If it has the opportunity to store, it will!
40
What is the estimated efficiency of fat storage as new tissue?
0.96
41
How much of TDEE is Resting metabolic rate (RMR)
~60-75%
Low variability
42
How much of TDEE is Thermic effect of food (TEF) (aka “DIT”)
~10%
43
How much of TDEE is Energy expenditure for activity (EEA) [thermic effect of exercise (TEE) + Non exercise activity thermogenesis (NEAT)]
~15-30++ % of TDEE
Highly variable
44
What are 3 ways to estimate TDEE? Maybe 4th?
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)
45
What is Doubly Labeled Water?
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
46
What is the input and output of Doubly Labeled Water
Input: 2H2 18O Dose, food & water, atmospheric water vapor
Output: Water, water + CO2
18O elimination (water + CO2) - 2H2 elimination (water) = CO2 Production
47
What are the 2 ways hydrogen leaves the body?
Sweat and urine, but we only measure urine
48
How does Doubly Labeled Water work?
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
49
What's the difference between BMR and RMR?
* 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.
50
How do you measure RMR?
* 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
51
What is RMR and what are the 3 ways it is measured?
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)
52
What is the conversion of lbs to kg?
Multiply by 2.2 (1kg = 2.2lbs)
53
What influence does body temperature have on BMR?
There is a 12% increase in BMR with every 1degree increase in body temperature
54
What is Thermogenesis made up of
Obligatory and facultative
55
What is Obligatory thermogenesis?
The energy required to digest, absorb and metabolize nutrients (ex. BMR)
It is independent of ambient temperature
56
When does facultative thermogenesis increase?
Colder temperatures
57
What is Facultative thermogenesis?
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)
58
What are the 2 effects of PA on RMR?
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
59
What are the 6 organs that use RMR in order of most to least?
Heart, Kidney, Brain, Liver, Muscle, Adipose Tissue. First 4 are ~60%RMR, ~6%BW
60
For EPOC, how many kcals are burned for L of O2?
1L = 5kcal
61
What is diet-induced thermogenesis and how is it measured?
Energy needed to digest, absorb and store.
Indirect calorimetry or estimated from formulas.
62
What influences diet-induced thermogenesis to change?
Type of macronutrients – protein requires the most energy
Exercise
63
What effects does exercise have on diet-induced thermogenesis?
*magnitude of DIT proportional to energy and protein content (less food, less DIT)
*glycogen-depleting exercise may elevate DIT
64
What % of DIT is thought to be obligatory
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
65
What happens to DIT with age?
DIT lowers with age
66
What is the heat increment of CHO as body fat
0.20
67
What is the heat increment of CHO as glycogen
0.05
68
What does a β-adrenergic blockade do to RMR?
Decreases RMR ~12%
69
What is EEA?
Energy Expenditure for Activity
Energy needed for all activities (skeletal muscle)
* planned workouts
* spontaneous physical activity or NEAT
70
What does NEAT stand for and include?
Non exercise activity thermogenesis
Includes occupation, leisure, sitting, standing and ambulation.
71
What are 5 ways to estimate EEA?
- Indirect calorimetry
- Heart rate
- Pedometers, accelerometers
- Questionnaires (METs)
- PAL (Ratio of TDEE:RMR)
72
What is the equation for EEA?
(METS × kg BW ) × (time (min) / 60 min)
73
1MET =
3.5 mLO2 / kg / min
74
Where did the MET come from and is it representative?
A 70kg, 40 year old male. Not representative! 3.5ml/kg/min is overestimated by 20%. Body comp accounted for ~60% variability. ~age 14
75
What is underestimated about the MET?
The energy cost of PA
76
What does EEA depend upon?
Frequency
Intensity
Time
Type
77
What are 3 other factors that effect EEA?
*Improved efficiency with training
*EPOC
*Exercise may affect NEAT?
78
What is NEAT?
The energy expended for everything that is not sleeping, eating, or sports/exercise-like activities
79
What activities does NEAT include?
* Typing
* Performing yard work
* Walking at the office
* Fidgeting
80
What are 7 ways to measure Activity Energy Expenditure (AEE)?
Indirect calorimetry
Heart rate monitoring
Accelerometry
Global Positioning System
Pedometry
Questionnaires
Observation
81
If overfed 1000 calories a day, what would happen to fat mass?
Fat gain varied and was inversely related to the increase in total daily energy expenditure. NEAT causes the difference.
82
Are we even in balance?
No. You are either too high (after eating) or too low (right before eating).
83
How is the setpoint of balance achieved?
- 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
How is the settling point of balance achieved?
- 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
How is steady state balance achieved?
- 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
What are passive compensatory changes?
Increase in energy expenditure with an increase in body size
87
What are active compensation changes?
Changes in food intake after exercise.
- Occurs over the longer term – variability in weight loss with exercise interventions
88
How is energy balance achieved through regulation?
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
Hoe does body weight generally change over time?
There is often a systematic increase in body weight fat with age
90
What are 6 variables associated with body fat that may be regulated?
1. body weight
2. body fatness
3. body temperature
4. energy intake
5. energy expenditure
6. energy balance
91
What is hedonics?
The pleasantness of food
92
What are 3 emergency circuits?
Hypoglycemia, stress, inflammation
93
What is one biological reason we eat or spend energy?
Homeostasis (maintaining balance/stability)
94
Why is set point unlikely?
- 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
Why is settling point unlikely?
Doesn’t take into account biological regulation of weight control
96
What are the 2 theories on food / weight regulation?
The set point and the settling point
97
What are 3 ways we measure appetite?
Hunger, Satiation, Satiety
98
What is hunger?
Sensations that promote food consumption. A multidimensional attribute with metabolic, sensory, and cognitive facets. (before a meal)
99
What is satiation?
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
What is satiety?
Sensations that determine the intermeal period of fasting are termed satiety (in between meals)
101
What is Orexigenic?
Having a stimulating effect on the appetite (eg. Ghrelin)
102
What is Anorexigenic (anorectic)
Causing loss of appetite
103
What is an Agonist (in Biochemistry)
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
What is an Antagonist (in Biochemistry)
A chemical substance that interferes with the physiological action of another, especially by combining with and blocking its nerve receptor
105
What are 4 ways to measure appetite that have limitations?
1. Brain Imaging
2. Biomarkers
3. Food intake
4. Questionnaires
106
What is the most common way to measure appetite?
Visual analogue scales (VAS)
107
What questions are on the Visual analogue scales (VAS)?
* 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
What is the correlation between VAS and EI?
Weak/moderate
109
How does the brain adapt to maintain fat stores?
- Eating food inhibits the rewarding properties of food.
- When you starve, the rewarding properties of food increase and satiety signals decrease.
110
For Leptin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI
- 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
For Insulin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI
- 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
For Ghrelin:
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI
- Peptide
- Synthesized predominantly in stomach
- Stimulates growth hormone (GH), levels rise with fasting and fall with feeding
- Increases food intake (orexigenic)
113
For Peptide YY (PYY):
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI
- Peptide
- Secreted from small and large bowel
- Released after feeding and leads to reduced food intake
- Anorexigenic (reduces EI)
114
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
- 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
For Cholecystokinin (CCK):
- What it is
- Where it is secreted
- When it is secreted
- How does it affect EE or EI
- Hormone
- Gut
- Stimulates digestion of fat, secreted by the small intestine
- May synergize leptin’s action (decrease food intake)
- Inhibits feeding
116
What happens with brain insulin injections vs peripheral insulin injections?
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
What is the history of Glucagon-like-peptide-1 (GLP-1)?
* Originally approved for type 2 diabetes
* Now approved for weight loss
- slows gastric emptying
118
What is energy availability?
The amount of dietary energy remaining after exercise, available for other physiological functions such as growth, muscle recovery and homeostasis.
119
What is the EA (energy availability) equation?
dietary intake (kcal) - exercise energy expenditure (kcal)/ fat free mass (kg)
120
Why is energy availability important in sport?
Sufficient energy availability and quality of nutrition are essential to support health and desired adaptations.
121
What is considered low energy availability? Moderate energy availability? Adequate energy availability?
Low: 20kcal/kg/fm
Moderate: 30kcal/kg/fm
Adequate: 45kcal/kg/fm
122
What are the performance consequences of LEA?
Decreased endurance performance, increased injury risk, decreased training response, impaired judgement, decreased coordination, irritability, decreased concentration, depression, decreased glycogen stores, decreased muscle strength
123
What is LEA associated with?
The majority of consequences of relative energy deficiency in sport (RED-S), the Female Athlete Triad, and health / performance consequences.
124
What are 3 risk factors for developing low energy availability?
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
What sports are at risk for LEA?
- 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
What is intentional low energy availability?
Restricting energy intake in the hope that becoming even leaner might improve performance
127
What is adequate energy availability?
Continually adapting energy intake to match training load
128
What is unintentional low energy availability?
Failing to increase energy intake to match a higher training load
129
Can loosing weight increase performance?
To an extent, negative health outcomes can be masked by increased performance. Will only be masked for a certain amount of time
130
What are the signs and symptoms of LEA?
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
What is obesity?
Disease in which excess body fat has accumulated such that health may be adversely affected
132
What risks are associated with obesity?
- Diabetes
- Hypertension
- “Metabolic syndrome”
- Others: Mental health, Osteoarthritis, Cancer
133
What blood glucose level do you have to be at at any point of the day to be considered type 2 diabetes?
2hPG in a 75 g OGTT >= 11.1mmol/L
134
What are the risk factors for type 2 diabetes?
Low PA
Aging
Genetics
Obesity (abdominal obesity)
135
What % of the population has T2DM
5-10%
136
What % of overweight / obese have T2DM
10-20%
137
What is lipolysis
Breakdown of lipids
138
How is excess fat in the liver a proposed explanation for the link between obesity and T2DM?
Increase gluconeogenesis, dyslipoproteinemia – abnormal levels of lipoproteins in blood
139
How is excess fat in adipose tissue a proposed explanation for the link between obesity and T2DM?
Reduce antilipolytic effect of insulin – results in greater breakdown of fats to release FFAs
140
How is excess fat in skeletal muscle a proposed explanation for the link between obesity and T2DM?
Insulin resistance, reduced glucose uptake, reduced oxidative potential
141
How is excess fat in the pancreas a proposed explanation for the link between obesity and T2DM?
Hyperinsulinemia and potential beta-cell “failure”
142
What blood pressure is considered hypertension?
Systolic BP (SBP) is ≥140 mmHg and/or
Diastolic BP (DBP) is ≥90 mmHg
143
What % of people have hypertension? Obese people?
16%, 40%
144
How can obese people reduce hypertension?
Weight loss and salt restriction
145
What is primary vs. secondary hypertension?
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
What is Adiponectin?
- Secreted “exclusively” by adipocytes
- Inversely proportional to %body fat (more likely adipocyte size)
- Weight (fat) loss increases adiponectin concentrations
147
What effect does Adiponectin have?
Increased insulin sensitivity
148
What are the different definitions of metabolic syndrome?
o IDF
o WHO
o EGIR
o NCEP
o American Heart Association/Updated NCEP
149
What is metabolic syndrome AKA
- Plurimetabolic syndrome, cardiometabolic syndrome
- Syndrome X, Reaven’s Syndrome
- Insulin resistance syndrome, CHAOS (Coronary artery disease, Hypertension, Atherosclerosis, Obesity, and Stroke)
150
What is the cutpoint for elevated BP?
Systolic >= 130mmHg and/or diastolic >=85mmHg
151
What is the cutpoint for elevated FPG?
>=5.6mmol/L
152
How does cancer increase with obesity in men and women?
52% ↑ men
62% ↑ women
153
What is Osteoarthritis? What is the number one preventable risk factor?
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
What are the biological mechanisms of obesity?
* FFA
* Ectopic fat
* Insulin resistance
* Adipocytes as endocrine cells (inflammation)
* Inflammation
155
What is Visceral fat?
“hidden” and stored deep in the belly around the organs (intestines & liver). Carries significant health risks.
156
What is Abdominal obesity?
A condition where excessive visceral fat around the stomach has built up (apple shape / beer belly)
157
What is Ectopic fat?
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
What is insulin resistance?
A physiological condition where the natural hormone insulin becomes less effective at lowering glucose
158
What is insulin resistance?
A physiological condition where the natural hormone insulin becomes less effective at lowering glucose
159
What are potential mechanisms of insulin resistance?
- FFA, ectopic fat
- Inflammation***
- Adipokines (Cytokines produced by adipose tissue)
- Adiponectin
160
What is the relationship between sleep and BMI?
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
What is the relationship between sleep and food intake?
Sleep deprivation increases food intake
162
What happens if you have a decrease in leptin?
You want to eat more
163
What happens if you have an increase in ghrelin?
You want to eat more
164
What is cortisol?
- Is known as “the stress hormone”
- Short term beneficial, long term not
- Is the most potent glucocorticoid
- Causes insulin resistance
165
What is Cushing’s syndrome?
Excess cortisol of any cause
166
What are 5 links / results between Cushing's syndrome / metabolic syndrome?
Abdominal Obesity
Hypertension
Hyperglycemia
Insulin resistance
Dyslipidemia
167
What was the response to chronic psychological stress and what was the overall effect?
~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
Even if the cortisol response is the same, why will weight change will be different?
There are responders and non-responders
169
What is the acute effect of stress/cortisol on food intake?
On stress day, high reactors ate more calories after test. This explains why some people gain / loose weight when stressed.
170
What are some food eating implications?
* Restrained Eaters
* Night eating syndrome
* Binge eating syndrome
* Emotional eating
* Smoking and alcohol consumption
* Implications for use of food/ PA diaries
171
What is Assortative mating?
Lean individuals mate with lean individuals; individuals with obesity mate with individuals with obesity.
172
What is Epigenetics?
How your genes express themselves
173
What is 1kg in lbs?
2.2lbs
174
What was the Quebec 100-day overfeeding experiment with twins?
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
What is NEAT? What does it represent?
Non exercise activity thermogenesis. - Metabolism that is not due to exercise (fidgeting, etc)
176
What was the Quebec negative energy experiment with twins?
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
What genetic trait has direct transmission and a high effect size?
Mendelian disease
178
What genetic trait is a gene that significantly affects a heritable characteristic >=5%?
Oligogenes
179
What genetic trait is a gene that has a small effect on heritable characteristics (<5%) and has the most frequency?
Polygenes
180
What are 5 genetic genes for obesity? What do they mean?
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
What are Gene-Gene Interactions?
Expression of one gene affects expression of another gene. Seen at an individual level.
182
What are Gene-Environment Interactions?
The interactions between genes and their environment that necessitate a cellular response. Usually seen at a population level.
183
What is Epigenetics?
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
What is the percentile cut off point for at risk for overweight in youth?
85th percentile
185
What is the percentile cutoff for being overweight in youth?
95th percentile
186
What happens if you are exposed to a famine in TM1 or TM2?
Increased risk of obesity at 19years - resetting appetite, metabolism, etc.
187
What happens if you are exposed to a famine in TM3?
Lower rate of obesity at 19 years (usually laying down fat in TM3, doesn't effect metabolism as much)
188
What happens if you have early, excessive weight gain in early pregnancy?
May alter in utero environment to promote obesity. Linked to gestational diabetes, postpartum weight retention and childhood obesity
189
What birthweight has a risk of being overweight?
>4000g
190
What pregnancy complications can you get?
GDM
Preeclampsia (high blood pressure)
191
What effect does exercise have on pregnancy?
Lower rates of high birthweight
192
What effect does smoking have on pregnancy?
Higher BMI in childhood
193
What effect does breastfeeding have on pregnancy?
Associated with slightly lower BMI throughout life
194
What are 12 ways to distinguish bad science?
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
What are 12 ways to distinguish bad science?
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
The coefficients of digestibility of CHO and fats are consistently over what?
90%
196
Explain the chart linking obesity and T2D
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
How do increased adipocytes lead to inflammation?
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.
