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6-Clinical Nutrition 1 > Dyslipidemia and CVD Part 2 > Flashcards

Dyslipidemia and CVD Part 2 Flashcards

1
Q

What are the benefits of weight loss of 2-7kg in terms of blood lipid profile?

A
  • decreased LDL-C by 0.1 mmol/L initially, variable afterwards
  • decreased HDL-C by 0.03 mmol/L during loss, then increase by 0.4 mmol/L during maintenance
  • decreased TG by 0.07 mmol/L
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2
Q

What are the benefits of physical activity in terms of blood lipids?

A
  • 1200-2000 kcal/week
  • decreased TG by 4-37%
  • increased HDL by 2-8%
  • decreased LDL by 0-7%
  • improvements accentuated with weight loss
  • volume/intensity of exercise has the greatest benefits
  • resistance has little effect
  • modest exercise can prevent deterioration
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3
Q

What are the predictive equations of effects on diet on serum total cholesterol?

A

KEYS

HEGSTED

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4
Q

What are the limitations of Predictive Equations?

A
  • different have different effects
  • predicts total cholesterol only - not lipid functions
  • assumes MUFA and CHO are neutral
  • effects on total cholesterol may not be linear
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5
Q

What is the 7 countries study?

A
  • east Finland had the highest coronary deaths
  • Ushibuka has the lowest coronary deaths
  • Focus was Crete - mediterranean diet!!
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6
Q

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

A
  • found only in animal foods
  • less of an effect on raisin blood cholesterol than saturated fats but may be significant in some individuals
  • very heterogenous responses to dietary cholesterol
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7
Q

What are the independent mechanisms of dietary cholesterol?

A

– Decreased synthesis and activity of hepatic LDL receptors
– Increased cholesterol in chylo and chylo remnants –> more atherogenic and increased chol delivery to liver
– Increased cholesterol in VLDL and VLDL remnants –> more atherogenic
– Cholesterol release to arterial wall during TG hydrolysis
– Interferes with ability of HDL to clear cholesterol

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8
Q

Saturated fats reduce the activity of LDL receptors by?

A

– Decreasing transcription of LDL receptor gene
– Altering PL composition of cell membranes to decrease binding
– Altering LDL itself and delays binding to receptors

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9
Q

What are the major sat. fat sources in the diet?

A

baked goods and processed foods

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10
Q

What are medium chain sat fats?

A

caprylic (8)

caproic (10)

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11
Q

What are intermediate chain sat fats?

A

lauric (12)

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12
Q

What are long chain sat fats?

A

myristic (14)
palmitic (16)
stearic (18)

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13
Q

How do sat fats affect blood LDL levels?

A

Different SFAs have different effects on blood LDL-C levels
– SFAs from dairy products ↓CVD risk compared to meat
– SFAs from cheese ↓LDL compared to butter

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14
Q

Which sat fats increase LDL?

A

– Lauric: may increase HDL-C more, thus ↓LDL/HDL ratio
– Myristic
– Palmitic: may ↑LDL-C only in presence of high dietary cholesterol

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15
Q

What is the effect of omega 6 on LDL and HDL levels?

A

increases LDL clearance

>10% may decrease HDL

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16
Q

What is the intake goals for omega 6?

A

5-10% of calories

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17
Q

What are the food sources of omega 6?

A

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

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18
Q

How does w-6 lower LDL?

A

LDL lowering effect is partly passive – removes the suppressing effect of SFA (similar to oleic acid and carbohydrates)

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19
Q

High intakes of w-6 might cause ___

A

– Immune suppression
– Increased oxidative damage to LDL
– Increased cancer risk (with very high PUFA intake)

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20
Q

What are the intake goals for MUFAs?

A

Goal is no more than 20% of total calories – assuming a lower saturated fat intake

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21
Q

PUFA vs MUFA on HDL

A

Compared to PUFA, oleic acid does not lower HDL

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22
Q

MUFA vs SFA on LDL

A

Compared to saturated fats (C:12 – C:16) oleic acid lowers LDL

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23
Q

What are the food sources of MUFAs

A

olive and canola oils, peanuts, meat and poultry

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24
Q

What are the advantage of MUFAs

A
  • mediterranean diet

– Do not decrease HDL as does PUFA and carbohydrates – Less susceptible to oxidation
– Do not increase triglycerides as carbohydrates often do – Do not increase cancer risk as high PUFA intakes could

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25
Q

What are omega-3 PUFAs

A

EPA: eicosapentanoic acid (fish)
DHA: docosahexanoic acid (fish)
ALA: Alpha-linolenic acid (canola, linseed, soybean oil)

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26
Q

How do w-3 affect TG levels?

A
  • Decrease TG in hyperlipidemic and hyperTG patients

* May reduce mortality in those with CVD

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27
Q

How do w-3 affect VLDL levels?

A

Do not reduce the number of VLDL particles being secreted by the liver but rather decrease the TG content of these particles

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28
Q

How do w-3 affect LDL levels?

A

Omega-3 PUFAs do not lower LDL-C concentrations except as their PUFA replace SFA in the diet

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29
Q

How do w-3 prevent coronary thrombosis?

A
  • Omega-3 PUFAs interfere with platelet aggregation and thereby prevent coronary thrombosis; retard proliferation of fibroblasts
  • Reduce plaque formation and growth as they reduce adhesion molecules
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30
Q

How do trans fats affect LDL and HDL levels?

A
  • Increase LDL-C, similar to saturated fats, but reduce LDL size (more atherogenic)
  • Reduce HDL-C
  • May ↑inflammatory markers and endothelial damage
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31
Q

How do trans fats occur?

A

Occur as a result of partial hydrogenation.

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32
Q

What are the food sources of trans fats?

A

hard margarines, partially hydrogenated oils used in many foods, small amounts in dairy (which may not have the same effects)

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33
Q

What are the intake goals of dietary fiber?

A

Goal is 20-30 g/day; about 50% of which should be soluble

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34
Q

How does dietary fiber affect total cholesterol and LDL?

A

Soluble fibers decrease Total-C and LDL-C – may be dependent on initial level of hypercholestorolemia

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35
Q

How does CHO affect HDL and LDL?

A

Decreases HDL formation and/or Apo-AI synthesis

Overproduction of VLDL-TG especially if sucrose, fructose, or high-fructose corn syrup

36
Q

What are the disadvantages of high CHO diet?

A

– Decreased HDL and increased TG
– Hyper TG in some populations
– Could increase blood glucose and hyperinsulinemia

37
Q

What are the benefits of red wine on blood lipid profile?

A

Elevate HDL-C

Red wine in particular may inhibit cell-mediated oxidation of lipoproteins – due to resveratrol (polyphenol) NOT alcohol – FRENCH PARADOX

38
Q

How does soy protein affect total cholesterol, TG and LDL?

A
  • Reduces T-C, LDL-C, and TG without an effect on HDL-C in patients with or without CVD
  • Due to isoflavones and phytoestrogens
39
Q

How do antioxidants affect the lipid profile?

A

May inhibit LDL oxidation thereby decreasing atherosclerosis risk – oxidized fat less capable of being removed

40
Q

What are the normal fasting concentrations of folate and B6?

A
  • Normal fasting concentrations: 6-12 umol/L

* If >14 umol/L à increased risk of heart disease

41
Q

What is the relationship between homocysteinemia, folate and B6?

A

Low levels of folate especially are associated with high homocysteine levels

42
Q

What are the recommendations for supplementation for homocysteinemia?

A

• Supplement only in persons with high levels or family history of
CVD: 500 μg folate/day (once B12 deficiency is ruled out )
• Low levels of B12 not associated with increased risk of CHD

43
Q

What are the food sources of folate?

A

fortified cereals, vegetables, citrus fruits/juices, legumes, organ meats

44
Q

What are phytosterols and where are they found?

A
  • Equivalent to plant cholesterol
  • Compete with cholesterol absorption: increase fecal excretion
  • Diet enriched with 2-2.5 g sterols/stanols reduced LDL-C by 6- 14%
  • This amount almost impossible to obtain from normal foods: fortified margarines are the main source
45
Q

What are the benefits of nuts?

A

• Rich in mono- and polyunsaturated FA, most low in SFA
• High in plant protein, soluble fibers, folic acid, antioxidants,
arginine (NO precursor)

46
Q

How do nuts affect lipid profile?

A 
High intake (30-60 g/d) reduces risk of CHD, moderate intake
reduces LDL-C and improves endothelial function
47
Q

What is the Dietary approach for dyslipidemia?

A

• Based on global cardiovascular risk (Framingham)
• 1st target: LDL-C, then factors of the metabolic syndrome
• TLC model = therapeutic lifestyle changes
- saturated fats and dietary cholesterol
Step I: <10% SFA and <300 mg cholesterol
Steps II and III: <7% SFA and <200 mg cholesterol
- physical activity
- weight management to reduce coronary risk

48
Q

What is the mediterranean diet?

A

– high in oleic acid (olive oil)
– high in fruits, vegetables, legumes
– high in fish, low red meat, moderate dairy (mostly cheese and yogurt)
– regular but moderate wine consumption

49
Q

What are the benefits of mediterranean diet?

A

– Primary prevention:
• PREDIMED trial: 30% ↓ in CV events, favorable lipid
profile compared to low fat diet: ↓ LDL-C, apo-B and
TG, ↑HDL-C
• Other studies: additive effects to statins, ↓
inflammatory markers, favors weight loss, 25%
↓mortality
– Secondary prevention: Lyon Study: 70% ↓mortality post-MI

50
Q

What is the portfolio diet?

A

– low in saturated fats

– high in phytosterols (1 g, margarine), soy protein (21 g), soluble fibers (10 g), almonds (14 g) (all/1000 kcal)

51
Q

What are the benefits of the portfolio diet?

A

– ↓ 29% in LDL-C vs. 31% with low-fat diet +statins vs. 8% low-fat diet, ↓CRP vs. low-fat diet, under controlled conditions
– In a clinical study: ↓13% in LDL-C in portfolio intensive vs. 13% in portfolio routine vs. 3% in diet low in SFA. 11% ↓ in FRS.
– But adherence to portfolio diet is low: about 40-45%

52
Q

What are the dietary goals for extremely high triglycerides (>11.00 mmol/L), major risk from pancreatitis (this is rare so
no pre-calculated diet is provided) e.g., Type I HLP?

A
  1. Attain or maintain ideal body weight
  2. 10-15% energy from fat (20-30 g/day)
  3. MCT oil may be used to provide extra energy 4. No alcohol
53
Q

What are the dietary goals for Blood cholesterol 3 75th percentile, e.g., Type IIa and IIb HLP?

A
  1. Attain or maintain ideal body weight
  2. Decrease total fat intake, primarily saturated fat with a partial substitution of polyunsaturated fat
  3. Decrease cholesterol intake
54
Q

What are the dietary goals for blood triglycerides 3 90th percentile, e.g., commonly elevated in uncontrollable diabetes, alcohol excess, Type IV and V HLPs

A
  1. Attain or maintain ideal body weight
  2. Decrease or eliminate alcohol
  3. Decrease or eliminate sugar
  4. Decrease total fat with modest addition of
    polyunsaturated fat
55
Q

What are the dietary goals for Severe type V HLP = triglycerides 3 11.00 mmol/L

A

Decrease total fat to 20% of total energy and eliminate alcohol

56
Q

What are the dietary goals for Combination - elevated blood cholesterol and triglyceride, e.g., obesity, diabetes, Type IV and Type III HLPs

A
  1. Attain or maintain ideal body weight
  2. Decrease total fat intake, primarily saturated fat with a partial substitution of polyunsaturated fat
  3. Decrease cholesterol intake
  4. Decrease or eliminate alcohol and/or added sugar
57
Q

What are the classes of drugs for treatment of hyperlipidemia?

A
  • HMG-CoA reductase inhibitors (statins)
  • Cholesterol absorption inhibitors
  • Bile acid sequestrants (BAS)
  • PCSK9 inhibitors
58
Q

What are the names of HMG-CoA reductase inhibitors

(statins)?

A 
atorvastatin (LipitorTM) 
lovastatin (MevacorTM) 
simvastatin (ZocorTM) 
rosuvastatin (CrestorTM) 
pravastatin (PravacholTM)
59
Q

What are the names of Cholesterol absorption inhibitors?

A

ezetimibe (EzetrolTM)

60
Q

What are the names of Bile acid sequestrants (BAS)?

A

cholestyramine (QuestranTM)

colestipol (ColestidTM)

61
Q

What are the names of PCSK9 inhibitors?

A

evolocumab (RepathaTM)

alirocumab (PraluenTM)

62
Q

What are the predicted effects of statins?

A

decreased LDL-C (18-55%)
decreased TG (17-30%)
increased HDL-C (5-15%)

63
Q

What are the predicted effects of Cholesterol absorption inhibitors?

A

decreased LDL-C (18% mono, 25% with statin)

64
Q

What are the predicted effects of Bile acid sequestrants (BAS)?

A

decreased LDL (15-30%)

65
Q

What are the predicted effects of PCSK9 inhibitors?

A

decreased LDL (about 50%)*

66
Q

What is the mechanism of statins?

A
  • Block cholesterol synthesis

- increases LDL receptor mediated removal

67
Q

What is the mechanism of Cholesterol absorption inhibitors?

A

Inhibit cholesterol GI absorption

68
Q

What is the mechanism of Bile acid sequestrants (BAS)?

A

Promote sterol excretion

increases LDL receptors

69
Q

What is the mechanism of PCSK9 inhibitors?

A

Prevent catabolism of LDL receptors
– enzyme that binds to LDL receptors and promote their degradation (instead of LDL recycling on the cell surface)
– Inhibitors are monoclonal antibodies that block PCSK9 action –> more LDL recycling

70
Q

What are the names of fibrates?

A

gemfibrozil (LopidTM)

fenofibrate (LipidilTM)

71
Q

What are the names of nicotinic acid?

A

nicotinic acid slow release (QuestTM, NiaspanTM)

72
Q

What are the predicted effects of fibrates?

A

decreased TG (20-50%)
increased HDL-C (15-35%)
decreased LDL-C (5-25%)

73
Q

What are the predicted effects of nicotinic acid?

A

decreased TG (20-50%)
increased HDL-C (15-35%)
decreased LDL-C (5-25%)

74
Q

What is the mechanism of fibrates?

A

Decreases VLDL synthesis, enhances LPL action

75
Q

What is the mechanism of nicotinic acid?

A

Decreases VLDL synthesis, increase LPL activity

76
Q

What are the adverse effects and interactions of statin?

A

myalgia and myopathy, increased liver enzymes and low risk of diabetes (liver enzymes should be monitored semi- annually)

interaction with grapefruit juice

77
Q

When is ezetimibe recommended?

A

Recommended as second-line Tx in patients with clinical CVD and targets not reached by maximal statin dose

78
Q

What are the adverse effects and interactions of ezetimibe?

A
  • Possible side effects: diarrhea, rash, fatigue, muscle weakness or pain
  • Contra-indications: liver disease or failure
79
Q

What are the adverse effects and interactions of BAS?

A
  • May decrease absorption of fat and liposoluble vitamins, Ca, Fe, Zn, Mg
  • Side effects: significant constipation
  • Contraindications: existing hemorrhoids, peptic ulcer, hiatus hernia, multiple drug use, extensive travel, hypertriglyceridemia
80
Q

When is PCSK9 recommended?

A

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

81
Q

What are the adverse effects and interactions of PCSK9?

A

diarrhea, muscle or joint pain, bruising around injection site

82
Q

What are the recommendations for treatment of TG?

A
  • No specific target level for high-risk
  • Lower triglyceride levels are associated with decreased CVD risk
  • Health behavior interventions are first-line
  • Fibrates may prevent pancreatitis in patients with extreme hypertriglyceridemia (>10 mmol/L)
83
Q

What are the recommendations for treatment of HDL?

A
  • Low HDL-C may pose no risk, depending on genetic type
  • Medications may not increase HDL-C to a clinically significant extent
  • Health behaviour interventions increase HDL-C
84
Q

When should fibrates be used?

A
  • For use in highly elevated TG (familial hyperTG)

* Not recommended to add to statin for CVD prevention when target has been reached

85
Q

What are the adverse effects and interactions of fibrates?

A
  • Side effects: GI reactions (taste changes, abdominal pain), muscle toxicity
  • May cause reversible increases in plasma creatinine
  • Contraindications: hepatic or renal dysfunction, gallbladder disease, combination Tx with simvastatin
86
Q

When should nicotinic acid be used?

A
  • Used for primary hypercholesterolemia and/or hypertriglyceridemia, and hypoalphalipoproteinemia
  • Not recommended as add-on to statins
87
Q

What are the adverse effects and interactions of nicotinic acid?

A
  • Side effects: only 50-60% tolerate nicotinic acid: GI distress, skin flushing and itching, hepatotoxicity, arrhythmias
  • Monitor uric acid levels
  • Contraindications: active peptic ulcer, hepatic disease, gout, hyperuricemia

6-Clinical Nutrition 1 (21 decks)

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