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HLTH 331 > Advanced Nutrition Midterm (1) > Flashcards

Advanced Nutrition Midterm (1) Flashcards

1
Q

What is experimental research?

A
  • Researcher manipulates a variable
  • Evaluates response of the change
  • Determines causation
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2
Q

What is observational research?

A
  • Researcher observes responses in natural conditions
  • Determine the association between variables (NOT causation)
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3
Q

Statistical Significance

A

If the value is within the 95% confidence interval (within the threshold) then the null hypothesis is true: if the p value is less than 0.05, it is significant. If it is on the outside or greater than 0.05, it is not true.

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4
Q

Effect Size

A

Measures the strength of a relationship between two variables in a population.
Effect Size (Cohen’s D)
- Ignored (0-0.2)
- Small (0.2-0.49)
- Medium (0.5-0.79)
- Large (greater than 0.8)

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5
Q

Hazard Ratio

A

Ratio of the risk of an outcome in one group to the risk of that outcome in another group, occurring at any given interval of time

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6
Q

Relative Risk

A

Risk of an event in the exposure group to the risk of that event in the non-another group

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7
Q

Forest Plot

A

Effect size - represented by the square or diamond: position along the horizontal axis indicates the magnitude
Vertical line - represents the null hypothesis (no effect)
If diamond touches or crosses the line, it is not statistically significant, if it is on either side it is significant

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8
Q

Third variable problem

A

Type of confounding variable that leads to a mistaken causal relationship between 2 others
Example: hot weather (mediator) causes sunburns but also increases ice cream sales. They are correlated but not causally related

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9
Q

Types of third variables

A

Confounder = variable that influences both dependent and independent variable. Moderator = modifies the form or strength of the relationship between an independant and dependant variable. Mediator = x causes the mediator M. and M causes Y, x-m-y

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10
Q

Confounder example exercise

A

Confounder = diet. Independent variable = exercise
Dependent variable = weight loss

BUT exercise does not cause weight loss.

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11
Q

Mediator example

A

Sleep quality causes stress (the mediator) and that influences mental health

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12
Q

Moderator example

A

Caffeine consumption (independent) influences sleep quality - caffeine addiction, which in turn influences cognitive performance

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13
Q

Why is nutrition research difficult?

A
  • Varies between populations
  • DIetary restrictions
  • Biased research
  • Lifestyle factors (those who eat healthy typically exercise more often)
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14
Q

Research design differences

A

Feeding Trial
- Provided with all meals, snacks, etc (controlled)

Randomized Controlled Trials
- Participants asked to follow a diet but are not provided with meals (guided)

Observational studies
- Compare individuals who self select to consume a specific diet (no intervention)

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15
Q

Feeding Trials

A
  • Expensive
  • High adherence (main advantage)
  • Short duration
  • Lots of work to organize
  • No generalizability
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16
Q

Randomized Controlled Trials (RCT)

A
  • Average cost
  • Must adhere themselves
  • Last for several years
  • Still lots of labor
  • Somewhat generalizable
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17
Q

Observational Trials

A
  • Cheaper than others
  • N/A for adherence
  • 10+ years for study time
  • Less work to organize
  • Very generalizable
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18
Q

Which variables would affect how someone would respond to a diet?

A
  • Exercise
  • Sleep
  • Hormones
  • Lifestyle
  • Medications
  • Age
  • Sex
  • Socioeconomic status
  • Time of eating
  • Cost of food
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19
Q

What are primary research papers?

A
  1. Randomized control trials
  2. Peer reviewed papers
  3. Cohort studies

They require an active statement - testable question, methods, results, discussion, and provides first hand evidence

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20
Q

Metabolic Health (5)

A

Defined as having optimal levels of:
1. Blood sugar levels
2. Triglycerides
3. High density lipoprotein (HDL)
4. Blood pressure
5. Waist circumference (lower)

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21
Q

Metabolic health - blood pressure

A

> _ 130/85 mmHg or BP lowering medication

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22
Q

Metabolic health - triacylglycerols

A

> _ 1.69 mmol/L or lipid lowering medication

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23
Q

Metabolic health - HDL cholesterol

A

< 1.04 mmol/l for men
< 1.29 mmol/l for women

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24
Q

Metabolic health - fasting glucose

A

> _ 6.1 mmol/L or prevalent diabetes

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25
Q

Metabolic health - waist circumference

A

> 102 cm men (greater than)
88 cm for women

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26
Q

Biomarker

A

Biomarkers are objective, quantifiable characteristics of biological processes. They are surrogate endpoints? Example, tumor size reduction in cancer patients

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27
Q

Clinical endpoint

A

They are a variable that reflects of characterizes how a subject in a study or clinical trial “feels, functions, or survives”bio

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28
Q

Biomarker Examples

A

Marker = fasting blood glucose (FBG). Explanation = concentration of glucose in the blood, provides information on blood sugar. Risk = diabetes

Marker = Low density lipoprotein cholesterol. Explanation = provides information on lipid metabolism (measures the amount of atherogenic lipoproteins in the blood). Risk = cardiovascular disease

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29
Q

Mediterranean diet confounders

A

Randomly assigned - diet or no diet. Follow up assessments at 6 and 12 weeks. Outcome - diet group had improved cholesterol and greater reductions in BMI.

Confounders: Length of the study. Could have had problems with adherence

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30
Q

Why do we gain weight?

A

All about energy. Energy in versus energy out.

For example, if our calories consumed is relative to energy expenditure, weight remains relatively constant

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31
Q

Balanced weight

A

Energy consumed = energy expended

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32
Q

Gained weight

A

Energy consumed is greater than energy expended

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33
Q

Lost weight

A

Energy consumed is less than energy expended

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34
Q

Energy In

A

Food consumption

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35
Q

Energy out

A

Divided into 4 categories:
1. Basal metabolic rate (BMR)
2. Exercise activity thermogenesis (EAT)
3. Non exercise activity thermogenesis (NEAT)
4. Thermic effect of food (TEF)

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36
Q

Non exercise activity thermogenesis (NEAT)

A

Energy expended from everything we do that is not sleeping, eating or sports-like exercise. Results from spontaneous physical activity that is not the result of voluntary exercise. Ie, moving arms when speaking, cooking, typing, singing, shoveling snow, gardening, cleaning

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37
Q

Exercise activity thermogenesis (EAT)

A

Number of calories burned when they’re purposefully trying to break a sweat (training, exercise). Purposeful exercise

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38
Q

Basal metabolic rate (BMR)

A

Calories burned while your body performs basic (basal) life sustaining functions

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39
Q

Thermic effect of food (TEF)

A

Metabolic rate after ingestion of a meal (protein is the highest). Reflects the energy cost (burned) during food digestion, absorption, and storage

ATP = energy to break down bonds

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40
Q

Total energy expenditure

A

65% of calories burnt are from BMR.
20% from neat.
10% from eat.
5% from tef.

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41
Q

Resting energy expenditure (REE) vs basal metabolic rate (BMR)

A

Biggest difference lies in the strictness of conditions.

RER = amount of energy required by the body in the resting condition. BMR = amount of energy needed to maintain basic life metabolic processes at rest

RER - measured under less strict conditions, fasted 3-4 hours, not following sleep, no exercise 12 hours prior to test, 10% higher than BMR (less accurate)

BMR - measured under very strict conditions, overnight fast, morning following sleep, no exercise 24 hours prior, 10% lower than BMR (more accurate)

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42
Q

Which factors affect BMR?

A
  1. Gender/sex
  2. Muscle mass/fat free mass (higher metabolic rate than fat mass)
  3. Pregnant
  4. Undereating
  5. Age
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43
Q

Energy out (physical activity)

A

Represents NEAT and EAT. All exercise and non exercise activities associated with daily living. The most variable energy output

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44
Q

NEAT and work

A

Burn more calories in a strenuous job compared to a seated one… NEAT associated with occuption.

Ex, working in agriculture is strenuous (burning almost 2500 calories), having a desk job is not (burning about 500).

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45
Q

NEAT comparisons

A

Figeting burns about 50 calories per day. Walking 3 mph about 250 calories. Sitting is like 10 calories

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46
Q

MET (Metabolic Equivalent of Task)

A

Ratio of the rate of energy expended during an activity to the rate of energy expended at rest. Amount of oxygen consumed while sitting at rest. We measure exercise through METs, higher the MET = more calories burned.

Gardening = 4, golf = 5.3, weightlifting = 6, ballet = 6.8, basketball = 8, martial arts = 10.3

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47
Q

Measuring energy expenditure

A

Measures of O2 and CO2 being consumed.
Food + O2 = CO2 + H2O + heat
Quantified by measuring the heat dissipated by the body

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48
Q

Food Consumption

A

Calorie = energy required to increase the temperature of 1g of water by 1 degree celsius

Carb = 4cal/g
Fat = 9cal/g
Protein = 4cal/g
Alcohol = 7cal/g

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49
Q

Complications of energy in vs energy out

A

Factors such as environment, genetic background, individual factors, all determine and impact other factors. Everything is intertwined

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50
Q

Obesity

A

A progressive chronic disease characterized by abnormal or excessive fat accumulation that impairs health. It is associated with type 2 diabetes, high blood pressure, heart disease, stroke, arthritis, cancer

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51
Q

Measuring Obesity (BMI)

A

Body mass index = universal definition of overweight and obesity. Mass in kg divided by height in m.

Underweight = less than 18.5
Normal = 18.5-24.9
Overweight = 25-29.9
Obese 1 = 30-34.9
Obese 2 = 35-39.9
Obese 3 = 40 and above

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52
Q

Limitations of BMI

A
  1. Does not consider body composition
  2. Gender and sex not considered
  3. No information on fat distribution
  4. Hard to interpret across different ethnic groups and age (elderly for example)
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53
Q

BMI - Body composition

A

Athletes considered obese with increased muscle. Some people may have high BMI but low body fat % (no increase in risk of cardiovascular disease). Low BMI with high body fat means there is an increased risk

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54
Q

Muscle mass and BMI

A

Graph shows that having high muscle and low fat, will give someone a higher survival probability than someone with low muscle and low fat. Most importantly, muscle mass is associated with more positive outcomes

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55
Q

Measuring Body Composition

A

Gold standards: MRI (magnetic fields and radio waves forming images), CT, DXA (x rays)

Indirect methods: Lab based - hydrostatic weighing, BodPod. Field methods - skin folds, BIA (electrical current through body)

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56
Q

Comparison of body composition methods

A

Slide 27 of lecture 2. Table

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57
Q

Fat distribution - who has the greatest risk of cardiovascular disease?

A

Internal adipose tissue - fat lining that lower gut area that goes around entire back too

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58
Q

Subcutaneous adipose tissue

A

External - anything you can pinch. Represents over 80% of total body fat. Responsive to external signals such as adrenergic stimulation and endocrine regulation. Used as energy storage

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59
Q

Visceral adipose tissue

A

More inflammatory and dangeous. Associated with a risk of metabolic and cardiovascular disease. About 5-20% of body fat. Protects organs - surrounds vital organs inside abdominal cavity. Secretes proinflammatory cytokines

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60
Q

Visceral adipose health risks

A

Associated with metabolic abnormalities that increase risks of disease… visceral adipocytes may mediate INSULIN resistance.

  1. Pro inflammatory cytokines. These alter hepatic function, insulin sensitivity, and cytokine production (small proteins).
  2. Portal theory. Proposes the liver is directly exposed to free fatty acids and cytokines increasingly released from visceral fat tissue into the portal vein, causing visceral fat accumulation, which is hazardous for the development of hepatic insulin resistance and type 2 diabetes
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61
Q

Waist circumference

A

Used alongside BMI to assess risk of obesity related complications. WC cut off points:
Men >_ 102 cm
Women >_ 88 cm
If above, you have an increased risk of developing health problems

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62
Q

More men have obesity than women

A

Graph shows it varies by age and sex, but men are more obese at every age besides youth. Massive increase in our 20’s then again at 35

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63
Q

Men and visceral accumulation

A

Men more likely to accumulate fat into the visceral area than women. They grow an apple shape

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64
Q

Women and subcutaneous accumulation

A

They gain more subcutaneous than men. Grow into a pear shape. Tend to gain more weight in legs and hips

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65
Q

Rates of Obesity Worldwide

A

Rates have tripled since 1975. 39% of adults overweight. 13% of those adults are obese
In Canada, 40% overweight, 25% obese

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66
Q

Why has obesity increased

A
  1. More sedentary behaviour, less moving in occupation, easier to drive
  2. Less exercise as a whole
  3. Not eating enough protein
  4. Portion sizes, variety of food, prices
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67
Q

Obesity - energy IN has increased over time (worldwide)

A

24% calorie increase since 1961. Average of 2880 to now 3600 calories per day. Diet consists of processed meals. Bigger portion sizes.

Happening even in developing countries! 2054 calories per day in 1965, 2980 in 2030

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67
Q

Obesity - declines in NEAT

A

Considering our occupation. Many people are doing sedentary work compared to in the past. Rates of moderate work have severely decreased. Total daily energy expenditure has declined

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68
Q

Changes in Energy Balance (bodyweight)

A

Predicted weight gain would be a 30-80 fold increase in body weight in adults. However, we have physiological processes helping to maintain our body weight so it doesn’t reach this point

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69
Q

Set point theory

A

Human body has a predetermined weight or fat mass set-point range. There exist compensatory physiological mechanisms to maintain and resist deviation from the set point

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70
Q

Factors that alter the set point (5 of them)

A
  1. Genetics
  2. Epigenetics
  3. Obesogens (chemicals which alter our bodies function - plastics for example)
  4. Diet and physical activity (adjust to eating too much or too little)
  5. Disease
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71
Q

Set Point Theory Breakdown

A

Signals to the brain (hypothalamus) does BMR need to be adjusted?

Neutral energy balance = calories you take in is equal to what you expended.

Negative energy balance = you expend more energy than you take in (causing weight loss)

Positive energy balance = you take in more calories than you expend (causing weight gain)

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72
Q

Light Activity

A

Idea that light physical activity can prevent obesity - linked with a substantially reduced risk of death in a dose-response manner

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73
Q

Two responses to cause changes to BMR

A
  1. Obligatory - function of losing weight (we can lose both muscle and body fat). BMR should decrease. When you weigh less, you require less energy
  2. Adaptive - physiological mechanisms employed for maintaining weight (set point) independent of obligatory mechanisms
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74
Q

Energy restriction (REE)

A

REE = resting energy expenditure - amount body uses at basal rest.

Obligatory = decrease in metabolically active tissue (skeletal muscle and organ mass)

Adaptive = increase in adaptive thermogenesis by reduced substrate cycling in skeletal muscle (body attempts to preserve energy stores in an energy crisis - underfeeding)

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75
Q

Energy restriction (EAT)

A

Obligatory = decrease in energy cost of movement proportional to reduced bodyweight

Adaptive = increase in skeletal muscle work efficiency

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76
Q

Energy restriction (NEAT)

A

Obligatory = decrease in energy cost of movement proportional to reduced bodyweight

Adaptive = increase in spontaneous physical activity (pacing, etc)

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77
Q

Energy restriction (TEF)

A

Obligatory = decrease in postprandial (after a meal) response due to reduced energy intake

Adaptive = increase in adaptive postprandial response associated with overfeeding only

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78
Q

Adaptive Thermogenesis

A

Thermogenesis is the process of heat production in organisms.

Adaptive thermogenesis is underfeeding associated fall in REE independent of changes in FFM (free fat mass) and FM (free mass). During underfeeding BMR goes down to burn less, during overfeeding it goes up to burn more

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79
Q

Role of NEAT in overfeeding

A

Those more resilient to weight gain (spendthrifts), their NEAT (spontaneous movements) increase when they overeat. They are less susceptible to obesity.

People unable to respond to a continued energy surplus with NEAT (thrifty). Represent the majority of the population. They are diet resistant

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80
Q

Adipose tissue fibrosis

A

Lean tissue has less fat between (skinny lines) whereas obese tissue has bigger fat stores (thicker gaps between)

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81
Q

Calorie is just a calorie

A

Idea that the effect of eating carbs, proteins, fats, will all have the same effect on the body. States that diets high in added sugar or processed foods should have no adverse effects on metabolism or body composition, after considering total calorie consumption

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82
Q

Protein and obesity

A

Does not contribute to obesity (barely) because it is satiating, promotes lean mass, and has thermogenic effects (takes more calories to burn), is nutrient dense

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83
Q

Comparing a meal rich in protein and one rich in fat

A

Diet induced thermogenesis was significantly higher (3 fold) after consumption of the protein rich meal

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84
Q

Two theories of calorie is just a calorie

A

1) conventional model
2) carbohydrate insulin model

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85
Q

Conventional Model

A

Eating too much = weight gain
Eating too little = lose weight

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86
Q

Blood glucose regulation

A

Bodies response to sugar:
Body does not want to have high resting blood glucose levels.

Eating cake = spike in blood sugar. Signals to pancreas to release insulin and stimulate glucose uptake and glycogen.

Haven’t eaten = low blood sugar. Signals to pancreas to release glucagon and signals to liver release glycogen

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87
Q

Carbohydrate insulin model

A

Depending on the food we eat, it has a different effect on metabolism. Eating something high in sugar = spike in insulin. Insulin stimulates fat storage. Increase in energy intake = hungry and wanting more food. This leads to a decrease in expenditure and increase in weight

Idea that dietary quality can change hormonal responses to shirt partitioning of calories consumed toward deposition in fat tissue. Fewer calories remain in blood stream which drives hunger and overeating. saying certain foods prompt fat storage, etc

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88
Q

Carb devil study

A

Showed that even with a decrease in eating carbs, obesity is still on the rise. Supports argument that calorie is just a calorie

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89
Q

Cell Metabolism Study

A

Showed cutting fat in a diet resulted in more body fat loss compared to cutting carbs. Showed more cumulative weight loss with reduced fat diet - but difference wasn’t very meaningful? But really no difference between diets - confused here

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90
Q

Low fat vs low carb diet

A

Study showed low fat diet was only -28 calorie difference, meaning it is clinically meaningless…

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91
Q

Processed vs unprocessed foods

A

Ad libitum = allowed to eat whatever they want. Bodyweight significantly changed with ultra processed foods (gained), for unprocessed foods (lost some weight).

Basically saying that refined carb intake may accelerate weight gain?

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92
Q

When it comes to weight loss, is a calorie just a calorie?

A

In this case yes. both increased carb and fat intake are driving weight gain… when it comes to weight loss calorie is just a calorie

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93
Q

Carbohydrate classification

A

Organic molecules that contain carbon, hydrogen, oxygen

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94
Q

Monosaccharides

A

One sugar molecule:
Glucose
Fructose
Galactose

95
Q

Disaccharides

A

Two sugar molecules:
Sucrose (gluctose + fructose)
Lactose (glucose + galactose)
Maltose (glucose + glucose)

96
Q

Oligosaccharide

A

2-10 sugar molecules:
Raffinose
Stachyase

97
Q

Polysaccharide

A

10 or more sugar molecules:
Starch
Glycogen
Cellulose

98
Q

Metabolic fate of carbohydrates

A

They are the primary energy source. Yield ATP to perform daily functions.

Liver and muscle is where glycogen is stored. When we have too much glucose it is converted into fat or triglycerides

99
Q

Carbohydrate digestion

A

If we digest bread, saliva (amylase) breaks it down into poly then oligosaccharides. It does through the esophagus to stomach which ends in the small intestine. Broken into disaccharides which are further broken down into absorbable monosaccharides

100
Q

Carbohydrate absorption

A

Monosaccharides are broken down into their smallest form. They go through microvilli (to increase surface area) and reach other systems

101
Q

Carbohydrate metabolism

A

The conversion of glucose to other forms.

Glucose-6-phosphate is converted to glycogen through glycogenesis (after eating)

Glycogen is depleted when fasting or working out (so we must eat more carbs to replenish)

Gluconeogenesis is the conversion of other macronutrients to form glucose (from fats and proteins)

102
Q

Glycogen

A

Stored in the muscle (350-750g) and parts of the liver (100-200g)

103
Q

Glycogenesis

A

Conversion of excess glucose to glycogen for storage. It allows your body to manage and regulate blood glucose levels efficiently (glucose homeostasis).

Glucose comes from food we eat, when there is excess it is converted for storage (happens in liver or muscle), enzyme action (hexokinase in muscle, glucokinase in liver), glycogen serves as energy reservoir, insulin helps regulate glycogenesis.

The first step involves phosphorylation of glucose to glucose-6-phosphate by the enzyme hexokinase or glucokinase, depending on the tissue. Glucose-6-phosphate is then converted to glucose-1-phosphate. Converted to glycogen

104
Q

Glycogenolysis

A

The reverse of glycogenesis - it is breaking down glycogen.

Body needs a quick supply of glucose (during PA or between meals). Glycogen phosphorylase (enzyme) breaks bonds between glucose molecules. As phosphorylase breaks the bonds, glucose molecules are released into the bloodstream. Rapid increase in blood glucose. Used by body for immediate energy needs

105
Q

Glycogen

A

Emergency glucose storage

105
Q

Skeletal muscle and glucose

A

Muscle maintains blood glucose homeostasis. Can be broken down to lactate which can be transported to the liver and via gluconeogenesis contribute to maintaining euglycemia

106
Q

Gluconeogenesis

A

Process where your body makes new glucose (sugar) from non-carbohydrate sources such as amino acids and glycerol. When we need energy our body forms glucose, if we have too much it forms glycogen.

Gluconeogenesis starts with amino acids (protein building blocks), lactate (from muscles), glycerol (from fats). Enzymatic reactions in the liver and sometimes kidneys, these non carb precursors are converted to glucose. Process is regulated by hormones such as glucagon and cortisol, which signal the need for more glucose in blood.

SO when on a low carb diet, this helps create glucose and meet energy demands

107
Q

Blood Glucose Regulation

A

Regulation of the body’s blood sugar. Primary organ that uptakes blood glucose is muscle!!!

Post meal: blood glucose rises, signals to pancreas to release insulin (hormone). Cells use glucose for energy or store it. Insulin works until blood glucose returns to normal.

Between meals: body needs energy so pancreas releases glucagon. Signals to liver to breakdown stored glycogen into glucose and release into blood

108
Q

Factors to consider when choosing a carbohydrate source

A
  1. Nutrient density
  2. Glycemic index
  3. Fructose content (simple vs complex carbs)
  4. Fiber content
109
Q

Nutrient density

A

Nutrients per reference amount of food, typically 100cal or g per serving. In graph most nutrient dense food is liver. Least are refined grains

110
Q

Glycemic Response

A

Depending on the food you eat, it will cause spikes in blood sugar. High spikes and low crashes are not good, but makes sense to fluctuate a bit (green area).

111
Q

Glycemic Index

A

Glycemic response: change in blood glucose after eating a carbohydrate containing food. Glycemic index: scale that ranks carbohydrate-containing foods/drink by how much it raises blood glucose. Important parameter in controlling blood glucose homeostasis, insulin release, and obesity. Persistent elevation = development of chronic diseases

High GI: Quickly digested and absorbed, rapid rise in blood glucose and insulin. Sugary drinks, white bread, potatoes

Low GI: Slow rise in blood glucose and insulin. Slowly digested and absorbed (better out of two). green veggies, carrots, chickpeas

112
Q

Glycemic Load

A

Considers the amount of carbs ingested. GL = GI x grams of carbs

113
Q

Glycemic index and health outcomes

A

Low GI diets are associated with a lower risk of developing type 2 diabetes and cardiovascular disease.

High GI diets are associated with greater risk of developing type 2 diabetes and cardiovascular disease.

114
Q

Reactive Hypoglycemia

A

Condition where your blood sugar levels drop lower than normal after eating.

Eat meal = breaks down carbs and causes spike in glucose and rapid increase in blood sugar = pancreas releases insulin to use glucose for energy = can release too much insulin which causes blood sugar levels to drop below normal (glucose crash) = in turn induces hunger and more energy intake (increases risk for obesity, T2 diabetes, heart disease because events can promote beta cell dysfunction and endothelial dysfunction)

115
Q

Clinical trials that investigate low vs high GI diets on insulin sensitivity and cardiovascular disease report diverse results… why?

A
  1. Changes in total carbs and fiber intake
  2. Weight loss (has a group gained or lost weight/it impacts their insulin sensitivity (higher the better) and resistance (not good))
  3. Presence and use of treatments for diabetes (help manage their blood glucose levels)
116
Q

Energy intake and glycemic index

A

When total energy intake is used as a confounder, the association between glycemic index/load and insulin sensitivity is removed

117
Q

GI Insulin resistance and weight loss

A

Graph compares a high fat, low GI diet, and high GI diet…

Insulin sensitivity improved in all 3 groups. They lost the same amount of weight? As long as energy restriction is the same, weight loss is the same

118
Q

Glycemic Index and Weight Management

A

Comparing low GI diets and high GI diets for weight loss… Results show low GI were generally no better than high GI diets for reducing body weight or body fat. They compared various genders and ethnicities.

119
Q

Type 2 diabetes and fibre intake

A

Idea that as you increase your fiber intake, you lessen your glycemic index. As you decrease your fiber intake, you increase your glycemic index

120
Q

Fibre and Diabetes

A

Graph shows that a high fiber diet is a huge confounder to limit the chance of diabetes. Can help to prevent it!

121
Q

Baseline characteristics of glycemic index

A

Diet is more important for certain populations than others (normal BMI versus obese). Idea that we should just include more fiber?

Lower insulin means you are not super insulin resistant. So following the glycemic index comes down to whether it is a personal issue or for someone else

122
Q

Glycemic Index Review

A
  1. When calorie intake is controlled, low GI and high GI diets report similar outcomes
  2. Large variability between study findings for weight loss
  3. Fiber content is a large confounder (more positive effects on health when eating more fiber)
  4. Baseline characteristics matter (finding what diet is best for you)
123
Q

Limitations of glycemic index

A
  1. Intra and inter-variability
  2. Lifestyle factors
  3. Growing conditions and meal preparation after GI
  4. GI is assessed on an empty stomach and without other foods (might feel blood glucose rising when eating candy on an empty stomach)
124
Q

Intra and inter variability

A

Inter variability - variability within a single group or entity

Intra variability- variability or fluctuations within a single individual across different measurements (the idea of different responses)

Ex, if someone is more insulin sensitive it will yield different effects

125
Q

Glycemic index in a meal

A

Protein, fiber, lipids = lower glycemic index

Fiber can lower glycemic index as it’s not absorbed. Can mix high and low GI foods to lower glycemic index

126
Q

Culinary techniques and glycemic index

A

Degree of processing causing increased GI. More cooking time = increased GI. More time in storage and then microwaving= increased GI outcome.

Lack of processing exposes nutrients to the food matrix. Chewing and digestion breaks down structure to facilitate nutrient absorption which requires more energy to break bonds

127
Q

Order of Consumption

A

Have the lowest glycemic response when starches are eaten last. Start with veggies, then protein, then starch?

Eating candy then rice will have a different effect on blood glucose levels than vice versa

128
Q

What are CG-M’s? Continuous glucose monitor

A

Helpful tool for diabetics. Get blood glucose levels in real time. Glucose is measured but not insulin usually. Helpful to better manage glucose levels.

Persistent elevated blood glucose and insulin levels are linked with obesity and development of chronic diseases.

129
Q

Sugars

A
  1. Glucose
  2. Fructose
  3. Galactose

Maltose = glucose x2
Lactose = galactose + glucose
Sucrose = fructose + glucose (50/50)

130
Q

Added Sugars

A

Are associated with negative health outcomes.

131
Q

Fructose

A

Fructose metabolism is said to contribute to cardiovascular disease risk factors.

High fructose intake = gut dysbiosis (imbalance of gut diversity - disturbance), de nevo lipogenesis (inflammation and obesity), abdominal adiposity and hypertension (fat), insulin suppression

132
Q

Exogenous fructose metabolism

A

How the body handles fructose from consumption (drinking pepsi for ex).

Consuming high fructose, it is absorbed in small intestine and enters the bloodstream. Carries to liver to be converted to glucose. Enzymes such as fructokinase and aldolase are involved in the breakdown. Excess fructose can be converted to fat in the liver, contributing to metabolic conditions

Some people cannot absorb fructose and experience pain, gas, diarrhea - malabsorption

133
Q

Fructose vs glucose metabolic fates

A

Difference between the two sugars, is that fructose is metabolized by fructokinase and requires ATP for phosphorylation. Results in rapid generation of uric acid (which is fine in moderation).

Fructose undergoes more processing in the liver and has a higher likelihood of being converted to fat.

134
Q

Feedback Mechanism Fructose

A

Fructokinase does not have a negative feedback loop (can’t self regulate like temperature through bodily signals). Means this process will continue to occur. ADP is converted to AMP which could cause a person to experience more fatigue

135
Q

High doses of uric acid has what implications?

A

Idea that fructose has negative effects.

Blood pressure
- More oxidative stress
- More vascular smooth muscle cell proliferation

Type 2 diabetes
- More gluconeogenesis
- Less insulin secretion
- More oxidative stress

Obesity
- Less fatty acid oxidation (causes more fats and decrease in ATP)
- Greater triglyceride accumulation

136
Q

Metabolic outcomes in animal models (biomarkers for metabolic syndromes)

A
  • Visceral fat
  • Triglycerides
  • Insulin resistance
  • Uric acid
  • Non alcoholic fatty liver disease
137
Q

Animal: Paired feeding studies

A
  • Mice forced to eat the same amount of food
  • One ate a diet of 40% sucrose, the other isocaloric starch (equal calories from protein, fat, carbs)
  • Demonstrates how fructose is not good for you
  • Causes fatty liver?
138
Q

Animal studies - increased energy intake

A

Rats who at the fructose diet became leptin resistant. Leptin suppresses hunger, meaning they just continued eating. So they’re food intake and body weight both increased

Leptin group ate less!

139
Q

Animal Study Limitations

A
  1. Unbalanced calorie intake between group treatments.
    - Weight gain causes metabolic health issues overall, so it is hard to know the effects independent of weight gain
  2. Fructose intake is unrealistically elevated as a percentage of energy intake
    - Concentration that was administered to rats was 60-70% of diet, whereas an average beverage is 10-30%
    - So need to consider, would these effects occur if consuming lower fructose quantities?
140
Q

Fructose survival hypothesis

A

Process of fructose metabolism:
1. Fructose is broken down by fructokinase
2. ATP is converted to ADP. Fructose metabolism depletes ATP reserves
3. ADP is used to create uric acid (BAD) which causes mitochondrial damage WHICH signals to activate the survival switch

The Switch:
- In the past, ancestors faced periods of food scarcity and needed to maximize energy intake when food was available. For them storage of sugars served as backup fuel
- Prepares body for times of food scarcity (ie, Winter, starvation)
- Now food is more abundant, in which eating fructose will contribute to overconsumption and potentially obesity
- Now not necessary to activate switch
- Causes increased fat, reduced energy, can’t fight infection

141
Q

Fructose survival hypothesis (normal vs fructose)

A

Normal weight regulation
- Different types of diets cause the body to self correct and result in more ATP than fat

Fructose survival pathway
- Consuming fructose, reduces ATP production, causing insulin resistance and then a greater percentage of fat than ATP as a result

142
Q

Hypercaloric diet VS isocaloric diet

A

Hypercaloric diet
- Total calorie intake exceeds amount expended by the body
- Causes weight gain

Isocaloric diet
- consuming the same amount as the body expends
- stable weight
- No weight gain

143
Q

Fructose and weight gain

A

Overeating = increased energy intake = circulating metabolic fuels = increased fat storage.

Idea that calorie is just a calorie. Energy in = energy out. That eating more will cause a person to gain weight

144
Q

Does fructose lead to overconsumption in humans?

A

Soft drink consumption and energy intake: longitudinal studies say there is a positive association between soft drink consumption and overall energy intake - might stimulate appetite. Long term studies showed individuals did not compensate for the extra energy consumed, causing weight gain.

145
Q

Fructose and lipogenesis

A

After consuming fructose it is absorbed into the bloodstream. Unlike glucose, a significant portion of fructose is transported to the liver. Fructose is converted to acetyl-CoA through enzymatic reactions. Acetyl CoA serves as a precursor for de novo lipogenesis, where the liver synthesizes new fatty acids. New fatty acids combine with glycerol to form triglycerides which are packed into VLDLs. Contributes to an increase in fat body stores

146
Q

More fructose in weight gain

A

Studies showed fructose and glucose diets gain the same amount of weight BUT visceral adipose tissue increased more in the fructose group!

147
Q

Fructose Conclusions

A
  1. Fructose diet led to an increase in visceral adipose tissue (VAT) compared to the glucose group which had larger increases in subcutaneous adipose tissue (SAT)
  2. Fasting ApoB was increased in the fructose group and not glucose group (Fasting ApoB levels refer to the measurement of ApoB protein in the blood after a period of fasting. Elevated levels are correlated with risks of cardiovascular disease - associated with VLDL and LDL)
  3. Measures of insulin sensitivity decreased in fructose group compared to glucose group (reduced effectiveness of insulin which can lead to high blood sugar)

Limitations
1. Glucose vs fructose - hard to separate because fructose is usually in combination with glucose

148
Q

Limitations of fructose and insulin resistance study

A
  1. Small sample size
  2. Narrow demographic
  3. Short duration (10 weeks)
  4. Poor study quality
149
Q

Ectopic fat deposition

A

Liver fat - refers to abnormal accumulation of fat in organs where fat is not usually stored. Storage of excess lipids in liver and muscle

Study compared an isocaloric diet and high fructose diet between a control group and offspring T2D (parent has diabetes so they might too). Offspring were more susceptible to the effects of fructose - again showing it’s all about a person’s personal risks

150
Q

Limitations of Human Research on Fat Deposition

A
  1. Duration of studies often less than a few weeks (not long enough to observe significant changes)
  2. Fructose intake is unrealistically elevated as a percentage of energy intake (had over 25% energy intake from sugar sweetened beverages)
151
Q

Dietary fiber

A

Non digestible carbs and lignin (by human digestive enzymes) that are intact and intrinsic in plants
Ex: cellulose, pectins, fructans, lignin, gum, hemicellulose, B-glucans, resistant starches

152
Q

Functional fiber

A

Are isolated, extracted, or manufactured non-digestible carbs that have been shown to have positive physiological effects in humans. Usually added to foods and found in supplements

Ex, fructans, pectins, psyllium, gums, B-glucans

153
Q

Total fiber

A

Refers to dietary fiber present within the food and the functional fiber that has been added to the food.

154
Q

Resistant starch

A

Starch that cannot be or not easily enzymatically digested

Four main types:
1. RS1 (starch that is physically inaccessible to digestion due to its location)
2. RS2 (starch that resists digestion because it is tightly packaged inside of granules within foods)

RS1 and RS2 are dietary fibers.

  1. RS3 (formed with moist-heat cooking and cooling of starches that has gelatinized)
  2. RS4 (results from chemical modification of starches)

RS3 and RS4 are functional fibers.

155
Q

Recommended fiber intake

A

Women : 25 grams per day
Men : 38 grams per day

Projected that 50% of population are not eating the recommended amounts (not enough around the globe)

156
Q

Properties of fiber (3)

A
  1. Solubility in water
  2. Viscosity and gel formation
  3. Fermentability
157
Q

Solubility in water (fiber)

A

Water insoluble fibers
- Does not dissolve in hot water
- Whole grain products, bran, legumes, seeds, some veggies (cauliflower, green beans)
- Said to decrease intestinal time and increase fecal weight to positively impact lactation

Water soluble fibers
- Dissolves in hot water
- Oats, barley, rye, chia, flaxseeds, most fruits
- Said to delay gastric emptying to positively impact blood glucose and lipid concentrations

Some inconsistencies in findings!

158
Q

Viscosity and gel formation (fiber)

A

Viscosity: the ability of fiber to both bind or hold water and to form a gel (think of it as a sponge that hydrates and moves through digestive tract - soaks up) to form a gel

  • Most fibers can hold water to some extent
  • Not all fibers form a viscous fel when interacting with fluids

Associated with positive health outcomes: longer intestinal transit time that can increase satiety and fullness, reduced nutrient digestion (slower release of glucose to stabilize blood sugar), reduced micelle formation, decrease nutrient diffusion rates (gradual release)

159
Q

Fermentability (fiber)

A

Fermentability of dietary fiber refers to how quickly and efficiently gut microbes can degrade fiber through fermentation.

Bacteria ferments the fiber… can increase fecal bacteria mass which can attract water to enhance stool size. Can also act a prebiotic

160
Q

Diets in high fiber

A

Associated with reduced risk of death from cardiovascular disease. All concerned with the weight of stool

161
Q

Health benefits of fiber

A
  1. Diabetes
  2. Cardiovascular disease
  3. Appetite and satiety (perceived fullness after meal) and weight control
  4. Gastrointestinal disorders
162
Q

Lipid Classification

A
  1. Simple lipids
  2. Compound lipids
  3. Derived lipids
163
Q

Simple Lipids

A

Contain hydrogen, oxygen, and carbon.

  1. Waxes
  2. Triglycerides

Triglycerides further broken down into:
1. Fatty acids
2. Glycerol

Fatty acids further broken down into:
1. Saturated fatty acids
2. Unsaturated fatty acids

Unsaturated fatty acids further broken down into:
1. Monounsaturated fatty acids
2. Polyunsaturated fatty acids

164
Q

Compound Lipids

A

Contain additional elements such as phosphorous, nitrogen or sulfur.

  1. Phospholipid
  2. Glycolipid

Glycolipid further broken down into:
1. Cerebrosides
2. Gangliosides

165
Q

Derived Lipids

A

Combined simple and compound lipids through hydrolysis, the produced chemical is derived lipids.

  1. Steroids
  2. Sterols
  3. Carotenoids
166
Q

Triglycerides

A

Contains 3 fatty acids with a glycerol backbone.

Saturated = no double bonds
Monounsaturated = one double bond
Polyunsaturated = bunch of double bonds

167
Q

Sterols and Cholesterol

A

Cholesterol is the most common sterol. Has a 4 ring steroid nucleus and at least one hydroxyl group.

168
Q

Cholesterol

A

The precursor for various hormones and substances (sex hormones, vitamin D, bile salts - digestion, etc). It is required for may different functions in our body.

LDL = bad
HDL = good

169
Q

Triglyceride Digestion

A

Process of breaking down dietary fats into components that can be absorbed.

  1. Ingest fats, lingual lipase breaks it down into triacylglycerols, fatty acids, diacylglycerols
  2. Those go to the stomach, which gastric lipase is released
  3. Enter small intestine (where most digestion occurs) where bile is released (produced by liver stored in gallbladder). Bile emulsifies fat globules into smaller droplets
  4. Emulsified triacylglycerols, fatty acids, and diacylglycerols micelles go through enzymatic digestion from pancreatic lipase
  5. Results in monoacylglycerols and fatty acids
170
Q

Micelles

A

Lipid molecules that arrange themselves with a hydrophobic core and hydrophilic shell, this allows lipids to travel through a polar solvent (ie, water).

Micelles are hydrophobic = do not dissolve in water.

Triglycerides, diacylglycerol, cholesterol, and cholesterol esters combine with bile salts to form a micelle

Can dissolve naturally in aqueous solution…

171
Q

Chlyomicron

A

large lipoprotein particles that transport dietary fats, including triglycerides, from the small intestine to various tissues in the body. Bypasses the liver so it can circulate to other parts of the body

172
Q

Lipid Absorption - Chylomicrons

A

From lymphatic vessels, chylomicrons travel to the left subclavian vein and diffuses into circulation. Bypasses the liver where they would be catabolized (if they were to enter the hepatic portal vein)

173
Q

Lipid transport - lipoproteins

A

Lipids are transported in the blood as components of lipoproteins.

Types of lipoproteins
1. Chylomicrons
2. Very low density lipoproteins (VLDL)
3. Low density lipoproteins (LDL) - bad cholesterol
4. High density lipoproteins (HDL) - good cholesterol

Each type of lipoprotein has different proteins attached to it.

174
Q

Lipoproteins - difference between them?

A

Graph shows a chylomicron is 82% triglycerides, etc.

LDL is 47% cholesterol, 23% phospholipids, etc.

VLDL is 52% triglyceride, 22% cholesterol

HDL is 50% protein, 19% cholesterol, 28% phospholipid, 3% triglyceride

Illustrates concentrations changing between lipoproteins (density)

175
Q

Which proteins are transported

A
  1. Triglycerides
  2. Cholesterol
  3. Phospholipids
176
Q

Where are the lipids delivered?

A
  1. Liver
  2. Skeletal muscle
  3. Adipose tissue
177
Q

Lipoproteins metabolic fate

A

Play a role in helping the body to utilize fats/lipids.

178
Q

Three systems responsible for different types of fats being transported in the blood

A
  1. Exogenous lipid transport
  2. Endogenous lipid transport
  3. Reverse cholesterol transport
179
Q

Exogenous lipid transport

A

Function: transport of dietary lipids (triacylglycerols) from the intestine to peripheral tissues for storage or energy utilization

Lipoprotein: chylomicron

Operates only after a fat containing meal. Chylomicrons disappear after all dietary triacylglycerols are delivered to target tissues

180
Q

Endogenous lipid transport

A

Function: transport of triglycerides from the liver to peripheral tissues for storage or energy utilization

Lipoprotein:
VLDL, IDL, LDL

Just consumed something, transport of fatty acids from liver to rest of body when needed

181
Q

Reverse cholesterol transport

A

Function: ability to pick up excess cholesterol from peripheral tissues and deliver it to the liver for excretion from the body (via bile)

Lipoprotein: HDL

Body has a specific way of collecting cholesterol - picking it up and delivering to liver for excretion

Large HDL’s better for health - larger molecules means you can pick up cholesterol with more ease and fewer negative effects on the body

182
Q

Exogenous liquid transport system explained

A

Chylomicron enter the bloodstream through the lymphatic system? Confused

183
Q

Lipid metabolism in adipose tissue

A

?

184
Q

Lipid metabolism fatty meal

A

If you just ate a fatty meal, fatty acids will go into liver cell, forms triglycerides and goes into VLDL to systematic circulation and distribute to rest of the body (understanding diffusion process)?

185
Q

Endogenous liquid transport system explained

A

It is the reserve - what you already have in the body and transporting triglycerides from place to place for storage or energy utilization. Continuous process.

Begin with Nascent VLDL
- Gets rid of fatty acids and concentrations to become lower, IDL?
- LDL is excreted and destroyed in liver

186
Q

What can lead to an accumulation of LDL?

A

If LDL receptors in the endogenous liquid transport system stop working. It accumulates because there is no way to get rid of them

187
Q

Reverse cholesterol liquid transport system explained

A

Idea that it transports accumulating cholesterol. Receptors signal to HDL, I have cholesterol to give you in which it continues to collect.

Refers to the ability of circulating HDL to pick up excess cholesterol from peripheral tissues and deliver it to the liver for excretion from the body via bile. All cells can synthesize cholesterol but not degrade it (liver must do this hence why transport is important)

188
Q

Cholesterol and cardiovascular risk

A

High proportion of large HDL is associated with a LOWER risk of cardiovascular disease.

High proportion of LDL is associated with a high risk.

Says its because larger HDL means greater ability to gather cholesterol and deliver it to the liver.

189
Q

FULL VERSION: Reverse cholesterol liquid transport system (slide 22)

A
  1. Lipid-free ApoA-1 is secreted by the liver and intestine. It is also released from chylomicrons and VLDL during TAG hydrolysis.
  2. ApoA-1 acquires PL and C from interaction with liver ABCA1, resulting in nascent HDL particles.
  3. Nascent HDL acquire additional PL and C via ABCA1 and additional C via SR-B1 in peripheral tissues.
  4. The enzyme LCAT, carried on HDL particles, esterified C to CE that migrate to the particle core.
  5. Lipid-free ApoA-1 is secreted by the liver and intestine. It is also released from chylomicrons and VLDL during TAG hydrolysis.
  6. LCAT continues to esterify C to CE, forming larger HDL
  7. Some CE are transferred to VLDL and LDL, mediated by CEPT
  8. Liver SR-B1 binds HDL. CE may be selectively removed, or the HDL particle may be internalized and degraded.
190
Q

Saturated fats

A

Just the single lines in picture
- Raise HDL cholesterol
- Butter, bacon, cheese

191
Q

Unsaturated fats

A

Double bond (indicating break in bond)
- Omega 3 fats

192
Q

Atherosclerosis

A

Caused by the buildup of plaque in the lining of an artery. Plaque is composed of fats, cholesterol and other substances. It is the progressive narrowing of the arteries due to plaque formation and considered the major cause of cardiovascular disease. Elevated levels of LDL cholesterol and apolipoprotein (apoB) are directly associated with the risk for cardio events.

  1. Dysfunctional endothelial cells and retention of ApoB-containing lipoproteins
  2. Triggers an inflammatory response (when inflammation spreads through the arterial wall it weakens and scars leaving it stiff)
  3. Fatty streak formation
193
Q

Atherosclerosis Pathogenesis (fatty acid)

A

Damage to endothelium (caused by smoking, high blood, etc). Body initiates an inflammatory response for the damage. White blood cells attracted to damaged site. LDL enters damaged area. Can become oxidized and trigger an inflammatory response. Causes formation of plaque. Accumulation can create proteoglycans. Immune cells (macrophages are attracted to the site) and engulfs LDL cholesterol. Lipid droplets give it a foamy appearance (foam cell). Foam cells recruit inflammatory markers

194
Q

Atherosclerosis Pathogenesis (plaque progression)

A

Foam cells trigger an inflammatory response = progression of atherosclerosis. Eventually get smooth muscle formation from the inflammatory response. Causes fibrous cap over fatty acids. Foam cells cause plaque instability in which it can rupture. Erosion of plaque can lead to blot clots and cardiovascular events

195
Q

LDL and Atherosclerosis

A

Excessive secretion of LDL by the liver and/or ineffective clearance of plasma LDL = circulating levels of LDL rise = results in the initiation and development of atherosclerotic plaques

196
Q

The lipid hypothesis

A

Increased plasma cholesterol (LDL cholesterol) causes atherosclerosis. States that elevated plasma (LDL) has a causal role in the development of coronary heart disease, etc

Dietary cholesterol does not lead to increased blood cholesterol which leads to atherosclerosis.

Dietary lipids can alter blood lipid levels

197
Q

The lipid hypothesis numbers

A

Dangerous:
Total cholesterol = 240 and higher
LDL cholesterol = 160 and higher
HDL cholesterol = under 40 male, under 50 female

Healthy range:
Total cholesterol = under 200
LDL cholesterol = under 100
HDL cholesterol = 60 and higher

KEY NUMBER: Cholesterol makes up 47% of LDL, whereas cholesterol only makes up 19% of HDL

198
Q

Atherosclerosis Study

A

Lower the concentrations of LDL, lower the risk of cardiovascular disease . Implies LDL has a causal and cumulative effect on the risks

199
Q

Saturated fats and cardiovascular disease

A

Regular diet: not high in saturated fats, fat is converted to IDL then LDL which leaves the body

Saturated diet: eat, IDL converted to LDL, but receptors are not picking it up causing it to linger in the bloodstream

200
Q

Contradictory findings of fats

A
  1. Does dose matter?
    - More is usually worse
  2. Does nutrient replacement matter?
    - Ex, will reducing fat intake and replacing with added sugar have an effect
    - No
  3. Does source matter?
    - The type of food have an effect?
    - Yes
201
Q

Does does matter?

A

Not eating a lot = should be okay.
Eating 7% energy from saturated fat vs 10% has a huge difference. But other numbers illustrate capping effect - from 10% fat intake to 13%, they pretty much have the same effects on health.

When replaced saturated foods, pick fiber?

202
Q

Does nutrient replacement

A

Significant effect

203
Q

Does source matter?

A

Vegetable sources have lower hazard ratios compared to animal fats.

204
Q

What are Omega 3’s

A

Polyunsaturated fatty acids.

3 types:
1. Alpha-linolenic acid (ALA) : plant based
2. Eicosapentaenoic acid (EPA) : Fatty fish. Known for anti inflammatory properties
3. Docahexanoic acid (DHA) : found in fatty fish, helps with development

205
Q

Roles of Omega 3s

A
  1. Components of phospholipids (membrane order)
  2. Precursor for anti-inflammatory molecules (resolvins, protectins, maresins)
  3. Cardiovascular benefits

Saturated FA is pictured tightly together, unsaturated FA has breaks in it

206
Q

Sources of Omega 3s

A

Salmon and fish are great sources. Mackerel.

Flaxseeds, chia seeds, walnuts also good

207
Q

Recommended Intake (AI) for ALA - alpha linolenic acid

A

Men 19+ = 1.6g/day
Women 19+ = 1.1g/day

Children 0-12 = 0.5g/day
Boys 14-18 = 1.6g/day
Girls 14-18 = 1.1g/day

208
Q

American Heart Associationn

A

Patients without CHD, recommends 2 servings of oily fish per week.

Patients with documented CHD, consume about 1g of EPA and DHA per day, preferably from oily fish

CHD=congenital heart defects

209
Q

History of Omega 3 literature

A

Cross sectional: showed greenland eskimos had an EPA of 7 compared to white people with EPA of 0.7. Difference is from eating more fish. So eskimos had the lowest risk of cardiovascular disease

Case control: Idea that those who ate more fish per week had less heart attacks

Recommended to eat fish 2x/week.

210
Q

Limitations of Omega 3 studies

A

All correlational; doesn’t mean it is causing cardiovascular disease. Maybe they are wealthier, fish is expensive

211
Q

Omega 3 Index

A

The level of EPA and DHA in erythrocyte phospholipids to determine risk for coronary heart disease.

High risk = less than 4%
Moderate risk = 4-8%
Lowest risk = above 8%

Higher you are on the index, greatest protection of cardiovascular disease. Idea that we want healthy intakes of EPA and DHA, more than less

212
Q

Primary prevention

A

Intervening before the health effect occurs

213
Q

Secondary prevention

A

Screening patients for previous CVD, CHD. Then use treatment to help them return to baseline. Might have already had a cardiovascular event, stroke, etc

214
Q

Primary outcome measures

A

Cardiovascular outcomes:
- Coronary outcomes (event or death). Ex, myocardial infraction, coronary artery bypass graft, sudden cardiac arrest

All cause mortality
Hospitalization or readmission for cardiovascular reasons

215
Q

Omega 3 Meta Analysis

A

Showed that omega 3s had no significant association with fatal or nonfatal coronary heart disease or any major vascular events. Shows no support for recommendations of supplements in people with a history of heart disease

216
Q

Omega 3 supplementation

A

Idea that if you already consume fish, do not spend the money on Omega 3s as there isn’t truly a benefit. If you don’t eat fish (low consumption) it could help

217
Q

Post 2018 Major Trials

A

Showed that Omega 3s do have benefits on cardiovascular disease.

Cochrane review (gold standard in evidence based health care) says increasing intake might reduce cardiovascular events.

218
Q

Omega 3 Literature Limitations

A

Support for the benefits of Omega 3s comes from low quality studies. Ex, cross sectional and case reports rather than systematic reviews and RCTs (top of pyramid)

219
Q

Omega 3 Limitations - control of pills

A

Issues with control pills and Omega 3 pills. Studies can cause placebo effect. Fishy taste (people are not a fan). Can tell which pill is control vs which is placebo

220
Q

Omega 3 Limitations - analysis not controlled

A

Analyses are not controlled for all variables. More studies are needed!

Ex, protein consumption plays a role, SES, education

221
Q

Omega 3 Limitations - generalizability

A

Generalizability limitations. Only a specific population will benefit. No standardized dose to have an effect

222
Q

Omega 3 and skeletal muscle

A

Data shows that omega 3s confer a higher sensitivity to insulin regulated amino acid and glucose disposal and that these responses occur in part in the skeletal muscle

223
Q

Omega 3 fatty acid supplementation increases EPA and DHA composition of skeletal muscle

A

Eating more omega 3s = increases concentration of EPA and DHA in skeletal muscle.

This increases permeability which may improve strength

224
Q

Fish oil supplementation potentiates muscle protein synthesis (MPS) in response to an amino acid infusion

A

There is a larger spike in MPS when we have Omega 3s in the body = theoretically improves muscle mass.

DHA and EPA can improve skeletal muscle composition in just 2 weeks. Improves strength

225
Q

Effect of krill oil supplementation (another omega 3) on skeletal muscle function in older adults

A

Resulted in an increase in grip strength which is a predictor of health and longevity in older adults. Supplementation for 6 months resulted in significant increases in muscle function

226
Q

Omega 3 and muscle quality

A

Fish oil supplementation enhances strength training in elderly women. Difference between muscle quality of placebo vs real.

227
Q

Omega 3 muscle effects in women vs men

A

Men may not have the same benefit with supplementation. Women might be more susceptible to the effect.

228
Q

Omega 3 and lean body mass

A

Studies favor omega 3s. Lots of studies done in older populations

229
Q

What causes you to lose muscle mass

A
  • Inactivity
  • Aging
  • Lack of protein
  • Illness
  • Weight loss
  • Injury
230
Q

Fatty acid intake to protect against muscle disuse atrophy

A

Had people wear a cast and measured muscle size. Omega 3 group lost less skeletal muscle than the control group. Good to know if you are injured you can supplement with Omega 3s to save muscle mass - speedier recovery

231
Q

Take Home Lipids Points

A
  1. EPA appears to have benefits towards CV health, but when combined with DHA
  2. Beware of study design limitations and conclusions
  3. Omega 3 fatty acids may enhance muscle anabolism (build and repair of muscle)
232
Q

Obligatory Changes

A

Obligatory changes refer to the immediate, unavoidable reductions in Total Energy Expenditure that occur in response to energy restriction.
Basal Metabolic Rate (BMR): BMR is the amount of energy expended by the body at rest to maintain basic physiological functions such as breathing, circulation, and cellular processes. During energy restriction, BMR typically decreases as the body adjusts to lower calorie intake. This reduction in BMR is an obligatory change that helps conserve energy and maintain vital bodily functions.
Thermogenesis: Thermogenesis refers to the production of heat by the body. During energy restriction, thermogenesis may decrease as the body conserves energy. This reduction in thermogenesis contributes to the obligatory decrease in Total Energy Expenditure.

233
Q

Adaptive Changes

A

Adaptive changes refer to the longer-term adjustments in Total Energy Expenditure that occur in response to energy restriction.
Physical Activity: In response to decreased calorie intake, individuals may unconsciously reduce their levels of physical activity, such as walking less or engaging in fewer activities that require energy expenditure. This reduction in physical activity contributes to the adaptive decrease in Total Energy Expenditure.
Metabolic Efficiency: Over time, the body may become more efficient at utilizing energy, meaning it can accomplish the same tasks while expending fewer calories. This increased metabolic efficiency is an adaptive change that helps the body conserve energy during periods of energy restriction.

HLTH 331 (3 decks)

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