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Clinical nutrition 1 > Dyslipidemia and CVD > Flashcards

Dyslipidemia and CVD Flashcards

1
Q

dyslipidemia is a disease. true or false

A

FALSE, it isn’t a disease but a major risk factor for developing cardiovascular diseases

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2
Q

what has caused the important decrease in mortality from CVD in Canada? (40% decrease)

A
  • improvements in control of CVD risk factors and medical management of patients with CVD
  • new clinical data available -> may enhance prevention and management of CVD
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3
Q

what are the roles of the cardiovascular system

A
  • regulate blood flow to tissues
  • thermoregulation
  • hormone transport
  • maintenance of fluid volume
  • regulation of pH
  • gas exchange
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4
Q

why is it important to regulate blood flow to tissue?

A
  • delivers oxygenated blood and nutrients

- retrieves waste products

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5
Q

what are the major forms of cardiovascular disease?

A
  • hypertension
  • atherosclerosis
  • coronary heart disease (CHD)
  • peripheral vascular disease
  • congestive heart failure (CHF)
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6
Q

what are examples of peripheral vascular disease

A
  • cerebrovascular disease (stroke)

- deep vein thrombosis

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7
Q

what is atherosclerosis

A

the thickening of the blood vessel walls caused by presence of atherosclerotic plaque

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8
Q

what is the effect of atherosclerotic plaque

A

results in restriction of blood flow due to reduced radius/diameter of blood vessel

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9
Q

what can atherosclerosis be associated with?

A
  • myocardial infarction (MI)
  • cerebrovascular accident (CVA; stroke)
  • peripheral vascular disease
  • CHD
  • CHF when severe CHD or MI occurs
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10
Q

what does atherosclerosis involve?

A
  • endothelial cells
  • smooth muscle cells
  • platelets
  • leukocytes
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11
Q

how does atherosclerosis begin?

A

begins as a response to endothelial lining injury caused by HTN/high BP that results in an inflammatory process

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12
Q

atherosclerosis is _____ until it progresses to ____

A

asymptomatic until it progresses to ischemic heart disease [lack of blood supply to heart]

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13
Q

explain process of formation of the atherosclerotic plaque

A
  • monocytes (phagocytic white blood cells) circulate in the bloodstream and respond to injury on the artery wall
  • monocytes slip under blood vessel cells and engulf LDL cholesterol which also infiltrate the wall either between cells or through diffusion in cell membrane => LDL OXIDATION [atherogenic]
  • they become foam cells. The thin layers of foam cells that develop on artery walls are known as fatty streaks and generates inflammation
  • a fatty streak thickens and forms plaque as it accumulates additional lipids, smooth muscle cells, connective tissue, and cellular debris
  • the artery may expand to accommodate plaque. when this occurs, the plaque that develops often contains a large lipid core with a thin fibrous covering and is vulnerable to rupture and thrombosis
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14
Q

with atherosclerosis there is a moderate elevation of ____. what is it a good indicator of

A

CRP protein levels - good indicator of inflammation because cytokines, secreted due to inflammation caused by foam cells, generate CRP synthesis in the liver

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15
Q

what is the atherosclerotic plaque made up of

A

smooth muscle cells, LDL-c, monocytes, mixture of lipids, connective tissue, calcium

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16
Q

what is more dangerous that then restriction of the blood flow caused by atherosclerotic plaque?

A

the rupture of the plaque -> release of all component sin blood which could block small capillaries/vessels
HTN is a risk factor for rupture

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17
Q

what are the potential primary causes of damage to endothelial wall

A
  • high BP
  • chemicals from tobacco
  • oxidized LDL
  • glycated proteins
  • decrease in nitric oxide
  • angiotensin 2 [decrease levels of NO which is protective to endothelial wall]
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18
Q

what are the tow hypothesis of atherogenesis?

A
  1. endothelial-injury hypothesis
  2. lipid-infiltration hypothesis
    but they are LINKED
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19
Q

why are the 2 hypothesis of atherogenesis linked?

A

lipid-infiltration causes LDL to be oxidized by macrophages and in turn causes endothelial-injury + fatty streak caused by foam cells from lipid-infiltration also causes endothelial injury

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20
Q

as ratio of LDL:HDL >3:1 increases, there will be high risk for ____

A

atherosclerosis

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21
Q

what are the risk factors of atherosclerosis

A
  • family history
  • age and sex
  • obesity
  • dyslipidemia
  • hypertension
  • physical inactivity
  • diabetes mellitus/pre-diabetes
  • smoking
  • obstructive sleep apnea [hypoxia]
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22
Q

there is a genetic factor in development of atherosclerosis. true or false

A

true, there is predisposing genes

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23
Q

atherosclerosis is more prevalent in ___. why?

A

in men [like any cardiovascular disease]

because estrogen has a protective effect just like in HTN

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24
Q

why is HTN a big risk factor in developing atherosclerosis

A

it may initiate atherosclerotic lesion and can also cause plaque to rupture

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25
Q

what are the specific risk factors of dyslipidemia?

A
  • hyperlipidemia (LDL-c)

- low HDL-c (<1.0mmol/L for men and <1.3 for women)

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26
Q

normal HDL levels are the same for men and women. T or F

A

False: women naturally have more HDL-c

men: >1.0mmol/L
women: >1.3mmol/L

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27
Q

about chylomicrons

A
  • Apo B-48!!! [only found in CM because synthesized by intestine]
  • produced and packed in intestine
  • high content in TG coming from diet
  • biggest of all lipoproteins
  • circulates throughout body/tissues/blood vessels
  • Apo C-2 stimulates activity of lipoprotein lipase which hydrolyzes TG in CM to FFA taken up by tissues -> decrease size of CM => CM remnant with less TG and more cholesterol esters
  • remnants comes back to liver where it is completely disaggregated and cholesterol and TG are repacked in VLDL
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28
Q

circulation of CM

A

CM goes through lymphatic system [much larger vessles] where it is broken down into CM remnants before they go into the liver

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29
Q

about VLDL

A
  • Apo B-100!!!
  • VLDL is synthesized in liver and secreted
    contains alot of TG [from both diet from de novo lipogenesis bu liver and from FFA coming from adipose tissue to the liver] but in less amounts than in CM
  • smaller than CM
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30
Q

metabolism of VLDL

A

VLDL is secreted from liver as lipoprotein and in the circulation, there are interactions and exchanges between HDL and VLDL where HDL exchanges cholesterol from reverse cholesterol circulation transport and TG from VLDL to HDL
=> mature VLDL particle which circulates into all tissues, app C2 activates LPL and FFA taken up by tissue and stored in adipose tissue
-> remnant either becomes LDL or is taken up by liver

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31
Q

how is VLDL remnant taken up by liver

A

recognition of LDL receptor with interaction of Apo E and Apo B-100 - endocytosis with receptor

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32
Q

how is VLDL remnant turned into LDL

A

VLDL remnant is hydrolyzed by hepatic triglyceride lipase -> LDL with less TG content and more cholesterol

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33
Q

characteristic of LDL

A

has Apo B100
low TG
high CE

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34
Q

characteristics of HDL

A
  • Apo A1!!!
  • highly dense
  • small
  • has alot of Apo protein and phospholipids on its surface
  • contain mostly cholesterol from reverse transport
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35
Q

difference between nascent HDL and HDL

A

nascent HDL has unesterified cholesterol - transformed into cholesterol esters by LCAT -> HDL

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36
Q

transfer and exchanges between HDL and VLDL

A

HDL transfers cholesterol esters to VLDL

VLDL exchanges TG to HDL

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37
Q

what is the fate of cholesterol

A

cholesterol is mainly excreted through feces but it also excreted through its conversion in bile acids which is secreted in intestine [recycling/reabsorption of cholesterol]

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38
Q

target for total cholesterol levels in serum

A

<5.2 mmol/L

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39
Q

target for HDL cholesterol levels in serum

A

1.0-1.5 mmol/L
>1.0 men
>1.3 women

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40
Q

target for LDL cholesterol levels in serum

A

<2.6 mmol/L

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41
Q

target for triglyceride levels in serum

A

<1.7 mmol/L

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42
Q

can you measure LDL-c levels directly?

A

no - indirect measurement using equation => substation of other measures
comes from Total cholesterol, HDL, and TG levels

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43
Q

when is LDL-c equation not recommended/valied

A

when TG are higher than 4.5mmol/L

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44
Q

what are the functions of apoproteins

A
  • synthesis/secretion of specific lipoproteins [apo B-100 stimulates synthesis and secretion of VLDL]
  • stabilize surface coat of lipoproteins
  • activate enzymes (apo C-2 activates LPL)
  • interact with cell surface receptors (B-100 and LDL receptors on liver)
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45
Q

apoproteins are the primary determinants of the ____ of lipoproteins

A

metabolic fate

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46
Q

apoproteins reflect changes in ______ and is indication of ______ in plasma

A

lipoprotein composition

lipoprotein concentration

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47
Q

which is the better predictor of heart disease: apoprotein levels or lipid levels (LDL)

A

apoprotein levels - better diagnosis o lipoprotein disorders and risk for developing CHD and CVD because they are indicative of lipoprotein concentration and reflect changes in lipoprotein composition

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48
Q

lipoprotein and they’re associated apoproteins

A

chylomicrons - B-48
VLDL - B-100
LDL - B-100
HDL - A-1, A-2

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49
Q

which are the most frequent genotypes of Apo-E

A

E-3/E-3
E-3/E-4
=> associated with better binding of the poE with LDL receptors

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50
Q

how many alleles are associated with apoE

A

4

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51
Q

E-4/E-4 is associated with ____

A

dementia

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52
Q

E-2/E-2 genotype is very rare. why is it not a good genotype to have?

A

Apo E-2/E-2 does not bind to LDL receptors -> increase in VLDL remnants => very high triglyceridemia

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53
Q

what are the two classification of dyslipidemia?

A

primary and secondary, secondary being the most common one

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54
Q

what is primary dyslipidemia

A

single or polygenic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia

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55
Q

what is the diagnosis for primary dyslipidemia based on

A
  • history (age at onset, family members)
  • physical signs (xanthomas)
  • lab analysis: really high lipid profile values, absence or presence of apoproteins, LPL activity
  • appearance of serum
  • genetic sequencing for rare cases
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56
Q

what are xanthomas

A

accumulation of small bubbles of connective tissue mixed with cholesterol

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57
Q

what is secondary dylipidemia

A

from environmental causes +/- predisposition

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58
Q

which are the three types of hypolipoproteinemias associated with primary dyslipidemia

A
  • abetalipoproteinemia
  • familial hypobetalipoproteinemia
  • familial alpha-lipoprotein deficiency
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59
Q

what is abetalipoproteinemia

A
  • defect in apoprotein B synthesis

- no chill, VLDL, LDL formed and TAG accumulate in liver and intestine

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60
Q

what is familial hypobetalipoproteinemia

A
  • LDL concentration in 10-50% of normal but chylomicron formation occurs
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61
Q

what is familial alpha-lipoprotein deficiency (Tangier disease)

A
  • virtual absence of HDL (Apo-A1), CE accumulates in tissues
  • Chylo, VLDL, LDL are all normal
  • moderate hyperTG
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62
Q

what are the 2 most common phenotypes of hyperlipoproteinemia?

A

IIb and IV

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63
Q

which lipoprotein(s) is/are affected my phenotype 2b of hyperlipoproteinemia and what are the specific markers?

A

higher LDL and VLDL

mutation of LDL receptor or Apo B

64
Q

which lipoprotein(s) is/are affected my phenotype 4 of hyperlipoproteinemia and what are the specific markers?

A

high VLDL

no marker [no gene/marker]

65
Q

which phenotype(s) of hyperlipoproteinemia is/are associated with high CVD risk? why?

A

2b and 3

because of accumulation of LDL in circulation

66
Q

phenotype 4 of hyperlipoproteinemia is also known as ____

A

hypertriglyceridemia

67
Q

phenotype 2b of hyperlipoproteinemia is also known as ____

A

combined hyperlipoproteinemia

68
Q

which lipoprotein is the most atherogenic

A

LDL-cholesterol

69
Q

what are the major causes of secondary dyslipidemia

A 
Lifestyle factors:
- diet
- alcohol
- smoking
- lack of PA 
Diseases:
- diabetes - hyperthyroidism - renal failure - obesity - cirrhosis - myelomas - Cushing syndrome
Medications
70
Q

what are the effects of obesity on lipoprotein metabolism

A

INCREASE TG LEVEL AND OVERPRODUCTION OF VLDL
there is an increased substate flux of CHO and FAT to the liver due to increased total intake
-> postprandial (lipogenesis from excess CHO) and postabsorptive due to high adipose tissue and hormone-sensitive lipase activity resulting in increased FFA fluctuations to liver + ethanol blocks oxidation of acetyl-coA -> more production of TG

71
Q

during obesity, lipolysis of excess VLDL is increased therefore TG levels are _____ but there’s an accumulation of ___ in tissues

A

TG levels are maintained/normal

FFA/fat accumulation in tissues

72
Q

VLDL lipolysis can be inhibited due to ____. what are the consequences

A

inhibited due to insulin resistance, inflammation , inflammatory factors affect LPL activity
see accumulation of VLDL and TG in circulation => hypertriglyceridemia (commonly seen but not in every person who is obese)

73
Q

what characterizes dyslipidemia associated with obesity?

A

hypertriglyceridemia

74
Q

what causes hypercholesterolemia

A

due to increased total calories there is an overproduction of VLDL particles + reduced activity of LDL receptors due to dietary factors (saturated FA, cholesterol intake) overall leading to an accumulation fo VLDL and LDL in the circulation

75
Q

with increased triglyceridemia we usually see ____. why?

A

HDL-c lowering
increased transfer of CE from HDL to VLDL changing density and physical aspects of HDL favouring their uptake by liver + favour their uptake/catabolism by adipose tissue

76
Q

Both ___ and ___ are associated with low HDL-c

A

severity (high BMI) and distribution (abdominal) obesity

77
Q

what are the possible mechanisms of reduced HDL-c in obesity

A
  • increased Vldl pool so increased transfer of Tg from VLDL to HDL stimulating hepatic lipase and in turn liver uptake of HDL
  • increase uptake of HDL2 by adipocytes
  • increased clearance of apolipoprotein A1 -> HDL catabolism
78
Q

who should be screened for prevention of CVD

A

men and women >40yo or postmenopausal

or all patients with an existing condition that could be a risk factor

79
Q

how do yo screen for CVD

A
  • blood tests containing all lipid fractions NON-FASTING
  • non-HDL-c
  • estimated glomerular filtration rate
80
Q

LDL-c is the ____ but is not _____

A

target (we want to reduce the value) but is not part of the risk factor

81
Q

high risk patients are automatically prescribed ____ to treat hyperlipidemia

82
Q

what are alternate targets to LDL-c

A

non-HDL-c and apo-B

83
Q

what are non-HDL-c?

A

total cholesterol minus HDL-c

=> atherogenic Apo B-containing lipoproteins

84
Q

interest around Lp(a)

A

highly atherogenic particle, mostly determined by genetic predisposition => should be measured once in a lifetime to see where person stands

85
Q

what are the target values for LDL-c, Apo-B, non-HDL-c

A
  • LDL-c < 2.0mmol/L or >50% reduction
  • Apo B < 0.8g/L
  • non-HDL-C < 2.6mmol/L
86
Q

how does weight management/loss affect dyslipidemia

A

a weight loss of 2-7kg decreases LDL, TG, and HDL before increasing HDL during maintenance

87
Q

how does physical activity affect dyslipidemia

A

it decreases TG majorly and LDL, and increases HDL

88
Q

what kind of physical activity has the greatest effect on lipid profile improvement

A

higher volume and high intensity has the greatest effect rather than resistance exercise

89
Q

changes in lipid profile tell you the risk of developing CVD. True or false

A

False, there are a multitude of factors determining CVD risk

90
Q

what Is the relationship between high cholesterol intake and serum cholesterol levels

A

positive relationship

91
Q

which factors are considered to evaluate/predict the changes in serum cholesterol

A
  • cholesterol
  • saturated fats
  • polyunsaturated fats
92
Q

which factor contributes the most to change in serum cholesterol

A

dietary saturated fatty acids

93
Q

what are the limitations of the predictive equations of changes in serum cholesterol

A
  • different saturated FA have different effects
  • predicts total cholesterol only, not lipid fractions [different lipoprotein fractions are more important to consider]
  • assumes MUFA and CHO are neutral
  • effects on total cholesterol may not be linear
94
Q

where is dietary cholesterol found

A

ONLY in animal products, especially organ meats

95
Q

what are the mechanisms of dietary cholesterol regarding lipid profile

A
  • decreased synthesis and activity of hepatic LDL receptors
  • increased cholesterol in chylo and chylo remnants -> more atherogenic and increased cholesterol delivery to liver
  • increased cholesterol in VLDL and VLDL remnants -> more atherogenic
  • interfered with ability of HDL to clear cholesterol
96
Q

cholesterol in food isn’t proportional to ____

A

fat content

97
Q

what is more important than amount of fat intake

A

the type/quality of fat

98
Q

which factor has the greatest impact on serum cholesterol

A

saturated fats

99
Q

why do saturated fatty acids have the greatest impact on serum cholesterol

A

they reduce the activity of LDL receptors by: decreasing transcription of LDL receptors genre, altering phospholipid composition of cell membranes to decrease binding [decreased fluidity], altering LDL itself and delays binding to receptors

100
Q

what is the contribution of SFA in Canadians’ diet

A

10% of total energy

101
Q

diets high in SFA -> ____

A

increase LDL-C

102
Q

higher LDL-C -> _____

A

increase CVD risk

103
Q

what happens when 5% of energy from SFA is replaced by PUFAs?

A

here is a 10% reduction in CVD risk

104
Q

what are the recommendations regarding saturated fats in diet

A

no limit on SFA instead focus on healthy balanced diet because different lengths of SFA have different effects on health

105
Q

which SFA increase LDL-C

A

Lauric, myristic, palmitic

106
Q

SFA have no effect on ___

107
Q

what are the effects of reducing dietary SFA on LDL-C and HDL-C

A
  • reduces LDL-c: primarily the large LDL particles, not the smaller more atherogenic particles
  • reduces HDL-c: small effect on the ratio total-c/HDL-c
108
Q

SFAs from dairy products ___ CVD risk compared to SFA from meat

109
Q

SFAs from cheese vs. butter

A

less increase in LDL-c compared to butter

110
Q

what are the effects of trans fatty acids

A
  • increase LDL-c, similar to saturated fats, but reduce LDL size making them more atherogenic
  • reduces HDL-c
  • may increase inflammatory markers and endothelial damage
111
Q

omega-9 unsaturated FA of the diet

A

oleic acid

112
Q

omega-6 unsaturated FA of the diet

A

linoleic acid -> arachidonic acid

113
Q

omega-3 unsaturated FA of the diet

A 
linolenic acid
eicosapentaenoic acid (EPA)
docosahexaenoic acid (DHA)
114
Q

effects of omega-6 linoleic acid

A

increases LDL clearance [removes suppressing effect of SFA]

115
Q

what is the goal of calorie intake from omega-6 PUFA

A

5-10% of calories [corn, sunflower, safflower, soybean oils, walnuts, sunflower seeds]

116
Q

what is the derepression effect of omega-6 PUFA

A

derepression of LDL-receptor synthesis on liver - removes suppressing effect of SFA

117
Q

what is the calorie goal of MUFA (omega-9) consumption

A

no more than 20% of total calories [olive and canola oils, peanuts, meat and poultry]

118
Q

compared to PUFA, oleic acid _____

A

does not lower HDL-c

119
Q

compared to saturated fats, oleic acid _____

A

lowers LDL-c

120
Q

Why is it better to substitute SFA with MUFA rather than PUFA

A

because MUFA, unlike PUFA, does not impact HDL levels

121
Q

what are the advantages of MUFAs

A
  • do not decrease HDL as does PUFA and CHO
  • less susceptible to oxidation than PUFA
  • do not increase TG as CHO often do
  • DO not increase cancer risk as high PUFA intakes could
122
Q

effects of omega-3 pUFA

A

decrease triglyceridemia in hyperTG patients at high doses (supplements) but not CVD benefit in primary or secondary prevention

123
Q

omega-3 PUFA do not reduce number of ____ secreted by liver but rather decrease ____ of these

A

VLDL particles

reduce TG content of these particles

124
Q

omega-3 PUFAs interfere with platelet aggregation and thereby prevent _______

A

coronary thrombosis

125
Q

which type of fibre is recommended for consumption. what is the mechanism of action

A

soluble fiber, Acts in intestinal lumen and binds some bile acids and cholesterol being excreted to be excreted into feces thereby reducing total-c and LDL-c

126
Q

what is the recommended intake of fiber

A

20-30g/day of which 50% is soluble

127
Q

food sources of dietary soluble fiber

A

oats, legumes, pectins, psyllium, gums

128
Q

___ and ___ both increase production of TG by liver

A

carbohydrates and fats

129
Q

simple carbohydrates decrease HDL-c levels, why?

A

due to overproduction of TG, TG will be transferred to HDL causing HDL to be taken up more by the liver and adipocytes to be catabolized, decreasing heir levels

130
Q

disadvantages of high CHO diet

A
  • decreased HDL and increased TG
  • hypertriglyceridemia
  • could increase blood glucose and hyperinsulinemia
131
Q

what is the recommendation around alcohol consumption

A

consume in moderation (1-2drinks/day)

132
Q

alcohol consumption shows no benefit. true or false

A

false, it has been seen to increase HDL-c levels when consumed in moderation + polyphenols present in rede wine reduce oxidation of lipoproteins

133
Q

which polyphenol found in red wine inhibits cell-mediated oxidation of lipoproteins

A

resveratrol

134
Q

when is alcohol consumption completely not recommended

A
  • not specifically recommended especially for those with established Congestive Heart Disease
  • if there is hypertriglyceridemia because of its effect on inhibiting oxidation of acyl-coA and therefore moving the use of excess CHO and fats to produce TG
135
Q

soy protein, when consumed in sufficient amounts, reduces _______ without lowering _____ in patients with or without CVD

A

Total cholesterol, LDL-c, and TG without reducing HDL-c

136
Q

what are food sources of soy protein?

A

tofu, soy beverage, soy protein isolates, tempeh

137
Q

why have antioxidants shown interest in reducing congestive heart disease?

A

they may inhibit LDL oxidation which could therefore decrease the risk of atherosclerosis [vit C, E, beta-carotene]

138
Q

_____ is a marker for cardiovascular risk aka ___ levels of it translate to an increased risk of heart disease

A

homocysteine

higher levels [>14 micomol/L] -> increased risk of heart disease

139
Q

which nutrients are targeted when there is hyperhomocysteinemia. why?

A

FOLATE, vitamins B6 and B12 because they are involved in the metabolism/recycling of homocysteine

140
Q

low levels of ____ especially are associated with high levels of homocysteine

141
Q

what are some food sources of folate

A

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

142
Q

how do phytosterols and stenols impact our serum cholesterol?

A

they are the plant equivalent of animal cholesterol. they compete with cholesterol absorption, increasing fecal excretion -> Diet enriched with 2-2.5 g sterols/stanols reduced LDL-C by 6-14%
However, they are hard to find so diet must be enriched with these (fortified margarines)

143
Q

what is the impact of nut consumption

A

high intake (30-60g/d) it reduces risk of CHD, moderate intake reduces LDL-c and improved endothelial function

144
Q

nuts are rich in ____ and low in ____

A

high in MUFA/PUFA low in SFA

145
Q

which type of nut is rich in SFA

A

Brazil nuts

146
Q

nuts are a good source of arginine, why is this of interest?

A

arginine is a precursor of nitric oxide which acts as a vasodilator

147
Q

what is the first target for the dietary approach for dylipidemia?

A

LDL-c by reducing SFA and cholesterol intake

148
Q

observations around Mediterranean diet

A
  • lowers CVD risk
  • improves lipid profile
  • reduced mortality
149
Q

omega-3 PUFA supplement should be used to reduce CVD risk. T or F

A

FALSE, SHOULD NOT be used to reduce CVD risk

150
Q

with what should SFA be replaced with

A
  • MUFA and PUFA from plant source

- CHO that is whole grain or with low Glycemic Index

151
Q

characteristics of mediterranean diet

A
  • high in oleic acid (olive oil)
  • high in fruits and vegetables
  • high in fish, low in red meat, and moderate dairy from cheese and yogurt
  • regular but moderate wine consumption
152
Q

the Mediterranean diet has an additive effect with which medication?

153
Q

characteristics of portfolio diet

A
  • low in SFA
  • high in phytosterols, soy protein, soluble fibres, almonds
  • vegetarian diet
154
Q

what are the specific recommendations for those with familial dyslipidemia (primary hypyperlipidemia and hypertriglyceridemia)

A
  • no alcohol intake
  • eliminate simple sugars
  • dietary therapy WITH medication always
  • low fat intake (10-15% energy from fat)
155
Q

which factors increase HDL-c

A
  • saturated fats
  • dietary cholesterol
  • alcohol
    (don’t only have negative effects)
  • long-term aerobic exercise
  • female sex (estrogen)
156
Q

which factors decrease HDL-c

A
  • simple sugars/high carb diet
  • PUFA, high (>10%)
  • abdominal obesity
  • male sex (androgens)
  • anabolic steroids
  • some antihypertensive drugs
  • diabetes
  • smoking
157
Q

there are no medications that will target HDL-c. T or F

A

TRUE, all medications target LDL or TG

Clinical nutrition 1 (7 decks)

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