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Hold LDL constant and high to low HDL...
10 fold increase in CV disease risk
Hold HDL constant and low to high LDL...
3 fold increase in CV disease risk
What is atherosclerosis?
formation of plaques that can block arteries
blockage of coronary arteries
blockage of cerebral arteries
Seven steps of plaque formation
- 1. oxidized lipoproteins aggregate and stick to extracellular matrix
- 2. monocyte attracted to area of oxidized lipoproteins
- 3. monocyte differentiates into macrophage
- 4. foam cell ingests lipoproteins
- 5. free cholesterol accumulates in membranes, forms droplets
- 6. apoptosis, necrosis, tissue damage
- 7. cholesterol-rich plaque forms
What are the three defects or mutations in familial hypercholesterolemia?
- 1. defective LDL uptake leading to high serum cholesterol
- 2. mutation in gene encoding LDL receptor
- 3. mutation in gene encoding Apoprotein B (ApoB) which is part of LDL that binds to receptor
Heterozygotes of hypercholesterolemia
dominant phenotype of elevated risk for atherosclerotic heart disease
homozygotes for hypercholesterolemia
develop atherosclerosis during childhood
True/False: Restricting total intake alone can affect the rate of CV, obesity, or cancer.
AMDR for lipids, carbs, proteins
- lipids: 20-35%
- carbs: 45-65%
- proteins: 10-35%
Average dietary intake of cholesterol
200-300 mg per day
True/False: There is no correlation between dietary cholesterol and risk for CV disease
Main finding of Siri-Tarino, 2010 study
Relative increase in risk for CV disease with high intake of saturated fatty acids was 1.07 and not statistically significant
Significance of Masai people of East Africa
- consume at least 1/3rd of calories for saturated fats (milk, meat, blood)
- remarkably low CV disease
- replaced diet with flour, sugar, shortening and atherosclerosis increased
Findings of Micha and Mozaffarian, 2010 study
- Replace SFA w/PUFA - 10% reduction of CV risk
- Replace SFA w/carbohydrate - no effect
- Replace SFA w/MUFA - mixed results
Two biggest sources of SFA in U.S.
dairy and cheese
Milk fat content
- 69% SFA
- 25% MUFA
- 2% PUFA
- poor source of PUFA
NAS recommendation for SFA
SFA should be no more that 10% of total calories
How are trans fats formed?
Hydrogenation of unsaturated fatty acids in vegetable oils converts them to saturated fatty acids and produces large amounts of trans fatty acids as a byproduct
What is the risk with trans fats?
Increased risk of CV disease
What are the two essential fatty acids?
linoleic acid and linolenic acid
Why are the two essential fatty acids considered essential?
Humans lack the Δ12 and Δ15 desaturases to make them
Outline linoleic acid
Linoleic acid (ω-6) - [Δ5, Δ6 desaturases + elongation + Acetyl-CoA] - arachidonic acid -> eicosanoids (prostaglandins); paracrine hormones (signal transduction)
Outline linolenic acid
Linolenic acid (ω-3) - [Δ5, Δ6 desaturases + elongation + Acetyl-CoA] - eicosapentaenoic acid - [elongation + desaturase activity] - docosaenoic acid/phospholipids (important component of cell membranes and nervous system)
Good dietary source of linoleic acid
sunflower oil, corn, seeds, nuts
Good dietary source of linolenic acid
Good dietary source of arachidonic acid
Increasing which has shown to be better: ω-6 or ω-3?
What do nuclear receptors PPAR alpha and PPAR gamma do? What are two good ligands?
- They bind to (unsaturated) fatty acids and regulate genes involved in fatty acid and lipoprotein metabolism
- EPA and DHA are good ligands