Diet Atherosclerosis Flashcards
(21 cards)
What are the concerns related to high intakes of N6 (5)
Increase in arachidonic acid synthesis
Inhibition of alpha linoleic acid desaturation to EPA and DHA
Increase in AA is said to increase production of pro-inflammatory eicosanoids
May prevent protection against atherogenesis
Jakobsen 2009 SFA replacement review (5)
Investigated associations between energy intake from MUFAs, PUFAs and carbs (instead of SFA)
Findings suggest SFA should be replaced with PUFAs in order to reduce heart disease risk
Harcombe 2015 meta-analysis (6)
Examined evidence from RCTs available in 1983
National guideline implemented between 1977 and 1983
Main findings were no significant differences in all cause mortality or CHD mortality between intervention and control groups
Despite sig reductions in cholesterol in intervention groups
Limitation of the review is that most of the studies did not detail fat composition
What are the implications of the Harcombe 2015 findings?(2)
Undermines the role of cholesterol levels in the development of CHD
Goes against the theory that reducing SFA particularly reduces risk of CHD
Diet-cholesterol hypothesis (3)
Hypothesised that increased LDL cholesterol is a major factor CVD
Dietary SFAs increase plasma LDL cholesterol
Therefore reducing SFAs in diet will reduce risk of CVD
Keys 1970 countries study (5)
Examined the effect of potential lifestyle risk factors and disease rates between various populations
Study demonstrated strong associations between SFA intake, cholesterol levels and CHD rates
Limitation is the selection of the different geographic areas
What are the major clinical outcomes of atherosclerosis?(3)
Stroke
Coronary heart disease
Peripheral vascular disease
CVD is caused by a combination of which conditions?(2)
Atherosclerosis
Thrombosis
Events associated with atherogenesis via platelet aggregation (6)
Endothelial injury
Reduction in prostacyclin
Platelet aggregation increase
Increase in thromboxanes and platelet derived growth factor
Stimulates smooth muscle cell proliferation
Contributes to hardening of fibrous plaque
Events associated with atherogenesis via increased permeability (4)
Endothelial injury
Increased permeability
Increased LDL uptake
Foam cell formation
Events associated with atherogenesis via monocytes attraction (7)
Endothelial injury
MCP attracts monocytes to injury in artery
VCAM-1 attaches monocytes to vasculature
Monocytes converted to macrophages
Formation of foam cells
Cell death / extra cellular cholesterol deposition
Contribution to fibrous plaque
Calcification of plaque (2)
Part of the scarring process
Lesion becomes very unstable and more likely to rupture
Thrombosis (6)
When a rupture of the lesion occurs
Sub-endothelial layer becomes exposed to the blood
Coagulation occurs in attempt to close rupture
This causes platelet aggregation and thrombus is formed
If thrombus blocks artery then thrombosis occurs
This brings on clinical event
Lipid accumulation (5)
Cholesterol ester accumulates in macrophages
Cholesterol comes from LDL in circulation
Macrophage fills up with too much cholesterol and die
Lipid deposited in extra cellular matrix
Scar tissue forms over plaque
Why does cholesterol accumulate in macrophages?(5)
Typically high LDL cholesterol leads to down regulation of LDL receptor
However LDL is oxidised when it enters the intima
Oxidised LDL is taken up by scavenger receptors
In an uncontrolled manner
Excess cholesterol accumulates eventually leading to cell death
Fatty streaks play a major role in _______
Atherosclerosis
What are fatty streaks?(6)
Collections of foams cells in the arterial intima
Which leads to the development of atherosclerotic plaque
They appear early in life
The development of early fatty streaks are similar between populations
Regardless of CVD prevalence
However rate of progression differs later in life
CVD essay plan (18)
CVD overall cause Clinical outcomes Fatty streaks Cause of endothelial injury Endothelial injury - monocytes attraction Increased permeability Lipid accumulation OxLDLs Platelet aggregation Thrombosis Keys 1970 Diet-cholesterol hypothesis Harcombe 2015 Jakobsen 2009 Ramsden 2013 Arachidonic acid / N3 Liou 2007 LA:ALA ratio study
Causes of endothelial injury (3)
Mechanical damage due to high BP
Chemical toxins from smoking
High plasma lipids
Ramsden 2013 (5)
Conducted a RCT to investigate the use of LA for CHD prevention
Intervention group replaced SFA with LA
The intervention group had high rate of CHD, CVD and all cause mortality
Liou 2007 LA:ALA ratio study (4)
Liou 2007 demonstrated that an increase LA:ALA ratio reduced EPA
But increased DHA by same amount
There were no effects of high LA on inflammatory markers or platelet aggregation
