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Clinical Nutrition 1 > Dyslipidemia & CVD 2 > Flashcards

Dyslipidemia & CVD 2 Flashcards

1
Q

Lifestyle modification approach for tx of dyslipidemia

A
  • diet
  • weight management : healthy and sustainable
  • physical activity
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2
Q

Benefits of weight loss of 2-7kg in terms of blood lipid profile?

A
  • decrease LDL-C by 0.1 mmol/L
  • decrease HDL-C by 0.03 mmol/L during loss and then increase by 0.04 mmol/L during maintenance
  • decrease TG by O.07 mmol/L
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3
Q

Benefits of physical activity (1200-2200kcal/week) in terms of blood lipids?

A
  • decrease TG by 4-37%
  • increase HDL-C by 2-8%
  • decrease LDL-C by 0.7%

=> accentuated with weight loss

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4
Q

Effect of resistance exercise

A

Little effect

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5
Q

Which PA has the greatest benefits (kcal spent)

A

Volume/intensity of exercise

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6
Q

Which PA has little effect on lipid profile

A

Resistance exercise

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7
Q

Limitations of predictive equations

A
  • different SFA have different effects
  • predicts total cholesterol only
  • assumes MUFA and carbohydrates are neutral
  • effects on total cholesterol may not be linear
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8
Q

Studies in 60s, 70s show:

A

Increased cholesterol in diet increases serum cholesterol levels
(don’t distinct LDL versus HDL)

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9
Q

The 7 Countries Study =

  • by who
  • result
A
  • Ancel Keys
  • result:
  • east Finland has the highest coronary deaths (on regressive line)
  • Ushibuka has the lowest coronary death (on regressive line)
  • Crete (mediterranean diet) = outlier not on regressive line,
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10
Q

What +ve relationship was found by Keys?

A

+ve relationship between serum cholesterol and mortality due to heart disease

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11
Q

What is dietary cholesterol and what is its impact on blood cholesterol levels

A
  • found only in animal foods
  • less effect on raising blood cholesterol than saturated fats but may be significant in some individuals
  • very heterogenous responses to cholesterol
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12
Q

How is the response to dietary cholesterol heterogenous ?

A

There are compensators (2/3) and non-compensators (1/3)

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13
Q

T/F

Dietary cholesterol has a higher effect on raising blood cholesterol than saturated fats

A

False

But could be significant in non-compensators

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14
Q

Average amount of cholesterol consumed

A

200-300mg/day

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15
Q

What happens when non-compensators ingest cholesterol?

A

Increases synthesis and activity of LDL receptors

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16
Q

Independent mechanisms of dietary cholesterol

A
  • decreased synthesis and activity of hepatic LDLr
  • increased cholesterol in chylo and chill remnants –> more atherogenic and increased cholesterol delivery to liver
  • increased cholesterol in VLDL and VLDL remnants –> more atherogenic
  • interferes with ability of HDL to clear cholesterol
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17
Q

T/F

Cholesterol content is directly proportional to fat content

A

False

ex: high cholesterol in kidney, pancreas, liver but low fat
ex2: high fat in beef, lamb, pork, veal but low cholesterol

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18
Q

Highest source of cholesterol

A

Brains > pancreas > kidney > liver

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19
Q

Highest cholesterol content in fish & shellfish is in _

A

shrimp

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20
Q

Total kcal from fat goal = _

A

25-35% of calories

Also helps to reduce T calories and saturated fat intakes

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21
Q

Current intake in North America

A

34-37% of T kcal

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22
Q

Which type of diet may decrease HDL-C which is not beneficial?

A

Very low-fat diet

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23
Q

Is quantity or type of fat important?

A

Type of fat (or quality)

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24
Q

How do saturated fatty acids reduce activity of LDL receptors?

A
  • decrease transcription of LDL receptor gene
  • alter PL composition of cell membranes to decrease binding
  • alter LDL itself and delays binding to receptors
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25
Q

What was the first recommendation by NCEP and USDA for SFA?

A

Goal was less than 10% of T kcal from SFA

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26
Q

Major sources of SFA (US)

A
  • highly processed foods
  • processed meats
  • baked goods (cakes, cookies, donuts)
  • pizza
  • cheese
  • ice cream
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27
Q

Primary contributor to total SFA intake in Canada

A

“All other foods” category which is not part of the CFG

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28
Q

New recommendations by Heart and Stroke Canada, CFG in terms of saturated fats are _

A

no limit on saturated fats but focus on a healthy balanced diet

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29
Q

Substitution of SFA to improve lipid profile and reduce CVD risk

A
  • replacing SFA with MUFAs and PUFAs
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30
Q

T/F

Replacing SFA with carbohydrates is beneficial in CVD risk

A

F

depends on source of carb

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31
Q

How dietary SFA affects lipid profile

A

increases LDL-C

increases HDL-C (depends on source)

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32
Q

Medium chain SFA

A

Caprylic (8)

Caproic (10)

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33
Q

Intermediate chain SFA

A

Lauric (12)

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34
Q

Long chain SFA

A

Myristic (14)
Palmitic (16)
Stearic (18)

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35
Q

Which SFA are directly absorbed into portal vein and don’t go through CM

A

Medium chain SFA (<10)

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36
Q

SFA that increase LDL-C

A
  • Lauric
  • Myristic
  • Palmitic (in presence of high cholesterol)
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37
Q

Stearic effect

A

neutral effect

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38
Q

Effects of medium chain SFA (<10) on serum cholesterol

A

No effect

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39
Q

Effect of SFAs on VLDL

A

None

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40
Q

Effects of SFAs from dairy products

A

decrease CVD risk (compared to SFA from meat)

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41
Q

Effects of SFAs from cheese

A

less increase LDL compared to butter

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42
Q

Highest SFA in :

  • coconut oil
  • butter
  • palm oil
A
  • coconut oil = high lauric
  • Butter = high palmitic
  • palm oil = very high palmitic
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43
Q

Coconut Oil vs butter

A
  • Co has higher %SFA than butter
  • Co has high lauric acid
  • B has high palmitic acid
  • Co better than butter but worse than other vegetable oils
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44
Q

Trans FA impact on lipid profile

A
  • increase LDL-C
  • reduce LDL size
  • reduce HDL-C
  • increase inflammatory markers (+endothelial damage)
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45
Q

Consumption of trans FA

A

3% T kcal (decreasing)

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46
Q

Sources of trans FA

A
  • heard margarine
  • partially hydrogenated oils
  • dairy (small amounts, better effect)
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47
Q

Trans fat consumption should be _

A

avoided

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48
Q

Trans fat occurs as a result of _

A

partial hydrogenation

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49
Q

Unsaturated fatty acids in the diet

A
  • Omega 9 (oleic acid)
  • Omega 6 (linoleic acid)
  • Omega 3 (linolenic acid, EPA, DHA)
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50
Q

Omega-6 effect on lipid profile

A
  • increases LDL clearance

- may decrease HDL formation and/or Apo-A1

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51
Q

Risk of high PUFAs

A

inflammation, increased oxidative damage to LDL

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52
Q

Omega-6 sources

A

corn, sunflower, safflower, soybean oils, walnuts, sunflower seeds

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53
Q

Goal of omega 6 in diet

A

5-10% of calories

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54
Q

Main Mono-unsaturated FA

A

Oleic acid

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55
Q

Source of MUFAs

A

olive, canola oil, peanuts, meat, poultry

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56
Q

Effects of MUFAs on lipid profile

A
  • does not lower HDL-C
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57
Q

Goal of MUFA in diet

A

<20% of T kcal (assuming a lower saturated fat diet)

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58
Q

Advantages of MUFAs

A
  • don’t decrease HDL like PUFA and carbs
  • less susceptible to oxidation than PUFA
  • don’t increase TG as carbs often do
  • don’t increase cancer risk of high PUFA could
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59
Q

MUFAs are characteristic of __ diet

A

Mediterranean

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60
Q

Dietary sources of linoleic acid

A

safflower oil
soybean oil
corn oil
sunflower oil

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61
Q

Dietary sources of oleic acid

A 
olive oil
canola oil (rapeseed)
peanut oil
avocados 
nuts
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62
Q

Types of Omega-3 PUFAs

A
  • EPA: eicosapentanoic acid
  • DHA: docosahexanoic acid
  • ALA: alpha linolenic acid
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63
Q

DHA & EPA sources

A

fish

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64
Q

ALA sources

A

canola, linseed, soybean oil

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65
Q

Omega-3 effects on lipid profile

A
  • decrease TG in hyperlipidemic and hyperTG patients

- don’t lower LDL-C

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66
Q

T/F

CCS recommendations promote use of omega-3 PUFA supplements to reduce CVD events

A

False

they emphasise on good sources such as fish, omega 3 fortified eggs

67
Q

Omega 3s __ risk of mortality in those with CVD

68
Q

Omega 3s interfere with :

A

platelet aggregation and prevent coronary thrombosis

delay proliferation of fibroblasts

69
Q

Omega 3s reduce/ increase plaque formation and growth

A

Reduce (because they reduce adhesion of molecules)

70
Q

T/F

Omega 3s reduce the number of VLDL particles being secreted by the liver

A

False

Omega 3s decrease the TG content of the VLDL particles

71
Q

Goal of fiber in diet?

A

20-30g/day

50% soluble fiber

72
Q

Soluble fiber effect on lipid profile

A
  • decrease total-C
  • decrease LDL-C
    (depends on initial level of hyperchlesterolemia)
73
Q

Soluble fiber sources

A 
oats
legumes
pectins
psyllium
gums
74
Q

Carbohydrate effect on lipid profile

A
  • increased VLDL-TG production

- decrease HDL-C

75
Q

Disadvantage of high CHO diet (mostly simple CHO)

A
  • decreased HDL and increased TG
  • Hyper TG in some populations
  • increase BG and hyperinsulinemia
76
Q

Alcohol effect on lipid profile

A
  • increased HDL-C
77
Q

Is it okay to consume alcohol? How much?

A

OK if consumed in moderation

1-2 drinks/day

78
Q

Which alcohol may inhibit cell-mediated oxidation of lipoproteins? Why?

A

Red wine

Due to resveratrol (polyphenol)

79
Q

What is the French paradox?

A

That red wine polyphenols decrease risk of CHD (eventhough French have a high saturated fat diet)

80
Q

Why should alcohol be avoided COMPLETELY if have familial hypertriglyceridemia?

A

Because alcohol inhibits acylCoA oxidation in the liver (–> TG formation)

81
Q

Soy protein effects on lipid profile

A
  • reduces Total-C
  • reduces LDL-C
  • reduces TG
  • no effect on HDL-C
82
Q

Food sources of soy protein

A

tofu
soy beverage
soy protein isolates
tempeh

83
Q

US Health claim that __ g of soy protein, as part of a diet low in saturated fat and cholesterol may reduce the risk of heart disease

84
Q

Which compounds present in soy protein are beneficial

A

isoflavones

phytoestrogens

85
Q

3 antioxidants are

A

vitamin C
vitamin E
beta-carotene

86
Q

Antioxidants effect on lipid profile

A

May inhibit LDL oxidation (decreases atherosclerosis risk-

87
Q

Are antioxidant supplements recommended

88
Q

Hyperhomocysteinemia increases/decreases incidence of CVD ? At which amount?

A

INCREASES

> 14umol/L –> increased risk of heart disease

89
Q

What is hyperhomocysteinemia caused by?

A

deficient folate and B6 causes high homocysteine

90
Q

in which patients does hyperhomocysteinemia appear?

A

in up to 40% of patients with CVD

91
Q

Does B12 deficiency elevated homocysteine?

92
Q

Which deficiencies elevated homocysteine?

93
Q

What are recommendations to avoid hyperhomocysteinemia

A
  • increase food sources of folate

- supplement (500yg/d ONLY if high levels or family history of CVD

94
Q

Before supplementing folate which deficiency should you be careful about?

A

B12 deficiency could be masked

95
Q

T/F

Low levels of B12 are associated with increased risk of CHD

96
Q

Food sources of folate

A 
fortified cereals
vegetable
citrus fruits/juices
legumes
organ meats
97
Q

What are phytosterols/stanols?

What do they compete with?

A
    • Are equivalent to plant cholesterol

- - Compete with cholesterol absorption : increase decal excretion

98
Q

Diet enriched with 2-2.5g sterols/stanols reduced __ by 6-14% ?

99
Q

Main source of stanols/sterols

A

Fortified margarine

100
Q

Nuts are rich in which FA ?

A

rich in: mono- and polyunsaturated FA

low in: SFA

101
Q

Nuts are rich in what other nutrients ?

A 
plant protein
soluble fibers
folic acid
antioxidants
arginine (= Nitric oxide precursor)
102
Q

High intake (30-60g/d) __ risk of CHD.

103
Q

Moderate intake of nuts reduces which lipid?

A

Reduces LDL-C and improves endothelial function

104
Q

T/F

Eating nuts has a notable effect on body weight

105
Q

NCEP =

A

National cholesterol education program (created the dietary approach for dyslipidemia)

106
Q

Dietary approach of dyslipidemia targets:

A

1st target = LDL-C

other targets = metabolic syndrome factors (TG, HDL, waist circ)

107
Q

What model does the dietary approach of dyslipidemia follow?

A

TLD model = therapeutic lifestyle changes

108
Q

Therapeutic lifestyle changes decrease/ increase:

A
  • decrease saturated fats and dietary cholesterol
  • increase physical activity
  • weight management to reduce coronary risk
109
Q
  • Step 1 to decrease saturated fats and cholesterol

- Step 2 and 3

A

Step 1: < 10%SFA and < 300mg cholesterol

Step 2 and 3: <7% SFA and <200mg cholesterol

110
Q

Which diets (2) can be used for prevention or treatment of dyslipidemia ?

A
  • The Mediterranean diet

- The Portfolio diet

111
Q

The Mediterranean diet is high in

A
  • oleic acid (olive oil)
  • fruits, vegetables, legumes
  • fish
112
Q

The Mediterranean diet is low in

113
Q

The Mediterranean diet is moderate in

A
  • dairy (cheese and yogurt)

- wine consumption

114
Q

Results of Mediterranean diet

A
  • decrease in CV events
  • decrease LDL-C, app-B, TG
  • increase HDL-C
  • additive effect to statins
  • decrease inflammatory markers
115
Q

Mediterranean diet has a decrease in mortality of _ %

A

25%

= very high

116
Q

What is the Portfolio diet?

A
  • vegetarian diet
  • low in saturated fat
  • high in phytosterols, soy proteins, soluble fibres, almonds
117
Q

Results of Portfolio diet:

A
  • decrease in 29% LDL-C

- decrease CRP

118
Q

What is the problem with the portfolio diet?

A

Has a low adherence (40-45%)

Was done in a very controlled environment

119
Q

A low-fat diet with satins decreases LDL-C by _%. Is it more or less than the portfolio diet.

120
Q

CCS Guidelines 2016 in terms of dietary recommendations

A
  • healthy eating and activity and Mediterranean dietary pattern to lower CVD risk
  • omega-3 PUFA supplements should not be used to reduce CVD events
  • avoid intake of trans fats
  • decrease intake of saturated fats for CVD risk reduction (substitute SFA with PUFAs)
  • moderate energy intake to maintain/achieve a healthy body weight
  • adopt a healthy dietary patterns
121
Q

Healthy dietary patterns recommended by CCS Guidelines

A
  • Mediterranean
  • Portfolio
  • DASH
  • high in nuts (30g+/d)
  • high in legumes (4servings+/d)
  • high in olive oil (60mL+/d)
  • rich in fruits and veg (5servings+/d)
  • high in total fiber 30g+/d) and whole grains (3servings+/d)
  • low-glycemic load or low-glycemic index
  • vegetarian
122
Q

Dietary factors that increase HDL-C

A
  • saturated fats
  • dietary chol
  • alcohol (less han 2drinks/d)
123
Q

Dietary factors that decrease HDL-C

A
  • simple sugars/high carb diet
  • polyunsaturated fat, high
  • obesity
124
Q

Other factors that increase HDL-C

A
  • long-term aerobic exercise program
  • estrogens
  • female sex
125
Q

Other factors that decrease HDL-C

A
  • androgens
  • male sex
  • anabolic steroids
  • some antihypertensive drugs
  • diabetes mellitus
  • cigarette smoking
126
Q

What do Statins inhibit

A

HMG-CoA reductase

127
Q

Statins examples:

A
  • atorvastatin (Lipidor)
  • lovastatin (Mevacor)
  • simvastatin (Zocor)
  • rosuvastatin (Crestor)
  • pravastatin (Pravachol)
128
Q

Mechanism of statins

A

Block cholesterol synthesis

Increases LDL receptor mediated removal

129
Q

Predicted effect of statins

A
  • decrease LDL-C
  • decrease TG
  • increase HDL-C
130
Q

4 classes of drugs to treat hyperlipidemia

A
  • HMGCoA reductase inhibitors (Statins)
  • Cholesterol absorption inhibitors
  • Bile acid sequestrants (BAS)
  • PCSK9 inhibitors
131
Q

Cholesterol absorption inhibitor drugs

A

ezetimibe (Eztrol)

132
Q

Ezetimibe mechanism

A

Inhibit cholesterol GI (intestinal) absorption

133
Q

Ezetimibe predicted efect

A

Decrease LDL-C

134
Q

Which 2 drugs are commonly used together?

A

Ezetimibe + statin

135
Q

Bile acid sequestrant drugs

A
  • cholestyramine (Questran)

- colestipol (Colestid)

136
Q

Bile acid sequestrants mechanism

A
  • promote sterol excretion
  • increases LDL receptors
  • bind bile acids in the GI tract and prevent their reabsorption
137
Q

Bile acid sequestrants predicted effect

A
  • decrease LDL
138
Q

PCSK9 inhibitor drugs

A
  • evolocumab (Repatha)

- alirocumab (Praluen)

139
Q

PCSK9 inhibitors predicted effects

A
  • decreased LDL
140
Q

PCSK9 inhibitors mechanisms

A

prevent catabolism of LDL receptors

block PCSK9 action –> more LDL recycling

141
Q

2 classes of drug treatment of hypertriglyceridemia

A
  • fibrates

- nicotinic acid

142
Q

Fibrates mechanism

A

decreases VLDL synthesis

enhances LPL action

143
Q

Fibrates drugs

A

Gemfibrozil (Lopid)

Fenofibrate (Lipidil)

144
Q

Fibrates predicted effect

A

decrease TG
decrease LDL-C
increase HDL-C

145
Q

Nicotinic acid mechanism

A

decreases VLDL synthesis

increases LPL activity

146
Q

Nicotinic acid drug

A

Nicotinic acid slow release (Quest, Niaspan)

147
Q

Nicotinic acid predicted effect

A

decrease TG
increase HDL-C
decrease LDL

148
Q

Adverse effects of statins

A

myalgia, myopathy, increase liver enzymes, low risk of diabetes

149
Q

Which statin interacts with grapefruit juice

A

Simvastatin

150
Q

Side effects of ezetimibe?

A

diarrhea, rash, fatigue, muscle weakness, pain

151
Q

Contra-indications to prescribing ezetimibe

A

liver disease or failure

152
Q

When is it recommended to prescribe ezetimibe

A

As a second-line tx in patients with clinical CVD and targets not reached by maximal statin dose

153
Q

Side effects of bile acid sequestrants (cholestyramine)

A
  • constipation, pain, hemorrhoids

- may decrease absorption of fat and liposoluble vitamins, Ca, Fe, Zn, Mg

154
Q

Contra-indications to prescribing BAS

A

existing haemorrhoids, peptic ulcer, hiatus, hernia, multiple drug use, extensive travel, hypertriglyceridemia

155
Q

Side effects of PCSK9 inhibitors

A

diarrhea, muscle or joint pain, bruising around injection site

156
Q

PSCK9 =

A

enzyme that binds to LDL receptors and promotes their degradation (instead of LDL recycling on the cell surface)

157
Q

Why is PCSK9 rarely prescribed?

A

expensive (7000$/y)
injectable drug
recently approved

158
Q

PCSK9i recommended for who?

A

primary (familial) hypercholesterolemia with high LDL-C despite maximal statin dose

159
Q

Side effects of fibrates (gemfibrozil)

A

GI reactions (taste changes, abdominal pain), muscle toxicity

160
Q

Contra-indications to prescribe gembribrozil?

A

hepatic or renal dysfunction, gallbladder disease, combination tx with simvastatin

161
Q

Fibrates prescribed for which patients?

A

in highly elevated TG (familial hyperTG)

162
Q

Nicotinic acid side effects

A

Only 50-60% tolerance, GI stress, skin flushing and itching, hepatotoxicity, arrhythmias

163
Q

Contraindications to prescribe nicotinic acid

A

active peptic ulcer, hepatic disease, gout, hyperuricemia

164
Q

Nicotinic acid prescribed for which patients?

A

used for primary hypercholesterolemia and/or hyperTG, and hypoalphalipoproteinemia

Clinical Nutrition 1 (13 decks)

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