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NUTR 344: Clinical Nutrition 1 > 11. Dyslipidemia and CVD 2 > Flashcards

11. Dyslipidemia and CVD 2 Flashcards

1
Q

A general lifestyle modification approach to treat dyslipidemia is to reach and maintain a healthy body weight. Reductions in weight of _________ have been associated with:

  • lower LDL-C by 0.1 mmol/L initially
  • Lower HDL-C by 0.03 mmol/L during loss, then increase by 0.04 mmol/L during maintenance
  • Lower TG by 0.07 mmol/L
A

2-7 kg loss

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2
Q

Physical activity has variable effects for the treatment of dyslipidemia. When considering benefits, volume _____ intensity of exercise.

At levels of 1200-2200 kcal/week of exercise, we can witness:

  • Lower TG by 4-37%
  • Higher HDL-C by 2-8%
  • Lower LDL-C by 0-7%
A

Volume > Intensity

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3
Q

What are improvements to dyslipidemia associated with weight loss and physical activity?

A
  • Volume/intensity of exercise has greatest benefits (kcal spent)
  • Resistance exercise has little effect
  • Modest exercise can prevent deterioration
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4
Q

Why aren’t lipid profiles the only thing measured when identifying lipemia or CVD risk?

A
  • Lipid profile can change quickly with diet adaptations (3-4 weeks)
  • Changes in profiles don’t signify less risk in CVD events
  • Don’t tell the full story, but are good indicators/markers
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5
Q

What are dietary components that affect lipemia and/or CVD risk?

A
  • Dietary cholesterol
  • Total fat
  • saturated fat
  • trans fatty acids
  • PUFA
  • MUFA
  • Omega-3 fatty acids
  • Fibers
  • CHO
  • Alcohol
  • Antioxidants
  • Soy protein
  • Folate and B6
  • Phytosterols
  • Nuts
  • Natural health products
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6
Q

In earlier studies, predictive equations demonstrated that dietary cholesterol levels weren’t the biggest influencers in predicting serum cholesterol. What component of the diet WAS the biggest influencer on serum cholesterol?

A

Saturated fat intake

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7
Q

What were the limitations of predictive equations from earlier cholesterol studies?

A
  • Individuality of SFAs and their effects weren’t considered
  • Predicted total cholesterol only; not lipid fractions
  • Assumes MUFA and CHO are neutral
  • Assumed linear effects on total cholesterol
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8
Q

The Seven Countries Study was the first time the ________ diet was noticed as a healthier lifestyle including fats.

A

Mediterranean Diet

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9
Q

Dietary cholesterol is found in _______ foods only.

A

Animal

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10
Q

Dietary cholesterol has ____ effect on raising blood cholesterol than saturated fats (in most individuals).

A

Less

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11
Q

⅓ of individuals are non-compensators for dietary cholesterol. What are non-compensators?

A

This means they have issues self-regulating cholesterol levels.

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12
Q

What is the main mechanism of dietary cholesterols on lipoproteins?

A

Decreased synthesis and activity in hepatic LDL receptors

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13
Q

What are independent mechanisms of dietary cholesterol, other than the decreased synthesis/activity of LDL receptors?

A
  • increased cholesterol in chylo and chylo remnants (more atherogenic, increased chol delivery to liver)
  • increased chol in VLDL and VLDL remnants ( more atherogenic)
  • interferes with ability of HDL to clear cholesterol
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14
Q

Cholesterol components in food _____ (are/are not) of similar proportion to fat levels in foods.

A

are not

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15
Q

What seafood is high in cholesterol despite being low in fat?

A

Shrimp

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16
Q

What organ meats are highest in cholesterol?

A
  • brains
  • pancreas
  • kidney
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17
Q

Very low-fat diets may ______ HDL-C.

A

decrease

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18
Q

Type of fat (is/is not) ______ more important than total quantity of fat in diet.

A

is

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19
Q

What is the goal for fat consumption in the diet, in %?

A

25-35%

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20
Q

What component of food has the most impact on cholesterol levels?

A

Saturated fats

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21
Q

Why are saturated fats prominent in processed foods?

A
  • not as sensitive to oxidation/spoiling
  • longer shelf-life
  • better tastes/mouth feels
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22
Q

How do saturated fatty acids reduce the activity of LDL receptors?

A
  • decrease transcription of LDL receptor gene
  • alter PL composition of cell membranes (decreases binding)
  • alters LDL itself and delays binding to receptors
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23
Q

What is the recommendation for saturated fat intakes in the US (used to be for Canada as well)?

A

Less than 10% of total calories

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24
Q

Between “all other foods” and “protein foods”, which category is better to reduce intake of saturated fats? Why?

A

Reducing consumption of foods in “other foods” category (processed foods, baked goods, pre-prepared meals…) is a better method of reducing saturated fats intake. Protein sources are more nutrient dense and limiting those foods would decrease the intake of those nutrients.

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25
Q

There is strong evidence to support the following:

  • A diet ____ in saturated fats leads to higher levels of LDL-C
  • High levels of LDL-C lead to ______ risk of CVD

There isn’t strong evidence supporting:

High intakes of saturated fats leads to _____ risk of CVD

A
  • high
  • increased
  • increased
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26
Q

Why do studies examining saturated fats intakes replace saturated fats with MUFAs and PUFAs instead of just reducing total fat intake?

A

They don’t want to misconstrue the results with a decreased energy intake or body weight loss (potential confounder)

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27
Q

Dietary saturated fats show _____ HDL-C levels.

What is the potential effects of reducing saturated fats in the diet?

A
  • increased
  • a reduction in HDL-C levels
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28
Q

Studies have shown that replacing saturated fats with CHO have ____ ________ on CVD risk.

A

no benefit

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29
Q

What is the revised recommendations concerning saturated fats intakes in the new CFG?

A
  • no limit on saturated fats
  • focus on healthy diet instead
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30
Q

Replacing saturated fats with MUFAs and PUFAs has been shown to ____ lipid profile and linked with a ______ CVD risk.

A
  • improve
  • decreased
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31
Q

When ___% of energy from saturated fats is replaced by PUFAs, there is no effect on mortality risk, but there is a ____% reduction in CVD risk.

A
  • 5
  • 10
32
Q

How are fatty acid chains differentiated as short, medium, or long?

A
  • Short: 2-6 C
  • Medium: 8-12 C
  • Long: 14 + C
33
Q

Coconut oil is _____ in saturated fats than butter. It’s most prominent fatty acid is _____ acid.

A
  • higher
  • lauric
34
Q

Palm oil and butter are high in _____ acid.

A

Palmitic

35
Q

Which SFAs can increase LDL-C?

A
  • Lauric: may increase HDL-C more, thus lowering LDL/HDL ratio
  • Myristic
  • Palmitic: only in presence of high dietary cholesterol
36
Q

Reducing dietary SFAa decreases what kind of LDL-C? Does this have an effect on CV health?

A
  • Primarily decreases larger LDL-particles, not the smaller ones
  • The smaller LDL particles are more atherogenic; therefore the effect on CV health is very minimal
37
Q

Stearic acids have a ____ effect on blood LDL-C levels.

A

Neutral

38
Q

What length of fatty acids have no effect on serum cholesterol?

A

Medium chains; less than 10C

39
Q

SFAs have ____ effect on VLDL-TG

A

no

40
Q

Compared to butter, SFAs from cheese have _____ of an increase in LDL-C.

A

Less

41
Q

SFAs from dairy products have ____ risk of CVD compared to SFAs from meat.

A

less

42
Q

Yogurt and cheese intake is _____ associated with CVD risk.

A

inversely

43
Q

Dark chocolate is rich in _____ acid and thus has a _____ effect on CVD risk.

A
  • stearic
  • neutral
44
Q

Trans-fats naturally produced by ruminants have ____ effect on CVD.

A

no

45
Q

Trans fatty acids ____ LDL-C, but _____ LDL size. This makes it more ________.

A
  • increase
  • decrease
  • atherogenic
46
Q

Trans fatty acids _____ HDL-C and may _______ inflammatory markers and endothelial damage.

A
  • decrease
  • increase
47
Q

Trans fatty acids occur as a result of partial __________.

What are some food sources that contain trans fatty acids?

A
  • hydrogenation
  • hard margarines, partially hydrogenated oils, small amounts in dairy (different effect)
48
Q

What are the major unsaturated fatty acids found in the diet?

A
  • Omega 9: oleic acid (18:1)
  • Omega 6: linoleic acid (18:2)
  • Omega 3: linolenic acid (18:3), EPA (20:5), DHA (22:6)
49
Q
  • Which unsaturated fatty acids increase LDL clearance?
  • How does this occur?
A
  • Omega-6 (linoleic acid)
  • partially passive; removes suppressing effect of SFA when replacing SFA in diet
50
Q

Omega-6 acids may _____ HDL formation and/or ApoAI, especially if intake is >___% of total calories.

What are other risk of high consumption of PUFAs?

A
  • decrease, 10%
  • inflammation (cancer risk?) and increased oxidative damage to LDL
51
Q

What is the goal intake for Omega-6 fatty acids?

What foods are good sources of linoleic acid?

A
  • 5-10% of EI
  • corn, sunflower, safflower, soybean oils, walnuts, sunflower seeds…
52
Q

What types of fatty acids make up the bulk of consumed fats?

A

MUFAs

53
Q

What is the goal intake for MUFAs?

What does this suggestion assume (incorrectly)?

A
  • No more than 20% of total calories
  • Assumes decreased sat. fatty acid intakes (MUFAs often consumed alongside them)
54
Q

Compared to PUFAs, oleic acid (MUFA) _______ lower HDL-C.

Compared to SFAs, oleic acid _____ LDL-C.

What are food sources of MUFAs?

A
  • does not
  • lowers
  • olive and canola oils, peanuts, meat and poultry
55
Q

Which type of fatty acid is associated with the Mediterranean Diet?

A

MUFAs

56
Q

What are advantages of MUFAs in the diet?

A
  • do not decrease HDL like PUFAs and CHO
  • less susceptible to oxidation than PUFAs
  • do not increase TG (like CHOs do)
  • do not increase cancer risk as high as PUFAs can
57
Q

Omega-3 PUFAs EPA and DHA are found in _____. ALA is found in _____, ______, and ______.

A
  • fish
  • canola, linseed, and soybean oil
58
Q

Omega-3 PUFAs (EPA, DHA, ALA), _______ triglyceridemia in hyperTG patients at ____ doses (2-4 g/day).

There is _______ benefit in primary or secondary prevention of CVD, therefore, supplementation of omega-3s (are/are not) _______ recommended to reduce CVD events.

A
  • decrease
  • high
  • no
  • are not
59
Q

Do omega-3 PUFAs reduce the number of VLDL particles being secreted by the liver?

Do they lower LDL-C concentrations?

A
  • No; they decrease the TG content of those particles
  • No; levels of LDL-C are reduced only when SFAs are replaced by PUFAs in diet
60
Q

How do Omega-3 PUFAs prevent coronary thrombosis?

A

Interfere with platelet aggregation and delay the proliferation of fibroblasts

61
Q

How do omega-3 PUFAs reduce plaque formation and growth?

A

By reducing adhesion molecules (interference with platelet aggregation)

62
Q

What is the daily goal intake for dietary fibers? What % should be soluble?

A
  • 20-30g per day
  • 50%
63
Q

Soluble fibers _____ total-C and LDL-C.

A

Decrease

64
Q

Higher fiber intakes are usually associated with:

A
  • lower EI
  • lower fat intakes
65
Q

What are good sources of soluble dietary fibre?

A
  • oats
  • legumes
  • pectins
  • psyllium
  • gums
66
Q

Excess ____ can cause an overproduction of VLDL-TGs.

A

simple CHO (sucrose, fructose, HF-corn syrups)

67
Q

Excess simple CHOs are linked with a ____ in HDL-C levels.

What other disadvantages are possible in high CHO diets?

A
  • decrease

Disadvantages:

  • decreased HDL and increased TG
  • Hyper TG in some populations
  • could increase blood glucose and hyperinsulinemia
68
Q

Alcohol _____ acylCoA oxidation in the liver, and should be _____ if the individual has hypertriglyceridemia.

A
  • inhibits
  • avoided
69
Q

Alcohol ______ HDL-C levels.

A

elevates

70
Q

Resveratrol (polyphenol) in red wine may ______ cell-mediated oxidation of lipoproteins.

A

inhibit

71
Q

What food source has shown to reduce TC, LDL-C and TG without effecting HDL-C in patients with/without CVD?

A

Soy protein

72
Q

What non-energy food component may inhibit LDL oxidation and therefore decrease atherosclerosis risk?

A

Antioxidants (Vit C, E, and beta-carotene)

73
Q

If levels of folate and B6 are > _____, there is an increased risk of heart disease. Each increase of ____ umol/L in fasting concentrations increases the incidence of CVD by 1.6-1.8 fold.

A
  • 14 umol/L
  • 5 umol/L
74
Q

Elevated homocysteine levels (folate and B6) appear in up to ____% of patients with CVD.

A

40

75
Q

How is homocysteine synthesized in the body?

A

NUTR 344: Clinical Nutrition 1 (15 decks)

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