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CVD > Role and mechanism of dietary fats > Flashcards

Role and mechanism of dietary fats Flashcards

1
Q

What is one of the most important risk factors for CVD?

A

Increased plasma cholesterol

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2
Q

What has epidemiology shown with total cholesterol and CHD?

A

A very strong relationship with total cholesterol and CHD mortality independent of other risk factors

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3
Q

How is this causal relationship proven?

A

Causal relationship is proven by the fact that intervention studies showing reduction of total and LDL cholesterol demonstrate a significant reduction in CHD mortality

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4
Q

What is the total cholesterol recommendation?

A

NHS: Healthy adults – 5mmol/l or lower

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5
Q

What is total cholesterol consumption?

A

Average in the UK: 5.5mmol/l (men) and 5.6 mmol/l (women)

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6
Q

What does the evidence say about serum LDL-C and CVD risk/mortality?

A

Over 100 years of supporting evidence for raised serum LDL-C and increased CVD risk and mortality . This is the consensus from EU Atherosclerosis Society (2017) (Ference et al. 2017). Serum LDL causally related to atherosclerotic CVD

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7
Q

What might SFA do?

A

Raise serum LDL-C which increases atherosclerosis and CHD. This is the basis for UK recommendations to reduce SFA intake

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8
Q

What should LDL ideally be?

A

Lower than 100mg/dL (2.6mmol/l)

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9
Q

Describe the lipoprotein Chylomicron and its major protein and major lipid?

A

apoB

TG

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10
Q

Describe the lipoprotein VLDL and its major protein and major lipid?

A

apoB

TG

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11
Q

Describe the lipoprotein IDL (intermediate) and its major protein and major lipid?

A

apoB

CE

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12
Q

Describe the lipoprotein LDL and its major protein and major lipid?

A

apoB

CE

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13
Q

Describe the lipoprotein HDL and its major protein and major lipid?

A

apoA-I

CE

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14
Q

What is apo?

A

Apolipoprotein

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15
Q

What is CE?

A

Cholesteryl ester

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16
Q

What does the exogenous pathway of synthesis and transport of fats refer to?

A

The absorption of dietary lipids by intestinal epithelial cells

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17
Q

How does the exogenous pathway work? Step 1

A

Ingested lipids are packaged into chylomicron particles, which consist mainly of triglycerides, phospholipids and cholesterol, and are coated in the protein apolipoprotein B- 48.

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18
Q

What is the major role of chylomicrons?

A

To transfer energy, in the form of fatty acids, to peripheral cells, mediated by the hydrolysis of triglycerides contained in circulating chylomicrons by lipoprotein lipase (producing glycerol (returned to liver for glucose synthesis) and fatty acids (used for resynthesis and storage mainly in adipose tissue)

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19
Q

How does the exogenous pathway work? Step 2

A

The resulting chylomicron remnant particles are then reabsorbed by the liver and the cholesterol content is either used to generate new lipoprotein particles or excreted through the bile duct

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20
Q

What is the endogenous pathway responsible for?

A

The majority of cholesterol in circulation, requires the synthesis of cholesterol by the liver, resulting in secretion of VLDL particles

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21
Q

What is the rate limiting enzyme in the endogenous process?

A

3- hydroxy-3-methyl-glutaryl-CoA (HMG Co-A) reductase, the key target of statin drugs which are used for cholesterol lowering

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22
Q

How does the endogenous pathway work? Step 1

A

VLDL particles consisting of fatty acids, free cholesterol and TAG are packaged by and coated with the apolipoprotein apoB100, which is secreted from hepatocytes in the liver

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23
Q

How does the endogenous pathway work? Step 2

A

Like chylomicrons, circulating VLDL is acted upon by lipoprotein lipase resulting in VLDL remnants termed IDL (intermediate density lipoprotein) particles.

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24
Q

How does the endogenous pathway work? Step 3

A

IDL then returns to the liver where it is hydrolysed by hepatic lipase resulting in particles referred to as low-density lipoprotein (LDL).

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25
Q

How does the endogenous pathway work? Step 4

A

The major apoprotein of LDL remains the same: apoB100.
The apoB-100 surface protein of LDL is recognised by tissue cells by the LDL receptor (LDLr), which is expressed on the surface of cells requiring cholesterol for membrane building.

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26
Q

What happens to excess cellular cholesterol?

A

It may be subjected to the reverse cholesterol transport (RCT) pathway mediated by the ATP-binding cassette A-1 transporter (ABCA1), which enables the uptake of cholesterol by apo-AI, the main surface protein of HDL particles.

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27
Q

What is HDL recognised by?

A

HDL receptors expressed by the liver are taken up and the cholesterol is recycled to be reintroduced to new VLDL particles, or excreted by means of the bile duct

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28
Q

What is a prediction of the diet-heart hypothesis?

A

Serum cholesterol lowering effects of replacing saturated fat with vegetable oil rich in linoleic acid will diminish deposition of cholesterol in the arterial wall, slow progression of atherosclerosis, reduce coronary heart disease events, and improve survival

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29
Q

What supports this prediction?

A

Evidence from RCTs showing that replacement of saturated fat with linoleic acid lowers serum total cholesterol and low density lipoprotein - observational evidence linking serum cholesterol to coronary heart disease events and deaths

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30
Q

What goes against these compelling relations?

A

no RCT has shown that replacement of saturated fat with linoleic acid significantly reduces coronary heart disease events or deaths

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31
Q

What are key facts to remember regarding SFA and CVD?

A
  • At population level, high SFA consumption per se is not linked to higher CVD incidence and mortality
  • However, replacement of SFA with a macronutrient does change CVD risk
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32
Q

How is LDL uptake into the liver?

A

via the LDL receptor (called LDL-receptor mediated endocytosis). The LDL receptors are in clusters and form vesicles that carry LDL into the cell.

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33
Q

What happens once inside cell?

A

receptors dissociate from cholesterol and then fold back to translocate to cell surface (receptor recycling). Lysosomal hydrolysis releases free cholesterol which can be incorporated into cell membranes or metabolized into steroids or bile acids.

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34
Q

What does excess cholesterol cause?

A

will inhibit de novo cholesterol synthesis (via inhibition of HMGCoA reductase), inhibit LDL receptor synthesis and stimulate cholesterol storage (as cholesteryl ester).

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35
Q

What happens with high con of cholesterol in liver?

A

uptake will adapt (lower) and LDL particles remain higher in the circulation which exposes a higher CVD risk.

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36
Q

What happens if LDL cannot get cleared through liver?

A

if the levels are too high, this increases CVD risk.

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37
Q

In summary, what is lipoprotein recovery?

A
  • Remnants of lipoproteins (CR, LDL) are recovered by the liver
  • Uptake of cholesterol in liver cells
  • LDL receptors are regulated by free cholesterol within cells
  • Increase in LDL receptors on membrane reduces plasma LDL concentrations
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38
Q

How was the link between cholesterol and heart disease first recognised?

A

through the study of individuals with familial hypercholesterolemia

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39
Q

What do individuals with familial hypercholesterolemia have?

A

several-fold higher levels of circulating LDL due to a defect in the function of their LDL receptors (Autosomal dominant mutation in LDL receptor - heterozygote: 1:500; homozygote: 1:1Mio

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40
Q

What happens without functioning LDL receptors?

A

LDL is not cleared from the circulation. As well, because cholesterol cannot get into cells efficiently, there is no negative feedback suppression of cholesterol synthesis in the liver.

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41
Q

What happens to Heterozygotes in terms of health outcomes?

A

increased plasma cholesterol with first heart attack at 30-40years old (50% LDL deficiency causes 2x higher plasma cholesterol)

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42
Q

What happens to Homozygotes in terms of health outcomes?

A

increased cholesterol and VLDL, with increased risk of cardiovascular disease/obesity (6-10fold increased LDL Chol)

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43
Q

What happens if familial hypercholesterolemia is undiagnosed?

A

Males can have first heart attack at ~2years (females protected ~20years old) – depends on severity of mutation (partial/total)

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44
Q

What is the need for cholesterol in the body?

A
  • Cholesterol is a fundamental component of cell membranes
  • Cholesterol is a fundamental component of lipoproteins
  • Cholesterol is a precursor of bile acids, steroid hormones and vitamin D (activated by UV)
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45
Q

How much cholesterol does the body produce?

A

Body produces around 75% of the cholesterol required

A man with 70kg body weight produces ~1g/d, total body cholesterol is 35g

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46
Q

How much cholesterol is from the diet?

A

25%

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47
Q

What is the average intake of cholesterol from the diet per day?

A

Dietary cholesterol intake approx 200-300mg/day
(150-250mg cholesterol per egg yolk,
Absorption 40-60%)

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48
Q

What happens if dietary intake is high?

A

The body correspondingly decreases cholesterol synthesis in liver

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49
Q

What happens if dietary intake is low?

A

at lower intake levels linear and above 300-400mg/day – hyperbolic response

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50
Q

What happens for every 100mg increase?

A

Rise of 10mg/dL

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51
Q

What happens for every 200mg/day reduction?

A

Decrease of 10mg/dL (approx. 5%)

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52
Q

What is the difference between animals and humans?

A

humans do not develop severe hypercholesterolaemia when fed high cholesterol diets

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53
Q

In the intestine, how much of the cholesterol is dietary?

A

only about 20% of cholesterol in the intestine is dietary

54
Q

Where is cholesterol synthesised?

A

liver from carbohydrate

55
Q

How is cholesterol synthesised?

A

Acetate –> cholesterol

(3-hydroxy glutamyl coenzyme A
(HMG-CoA) reductase is rate limiting

cholesterol –> bile salts

Cholesterol-
-7-α-hydroxylase is rate limiting

56
Q

Will dietary cholesterol raise blood cholesterol levels?

A

Dietary cholesterol will not raise blood cholesterol levels in most people to a large extent

57
Q

What are compensators?

A

Some reduction in endogenous cholesterol synthesis in response to dietary intake
(except at very high levels >850 mg/d)

58
Q

What are non-compensators?

A

No ability to modify endogenous cholesterol and so plasma cholesterol rises with intake

59
Q

How do statins work?

A

They inhibit the first step in cholesterol synthesis (HMGCR –> Mevalonate) by inhibiting HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis

60
Q

What do statins cause?

A

Statins produce MASSIVE reductions in blood cholesterol – also supporting the idea the dietary cholesterol has a limited role.

61
Q

What can statins treat?

A

dyslipidemia

62
Q

What can plant sterols do?

A

Dietary cholesterol absorption can be reduced by consumption of plant sterols

63
Q

How do sterols and stanols work?

A

Sterols and stanols replace cholesterol in micelles in the intestine, preventing absorption of cholesterol

64
Q

How are sterols and stanols used commercially?

A

Commercially used in products like benecol and flora-proactive, with claims to reduce plasma cholesterol by up to 10-15%

65
Q

How many points of cholesterol regulation are there in its absorption?

A

3

66
Q

How does cholesterol absorption work?

A

When the micellar particle comes in the proximity of an enterocyte, cholesterol is transported into the enterocyte through a channel recently identified as NPC1L1. A fraction of this cholesterol is pumped back out of the enterocyte into the intestinal lumen by the complex ABCG5/G8, and the remainder is esterified by the enzyme acyl-coenzyme A:cholesterol acyltransferase (ACAT) into cholesteryl esters.

67
Q

What are the 3 points of regulation?

A

NPC1L1
Complex ABCG5/G8
ACAT

68
Q

How much of intestinal cholesterol is absorbed?

A

approx. 50%

69
Q

Stanols and sterols have a similar structure to cholesterol, what does this mean?

A

They mimic cholesterol, binding to micelles but with greater affinity, thereby displacing a cholesterol molecule, which is in turn lost in the feces.

70
Q

What happens if plant sterols and stanols enter enterocyte?

A

They are very efficiently pumped back out into the intestinal lumen by the heterocomplex ABCG5/G8, so that only traces of plant sterols ultimately enter the body.

71
Q

What is ezetimibe?

A

Ezetimibe is a member of a new class of drugs that blocks the assimilation (absorption) of cholesterol from micellar particles into the enterocyte, possibly by interacting with NPC1L1.

72
Q

What does inhibition of cholesterol absorption does ezetimibe cause?

A

Inhibition of cholesterol absorption by approx. 50% and lowers LDL-Chol conc by 15-20%

73
Q

What is benecol?

A

Contains plant sterols – that compete with cholesterol for uptake in the gut
Made from wood pulp residue – paper milling industry

74
Q

What is benecol proven to do?

A

Proven to reduce cholesterol uptake
Proven to decrease plasma cholesterol
but maybe not…proven to decrease your cardiovascular disease risk

75
Q

Who is benecol most effective for?

A

Most effective for those with high cholesterol levels

76
Q

Benecol effect is competitive, what does this mean?

A

eat more cholesterol - Benecol effect blunted with plateau at approx 2g/day

77
Q

How much will benecol reduce cholesterol by?

A

Benecol will reduce blood cholesterol 10-15%

78
Q

What is the question with benecol?

A

It will reduce blood cholesterol 10-15%, but is it enough to decrease CVD risk?
No studies showing that plant sterol esters have an impact on CHD mortality rates

79
Q

What else can inhibit cholesterol absorption?

A

Fibre consumption

  • Soluble fibre, e.g. oat fibre, can trap bile acids (formed from cholesterol synthesis in liver)
  • Bile acids not available for re-absorption
  • More hepatic cholesterol will be diverted to produce bile acids, therefore lowering plasma cholesterol
80
Q

What are 4 summary points of cholesterol?

A
  • Cholesterol synthesis is regulated by both synthesis and absorption
  • Inhibition of cholesterol absorption may be compensated by increases in synthesis
  • Plant sterols may lower cholesterol levels but have not shown to impact on CHD mortality
  • Optimal LDL lowering may best be achieved through inhibiting several pathways
81
Q

All cells produce cholesterol but what is the only thing that can degrade it?

A

liver

82
Q

Where does excess cholesterol need to go?

A

to the liver

83
Q

What does HDL show an inverse correlation with?

A

HDL shows inverse correlation with CVD, low HDL is strong independent risk factor

84
Q

What is important about the LDL:HDL ratio?

A

LDL:HDL ratio is a stronger predictor of CVD than elevated LDL alone

85
Q

What occurs if cholesterol is not removed?

A
  • There is accumulation in peripheral cells

- down regulation of LDL rec and reduced uptake of LDL from plasma

86
Q

What does high plasma TAG mean?

A
  • High plasma TAG are independent risk factor
  • High TAG in obesity and diabetes mellitus type II, therefore higher CVD risk
  • With Insulin resistance: reduced LPL – higher TAG
87
Q

What is the direct mechanism that causes high plasma TAG to be a risk factor?

A

CM and VLCL remnants contribute to atherosclerosis and blood clotting

88
Q

What is the indirect mechanism that causes high plasma TAG to be a risk factor?

A

TAG is transferred to HDL and LDL by CEPT in large amounts, formation of small dense HDL and LDL (sdHDL) through hydrolysis by hepatic lipase

  • sdHDL rapidly broken down (=decrease in HDL)
  • Poor recognition of sdLDL by LDL receptor, remains in circulation longer
89
Q

Give two facts about lipoprotein a?

A
  • Discovered 1963 by Kare Berg

- Lipoprotein subclass, carries CHOL and some TG

90
Q

What % of the population have high lipoprotein a levels?

A

20%

91
Q

Define lipoprotein in terms of health outcomes?

A 
High Lp(a) predicts risk of early atherosclerosis and has been confirmed as a risk factor for CHD, atherosclerosis, thrombosis and stroke.
Response to dietary treatments not clear, can be lowered by niacin
92
Q

How does fructose cause increased ACETYL-CoA?

A

Fructose is converted to Phosphofructokinase-1 through Ketohexokinase.
Phosphofructokinase-1 is converted to Pyruvate.
Pyruvate is converted to ACETYL-CoA by pyruvate dehydrogenase

93
Q

What effect does insulin have?

A

As fructose yields a relative decrease in insulin secretion, the inhibition on the metabolism steps in glycolysis is removed

94
Q

Why is there an excess of acetyl-coA?

A

adipose tissue is still broken down to release fatty acids

which leads acetyl-coA as well as the fructose chain

95
Q

What happens to the excess acetyl-coA?

A

Goes to lipogenesis

96
Q

Where does most lipogenesis occur?

A

Little fructose is absorbed by adipose tissue so most of the lipogenesis occurs in the liver only

97
Q

What is glucose metabolism?

A

Glucose –> Glucose -6-P

  • hexokinase (muscle) and glucokinase (liver) are rate limiting
  • irreversible reaction

Glucose -6-P –> Fructose-6-P
- by Phosphoglucose Isomerase

Fructose-6-P –> Fructose-1-6-P-BisP

  • Phosphofructokinase is rate limiting
  • irreversible

Fructose-1-6-P-BisP –> Dihydroxyacetone-P + Glyceraldehyde

98
Q

What is fructose metabolism?

A

Fructose –> Fructose-1-P

  • by fructokinase
  • irreversible reaction

Fructose-1-P –> Dihydroxyacetone-P + Glyceraldehyde
- by Fructose-1-Phosphate Aldolase

99
Q

What is the difference between fructose and glucose metabolism?

A

Fructose is less readily inhibited by intermediates

100
Q

What is fructose metabolism free from?

A

Fructose metabolism is free from any control steps – prevailing concentration governs fate. The more you eat, the more lipid you can produce

101
Q

What happens to fats and cholesterol synthesised in the liver?

A

Fats and Cholesterol synthesised from fructose are accumulated in the liver and then secreted as lipoproteins (very low-density lipoproteins) to deposit fats into adipose tissue

102
Q

What happens to lipoprotein concentrations when plasma lipids are decreased?

A

Synthesis rate goes up

Lipolysis rate goes down

103
Q

What happens to lipoprotein concentrations when Hypertriglyceridemia occurs?

A

Synthesis rate goes down

Lipolysis rate goes up

104
Q

What factors control synthesis?

A

Lipid intake (diet), Lipolysis rate (adipose release), Lipogenesis rate (carbohydrate consumption)

105
Q

What factors control breakdown?

A

Particle size, Lipolysis rate (Lipoprotein lipase activity), Metabolic rate, and possibly types of fatty acid

106
Q

What does atheroma formation depend on?

A

upon lipoprotein present in blood

107
Q

What will always reduce risk?

A

Steps to reduce ‘burden’ and ‘half-life’ will always reduce risk

This is partly the reason rodents are protected from cardiovascular disease

108
Q

Summarise the points so far?

A
  • Cardiovascular disease risk is coupled to plasma lipoprotein concentration (& duration)
  • The remnants of lipoprotein metabolism (CR, LDL) are recovered by the liver – specific receptors
  • LDL receptor is crucial to take up cholesterol
  • LDL subclass distribution of importance to determine risk
  • Steps to enhance removal can decrease risk
  • Sugar ‘can’ also contribute to CVD, but only through increased hepatic lipogenesis
109
Q

What is important regarding fat in CVD?

A

For CVD the type of fat eaten is more important

than the amount

110
Q

What do saturates do?

A

Increase body’s production of cholesterol

111
Q

What do mono/polyunsaturates do?

A

Decrease body’s production of cholesterol

112
Q

What is the effect of dietary saturated fat on serum cholesterol?

A

SFA is directly correlated with plasma cholesterol and mortality from CHD

Plasma cholesterol increases by a factor related to 2 x the level of intake

113
Q

Describe the variation with chain length?

A

C14:0 (myristic acid) and C16:0 (palmitic acid) are the most hypercholesterolemic

C18:0 (stearic acid) appears neutral or hypocholesterolemic

114
Q

What do SFA regulate?

A

SFA regulate expression of LDL receptors on hepatic cell membranes

115
Q

What do high level of fatty acids in membranes cause?

A

The down-regulation of LDL receptors

Consequence: reduced rate of removal of LDL from circulation

116
Q

What does SFA intake increase?

A

an increase in plasma HDL, but the effect is not as significant as LDL increase

Hence, ratio of LDL:HDL still increases

117
Q

What are saturated fatty acids proven to increase serum LDL-cholesterol levels in order of increasing magnitude?

A
  • Palmitic acid (C16): palm oil, cocoa butter, meat fat and dairy products.
  • Myristic acid (C14): coconut oil, butter and palm kernel oil.
  • Lauric acid (C12): coconut oil (45% of total fat content) and palm kernel oil. Despite the current consumer health trend, coconut oil is by far the biggest contributor of the most cholesterol-raising saturated fatty acid.
118
Q

Which FA had no impact?

A

stearic acid (C18) had no impact.

119
Q

What is the effect of dietary unsaturated fat on serum cholesterol?

A

MUFA and PUFA reduce total and LDL cholesterol

Plasma cholesterol decreases by a factor related to 1 x the level of intake

MUFA and PUFA at <10% have no effect on HDL plasma levels

120
Q

10% energy provided by SFA decreases LDL when replaced by what?

A

MUFA = 0.39 mmol/L

PUFA = 0.42 mmol/L

121
Q

What does unsaturated FA do?

A

increase expression of LDL receptors, so increased removal of LDL from circulation

122
Q

What is the effect of trans fatty acids?

A

consistently significant increase in LDL following trans fatty acid intake

10% change from oleic acid to trans-oleic acid increases LDL by
= 0.37 mmol/L

there is an additional reduction in HDL level

overall an increase in the LDL:HDL ratio

123
Q

What is the effect of fish oil (N-3 Fatty acid) intake and CVD?

A
  • Greenland Inuit have low rates of CHD despite similar total fat intake compared to Danes (Published in the 1970s)
  • Traditional diet: high in seal meat, whale meat and fish
  • Low in saturated fat, high levels of n-3 fatty acids (EPA, DPA, DHA)
124
Q

What is the effect of n-3 FA on plasma TAG?

A
  • Consistent hypotriacylglycerolemic effects with n-3 FA
  • 2-3g/day n-3 FA can reduce TAG levels by 25-30% in both, normolipidemic and hyperlipidemic individuals
  • Plant derived n-3 precursor FA alpha-linolenic acid has not been observed to alter TAG except with very high intake
  • Furthermore, reduction on postprandial lipaemic response (reduction in CM and CM remnants)
125
Q

How is fish oil linked to this?

A

Fish oil supplements (fish oil, cod liver oil) make up around 40% of supplement market

Fish oil seems beneficial for most people, sensory problem to intake large amounts

126
Q

What is the effect of fish oil on the main mechanisms of the development of atherosclerosis?

A

Increase in HDL-chol
- Therefore change in HDL/LDL-chol ratio

Decrease in thrombogenicity

Decrease in plaque formation

Decrease in VSMC proliferation

LDL might be more susceptible to oxidation

Extra double bond results in physical changes of lipoprotein, easier accessible for enzymes (composition of lipoprotein), more diffuse, change structure of lipoproteins

Production of eicosanoids

127
Q

Summary of : What is the effects of different dietary fatty acids on blood lipids?

A

SFA:
increase HDL and LDL

TFA:
decrease HDL increase LDL

Dietary cholesterol:
same or increase HDL , increase LDL

128
Q

What are the main facts of fatty acids?

A

SFA may increase LDL cholesterol levels and is probably equivalent to refined and high glycemic index carbohydrates with respect to CVD risk

Some evidence that increase in MUFA results in greater mortality and with coronary artery atherosclerosis

Cardioprotective effects of n-6 FA, in particular linoleic acid, might be confounded by significant levels of ALA, EPA and DHA

Unlikely that randomized controlled trials assessing dietary interventions will be able to determine definitely the effects of altering intakes of various fatty acids on CVD risk

We have to rely on epidemiological evidence and controlled clinical trials on surrogate markers

129
Q

What did the SACN report on saturated fats and health (2018) say?

A

Review saturated fats and health effects
Conclusion: new evidence supports and strengthens the original COMA conclusion
Therefore – no changes to current advice

130
Q

What is the conclusion of SACN?

A

confirmed the need to lower saturated fatty acid intake for improved serum lipid profiles and CVD and CHD events.

provides insight into the cause of much of the controversies surrounding saturated fat, namely the limitations and confounding factors within the current data which have been overlooked by those disputing national and global recommendations.

Although the evidence clearly indicates that replacement of saturated fat with PUFA and MUFA is the ideal, in the current environment of over-consumption and obesity, a public health message focus on lowering saturated fatsper semay be more impactful.

131
Q

Should the government encourage the population to replace the calories saved from the saturated fat reductions with more fat calories –from PUFA or MUFA?

A

NDNS indicates that PUFA and MUFA intakes are more than adequate and exceed recommendations

The obesity epidemic is not abating

The population needs to reduce their calorie intake rather than maintain it and fat is the most concentrated form of energy

So it may be more prudent for public health messages to focus advice on reductions in saturated fatty acid intakesper serather than actively encouraging a replacement of the calories with PUFA or MUFA.

CVD (12 decks)

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